---

Section A:

Drug information

Antibiotics ( Drug pharmacology and formulations in India).

Select drug.

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

---

Fosfomycin(FOS )

By M. Younus, BVSc, MVSc, SKUAST-K

• FOS is a spanish antibiotic.
• Second line antibiotic used in veterinary medicine mainly due to the lack of knowledge among veterinary professionals.
• Epoxide antibiotic that’s used to treat uncomplicated urinary tract infections
• Classified as a veterinary highly important antimicrobial agent.
• Approved for use as a veterinary drug in bacterial infections in broiler chickens and pigs.
• Used to treat Escherichia coli-related diarrhoea and salmonellosis in cattle.
• Rapidly absorbed in the small intestine and distributed widely to the tissues.
• Has a very low protein binding (<0.5%).

MOA:

• In Escherichia coli, fosfomycin enters bacterial cells through two methods: the L-alpha-glycerophosphate system and the hexose-6-phosphate transporter.
• Fosfomycin with in bacterial cell binds to a cysteine in the active site of the MurA enzyme, rendering it inactive.
• This prevents the condensation of phosphoenolpyruvate (PEP) with UDP-N-acetylglucosamine (UNAG), stopping the production of the peptidoglycan precursor UDP N-acetylmuramic acid (UDP-MurNAc).
• Ultimately, the first step of bacterial cell wall synthesis is disrupted.
• Fosfomycin affects cell adhesion by reducing the ability of bacteria to stick to cells. For instance, it lowers the adhesion of bacterial cells to urinary epithelial cells and also decreases the adhesion of Streptococcus pneumoniae and Haemophilus influenzae to respiratory epithelial cells.

Effects:

• Bactericidal action.

Side-effects:

• Diarrhea
• Inappetence
• An allergic reaction showing irregular breathing, rash, fever, puffiness and swelling around the face.

Drug combination:

• Fosfomycin shows synergestic effect with pencillins ,cephalsporins,aminoglycosides, chloramphenicol, tetracycline, erythromycin, cotrimoxazole and quinolones.

Species:

• Poultry. Pig , Dog and Cattle.

Indication:

1]. Poultry: Infectious coryza ,fowl cholera , fowl typhoid, colibacillosis, salmonellosis, ORT (Ornithobacterium Rhinotracheale Infection), CRD (Chronic Respiratory Disease).

2]. Pig: Infections caused by Salmonella sp., Escherichia coli, Pasteurella sp., Staphylococcus sp., Streptococcus sp., Haemophilus sp., Klebsiella sp. (good activity) and Pseudomona sp. (moderate activity).

3]. Dog : Urinary tract infection.

4]. Cattle: Escherichia coli-related diarrhoea and salmonellosis in cattle.

Dose:

• 150 pg/ml drinking water for five consecutive days in broilers.
• 20 mg/kg / IM OD for 3 days in cattle.
• 80 mg/kg SC and PO BD for 3 days in dogs.
• 15 mg/kg / IM OD and 30mg/kg / PO in pigs.

Contraindications:

• Not Known.

Brands:

• Fosin 1kg( 10% fosphomycin) powder(Konya Life Science India).

Human Brands:

Injectable:

• Fosfotas 4gm ( Fosfomycin Sodium )Inj vial( Intas India).
• Emucin 4gm ( Fosfomycin Sodium ) Inj vial( Emcure Pharaceuticals India).
• Fosfona 4gm ( Fosfomycin Sodium ) Inj vial( Alniche Life Science India).
• Fosfofic 4gm ( Fosfomycin Sodium ) Inj vial( Gufic Bioscience India).
• Fonyl 4gm( Fosfomycin Sodium ) Inj vial( Glenmark Pharmaceuticals India).

Oral prepration:

• Fosfobact 3gm sachet( Alostar India).
• Fosforex 8gm sachet ( Meditrex Pharma India).
• Fosfona 8gm sachet ( Alniche Life Science India).
• Fosfozyme 3g sachet (Steris Healthcare India).
• Fosfochem 3g sachet (Aristo Pharmaceuticals India).

---

Tulathromycin

By M. Younus, BVSc, MVSc, SKUAST-K

Tulathromycin( Macrolide).

Key features :

• Primarily bacteriostatic but bactericidal to some pathogens.
• At physiological pH, tulathromycin (a weak base) is approximately 50 times more soluble in hydrophilic than hydrophobic media.
• Absorption from injection is greater than 80% in cattle and pigs.
• Higher tulathromycin concentrations are observed in the lungs as compared to the plasma.
• The tissue half-life is 8 days in cattle and 6 days in pigs, respectively.This prolongs the drug concentration at the site of infection.
• The volume of distribution is greater than 10 L/kg.
• Tulathromycin is eliminated from the body primarily unchanged via biliary excretion.

MOA:

• Tulathromycin is positively charged molecule, it may penetrate gram-negative bacteria more easily than other macrolide antibiotics. It inhibits bacterial protein synthesis by binding to the ribosomal 50S subunit.

Effects:

• Tulathromycin is considered bacteriostatic, but it may have bactericidal properties in vitro.
• It is effective against Mannheimia haemolytica, Pasteurella multocida, Histophilus somni, and Mycoplasma bovis, and against Fusobacterium necrophorum and Porphyromonas levii in cattle.
• It is effective against Actinobacillus pleuropneumoniae, Pasteurella multocida, Bordetella bronchiseptica, Haemophilus parasuis, and Mycoplasma hyopneumoniae in pigs.

Side effects:

• Transient dyspnoea and transient hyperslivation.

Species:

• Cattle and Pig.

Indication:

• BRD, Pink eye and foot rot in cattle.
• SRD in pigs .

Dose:

• 2.5mg/kg Sc single dose in cattle .
• 2.5mg/kg IM single dose in pigs.

Contraindication:

• Hypersensitivity to drug.

Brands:

Not available in India.

Foreign brands:

• DRAXXIN 50ml( Tulathromycin 100mg/ml) inj ( Zoetis USA).
• DRAXXIN 100ml( Tulathromycin 100mg/ml) inj ( Zoetis USA).
• DRAXXIN 250ml( Tulathromycin 100mg/ml) inj ( Zoetis USA).
• DRAXXIN 500ml( Tulathromycin 100mg/ml) inj ( Zoetis USA).
• Tulissin 50ml( Tulathromycin 100mg/ml) inj ( Verbac USA).
• Tulissin 100ml( Tulathromycin 100mg/ml) inj ( Verbac USA).
• Tulissin 250ml( Tulathromycin 100mg/ml) inj ( Verbac USA).
• Tulissin 500ml( Tulathromycin 100mg/ml) inj ( Verbac USA).
• Vetdrax100ml( Tulathromycin 100mg/ml) inj ( Vet Pharma USA).
• Vetdrax100ml( Tulathromycin 100mg/ml) inj ( Vet Pharma USA).
• Increxxa 50ml ( Tulathromycin 100mg/ml) inj (Elanco USA).

---

Colistin

By M. Younus, BVSc, MVSc, SKUAST-K

Key features:

• Colistin (polymyxin E) is a cationic polypeptide antibiotic to treat bacterial infections, especially carbapenem-resistant Gram-negative bacteria.
• As the first-choice treatment for neonatal diarrhoea in piglets and veal calves.
• Systemic administration should be limited to acute condition because of its adverse toxic effects in calves.
• Oral administration, especially through drinking water, is the most common method for all species, particularly in poultry.
• Not absorbed in GIT.

MOA:

• Colistin interacts with the outer membrane of the organism. It especially affects lipopolysaccharide molecules. This interaction causes displacement of calcium and magnesium ions and destabilizes the outer membrane.
• This destabilization of the outer membrane causes the leakage of cell content and leads to cell death.
• Colistin also binds and neutralizes free LPS, conferring a considerable anti-endotoxin activity.

Effects: 

• Colistin is effective against various Gram-negative bacteria such as Acinetobacter baumanni, Enterobactercloacae, Klebsiella pneumonia, and Pseudomonas aeruginosa.
• Anti endotoxemic effect.

Side effects:

• Neurotoxicity, nephrotoxicity, and other ailments.

Dose:

•  75,000 IU/kg feed for poultry.
• 100,000 IU/kg feed or 3.75–5 mg/kg bw for calves, rabbits and pigs.
• Colistin can be given with feed, milk, water, or by injection. About 0.01–0.02% is taken in through milk and 25–50 mg/L through water.
• Colistin is added to feed at 20–40 M IU/100 g, and 0.2 mg is injected into chicks that are 1–3 days old.

Species:

• Calf , Piglet, Rabbit and Chick.

Indication:

• colibacillosis in poultry are localized (e.g., omphalitis) or systemic (e.g., colisepticemia).

Contraindication .

• Renal impairment .

Brand:

• Colinex 100g ( 100mg colistin sulphate/ g) powder( Star Vet Poul India).

• Colinex 200g ( 100mg colistin sulphate/ g) powder( Star Vet Poul India).

• Colinex 1000g ( 100mg colistin sulphate/ g) powder( Star Vet Poul India).

• Colimex 1kg ( 100mg colistin sulphate/ g) powder( USG Pharma India).

• Colistin Vet 200g ( 100mg colistin sulphate/ g) powder( Samsun Biotech India).

• Coligro 100g ( 100mg colistin sulphate/ g) powder ( Vet Line India).

• Coligro 200g ( 100mg colistin sulphate/ g) powder ( Vet Line India).

• Coligro 1000g ( 100mg colistin sulphate/ g) powder ( Vet Line India).

---

---

Section: Bacterial Diseases

Dog- Select disease

Cat – Select disease.

• *Bordetellosis
• Cat-fight abscess
• *Campylobacteriosis
• chlamydiosis
• Coxiellosis (Q Fever)
• FIA (Feline infectious anaemia)
• Helicobacter infection
• *Pasteurella infection
• *Pyoderma
• Pyelonephritis
• *Septicemia
• Septic Arthritis
• *Salmonellosis
• Tularemia

Cattle – Select disease.

---

Section A: Bacterial Diseases in Dogs

---

Canine Borreliosis (Lyme disease)- Disease description, drugs and formulations in India

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Borreliosis (Lyme disease) is a pervasive tick-borne illness affecting dogs worldwide, and it holds the potential to transmit zoonoses to humans. Borrelia species are spiral-shaped, Gram-negative bacteria, though Gram staining does not easily reveal this classification. Most Borrelia are obligate anaerobes, with some being aerotolerant.

Pathogenesis

Pathogenesis starts with an infected tick bite that transfers Borrelia burgdorferi bacteria to the dog’s skin. During this process, the bacteria change their gene expression to adapt to their new environment. They replicate and spread in the skin. Borrelia burgdorferi has an outer membrane similar to lipopolysaccharides and moves in a corkscrew-like manner using endoflagella. This outer membrane contains proteins that enhance its ability to cause disease. Once they colonize the skin, the bacteria use virulence proteins to invade blood vessels and spread to other tissues, leading to tissue colonization and an inflammatory response.

Clinical symptoms

Clinical signs of Lyme disease are fever, loss of appetite, painful or swollen joints, intermittent lameness, swollen lymph nodes, and lethargy. If left untreated, Lyme disease can inflict serious damage to the kidneys, nervous system, and heart. Kidney-related issues are the second most common manifestation in dogs and are often fatal. Additionally, cases affecting the nervous system have been linked to facial paralysis and seizure disorders, while heart complications are rare.

Diagnosis

Diagnosis by SNAP 4Dx—A simple blood test yields results in just eight minutes. Polymerase chain reaction (PCR) of blood, joint fluid, or lymph node samples is used to detect Lyme disease. CBC allows for a comprehensive assessment of overall health and helps rule out other conditions that may mimic Lyme disease. Urinalysis—A urine sample is analyzed for proteins, which can indicate kidney disease in dogs confirmed positive for Lyme disease. KFT should be performed to detect the status of kidney function.

Treatment

Treatment involves use of antibiotics like Doxycycline, Oxytetracycline and potentiated Amoxicillin.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Doxycycline: Drug of choice 10mg/kg PO BD for 30 days	Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).
Oxytetracycline: Alternative to doxycycline 10 mg /kg PO BD for 30 days. NB: Do not provide with milk. Avoid in young one having milk teeth.	Oxin 500mg (50omg oxytetracyclin) tab (Zoetis India). Oxytech 500mg (50omg oxytetracyclin) tab (Mediseller India). Himoxy 500mg (50omg oxytetracyclin) tab (Himal Bioscience India).
Amoxicillin +Clavulanate: 20 mg/kg by mouth, three times a day for 30 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg(400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).

---

Canine Leptospirosis – Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description

Etiology

Canine Leptospirosis is caused by L. interrogans and L. kirschneri. Many animal species, especially rodents, serve as reservoir hosts that contribute to environmental contamination and disease. It is an important zoonotic disease. Leptospira is Gram-negative and has a spiral conformation. Dogs get infected by ingesting rodents, the reservoir hosts. They also become infected through food and water contaminated by the infected urine of reservoir hosts.

Pathogenesis

Pathogenesis of Leptospira bacterium is due to its ability to adhere to tissues and evade the complement system. The outer membrane of Leptospira contains various lipoproteins and transmembrane proteins. Certain outer membrane proteins bind to the host’s extracellular matrix. Factor H helps Leptospira adhere to host tissues and evade the complement system. Leptospiral LPS exhibits low endotoxin activity. It activates host cells through TLR2 (Toll-like receptor). This effect is potentially due to its unique lipid A structure. Leptospirosis-affected dogs often have multisystemic illness but more commonly cause acute kidney injury (AKI) and liver disease in them. In hosts, Leptospira rapidly multiply. They cause an inflammatory response. This response can lead to conditions such as acute kidney injury, liver damage, and vasculitis. There is potential involvement of other organs like the pancreas, gastrointestinal tract, eyes, myocardium, and lungs.

Clinical symptoms

Clinical symptoms vary based on factors like the host’s age, genetics, infectious dose, and leptospira strain. Serologic surveys indicate widespread subclinical exposure. Only a small percentage of dogs exhibit illness post-infection. Pyrexia typically appears early in the illness. It may decrease within 24 to 48 hours. Fever is accompanied by lethargy, anorexia, vomiting, diarrhea, dehydration, and abdominal pain. Dogs may also experience increased thirst and urination. There may also be reluctance to move and show icterus, alongside potential ocular issues like uveitis or retinal hemorrhages. Additionally, respiratory distress can occur from pulmonary hemorrhage linked to anemia.

Diagnosis

Diagnosis is done through blood tests, immunological tests, urine tests, and PCR. In the initial 24 to 48 hours of illness, CBC and serum biochemistry panels may show normal results. Alternatively, there may be mild abnormalities. As the illness progresses, signs like anemia, leukocytosis, and various serum biochemistry changes such as azotemia and hypoalbuminemia may appear. Hyperkalemia is less common than normokalemia or hypokalemia. This is due to the influence of Leptospira endotoxin on kidney function. Urine examination reveals isosthenuria, proteinuria, glucosuria, and casts. The presence of glucosuria in the absence of hyperglycemia should always raise suspicion for leptospirosis, especially in unvaccinated dogs. Final diagnosis is made by assaying Immunoglobulin G (IgG) or Immunoglobulin M (IgM) by Microscopic Agglutination Test (MAT) and nucleic acid amplification tests by PCR-based assays. Examine urine specimens using darkfield microscopy. Yet, this diagnostic technique requires both expertise and a darkfield microscope.

Treatment

Treatment with doxycycline and supportive care, started at the earliest stage, can save the dog’s life. Supportive therapy for organ dysfunction includes IV fluids, proton pump inhibitors, and other medications.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Doxycycline: Drug of choice 5-10mg/kg PO IM BD for 14 days.	Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).
Ampicillin: recommended if doxycycline induces vomiting. 20 mg/kg IV TID OR QID adjusting dose down if severe azotemia is present.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).

---

Canine Salmonellosis – Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Salmonellosis is an enteric disease and is caused by the ingestion of food and water contaminated with Salmonella. Salmonella are rod-shaped, gram-negative bacteria that belong to the family Enterobacteriaceae. Dogs are usually carriers of the bacteria but become clinically affected when their immunity goes down, particularly in pups. Canine Salmonellosis has zoonotic importance as the most common serotypes of Salmonella causing gastroenteritis in humans are actually the same serotypes that most frequently occur in dogs. Salmonella enterica and Salmonella typhimurium are the two serovars that are associated with cases of salmonellosis in dogs. These serotypes invade the mucosa of the small intestine, where they multiply and produce enterotoxins. Later on, the damage extends to the serosal layer of the intestine. The net result is malabsorption and malfunctioning of the intestines.

Pathogenesis

Pathogenesis of Salmonella serotypes begins when the bacteria adhere to the host cell surface. After adhesion, they can enter the cells through phagocytosis or by directly invading both phagocytic and non-phagocytic cells. Phagocytosis involves complex mechanisms that depend on various receptors, including Pattern Recognition Receptors (PRRs) like toll-like receptors (TLRs) and cytosolic nucleotide-binding receptors, which detect pathogen-associated molecular patterns (PAMPs) such as lipopolysaccharides (LPS) and flagellin. This detection affects phagosome development, activates signaling pathways, and alters gene expression. Research indicates that the interaction between TLR and LPS in non-typhoidal Salmonella (NTS) species is crucial for the onset of septic shock. Salmonella employs superoxide dismutases and SodCI and SodCII enzymes to defend against reactive oxygen species, aiding its survival in the harsh conditions of the phagosome. Lipopolysaccharides are key components of the outer membrane of Gram-negative bacteria, crucial for triggering the innate immune response in the host, providing cell stability, and acting as a barrier. LPS consists of lipid A, core oligosaccharide (C-OS), and O-antigen polysaccharide (O-PS) and is important for the adherence and invasion of host epithelial cells.

Clinical symptoms

Clinical symptoms include diarrhea, which may be bloody, fever, anorexia, weight loss, lethargy, dehydration, and abortion in pregnant animals.

Diagnosis

Diagnosis is performed by conducting stool culture, blood culture, and PCR for Salmonella detection in the samples. Differential diagnoses for suspected Salmonella enterocolitis include various infections (canine and feline parvovirus, canine distemper virus), viral gastroenteritides, campylobacteriosis, clostridial diarrhea, salmon poisoning disease, giardiasis, tritrichomoniasis, cryptosporidiosis, whipworms, leptospirosis, dietary indiscretion, gastrointestinal foreign body, pancreatitis, inflammatory bowel disease, lymphoma, hypoadrenocorticism, hyperthyroidism, and toxins (including drugs).

Treatment

Treatment of Salmonella in diarrhoeic dogs and cats is debated, as many experts believe antibiotics should not be used for uncomplicated cases. Instead, antibiotics are recommended for animals showing signs of serious infection or those with weakened immune systems. Using antibiotics can lead to longer shedding of bacteria and may cause resistant strains. For septic dogs and cats, effective antibiotics include fluoroquinolones, chloramphenicol, trimethoprim-sulfamethoxazole, and amoxicillin. It is advisable to determine a susceptibility profile to choose the best antimicrobials.

Drugs and formulations available in India.

Drug and dose	Veterinary and human formulations
Enrofloxacin: Recommended drug 2.5 mg-5mg/kg IM/IV OD for 5-10days. 5mg-20mg/kg PO OD for 5-10 days. NB: Avoid in young animals. Provide supportive treatment as per requirement.	Veterinary formulations: Fortivir 30 ml (100mg Enrofloxacin/ml) inj vial( Verbac India). Floxidin 100ml (100mg Enrofloxacin/ml) inj vial (MSD india). Efx -LA 100ml (120mg Enrofloxacin/ml) inj vial(Parex India). Enolox-K 30ml (100mg Enrofloxacin and 60 mg Ketoprofen/ml)inj vial( Zenley Animal health). Enrovet 100ml (100mg Enrofloxacin/ml) inj vial ( Vets Pharma India). Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Ciprofloxacin: Recommended drug 20 to 25 mg/kg PO OD or 10-12.5mg/kg PO BD for 7–14 days. NB:  Avoid or reduce dosage in animals with severe renal failure, avoid in young animals or in pregnant or breeding animals.	Human formulations: Zoxan 250mg ciprofloxacin tab (FDC India). Lucipro 250mg ciprofloxacin tab (Lupin India). 250mg ciprofloxacin tab (Lupin India). Floxip 250mg ciprofloxacin tab (Abbot India). Ciplox 250mg ciprofloxacin tab (Cipla India). Ciprobid 250mg ciprofloxacin tab (Zydus India).
Ampicillin: 22 mg/kg IV /IM TID for 5-7 days.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).

---

Canine Staph Dermatitis (Pyoderma)– Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Staph Dermatitis is caused by Staphylococcus pseudintermedius that leads to a skin problem in dogs commonly called pyoderma. However, Staphylococcus schleiferi, Staphylococcus aureus, and Pseudomonas aeruginosa have also been identified as causes of canine pyoderma. Staphylococcus is spherical (cocci) Gram-positive bacteria and belongs to the family Staphylococcaceae. They form grape-like clusters. Staphylococcus species are facultative anaerobic organisms and are normally found in small numbers on the skin of all dogs. Predisposing factors like allergies, insect bites, or contact with harsh chemicals facilitate bacteria to invade deeper parts of the skin, and an infection can develop. Dogs with allergies or who have underlying diseases that weaken the immune system, such as hypothyroidism or Cushing’s syndrome, for example, can develop infections not only in their skin and ears but also in their respiratory, reproductive, or urinary tracts, as well as in other areas of their bodies. Puppies and senior dogs are more prone to staph infections. Additionally, staph infections can also be transmitted from dog to dog through direct contact, and while the risk of transmission to humans exists, it is considered rare.

Pathogenesis

Pathogenesis begins with skin injuries like cuts or abrasions, allowing pathogens to enter and cause a Staph infection. Skin disorders that cause itching or alter the skin environment can create conditions for Staphylococcus to grow and lead to disease. The bacterium increases skin inflammation through toxins and enzymes that harm the skin’s protective functions. Staphylococcus produces α-hemolysin and δ-hemolysin, disrupting the skin barrier and causing inflammation. These molecules activate many T cells, resulting in an exaggerated immune response that contributes to dermatitis. Staphylococcus also releases superantigens, leading to excessive T cell activation and cytokine production. The presence of S. aureus in inflamed skin increases inflammatory cytokines like IL-4 and IL-13, impairing skin barrier function and making it easier for pathogens to colonize, thereby raising infection susceptibility.

Clinical symptoms

Clinical symptoms of staph infection in dogs include redness, inflammation, itchiness, head shaking, abnormal ear discharge, and crusts or scabs in the ears, which can lead to further discomfort and distress for the animal. Deep pyoderma in dogs is characterized by pain, crusting, odor, and exudation of blood and pus.

Diagnosis

Diagnosis of pyoderma relies on identifying specific lesions, verifying bacterial presence, and excluding other causes of folliculitis, such as demodicosis and dermatophytosis, using methods like Wood’s lamp, hair examination, and fungal cultures. Negative deep skin scrapings can help rule out follicular demodicosis. Skin cytology is crucial for diagnosing pyoderma and detecting inflammatory cells and bacteria, as well as identifying Malassezia dermatitis. Bacterial culture and susceptibility testing are vital for recurrent pyoderma cases to address resistant infections and guide systemic antimicrobial therapy.

Treatment

Treatment for staph infections in dogs typically involves antibiotics, and in severe cases, additional support such as fluids for dehydrated pets, specialized topical treatments, or even a change in diet may be required to boost their immune system. Good hygiene practices, such as regular bathing, grooming, and keeping living areas clean, can significantly help prevent staph infections in dogs, ensuring they remain healthy. It is also encouraged for pet owners to be vigilant about their dogs’ skin health and to seek veterinary care if any unusual symptoms arise, as early intervention can lead to better outcomes.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Clindamycin: 10-12.50 mg /kg PO/SC OD for 4wks.	Clindapet 30ml( 25mg Clindamycin/ml ) inj vial( Offered by Vea Impex India loyal pet zone/ India loyal pet zone India). Clindapet 300(300mg Clindamycin) tab (offered by Vea Impex India/ loyal pet zone India). Clivet 150(150mg Clindamycin) tab( Corise India). Goclin 150 (150mg Clindamycin) tab (Veko India). Petclind 450 (450mg Clindamycin) tab (Pet care India). Petclind 600 (600mg Clindamycin) tab (Pet care India).
Amikacin: 15-30 mg/kg IM/IV/SC OD for 3-5days.	Kancin-vet 100ml( 250mg Amikacin/ml) inj vial( Morvel India). AmikaZep 100ml ( 250mg Amikacin/ml) inj vial (Rapid Life India). Amikin 30ml ( 250mg Amikacin/ml) inj vial ( Vets Pharma India).
Enrofloxacin: 2.5 mg-5mg/kg IM/IV OD for 5-10days. 5mg-20mg/kg PO OD for 5-10 days. NB: Avoid in young animals. Provide supportive treatment as per requirement.	Fortivir 30 ml (100mg Enrofloxacin/ml) inj vial( Verbac India). Floxidin 100ml (100mg Enrofloxacin/ml) inj vial (MSD india). Efx -LA 100ml (120mg Enrofloxacin/ml) inj vial(Parex India). Enolox-K 30ml (100mg Enrofloxacin and 60 mg Ketoprofen/ml)inj vial( Zenley Animal health). Enrovet 100ml (100mg Enrofloxacin/ml) inj vial ( Vets Pharma India). Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Cephalexin: 22mg/ Kg PO BD for 28 days.	Lexin 300mg cephalexin tab( Virbac India). Lexin 20g sachet( Virbac India). Lexin 30g powder( Virbac India). Vetalexin 300mg cephalexin tab ( Indian Immunological). Celex 250 oral dry syrup( Indian Genomix).
Cefpodoxime: 5- 10mg/kg PO OD for 7days.	CefPetXL 100 (100mg ) tab( Intas India). CefPetX 200 ( 200mg cefpodoxime) tab( Intas India). CefPetXL 30ml (12.95g cefpodoxime) dry syrup( Intas India). Hatpod DS 30ml (100mg cefpodoxime/ml) syrup( Hatvet India). Cef DP- 100 (100mg cefpodoxime) tab ( SkyEc India). Cefvet-200( 200mg cefpodoxime) tab ( Malick Licenses Private Limited India)
Cefovecin: 8mg/ Kg Sc OD single injection.	Convenia 10ml(80mg Cefovecin/ml) inj vial (Zoetis India).
Amoxicillin+Clavulanate: 20mg/kg PO QID for 5-7 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg(400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).
Marbofloxacin: 2.75- 5.5mg /Kg PO/ IM OD for 5- 10 days.	Marbidac 30ml(16% Marbofloxacin) Injection (Zydus India). Marbofloxacin 20 ml (10% Marbofloxacin) Injection Vial (Credence Remedies India). Marbofloxacin 50 ml (10% Marbofloxacin) Injection Vial (Credence Remedies India). Marbofloxacin 100 ml (10% Marbofloxacin) Injection Vial (Credence Remedies India). Marbomet 30ml(100 mg Marbofloxacin/ml ) injection Vial ( Intas Pharmaceutical India). Marbomet 50(50mg Marbofloxacin) tab ( Intas Pharmaceutical India).

---

Streptococcal infection with special reference to Necrotizing fasciitis (NF) in dogs – Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Streptococcal infection is caused by a group of species, including Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus dysgalactiae, Streptococcus equi subsp. zooepidemicus, and Streptococcus canis. These organisms are facultative anaerobes, characterized as β-hemolytic gram-positive cocci, and typically arrange themselves in pairs and chains. The β-hemolytic streptococci are known for their ability to completely lyse red blood cells. This ability results in a distinct zone of clearing around the colonies on blood agar. The streptococci found in the gastrointestinal tract are grouped as enterococci bacteria. They can also be isolated from the skin of healthy dogs. Streptococcus canis and S. equi subsp. zooepidemicus are the main disease-causing bacteria in dogs and are found normally on the skin and in respiratory tracts respectively.

Pathogenesis

Streptococcus canis and S. equi subsp. zooepidemicus pathogens invade tissues when host barriers are compromised. Streptococcus canis invades soft tissues under favorable conditions. These conditions include bites, injuries, a compromised immune system, and allergies. The invasion and growth result in necrotizing fasciitis (NF). Necrotizing fasciitis is a serious and aggressive skin infection. It affects soft tissue and results in necrosis of muscle fascia and subcutaneous tissue. The infection advances along the fascial planes. The infectious process can spread swiftly, resulting in secondary infections of the overlying and underlying skin, soft tissues, and muscle. Therefore, Streptococcus canis bacteria are also called flesh-eating bacteria. Organ failure may occur because of the release of pyrogenic exotoxins, which function as superantigens. NF can cause Streptococcal Toxic Shock Syndrome (STSS), marked by sudden shock and death.

Clinical symptoms

The main signs of NF are quick swelling, limping, and changes in skin color (usually from red to purple to black). It most often affects the skin on the legs and neck, but other body parts can also be affected. Systemic involvement shows symptoms of fever, vomiting, and hypotension. Death can occur within 48 hours. Streptococcus equi subsp. zooepidemicus causes severe pneumonia in dogs. This condition may escalate rapidly and present with signs of STSS. It may potentially lead to death within the same timeframe. In some cases, dogs may only show mild upper respiratory symptoms.

Diagnosis

The most common biochemical findings are a left shift, lymphopenia, hyponatremia, hypocalcemia, decreased bicarbonate, hypoalbuminemia, and elevated liver enzymes. Cytology performed on aspirates of the tissue may reveal septic suppurative inflammation with bacteria. Chains of cocci support the diagnosis. Blood cultures positive for S. canis support the clinical diagnosis of NF.

Treatment

For infections caused by members of the Streptococcus family, β-lactam drugs are typically used for treatment. Severe cases require broad-spectrum combinations like aminopenicillin with aminoglycosides. It is essential to initiate prompt fluid resuscitation for necrotizing fasciitis (NF). Human patients with NF and STSS receive high-dose penicillin and clindamycin. Clindamycin is particularly beneficial because it inhibits exotoxin production. However, the emergence of resistance is a concern. For streptococcal meningitis, alternatives include trimethoprim-sulfamethoxazole or ceftriaxone. Treatment of necrotizing fasciitis should also involve surgical management for debridement. Amputation may be required. Hospitalization for intravenous antimicrobial therapy, aggressive wound management, and monitoring is advised. Patients receiving fluoroquinolones may have worse outcomes. Therefore, it is recommended to avoid fluoroquinolones when necrotizing fasciitis is a differential diagnosis. Culture results should be obtained for further courses of action. Pain management is often required, but NSAID use is controversial.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Ampicillin: 22 mg/kg IV /IM TID for 5-7 days. NB: potentiated ampicillin is better option.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin ) Inj vial ( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).
Amoxicillin+Clavulanate: 20mg/kg PO QID for 5-7 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).
Gentamicin: 6-12mg/kg IM/IV / SC OD for 3-5 days. NB: should be combined with Ampicillin:	Gentamicin 100ml (40 mg Gentamicin/ml) inj vial(Zuche Pharmaceuticals India). Gentamicin 30ml(40 mg Gentamicin/ml) inj vial (Zuche Pharmaceuticals India). Genacyn LA 30ml(80 mg Gentamicin/ml) inj vial( Zenley Animal Health India). Gentamor Vet 100ml(40 mg Gentamicin/ml) inj vial( Morvel India).
Clindamycin: 10-12.50 mg /kg PO/SC OD for 4wks. NB:Use cautiously in patients with history of regional enteritis and antibiotic associated colitis.	Clindapet 30ml ( 25mg Clindamycin/ml ) inj vial( Offered by Vea Impex India loyal pet zone/ India loyal pet zone India). Clindapet 300 (300mg Clindamycin) tab ( offered by Vea Impex India/ loyal pet zone India). Clivet 150 (150mg Clindamycin) tab ( Corise India). Goclin 150 (150mg Clindamycin) tab (Veko India). Petclind 450 (450mg Clindamycin) tab(Pet care India). Petclind 600 (600mg Clindamycin) tab (Pet care India).
Chloramphenicol: 45-60mg/kg IM/IV BD.	Dotclor 30ml (100 mg Chloramphenicol/ml) inj vial (Dotcom Pharma India).

---

Canine Actinomycosis – Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine actinomycosis is caused by anaerobic or microaerophilic bacteria, mainly from the genera Actinomyces and Arcanobacterium, affecting primarily young large-breed dogs. Actinomycetes are gram-positive, non-acid-fast organisms that may appear branched, with dimensions less than 1 µm wide. Actinomyces spp. are normal inhabitants of the oral cavity, the airways, and the GI tract. Actinomycosis occurs when there is disruption of the host barriers. The cervicofacial region, thorax, abdomen, and subcutaneous tissue are common areas where infection stems from bite wounds or foreign bodies. Pulmonary infections may arise from the aspiration of contaminated material, and existing lung diseases can facilitate infection. Plant awns perforating the intestinal wall and traveling through the mesentery transmit infection into the peritoneal cavity. The central nervous system is infected by infected blood or extension of the infection from sinuses, otitis media/interna, or head trauma.

Pathogenesis

Pathogenesis of Actinomyces spp. is aided by other microbes that weaken the host’s defenses and lower oxygen levels. The microbes significantly increase the pathogenicity of Actinomyces. The bacteria involved are usually commensal organisms, particularly anaerobes, from the mouth or intestines. The fimbriae of Actinomyces can attach to specific cell receptors on other bacteria, like streptococci, and form a complex body. This interaction reduces neutrophil phagocytosis and the bactericidal effects on the bacterial group. This complex association also triggers an acute inflammatory response that activates neutrophils and macrophages, leading to an increase in B-lymphocytes, resulting in the formation of a typical actinomycosis lesion. Enzymes from these bacteria and immune cells break down connective tissue, allowing the disease to spread. The organisms cluster together to form “sulfur granules,” which can appear as small or large yellowish-brown colonies. Sometimes, this inflammation leads to significant scarring. Nodular lesions may develop, which can be confused for tumors and can vary in firmness and may drain or ulcerate, with potential muscle involvement.

Clinical symptoms

Symptoms include variable pain and fever, and radiographic findings may show new bone formation or osteomyelitis. Pneumonia, intra-abdominal actinomycosis, and meningoencephalitis are less frequent. Aspiration of firm lesions is typically unhelpful. Infections in the thoracic and abdominal regions lead to a velvety thickening of the pleura and peritoneum, often with localized lung involvement that may appear as a mass or consolidation. Affected masses can impact multiple internal organs and cause subcutaneous swelling with draining sinuses. In abdominal cases, often only one organ is involved, but masses typically affect nearby structures. Subcutaneous actinomycosis may also affect areas like the lateral thoracic wall, flank region, and limbs. Lesions on the thoracic or abdominal walls can extend from deeper actinomycosis. Key features include lameness, draining masses, and new bone formation in affected limbs. Actinomycosis in the thoracic or abdominal cavity typically presents as a chronic and progressive condition but can occasionally be acute. Symptoms may include severe weight loss, fever, coughing, and, less frequently, hemoptysis and tachypnea. It can affect the lung parenchyma and other thoracic structures, leading to soft tissue masses and possibly a draining sinus. Clinical features of abdominal actinomycosis include palpable masses and abdominal distention from ascites. Retroperitoneal actinomycosis can present with spinal pain and may lead to rear leg paresis or paralysis. A subcutaneous mass with a draining sinus in the caudal thorax or flank area is commonly observed.

Diagnosis

Diagnosis involves X-ray examination, CBC, serum biochemistry, and culture of the organism. Radiographic findings may show interstitial or alveolar infiltrates, pneumothorax, pleural thickening, and mass lesions, which may complicate diagnosis due to potential misinterpretation as other conditions. Radiographic and sonographic findings of the abdomen reveal peritoneal effusion and mass lesions affecting nearby structures, with ascites showing a flocculent appearance on ultrasound. CBC and serum biochemistry often reveal mild to moderate nonregenerative anemia, leukocytosis, hypoalbuminemia, hyperglobulinemia, and hypoglycemia. CSF analysis frequently indicates elevated protein and cellular fluid resembling pus. Actinomycosis is diagnosed through culture of the organism from affected tissues and additional findings, including a pyogranulomatous inflammatory response and specific accompanying microorganisms. Actinomyces spp. require anaerobic conditions for culture, and samples should be submitted using tissue, pus, or sulfur granules. Growth usually takes 5 to 7 days, with colonies showing various appearances. Accurate species identification necessitates 16S rRNA gene sequencing due to the challenges in traditional biochemical testing. Associated bacteria from the oral cavity or intestinal tract are common in specimens, complicating the isolation of Actinomyces. Histologically, infection shows neutrophils in fibrosing granulation tissue, and identifying sulfur granules is crucial for diagnosis. Granules indicate true actinomycotic infection, ranging from 30 to 3000 µm in size, while other stains reveal non-acid-fast branched filaments.

Treatment

Treatment of actinomycosis primarily involves prolonged use of high-dose penicillin, which is recommended for weeks to months. Other antibacterial options are available for those with penicillin sensitivity. The therapy should extend beyond the resolution of disease symptoms to prevent relapse, with some cases requiring treatment for over a year. Infections typically respond well to penicillin, but broader-spectrum antibacterials may be needed initially in some instances.

Drugs and formulations available in India.

Drug and dose	Veterinary and human formulations
Procaine Penicillin 100,000 U/kg IM, SC TID	Veterinary formulation: Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Clindamycin 5 mg/kg SC TID	Veterinary formulation: Clindapet 30ml ( 25mg Clindamycin/ml ) inj vial( Offered by Vea Impex India loyal pet zone/ India loyal pet zone India). Clindapet 300 (300mg Clindamycin) tab ( offered by Vea Impex India/ loyal pet zone India). Clivet 150 (150mg Clindamycin) tab ( Corise India). Goclin 150 (150mg Clindamycin) tab (Veko India). Petclind 450 (450mg Clindamycin) tab(Pet care India). Petclind 600 (600mg Clindamycin) tab (Pet care India).
Erythromycin: 10 mg/kg PO TID	Veterinary formulation: Eycin-Ws 100g (200mg Erythromycin/g)powder ( IPPL India). Althrocin Ikg(200mg Erythromycin/g) powder( Alembic India). Benison 250g/1kg(100mg Erythromycin/g) powder( Benison Farm Vet India). Human formulations: Livethromycin 500 mg tab( Livealth India). Erythromycin Lactobionate 500 mg Inj vial ( Livealth India).
Chloramphenicol: 50 mg/kg PO, IV, IM, SC TID	Dotclor 30ml (100 mg Chloramphenicol/ml)inj vial (Dotcom Pharma India).
Minocycline: 5–25 mg/kg IV, PO BD	Human formulations: Divaine 100mg (1oomgMinocycline) Inj (Cipla India). Minyum 100mg (1oomgMinocycline) Inj (Glenmark India).
Ampicillin: 20–40 mg/kg IM, SC, PO QID for 5-7 days .	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).
Amoxicillin: 20–40 mg/kg IM, SC, PO QID	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).

---

Bordetellosis in dogs – Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Bordetellosis is caused by Bordetella bronchiseptica, a respiratory pathogen that primarily with viral infection causes kennel cough in dogs. Bordetella bronchiseptica are gram-negative rods or coccobacilli, aerobic, motile, and non-spore-forming bacteria. It is a common commensal organism in many other species, including guinea pigs, rats, rabbits, mice, swine, cats, turkeys, and primates. Bordetellosis is a contagious infection and spreads through direct contact between dogs living in places like shelters and kennels. Puppies are especially vulnerable due to their weaker immune systems. The bacteria spread when dogs come into contact with each other’s noses or through caregivers and contaminated objects. It can also spread through tiny droplets in the air.

Pathogenesis

Pathogenesis of Bordetellosis – Bordetella bronchiseptica adheres to ciliated respiratory epithelium, producing adhesion and cytolytic toxins that lead to an inflammatory response, antiphagocytic activity, and dermonecrosis. This bacterium primarily targets the respiratory system, where it damages the respiratory lining by releasing various virulent factors that disrupt normal cellular function. These factors can promote a cascade of inflammatory reactions that further compromise the host’s defenses. Furthermore, the release of these toxins can potentially lead to ciliary dysfunction by paralyzing ciliary movement, which is crucial for clearing mucus and pathogens from the airways. As ciliary function diminishes, the clearance of respiratory secretions becomes increasingly inefficient, thereby increasing the risk of serious lower respiratory infections. In immunocompromised individuals or those with pre-existing respiratory conditions, the impact of Bordetella bronchiseptica can be particularly severe, resulting in prolonged illness and the potential for secondary complications, emphasizing the importance of understanding this pathogen’s mechanisms for effective prevention and treatment.

Clinical symptoms

The clinical picture includes a honking cough and nasal discharge, and sometimes symptoms of life-threatening pneumonia are also evident. In mild cases, dogs may show an acute nonproductive cough, while severe cases can cause fever and systemic illness.

Diagnosis

Diagnosis of Canine Bordetellosis includes radiography, bacterial culture, and PCR. Chest X-rays may appear normal for simple coughing but can show changes in lung patterns if pneumonia develops. Testing involves bronchoscopy and bronchoalveolar lavage to identify the bacteria. Cultures from the nose or throat usually return normal bacteria. PCR testing from swabs helps confirm the presence of Bordetella bronchiseptica.

Treatment

Treatment with antibiotics like Doxycycline, Enrofloxacin, or Marbofloxacin is most effective in curing Bordetellosis in dogs.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Doxycycline : Drug of choice 5 mg/kg PO BD for 5-10 days. 10 mg/kg PO OD for 5-10 days. NB: A).Some isolates of B bronchiseptica are doxycycline-resistant. B) Enrofloxacin or marbofloxacin , azithromycin, or Amoxicillin-clavulanate in case of resistance. C) . Doxycycline, Enrofloxacin or marbofloxacin readily cross the blood–bronchus barrier. D). Provide oxygen supplementation to patients with SpO2 < 92%-94%. Particularly ensure this if respiratory difficulty is evident. Increased respiratory effort warrants attention even with adequate oxygenation.	Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

Campylobacteriosis in dogs- Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Campylobacteriosis is caused by Campylobacter spp (C. jejuni, C. coli, C. helveticus, and C. upsaliensis) particularly C. jejuni, causes canine enteric disease in dogs. These bacteria are small, curved, Gram-negative bacteria that are microaerophilic. Young dogs under 6 months are commonly affected and shed C. jejuni at higher rates. This may be due to their limited space, greater exposure to feces, and an immature immune system. The Campylobacter bacteria are commonly found in infected animals’ intestines. They can be transmitted through ingesting raw white meat, contaminated food, or water. Contact with infected feces also spreads the bacteria. Campylobacteriosis is a zoonotic disease and is common in dogs, but symptoms are rare. Most affected dogs recover without treatment.

Pathogenesis

Gastric acid acts as a barrier, but bacteria must reach the small and large intestines to grow; C. jejuni invades epithelial cells and those in the lamina propria. Virulent Campylobacter spp. attach to and enter enterocytes after getting through the mucus layer. They survive in the cytoplasm of enterocytes and avoid lysosomal compartments. C. jejuni produces toxins that harm the gut lining. The disease caused by Campylobacter involves secretion systems and toxins, including the virulence factor CDT (cytolethal distending toxin). This results in symptoms such as diarrhea, loss of appetite, vomiting, and fever lasting from 3 to 7 days.

Clinical symptoms

Some dogs seem healthy, while others may show symptoms of systemic illness. Common signs include abdominal pain, fever, diarrhea, blood in feces, and inflammatory cells in the stool, indicating inflammation from C. jejuni jejuni. Diarrhea is usually acute, lasting 5–15 days, particularly in dogs under 6 months old, and can be watery or bloody, with mucus and sometimes bile. It may become chronic, accompanied by fever and increased white blood cell counts. In cases of C. jejuni enteritis, gross lesions include enlarged, fluid-filled ceca and proximal colons with thickened walls, and lymph nodes draining infected areas become enlarged. Certain strains of C. jejuni can cause bloody mucus exudates.

Diagnosis

Fresh feces placed in anaerobic medium are cultured on selective media for the recovery of Campylobacter. Conditions during incubation should be strict, with plates incubated at 37°C or 42°C. PCR is used for accurate and rapid diagnosis.

Treatment

Macrolides or quinolones are used when there is frequent diarrhea. Macrolides are preferred due to the possible resistance to quinolones.

Drugs and formulations available in India.

Erythromycin: First choice 10-20 mg/kg PO TID for 5 days.	Eycin-Ws 100g (200mg Erythromycin/g)powder ( IPPL India). Althrocin Ikg(200mg Erythromycin/g) powder( Alembic India). Benison 250g/1kg(100mg Erythromycin/g) powder( Benison Farm Vet India)
Tylosin: Another option 25mg/kg PO BD for 7 days.	Trox 50g /120g Powder ( Verbac India ).

---

Brucellosis in dogs – Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine brucellosis is a zoonotic disease caused by Brucella canis in dogs, with B. abortus and B. suis also involved. These Gram-negative bacteria are small, non-encapsulated, non-spore forming, and non-motile intracellular pathogens. They usually appear singly or in pairs and occasionally in short chains, but not in long chains. These aerobic bacteria grow on various media, including serum dextrose, blood, and chocolate agar. Dogs can get infected by consuming, inhaling, or having reproductive contact with contaminated environments. Infected dogs may shed the bacteria for years, and B. canis is particularly effective at invading host cells.

Pathogenesis

Brucella can cross the intestinal barrier through M cells without triggering the host’s immune response. The BvrR/BvrS regulatory system is crucial for Brucella spp. invasion in both phagocytic and non-phagocytic cells by activating GTPases like Cdc42. The rough strain Brucella canis, which lacks the O-polysaccharide chain in its LPS, invades host cells more effectively than smoother pathogenic Brucella species. The type IV secretion system (T4SS) of Brucella is vital for survival inside host cells, as it injects effector proteins into the host’s cytoplasm. However, B. canis causes a weak inflammatory response even in its main host, and it is less likely to cause inflammation compared to smoother pathogenic Brucella species, leading to lower IFN-γ production and fewer inflammatory lesions.

Clinical symptoms

Infected dogs may show lymphadenopathy, and pregnant females can abort late in gestation. Bacteria in post-abortion fetal contents can infect other dogs and humans. Other issues include stillbirth and difficulty in conceiving females, while males may experience epididymitis, prostatitis, orchitis, and infertility.

Diagnosis

Common diagnostic tests include the rapid slide agglutination test and agar gel immunodiffusion test. B. canis infection often results in bacteremia lasting 2–4 weeks, with levels up to 10^4 CFU/mL in blood. PCR tests of blood, urine, and clinical specimens help confirm infection.

Treatment

Treatment typically involves tetracyclines and aminoglycosides, with oxytetracycline for 4 weeks and streptomycin for the first week often being ineffective. If resistance occurs, doxycycline may be used, and enrofloxacin can help prevent abortion, though streptomycin is not recommended during pregnancy.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Oxytetracycline: 50 mg/kg initial dose followed by 25 mg/ PO kg OD for 4 weeks.	Oxin 500mg (50omg oxytetracyclin) tab (Zoetis India). Oxytech 500mg (50omg oxytetracyclin) tab (Mediseller India). Himoxy 500mg (50omg oxytetracyclin) tab (Himal Bioscience India).
Enrofloxacin:  5 mg/kg PO BD for 30 days.	Fnoro-vet 250ml (100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml (100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml (100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin) tab (Vetoquinol India).

---

Tuberculosis in dogs-Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Tuberculosis, a zoonotic disease, is caused by Mycobacterium bovis, Mycobacterium tuberculosis, and Mycobacterium microti in dogs. These are Gram-positive, **non-motile, aerobic, non-spore-forming, acid-fast bacteria. They may appear as cocci or as bacilli up to 6-8 μm long. Their cell wall is made with up to 60% lipid, contributing to their hydrophobic nature, slow growth, and resistance to desiccation, disinfectants, acids, and antibodies. They are grown on egg-based and agar-based solid media such as Lowenstein-Jensen and Middlebrook 7H10/7H11, as well as liquid media like Middlebrook 7H9. The majority of dogs are infected with M. bovis and only a relatively small number of dogs are infected with M. tuberculosis. M. bovis infections in dogs usually arise from the consumption of unpasteurized milk from infected cattle, while M. tuberculosis infections primarily result from human respiratory illnesses. M. tuberculosis usually causes pulmonary TB in dogs and less frequently involves other organs.

Pathogenesis

Following initial infection, a period of latency may occur, with the innate immune response controlling infection and the onset of clinical signs for an often-extended period of time (months to years). In some dogs infected with M. tuberculosis, the initial exposure event is suspected to have occurred many years prior to diagnosis. Upon entering the body, macrophages kill most of the mycobacteria, leading to the formation of granulomas, thus restricting further infection. However, some bacteria multiply in macrophages and are released when the macrophages die, spreading through lymphatics to lymph nodes and blood, causing disease in many organs. This often results in granulomas, sometimes with necrosis, in lymph nodes or other organs.

Clinical symptoms

Symptoms vary based on affected organs and illness severity, but common signs include weakness, weight loss, fever, and coughing, particularly with pulmonary infections resulting from inhalation. Lesions can be polymorphic, and in dogs, pulmonary TB symptoms can progress slowly. Cutaneous or subcutaneous issues may arise from bites or injuries, along with abdominal symptoms from ingestion. Rarely, neurological symptoms, weight loss, vomiting, and diarrhea may occur if the disease spreads to locations such as the CNS, liver, or kidneys.

Diagnosis

Diagnosis can be done using X-rays, USG abdomen, identifying mycobacteria with Ziehl-Neelsen staining or PCR on biopsy or cytology samples, and immunological tests like lateral flow and IFNγ assays. PM findings are generalized emaciation, granulomatous lesions in lymph nodes, lymphadenopathy, lung consolidation, exudative pleuritis, pleural adhesions, and disseminated lesions in organs like the diaphragm, liver, spleen, etc.

Treatment

Treatment is lengthy and challenging, and due to potential transmission risks from dogs to humans, most animals diagnosed with TB are euthanized. A daily triple-antimicrobial therapy including rifampicin, a macrolide/azalide, and a fluoroquinolone is used to treat canine tuberculosis. The choice of macrolide/azalide is based on cost and formulation.

Drugs and formulations available in India.

Drug and dose	Veterinary and human formulations
Rifampicin 10 mg/kg PO OD for 5-6 months.	Human formulations: R-Cin 200 ml (100mgRifampicin/5ml) Suspension (Lupin India). Cavidin 450mg (450mgRifampicin) tab (Wockhardt India). Monocin 450mg (450mgRifampicin) tab (Overseas health care India). Rimactane 450mg (450mgRifampicin) tab (Novartis India). Ticin 450mg (450mgRifampicin) tab (Themis Medicare India).
Azithromycin : combined with Rifampicin 10–15 mg/kg PO OD for 5-6 months .	Azithrohat 300mg ( 300mg Azithromycin)tab (Hatvet India). Azihv  500ml(40mg Azithromycin/ml ) oral suspension (Healthyvet Pharma India). Azithromex 100ml( 40mg Azithromycin/ml) oral suspension ( Vetmex Animal Health India). Azithromex 250ml( 40mg Azithromycin/ml) oral suspension ( Vetmex Animal Health India). Azivet 100ml( 40mg Azithromycin/ml) oral suspension (Hindustan Therapeutics India). Azivet 250ml( 40mg Azithromycin/ml) oral suspension (Hindustan Therapeutics India).
Or Clarithromycin: combined with Rifampicin. 7.5–12.5 mg/kg PO BD for 5-6 months.	Human formulations: stayhappi Clarithromycin 500mg Tab(Sarvagunaushdhi India). Urclar Clarithromycin 250 mg tab (Novartis India). Klarim Clarithromycin 250 mg tab (Morepen Labs India). Claricyl 30ml( 125mg /ml) dry syrup ( PCD pharma India). Eclarin 30ml( 125mg /ml) dry syrup ( Esquire India). Clarimax 30ml( 125mg /ml) dry syrup ( Janus Biotech India).
Enrofloxacin: combined with Rifampicin and Azithromycin or with Rifampicin and Clarithromycin. 10 mg/kg PO OD for 5-6 months.	veterinary formulations: Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Or Marbofloxacin : combined with Rifampicin and Azithromycin or with Rifampicin and Clarithromycin. 2–3 mg/kg PO OD for 5-6 months.	veterinary formulations: Marbomet 50(50mg Marbofloxacin) tab ( Intas Pharmaceutical India).
Or Moxifloxacin : combined with Rifampicin and Azithromycin or with Rifampicin and Clarithromycin. 10 mg/kg PO OD for 5-6 months.	Human formulations: Moxif-400( 400mg Moxifloxacin) Tab (Torrent Pharma India). Moximac 400 ( 400mg Moxifloxacin) Tab ( Macleods India). Moxicip 400 ( 400mg Moxifloxacin) Tab ( Cipla India).

---

Canine Colibacillosis- Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Colibacillosis is caused by Escherichia coli in dogs and has zoonotic importance. The occurrence of UTI caused by extraintestinal pathogenic E. coli is common in both humans and dogs, with documented transmissions between pets and their owners. Dogs may also acquire antibiotic-resistant E. coli from raw meat, posing a risk to both the dogs and the humans who prepare the food. Escherichia coli, a group of gram-negative, rod-shaped facultative anaerobic bacteria, lead to extraintestinal and gastrointestinal diseases. E. coli can infect any system within the dog’s body. In adult dogs, E. coli is the primary cause of diarrhea in canines. The important pathogenic strains are enteropathogenic E. coli (EPEC), enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enterohemorrhagic E. coli (EHEC), Shiga-toxin-producing E. coli (STEC), adherent-invasive E. coli (AIEC), and enteroaggregative E. coli (EAEC). The important pathogenic strains EPEC and ETEC are notably common in young pups with enteric disease. While E. coli typically resides beneficially in the lower intestine, it can cause illness in puppies under certain conditions. Bacteria can be transmitted to puppies through the mother during pregnancy or at birth or during nursing through her milk from an infected mammary gland. Enterococcus spp. and Pseudomonas spp. significantly cause urinary tract infections (UTI) in dogs, but E. coli continues to be the most prevalent pathogen responsible for UTI.

Pathogenesis

The pathogenesis of E. coli in dogs begins with its colonization of the gastrointestinal tract. The virulence factors like adhesins help the bacteria attach to the intestinal lining. Once attached, E. coli can disrupt normal functions, leading to symptoms from mild gastrointestinal upset to severe illness. The severity depends on the strain of E. coli and the dog’s immune status. As the bacteria grow, they may produce toxins that worsen the condition. Enterotoxins can lead to diarrhea, while some strains produce Shiga toxins, causing more serious issues like hemolytic uremic syndrome.

Clinical symptoms

Symptoms of E. coli infection in dogs vary but often include diarrhea, vomiting, loss of appetite, lethargy, and dehydration. UTI symptoms manifest as dribbling urine, painful urination, vaginal discharge, lethargy, and hematuria.

Diagnosis

E. coli is frequently isolated from the feces of healthy and diarrheic dogs using bacteriological media, with MacConkey agar serving as a differential medium. Gram staining and biochemical tests (catalase, methyl red, indole, and nitrate tests) are routinely conducted. Flotation tests and parvovirus (parvo) tests using samples of feces are performed to exclude parasitic infestation and parvovirus infection.Advanced techniques such as polymerase chain reaction (PCR) assays serve as essential instruments in diagnosis. These assays are capable of accurately detecting specific virulence genes within bacterial DNA, facilitating definitive diagnoses. PCR is particularly effective in identifying shiga toxin-producing strains, which are associated with severe health consequences, thereby emphasizing its vital importance in public health.

Treatment

Dogs suffering from severe diarrhea require intravenous therapy. Before initiating treatment, susceptibility testing is essential to select antimicrobials that effectively penetrate intracellularly. E. coli is generally susceptible to a range of antibiotics, including amoxicillin with clavulanic acid, doxycycline, rifampin, fluoroquinolones, and trimethoprim-sulfonamides. Vomiting should be controlled by maropitant and/or ondansetron. Antacids and gastroprotectants like famotidine, omeprazole, sucralfate, and antispasmodics should also be included in the treatment.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Enrofloxacin: 10 mg/kg PO OD for 5-6 days.	Floxavet 100ml (100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml (100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin) tab (Vetoquinol India).
Doxycycline : 5 mg/kg PO BD for 5-10 days. 10 mg/kg PO OD for 5-10 days.	Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).
Amoxicillin+Clavulanate: 20mg/kg PO QID for 5-7 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).

---

Canine Pasteurellosis—Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Pasteurellosis, a significant zoonotic disease, is attributable to various species of Pasteurella found in dogs. Pasteurella are Gram-negative, encapsulated, non-hemolytic, non-spore-forming, coccobacilli, and facultatively anaerobic bacteria. These bacteria are typically cultured on sheep blood agar or chocolate agar media. Several species, including P. multocida, P. canis, P. dagmatis, P. oralis, and P. stomatis, are normal inhabitants of the oral cavity, gastrointestinal tract, upper respiratory tract, and skin of dogs. While usually harmless, these organisms can become pathogenic, particularly when dogs experience stress or immunocompromised states, leading to non-zoonotic respiratory and digestive diseases. They are commonly implicated in zoonotic bite wound infections in dogs, with human infections arising from scratches and bites from dogs or from exposure to dog wounds. The bacteria are transmitted through bites or by licking open wounds, posing a risk of zoonotic bite wound infections. P. canis emerges as a primary causative agent of pyoderma and cutaneous abscesses in humans, often transmitted through dog bite injuries.

Pathogenesis

Pathogenic bacteria synthesize virulence factors that significantly enhance their capacity to evade host defense mechanisms, thereby facilitating their colonization and invasion of deeper tissues. Pasteurella spp., in particular, produce various substances, including a capsule that is crucial for adherence and invasion, as well as Outer Membrane Proteins (OMP) that play a pivotal role in eliciting the protective immune response. Additionally, adhesins are involved in colonization, while neuraminidase reduces the viscosity of respiratory mucus, permitting closer bacterial apposition to the cell surface. Lipopolysaccharide induces immune-mediated hypersensitivity that may exacerbate inflammation and tissue damage, and the leukotoxin elicits numerous biological effects, including the formation of pores in the cell membrane at elevated concentrations, leading to cell swelling and lysis. These virulence factors are integral to promoting adhesion, colonization, and proliferation of the organism, thereby playing a critical role in the pathogenesis and transformation of the organism from a commensal state to a pathogenic one.

Clinical symptoms

Clinical manifestations associated with P. canis infections include pyoderma, cutaneous abscesses in animals, and sometimes osteomyelitis; systemic bacteremia, septic arthritis, or symptoms of lower respiratory infections are also seen. Furthermore, P. multocida is known to cause meningitis in both dogs and humans, a condition characterized by symptoms such as nausea, nuchal rigidity, fever, headache, and altered levels of consciousness.

Diagnosis

Laboratory identification of Pasteurella species is achieved by culturing the bacteria (isolated from wounds) on sheep blood agar, resulting in pale gray mucoid non-hemolytic colonies that emit a “mousy odor” and exhibit a blue halo under oblique lighting. P. multocida is noted to be oxidase-positive, catalase-positive, ornithine decarboxylase positive, indole positive, mannitol positive, and urease negative, whereas P. canis is characterized as ornithine, indole, and mannitol negative.  PCR offers a highly sensitive approach, detecting bacterial DNA even in low concentrations.

Treatment

Pet owners must exercise caution when interacting with a dog’s mouth and prioritize the oral hygiene of their pet. Protective gloves and masks are essential when addressing a dog’s wounds. It is imperative to use sanitizers before and after handling any dog injuries. Scratches inflicted by pets should not be dismissed lightly; they must be thoroughly cleansed with antiseptic soap and appropriate germicides. Pasteurella species demonstrate susceptibility to a broad range of antibiotics, with penicillin derivatives such as potentiated amoxicillin, potentiated ampicillin, and penicillin G being the most effective treatment options. Tetracycline or chloramphenicol can be used in dogs that show a reaction to beta-lactam antibiotics.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Amoxicillin+Clavulanate: 20mg/kg PO QID for 5-7 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate) tab( Savavet India).
Ampicillin: 20–40 mg/kg IM, SC, PO QID for 5-7 days.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).
Procaine Penicillin 100,000 U/kg IM, SC TID	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).

---

Clostridial diarrhea in dogs —Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Clostridium difficile and Clostridium perfringens are two important bacteria among clostridia species that can cause acute hemorrhagic diarrhea and colitis in dogs. They are gram-positive, rod-shaped, spore-forming bacilli that act as significant enteropathogens in dogs and humans. The Clostridium organisms are obligate anaerobes and are capable of producing endospores. The endospores are green, bowling pin or bottle-shaped and are identified by the Schaeffer–Fulton stain (0.5% malachite green in water). Reinforced clostridial medium is a commonly used non-selective medium, while selective media like CCFA (Cycloserine-Cefoxitin-Fructose Agar) are used for Clostridium difficile isolation. Transmission occurs through fecal-oral routes, and infections are primarily linked to C. perfringens biotype A. Species of Clostridium inhabit soils and the intestinal tracts of animals, including humans. Contaminated food and water are the main sources of infection in dogs.

Pathogenesis

The Clostridium organisms based on the production of four major toxins (α, β, ι, and ε) are typed into five toxigenic phenotypes, A-E. Each type may also express a subset of at least 10 other established toxins, including C. perfringens enterotoxin (CPE), a well-characterized virulence factor whose production is co-regulated with sporulation. Most of C. perfringens isolates are type A, with 15% harboring the enterotoxin gene. C. difficile produces three types of toxins, viz toxin A (an enterotoxin), toxin B (a cytotoxin), and CDT (an ADP-ribosyltransferase). C. perfringens enterotoxins damage the intestinal lining, leading to diarrhea, abdominal pain, and potentially more severe complications called enterotoxemia. The damage to the intestinal cells leads to fluid and electrolyte loss and results in diarrhea. C. difficile toxins (toxin A, toxin B, and CDT) are thought to be responsible for the virulence of the bacterium and the major contributors to the pathogenesis of antibiotic-associated gastrointestinal disease. These toxins also damage the intestinal cells, leading to inflammation and diarrhea.

Clinical symptoms

There are no pathognomonic clinical signs indicative of C. perfringens-associated diarrhoea in dogs, and the spectrum of disease attributed to this organism varies greatly and can involve both the small and large intestine. C. perfringens-associated diarrhoea can also cause acute hemorrhagic diarrhoea in dogs. Clinical signs that have been associated with canine C. difficile infection range from asymptomatic carriage to a potentially fatal acute haemorrhagic diarrhoeal syndrome. There does not appear to be a specific anatomic intestinal localization of clinical signs.

Diagnosis

There is currently no gold standard for the diagnosis of canine C. perfringens-associated diarrhoea. The optimal diagnostic approach utilizes a combination of faecal CPE immunodetection and PCR for detection of the enterotoxin gene (cpe). Detection of CPE via ELISA in faecal specimens is the most widely used diagnostic tool for C. perfringens in humans and animals; however, the performance characteristics of this human-based assay have not been validated in dogs or cats. Routine diagnosis of C. difficile-associated diarrhoea has been made based on positive faecal ELISA assays for toxins A or B; however, the performance characteristics of the human-based immunoassays are unacceptably low in dogs.

Treatment

Metronidazole is the drug of choice for dogs with suspected C. difficile-associated diarrhoea. The second drug of choice is vancomycin; however, it is used only in cases of non-responsive clostridial infection or when metronidazole-resistant strains have been demonstrated.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Metronidazole 44 mg/kg PO followed by 22 mg/kg, QID	Veterinary formulations: CleanexL 220 mg (Nitrofurazone 60 mg+ Metronidazole 100 mg +Povidone Iodine 60 mg) Bolus (Boehringer). Human formulations: Metrogyl 100ml (5mg Metronidazole/ml) injection ( Intas India). Flagyl 100ml (5mg Metronidazole/ml) injection (Abbott India). Flagyl 400mg Metronidazole tab (Abbott India).
Vancomycin 3.5 mg/kg IV followed by constant rate infusion of 1.5 mg/kg/h then 10-20mg/kg PO QID for 7days.	Human formulation: Vanlid (250mg Vancomycin Hydrochloride) Cap (Cipla India). Vanking 500mg (500mg Vancomycin) Inj (Neon Labs India). Vancogram 500mg (500mg Vancomycin) Inj (Zydus India). Vancoray  500mg (500mg Vancomycin) Inj (Mylan Pharmaceuticals India). Vantox-CP 500mg (500mg Vancomycin) Inj (Samarth Life Sciences India). Vancotech CP 500mg (500mg Vancomycin) Inj (United biotech India).

---

Listeriosis in dogs —Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Listeriosis is a foodborne disease caused by Listeria monocytogenes in dogs. Listeria monocytogenes is a capsulated, motile, rod-shaped, gram-positive, facultative intracellular bacterium and lives as single cells or in short chains. Listeria monocytogenes is widely distributed in nature and stands as one of the leading causes of death from foodborne illness in the world. It is primarily transmitted through contaminated food. Listeria monocytogenes is highly resilient, able to survive and grow in refrigeration and high-salt conditions, posing challenges for control in food processing environments. It primarily affects vulnerable populations like senior dogs and young pups. Healthy dogs usually remain carriers and are less likely to exhibit any disease symptoms.

Pathogenesis

The bacteria can infiltrate various mammalian host cells by altering plasma membrane structure for engulfment. After entering the cell, they disrupt the internalization vacuole and move to the cytoplasm to replicate. The bacterium employs host cell actin filaments for movement and spreads between cells, manipulating host cell receptors, organelles, and the cytoskeleton to affect functions like ion transport, membrane trafficking, immune responses, and gene expression of host cells.

Clinical symptoms

Clinical listeriosis is infrequent in dogs and varies from mild symptoms to serious clinical signs like septicemia. Most common signs include fever, muscle aches, gastrointestinal symptoms, nervous signs, breathing problems, and urinary tract issues, depending on the organ system involved and the severity of the infection.

Diagnosis

Gram staining examination of blood, cerebrospinal fluid (CSF), or tissue biopsies can reveal the presence of purple gram-positive, rod-shaped bacteria. Clinical samples are cultured on selective media, such as PALCAM agar (Polymyxin, Acriflavine, LiCl, and Ceftazidime) for isolation of Listeria species, which can grow on this selective medium. Colonies with typical morphological characteristics (smooth, gray, small colonies) are further tested for identification. Polymerase Chain Reaction (PCR) is increasingly used for the rapid and specific detection of L. monocytogenes. (ELISAs can detect Listeria monocytogenes-specific antigens in clinical samples or food products.)

Treatment

Fortunately, the condition of the affected dogs tends to improve favorably with antibiotic therapy, particularly with potentiated ampicillin, enrofloxacin, and minocycline. Trimethoprim-sulfamethoxazole is an alternative antibiotic used for listeriosis, especially in cases of penicillin allergy or resistance to ampicillin. More serious cases of listeria may require the dog to be hospitalized and given immediate care, including IV fluids.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Ampicilline+ Salbactum 20–40 mg/kg IM, SC, PO QID for 5-7 days.	Veterinary formulations: Vetracillin 4.5gm ( Ampicilline+ Salbactum) Inj (Vetenza Animal Health Care India). Megaclox 3g ( Ampicilline+ Salbactum) Inj (megavet India).
Enrofloxacin: 10 mg/kg PO OD for 5-6 days.	Floxavet 100ml (100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml (100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin) tab (Vetoquinol India).
Minocycline: 5–25 mg/kg IV, PO BD	Human formulations: Divaine 100mg (1oomgMinocycline) Inj (Cipla India). Minyum 100mg (1oomgMinocycline) Inj (Glenmark India).

---

Nocardiosis in dogs — Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Canine Nocardiosis is a rare disease in dogs and most often causes infections of the skin, lymphatic system, and chest but sometimes spreads to multiple internal organs. It may be a zoonotic disease and is caused by Nocardia spp., which are gram-positive facultative intracellular bacteria belonging to the phylum Actinobacteria. They are ubiquitous, aerobic, and non-motile organisms. These organisms exhibit characteristic filamentous branching with fragmentation into bacillary or coccoid forms. They enter the body through the skin after an injury (such as dog bites or migrating plant material), contamination of wounds, or rarely by inhalation. Immunocompromised dogs with underlying disorders, for example, distemper, are commonly susceptible.

Pathogenesis

Nocardia strains enter host cells and disrupt host immune responses by preventing phagosome-lysosome fusion, neutralizing acidification, resisting oxidative stress, secreting superoxide dismutase, and modifying lysosomal enzymes in neutrophils and macrophages.

Clinical Symptoms

Common nonspecific signs are poor appetite, fever, lethargy, and weight loss. Infections beneath the skin are called mycetomas that have the appearance of nodules or tumors. Infection of lymph nodes is characterized by inflammation and swelling. There may be swelling and inflammation of the gums around the teeth and ulcers in the mouth accompanied by severe bad breath. Nocardiosis in the chest is characterized by pus-producing inflammation of the chest cavity leading to hypothermia, dyspnea, and weight loss. Occasionally, young dogs have a form of the disease that begins in the lower respiratory tract after inhalation of the organism and spreads throughout the body. In disseminated form, lesions are prominent within the body with abscesses in multiple organs.

Diagnosis

Wright-Giemsa staining and modified Kinyoun acid-fast techniques or histopathological examination by the Brown and Brenn method can show the presence of Nocardia organisms from sputum, pus, and tissue samples. PCR and RFLP can be used to confirm the diagnosis.

Treatment

Sulfonamides are the first-line antimicrobial drugs for the treatment of nocardiosis. Cefotaxime, Amikacin, and Imipenem-cilastatin are also effective. Prolonged use of antibiotics (5-6 months) is required for recovery from the disease.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Trimethoprim-sulfamethoxazole: 30–45 mg/kg, PO BID.	Human Formulation: Bactrim ( Trimethoprim- sulfamethoxazole) Syrup ( Abbot India). l Trim ( Trimethoprim- sulfamethoxazole ) Syrup (Leben Labs India). Bioprim ( Trimethoprim- sulfamethoxazole ) Syrup ( Zydus Cadila India). oysitrim( Trimethoprim- sulfamethoxazole ) syrup ( Oyster Labs India).
Cefotaxime: 25-50 mg/kg IV/IM/SC QID	Veterinary Formulations: Sitox -S 1500 mg ( 1500mg Cefotaxime and sulbactum) Inj ( Indian Genomix India).
Amikacin: 10-30 mg/kg IV/IM/SC OD	Veterinary Formulations: Kancin-vet 100ml( 250mg Amikacin/ml) inj vial( Morvel India). AmikaZep 100ml ( 250mg Amikacin/ml) inj vial (Rapid Life India). Amikin 30ml ( 250mg Amikacin/ml) inj vial ( Vets Pharma India).
Imipenem-cilastatin : 3-10 mg/kg slow IV TID .	Human Formulations: Zienam 250 mg Imipenem-cilastatin inj ( MSD INDIA). IMICRIT 250 mg Imipenem-cilastatin inj ( CIPLA INDIA). Zilamac 250 mg Imipenem-cilastatin inj ( Macleods INDIA). Zilamac 125 mg Imipenem-cilastatin inj ( Macleods INDIA). Cilaxter 250 mg Imipenem-cilastatin inj ( Alkem INDIA).

---

Yersinia infection in dogs-— Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Yersinia infection in canines is caused by Yersinia spp. such as Y. pestis, Y. enterocolitica, and Y. pseudotuberculosis. These are gram-negative facultatively anaerobic coccobacilli that belong to the family Enterobacteriaceae. Yersinia pestis serves as a vector-borne pathogen, transmitted through various flea species associated with rats and other rodents. While dogs are described as exhibiting resistance to plague infection, the occurrence of clinical illness in dogs is considered less frequent compared to that in cats. Diagnoses of yersiniosis in dogs occur much less often than in cats. The disease affects cats and dogs of all ages, though it appears to be more prevalent in adult animals. Although dogs are viewed as indicator species for plague surveillance, their association with human infections remains infrequent. In endemic regions, the presence of bubo-like lesions (lymphadenopathy) and hyperthermia should prompt immediate consideration of Yersinia pestis in free-roaming or hunting cats and dogs. The bubonic form of the disease is most commonly observed, typically affecting the mouth (resulting in necrotic stomatitis) and the mandibular or sublingual lymph nodes, especially when the infection is contracted through predation on infected rodents; drainage of abscesses is associated with a favorable prognosis.

Clinical Symptoms

Y. enterocolitica and Y. pseudotuberculosis have been identified in canine populations. Y. enterocolitica is also a commensal organism, often present in the feces of healthy dogs. Yersiniosis in canines may manifest as generalized, intestinal, or secondary focal infections. Clinical signs, including anorexia, cachexia, hematochezia, and lethargy, are noted in canines infected with Y. enterocolitica.

Diagnosis

Isolation and identification methods, such as quantitative direct culture, immunohistochemistry, autoagglutination, calcium dependency, and PCR, have been utilized in multiple studies to confirm cases of yersiniosis in dogs. Adult dogs have been diagnosed with hepatic yersiniosis due to Yersinia enterocolitica, which upon gross examination of the liver reveals white to yellow nodules comprising degenerated inflammatory cells, bacterial clumps, and cell debris, with histopathological findings indicating suppurative and necrotizing hepatitis confirmed by immunohistochemistry.

Treatment

Treatment typically involves the administration of broad-spectrum antibiotics, such as gentamicin and doxycycline.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Gentamicin: First drug of choice 6-12mg/kg IM/IV / SC OD for 3-5 days.	Veterinary Formulations: Gentamicin 100ml (40 mg Gentamicin/ml) inj vial(Zuche Pharmaceuticals India). Gentamicin 30ml(40 mg Gentamicin/ml) inj vial (Zuche Pharmaceuticals India). Genacyn LA 30ml(80 mg Gentamicin/ml) inj vial( Zenley Animal Health India). Gentamor Vet 100ml(40 mg Gentamicin/ml) inj vial( Morvel India).
Doxycycline : Second drug of choice 5 mg/kg PO BD for 5-10 days. 10 mg/kg PO OD for 5-10 days.	Veterinary Formulations: Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).
Trimethoprim-sulfamethoxazole: 30–45 mg/kg, PO BID.	Human Formulation: Bactrim ( Trimethoprim- sulfamethoxazole) Syrup ( Abbot India). l Trim ( Trimethoprim- sulfamethoxazole ) Syrup (Leben Labs India). Bioprim ( Trimethoprim- sulfamethoxazole ) Syrup ( Zydus Cadila India). oysitrim( Trimethoprim- sulfamethoxazole ) syrup ( Oyster Labs India).

---

Ehrlichiosis in dogs-— Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Ehrlichiosis is a serious disease impacting dogs, transmitted by the brown dog tick that carries the Rickettsiae bacteria, Ehrlichia canis (E. canis), a specialized bacterium that exclusively resides within other cells. This disease maintains a robust transmission cycle involving both ticks and dogs, with E. canis predominantly found in tropical and subtropical regions.

Clinical Symptoms

The disease presents in three distinct phases: an ‘acute’ phase, marked by early signs of illness; a ‘subclinical phase’ with no apparent symptoms; and a ‘chronic’ or long-term stage. The severity of the disease can vary significantly across these phases. The acute phase typically manifests 1 to 3 weeks after a tick bite and endures for about 2 to 4 weeks, showcasing symptoms such as fever, lethargy, swollen lymph nodes, anorexia, weight loss, and unusual bleeding or bruising. While some dogs may seem to recover completely from the acute phase, they can enter the subclinical phase, during which E. canis remains latent in the spleen or bone marrow for years, potentially leading to negative blood test results since the bacteria are not present in the bloodstream at this stage. Some dogs stay in this subclinical phase, while others progress to the chronic phase, exhibiting symptoms like fever, weakness, weight loss, pale gums, unusual bleeding, and discharge from the nose and eyes.

Diagnosis

A complete blood count (CBC) often reveals low hemoglobin levels and reduced platelet counts. Serology tests for Ehrlichia antibodies can remain positive for years, even after the infection has been cleared. The polymerase chain reaction (PCR) test is positive only during the active phase of the disease. Blood cultures are the definitive diagnostic test, requiring laboratory analysis for conclusive results, which may take up to eight weeks.

Treatment

Certain antibiotics, especially doxycycline, are highly effective; however, a prolonged treatment course, generally lasting four weeks, is essential. This treatment regimen is preferred due to its accessibility and general tolerability. Preventive measures are crucial in controlling tick populations, the primary vector of the disease. It is advisable to keep dogs away from tick-infested areas and utilize preventive medications from a veterinarian to mitigate the risk of infestation. Any ticks found on a dog should be removed promptly and correctly to prevent disease transmission. When removing ticks, use fine-pointed tweezers to grasp the tick’s head at the skin entry point, pulling it straight out without squeezing the body. If multiple ticks are present, seeking veterinary assistance for removal and examination of the dog is a prudent decision. Most dogs in the acute or subclinical phases will not require hospitalization and can be managed as outpatients at home with minimal supportive care (pain medications and appetite stimulants). Dogs with chronic ehrlichiosis may require hospitalization for aggressive supportive care that includes blood transfusions, steroids, IV fluids, and nutritional support.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Doxycycline : Drug of choice 5 mg/kg PO BD for 28 days. 10 mg/kg PO OD for 28 days.	Veterinary Formulations: Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

Section B: Bacterial Diseases in Cats

---

Feline chlamydiosis: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Feline chlamydiosis is caused by Chlamydophila felis and mostly affects the conjunctiva of cats. It is a contagious disease spread through eye discharge among cats that are in close contact. Kittens may become infected by their mothers during birth. C. felis is a gram-negative bacterium. It can also spread from the eye via the bloodstream to other organs such as the tonsils, lungs, liver, spleen, intestinal tract, and kidneys. So, infected cats’ urine, saliva, or other bodily fluids also serve as sources of infection. In most cats, conjunctival shedding ceases at around 60 days after infection, although some may continue to be persistently infected. Chlamydia spp. can infect the epithelial cells of the ocular, respiratory, gastrointestinal, and/or reproductive systems, although the association with disease in some of these systems is poorly understood. There is circumstantial evidence that Chlamydia spp. may cause reproductive disease.

Pathogenesis

Chlamydia spp. specifically target mucosal tissues, with C. felis primarily affecting the conjunctiva. This pathogen exists in two distinct forms: elementary bodies and reticulate bodies. The elementary bodies (EB) are minute, infective, extracellular entities capable of surviving in the external environment. In contrast, the reticulate bodies (RB) are larger, metabolically active forms that are non-contagious and serve a replicative function. Upon uptake of the infectious elementary bodies, they transform into reticulate bodies, which then replicate through binary fission within a membrane-enclosed vacuole in the host cell’s cytoplasm, successfully avoiding lysosomal fusion. Eventually, the reticulate bodies revert to the elementary body form, which are released into the extracellular space following cell lysis, thus enabling the infection of additional host cells. This entire replication cycle is efficiently completed in about 2 days. The incubation period prior to the onset of clinical signs typically ranges from 2 to 5 days, although it is worth noting that many cats remain asymptomatic following infection.

Clinical Symptoms

Unilateral eye disease often initiates but typically progresses to bilateral involvement. Severe conjunctivitis is characterized by pronounced redness of the third eyelid, squinting, and noticeable eye discomfort. Initially, eye discharges are watery, transforming later into mucoid or pus-like substances. Chemosis, or conjunctival swelling, is a common manifestation of chlamydiosis. While respiratory symptoms are generally mild with C. felis infections, they can include nasal discharge and noisy breathing. Ocular complications, such as conjunctival adhesions, may occur, but keratitis and corneal ulcers are usually not associated with chlamydia; should keratitis present, it is likely due to feline herpesvirus. Mild fever, loss of appetite, and weight loss may arise shortly after infection; however, the majority of cats maintain their health and continue to eat without issue.

Diagnosis

PCR techniques are now the preferred option for diagnosing chlamydial infections. PCR techniques are extremely sensitive and avoid problems with poor viability of the organisms. Ocular swabs are generally used as samples, but oropharyngeal, nasal, tongue, and vaginal swabs are also used for the detection of infection. Since the organism is intracellular, it is necessary to obtain good quality swabs that include the epithelial cells that the organisms have infected.

Treatment

Systemic antibiotics are more effective than topical treatments for chlamydial infections. Tetracyclines, especially doxycycline, are preferred because they require only one daily dose, usually 10 mg/kg orally, or 5 mg/kg twice daily if vomiting occurs. Doxycycline should be given with food or water to prevent esophagitis in cats. Treatment should last four weeks to fully eliminate the infection, as three weeks may not be enough. Sometimes, recurrence can happen after stopping the treatment. It’s also suggested to continue doxycycline for two weeks after clinical signs have resolved. While tetracyclines can have side effects in young cats, these are less common with doxycycline compared to oxytetracycline.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Doxycycline : Drug of choice 5 mg/kg PO BD for 28 days. 10 mg/kg PO OD for 28 days.	Veterinary Formulations: Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

*Septicemia in cats — Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Sepsis in cats presents a grave, life-threatening condition wherein the body’s response to infection incites widespread inflammation and subsequent organ damage. This syndrome is characterized by a systemic inflammatory response to infection that culminates in substantial morbidity, extended hospitalization, and alarmingly high mortality rates, especially among felines. Common bacterial pathogens responsible for septicemia in cats include Clostridium chauvoei and Streptococcus pyogenes.

Pathogenesis

The sequence of events commences with an infection that can originate from several sources, including bite wounds, penetrating trauma, or infections localized to organs such as the lungs, abdomen, or urinary tract. These bacteria can infiltrate the bloodstream (bacteremia) and proliferate. Upon detection of bacterial presence in the bloodstream, the body’s immune system initiates a systemic inflammatory response, marked by the release of inflammatory mediators, including cytokines (TNF-alpha, interleukins), that activate immune cells and promote inflammation. This inflammatory response can instigate significant alterations within the circulatory system; blood vessels may undergo dilation (vasodilation), resulting in low blood pressure (hypotension) and diminished blood flow to critical organs. Furthermore, damage to the endothelial lining of blood vessels may occur, leading to microthrombosis and exacerbating blood flow complications. Insufficient blood flow and oxygen delivery to organs can provoke organ dysfunction or failure, impacting vital systems such as the kidneys, liver, lungs, and brain. In severe instances, sepsis may advance to septic shock, a critical state characterized by profound circulatory, cellular, and metabolic derangements. The immune response to infection can become aberrant, leading to a phenomenon of immunoparalysis (immune dysfunction), making the cat increasingly vulnerable to secondary infections and deteriorating the overall prognosis.

Clinical Symptoms

Cats afflicted by sepsis frequently display symptoms including bradycardia (slow heart rate), hypothermia (low body temperature), hypotension (low blood pressure), and abdominal pain. The condition arises when the body’s inflammatory response to an infection becomes dysregulated, propagating throughout the system. Infections may stem from various sources, such as pneumonia, pyothorax (infection in the chest cavity), septic peritonitis (infection in the abdominal cavity), and open wounds.

Diagnosis

Diagnosis hinges on the assessment of clinical signs, including abnormal temperature, irregular heart rates, and increased respiratory rates. Blood analyses are pivotal, revealing critical markers such as abnormal white blood cell counts, anemia, diminished platelet levels, hyperglycemia, hypoalbuminemia, and elevated bilirubin levels. Additionally, critical evaluations encompass clotting assessments, blood gas analyses, and lactate testing. Urinalysis and imaging of the thoracic and abdominal regions via X-rays or ultrasound are indispensable, alongside cultures of blood, urine, or feces.

Treatment

Treatment protocols for sepsis in cats underscore the necessity of supportive care and the prompt management of the underlying infection. This includes the administration of intravenous fluids to stabilize blood pressure and enhance organ perfusion, coupled with antibiotics targeting infection eradication and oxygen therapy to mitigate tissue hypoxia. In extreme circumstances, the implementation of vasopressors and nutritional support becomes essential. Frequently employed antibiotics such as penicillin G, cefazolin, cephalothin, and cefotaxime play a critical role in addressing this condition. It remains imperative to conduct bacterial cultures and antibiotic sensitivity testing to ensure the accuracy and efficacy of antibiotic therapy.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Cefazolin: 20 mg/kg every 8-12 hours.	Human formulations: Reflin 250mg inj vial ( Sun Pharmaceuticals India). Reflin 500mg inj vial ( Sun Pharmaceuticals India). Reflin 1000mg inj vial ( Sun Pharmaceuticals India). Cezolin 250mg inj vial ( Lupin India). Cefadin 250mg inj vial ( Neon Labs India). Alcizone 250mg inj vial ( Alembic Pharmaceuticals India). Alcizone 500mg inj vial ( Alembic Pharmaceuticals India). Alcizone 1000mg inj vial ( Alembic Pharmaceuticals India).
Vancomycin 3.5 mg/kg IV followed by constant rate infusion of 1.5 mg/kg/h then 10-20mg/kg PO QID for 7days. .	Human formulation: Vanlid (250mg Vancomycin Hydrochloride) Cap (Cipla India). Vanking 500mg (500mg Vancomycin) Inj (Neon Labs India). Vancogram 500mg (500mg Vancomycin) Inj (Zydus India). Vancoray  500mg (500mg Vancomycin) Inj (Mylan Pharmaceuticals India). Vantox-CP 500mg (500mg Vancomycin) Inj (Samarth Life Sciences India). Vancotech CP 500mg (500mg Vancomycin) Inj (United biotech India).
Amoxicillin+Clavulanate: 10 mg/kg to 25 mg/kg BD for 5-7 days	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).

---

Cat-fight abscess— Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Cat fight abscesses arise from bite or scratch wounds incurred during altercations among cats. Such injuries, particularly those associated with biting, are susceptible to infection, resulting in the accumulation of pus beneath the skin, thereby forming an abscess. Isolated organisms may encompass aerobes including Pasteurella multocida, Actinomyces spp., staphylococci, rhodococci, enterococci, and streptococci, along with anaerobes such as Porphyromonas (formerly Bacteroides), Fusobacterium, and Peptostreptococcus sp.

Pathogenesis

In felines, an abscess is typically a consequence of a violent encounter. Cats’ teeth and claws are reservoirs for bacteria, and when a cat’s skin is perforated during a fight, these bacteria can be introduced into the subcutaneous tissue. An abscess forms when a bacterial infection is introduced beneath the skin’s surface. The bacteria proliferate, prompting an immune response characterized by inflammation, which in turn produces liquid pus, leading to the noticeable swelling associated with the abscess.

Clinical Symptoms

The abscess typically presents with significant pain and swelling, potentially leading to lethargy and reduced appetite in affected felines. A swelling on the skin, most commonly affecting the head, neck, limb, tail, or lower back. The skin around it is discolored, and pus oozes through the punctured wound.

Diagnosis

A physical exam of the swollen area and aspiration with a sterile needle confirm the presence of pus. X-rays show how much area is affected, while blood tests indicate whether there is a systemic issue. Culturing the pus helps to identify the type of infection and bacteria involved. If abscesses keep forming, further investigation is needed to rule out underlying conditions like retrovirus infection, osteomyelitis, or foreign body reactions. Chronic infections may be connected to actinomycetes, mycobacteria, bacterial L-forms, and fungi. Sending swab samples for bacterial culture can help identify the cause of the abscess, but if standard antimicrobial treatments based on sensitivity testing do not work, further investigation into the abscess’s causes is needed. Specific blood tests for feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) may be recommended, as these viruses can sometimes lead to more abscesses in some cats.

Treatment

The treatment protocol focuses on ensuring drainage, employing a chlorhexidine solution (0.5%) for flushing the abscess, in conjunction with systemic antimicrobial therapy continued over 5–10 days; standard agents include ampicillin, clavulanic acid, amoxicillin, and clindamycin, although penicillin G is also deemed effective in principle.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Amoxicillin+Clavulanate: 10 mg/kg to 25 mg/kg BD for 5-7 days	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).
Procaine Penicillin 30,000–50,000 U/kgIM, SC BID.	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Clindamycin: 10-15mg/kg IV/SC/PO ODor BID	Veterinary formulation: Clindapet 30ml ( 25mg Clindamycin/ml ) inj vial( Offered by Vea Impex India loyal pet zone/ India loyal pet zone India). Clindapet 300 (300mg Clindamycin) tab ( offered by Vea Impex India/ loyal pet zone India). Clivet 150 (150mg Clindamycin) tab ( Corise India). Goclin 150 (150mg Clindamycin) tab (Veko India). Petclind 450 (450mg Clindamycin) tab(Pet care India). Petclind 600 (600mg Clindamycin) tab (Pet care India).

---

Septic Arthritis in Cats— Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Feline septic arthritis is frequently instigated by bacteria such as staphylococci, streptococci, and coliforms. This condition may arise from infections disseminating through the bloodstream or as a consequence of trauma, including surgical interventions. Additional etiological factors include rickettsia and spirochetes.

Pathogenesis

The invading microorganisms elicit a significant inflammatory response within the joint. The host releases inflammatory cytokines (such as IL-1β and IL-6) and proteases, which have the potential to inflict damage on cartilage and surrounding joint tissues. The resulting increase in vascular permeability leads to the accumulation of fluid in the joint (edema), culminating in swelling, pain, and a diminished range of motion. In the absence of effective management of the infection and inflammation, these inflammatory mediators may further degrade cartilage and bone, resulting in irreversible joint damage and potential long-term disability. Elevated levels of matrix metalloproteinases (MMPs) exacerbate the destruction of cartilage. Bacterial surface proteins (MSCRAMMs) facilitate the adherence to and colonization of joint tissues by bacteria. Certain bacterial products serve to activate the host immune response, thereby contributing to tissue damage.

Clinical Symptoms

Clinical manifestations of septic arthritis encompass limping, swelling, joint pain, fever, fatigue, loss of appetite, and stiffness.

Diagnosis

Radiographic examinations may reveal fluid accumulation within the joint and potential damage over time. A joint fluid analysis typically indicates elevated white blood cell counts, particularly neutrophils, with the fluid often appearing purulent. Bacterial cultures are instrumental in confirming the diagnosis, while blood tests are conducted to investigate non-bacterial causes.

Treatment

Therapeutic interventions entail both intravenous and oral antibiotics, irrigation of the joint, and surgical intervention for severe cases. Septic arthritis presents a serious health challenge and may require several weeks for resolution. Prognosis varies depending on the timeliness of diagnosis and treatment. In cats, those with promptly diagnosed traumatic injuries generally require 6-8 weeks of antibiotics and demonstrate a favorable prognosis. Delayed intervention leads to enhanced joint damage and a poorer outcome. Cats experiencing severe septic arthritis that recover may be predisposed to chronic osteoarthritis. Additionally, felines with multiple joint complications may harbor an underlying blood infection, and those who undergo sepsis may ultimately recover, though they typically necessitate prolonged hospitalization and treatment.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Cefazolin: 20 mg/kg every 8-12 hours for 6-8 weeks.	Human formulations: Reflin 250mg inj vial ( Sun Pharmaceuticals India). Reflin 500mg inj vial ( Sun Pharmaceuticals India). Reflin 1000mg inj vial ( Sun Pharmaceuticals India). Cezolin 250mg inj vial ( Lupin India). Cefadin 250mg inj vial ( Neon Labs India). Alcizone 250mg inj vial ( Alembic Pharmaceuticals India). Alcizone 500mg inj vial ( Alembic Pharmaceuticals India). Alcizone 1000mg inj vial ( Alembic Pharmaceuticals India).
Clindamycin: 10-15mg/kg IV/SC/PO ODor BID for 6-8 weeks.	Veterinary formulation: Clindapet 30ml ( 25mg Clindamycin/ml ) inj vial( Offered by Vea Impex India loyal pet zone/ India loyal pet zone India). Clindapet 300 (300mg Clindamycin) tab ( offered by Vea Impex India/ loyal pet zone India). Clivet 150 (150mg Clindamycin) tab ( Corise India). Goclin 150 (150mg Clindamycin) tab (Veko India). Petclind 450 (450mg Clindamycin) tab(Pet care India). Petclind 600 (600mg Clindamycin) tab (Pet care India).

---

*Campylobacteriosis in Cats — Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Campylobacteriosis, caused by various Campylobacter species, is infrequently observed in cats; however, when it does arise, it predominantly affects kittens younger than six months. The bacteria responsible for this disease are commonly found in the gastrointestinal tracts of most healthy mammals and generally remain harmless. A significant portion of stray cats harbor campylobacter bacteria, which are excreted through feces, posing a risk to other species, including humans, who may inadvertently come into contact with it. The primary mode of transmission for cats is through kennels, where they can directly encounter contaminated feces. Ingesting tainted food or water represents another transmission pathway, particularly in settings with poor food hygiene, such as animal shelters or households with several pets. Additionally, younger animals face a higher risk of contracting the disease due to their developing immune systems and tendency to explore their surroundings by tasting or chewing on contaminated objects.

Pathogenesis

Gastric acid acts as a barrier, but bacteria must reach the small and large intestines to grow; C. jejuni invades epithelial cells and those in the lamina propria. Virulent Campylobacter spp. attach to and enter enterocytes after getting through the mucus layer. They survive in the cytoplasm of enterocytes and avoid lysosomal compartments. C. jejuni produces toxins that harm the gut lining. The disease caused by Campylobacter involves secretion systems and toxins, including the virulence factor CDT (cytolethal distending toxin). This results in symptoms such as diarrhea, loss of appetite, vomiting, and fever lasting from 3 to 7 days.

Clinical Symptoms

Typical symptoms include mucus-laden, watery, or bile-streaked diarrhea (with or without blood) lasting from 5 to 15 days; reduced appetite; abdominal pain; and occasional vomiting, with fever potentially present. Diarrhea can be persistent, lasting more than two weeks for some cats, particularly those under six months old, where it appears most severe.

Diagnosis

To diagnose campylobacteriosis, veterinarians will analyze the cat’s feces for signs of infection, with a fecal culture being the standard diagnostic method employed. After 48 hours, the veterinarian will assess the culture for leukocytes (fecal white blood cells) in the stool, an indicator of infection, which may also be present in the gastrointestinal tract, confirming the bacterium’s existence. A complete blood profile, including a chemical blood analysis, a complete blood count, and urinalysis, will also be performed to provide comprehensive insights into the cat’s overall health and guide treatment options.

Treatment

Mild cases typically warrant outpatient treatment, enabling the cat to recover in a familiar setting under the owner’s watchful eye. Conversely, severe cases of campylobacteriosis necessitate close monitoring to avert complications such as dehydration or secondary infections. Veterinarians often recommend isolating the affected cat to prevent transmission to others, ensuring it can recover fully without the risk of spreading the infection within a multi-pet environment. Administering oral fluid therapy to treat or fend off dehydration, along with providing antibiotics, forms a crucial part of an effective treatment strategy. In more serious instances, a plasma transfusion may become necessary to supply vital nutrients and bolster the compromised immune system, facilitating a swift recovery. Understanding campylobacteriosis dynamics in feline patients not only enhances treatment efficacy but also promotes better preventive actions to safeguard both pets and humans against this potentially harmful pathogen. Macrolides or quinolones are utilized when diarrhea is persistent, with macrolides being the preferred choice due to potential resistance.

Drugs and formulations available in India.

Erythromycin: First choice 10-20 mg/kg PO TID for 5 days.	Eycin-Ws 100g (200mg Erythromycin/g)powder ( IPPL India). Althrocin Ikg(200mg Erythromycin/g) powder( Alembic India). Benison 250g/1kg(100mg Erythromycin/g) powder( Benison Farm Vet India)
Tylosin: Another option 25mg/kg PO BD for 7 days.	Trox 50g /120g Powder ( Verbac India ).

---

Helicobacter infection in Cats— Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Helicobacter spp. are found in the stomachs of both healthy and vomiting dogs and cats, but their role is not fully understood. In humans, H. pylori infections are linked to gastritis and ulcers, but similar connections in dogs and cats have not been proven. These are spiral, gram-negative, motile bacteria, with species like H. canis, H. felis, H. heilmannii, and H. bizzozeronii more common in pets. At least 38 Helicobacter species exist in animals, and infected pets can carry multiple types at once. They are usually found in the gastric tissue of pets, especially in the gastric fundus and cardia, and also in the intestines and liver. Helicobacter has been seen in the liver of a dog with necrotizing hepatitis and in healthy cats as well as those with cholangiohepatitis. It’s unclear if the bacteria can transfer between dogs and cats, and no reservoir hosts have been identified. Most healthy dogs and cats test positive for Helicobacter, with similar results in vomiting pets.

Pathogenesis

Colonization of the gastric mucosa mainly occurs in the surface mucus and in gastric glands and parietal cells. Helicobacter organisms produce an enzyme called urease which turns urea into ammonia and carbon dioxide, helping them survive by neutralizing stomach acid. Their flagella allow movement on epithelial surfaces, while adhesins (outer membrane proteins) assist in sticking to cells. They also have a type IV secretion system that delivers the CagA protein into host cells, which increases inflammation, disrupts cell functions, and heightens cancer risk. Cytokines like IL-8 attract neutrophils and lymphocytes, leading to tissue damage. Persistent inflammation can cause ulcers in the stomach or duodenum by damaging the mucosa and reducing protective mucus. Another toxin, Vacuolating Cytotoxin A (VacA), is released by the bacteria into gastric cells, causing vacuolation and eventually cell death.

Clinical Symptoms

In dogs and cats, gastritis, vomiting, and diarrhea have been associated with Helicobacter infection, though a direct causal relationship has yet to be confirmed. Peptic ulceration is infrequent in relation to Helicobacter infections in these animals. The relationship between Helicobacter infection and the risk of gastric neoplasia in dogs and cats remains unclear.

Diagnosis

Diagnosing these infections usually involves upper GI endoscopy or exploratory laparotomy to collect surface mucus samples from the stomach. This method is sensitive due to the large sampling area. Organisms can be identified with a 100X oil-immersion lens. Biopsies should be taken from various areas due to the uneven distribution of organisms. Standard H&E staining is typically enough for identification, but special silver stains might be needed for organisms in glandular tissues. Infections may cause mucosal inflammation, glandular degeneration, and hyperplasia of lymphoid follicles. Although cytological and histological tests might not identify specific species, a rapid urease test can confirm the presence of Helicobacter or other urease-producing bacteria. However, since these tests are sensitive and specific for detecting Helicobacter infections, urease testing may not always add useful information. Research is ongoing for noninvasive tests for Helicobacter infection, such as urea breath tests, fecal antigen detection, and serological testing, which are not yet available commercially.

Treatment

Numerous veterinary studies have indicated that eradicating Helicobacter infections is often challenging. Recommended treatment regimens typically involve a combination of amoxicillin or tetracycline, metronidazole, bismuth subsalicylate, and a proton pump inhibitor (such as omeprazole) or H2-receptor blocker (such as famotidine) for a duration of 2–3 weeks. Other treatment combinations, like those involving omeprazole and azithromycin or clarithromycin, have also been documented. Oral treatment protocol for Helicobacter in cats includes a combination of clarithromycin 5 mg/kg q12h PO, amoxicillin 20 mg/kg q8h PO, and omeprazole 0.7-1.0 mg/kg q24h PO for two to three weeks. The other protocol uses a combination of amoxicillin (20 mg/kg q8h PO), metronidazole 10 mg/kg q8h PO, and famotidine 0.5-1.0 mg/kg q24h PO for two to three weeks, but this might be slightly less effective. Although many dogs and cats receiving these treatment combinations did not achieve long-term eradication of Helicobacter infection upon retesting, a notable reduction in the frequency of vomiting and gastric lesions was observed in many patients who underwent therapy.

Drugs and formulations available in India.

Amoxicillin; 20mg/kg PO BD for 2-3weeks	Mentin D S with Amoxicillin and Clavulanate 30 ML dry syrup (Corise India).
Clarithromycin: 5 mg/kg PO BD for 2-3weeks	Human formulation: Cloff 250(250mg Clarithreomycin ) dry syrup (Alembic India). Bioclar 125 (125mg Clarithreomycin ) suspension (Zydus India).
Tetracyclin : 10mg-33mg/kg PO BD for 2-3weeks	Tetracycline WSP 100gm (50 mg Tetracycline hydrochloride /g) sachet (MSD India).
Pantoprazole: 1mg/kg PO BD for v2-3 weeks.	Pantopet 20 (20mg Pantoprazole) Tablets (Sihil Animal Health India) Oriheal Palapan Vet 20 (20mg Pantoprazole) Tablets (Oriheal India).

---

Feline infectious anaemia (FIA) — Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Feline infectious anaemia (FIA) is a disease of RBCs and is caused by Mycoplasmas bacterias. These bacteria are called ‘Haemoplasmas’. The main types causing FIA are Mycoplasma haemofelis, Candidatus Mycoplasma haemominutum, and Candidatus Mycoplasma turicensis. M. haemofelis is most likely to cause severe anaemia, while the others can cause mild or no anaemia. Cats can be infected with more than one type at the same time, and many infected cats may not show symptoms unless their immune system is weakened, such as from infections like feline leukaemia virus (FeLV) or feline immunodeficiency virus (FIV). Haemoplasmas can stay in an infected cat for a long time, possibly for life. How these bacteria spread among cats is not entirely clear, but likely methods include blood transfusions, fighting, biting insects (like fleas), and transmission from mother cats to their kittens.

Pathogenesis

Haemoplasmas reside on the surface of red blood cells (RBCs) and are capable of invading the cell itself. By adhering to the RBC surface, they inflict damage, potentially leading to cell destruction referred to as haemolysis or red cell death. Consequently, if a significant number of RBCs are destroyed, it can result in the development of anaemia, characterized by a reduced red blood cell count. The cat’s immune system may play a crucial role in the destruction of the infected RBCs as it endeavors to eradicate the bacteria that are bound to them.

Clinical Symptoms

Acute infection with M. haemofelis can result in severe, sometimes life-threatening anemia, although many cats may exhibit only mild anemia. In severe cases, symptoms include a rapid heart rate, rapid breathing, and varying pulse strength, accompanied by heart murmurs. Jaundice is uncommon. enlarged lymph nodes and spleen can also be observed. Other signs of acute haemoplasma infections include lethargy, weakness, decreased appetite, dehydration, weight loss, and intermittent fever (greater than 39.2 °C). Chronic infections typically do not lead to significant anemia, and some cats may harbor the infection asymptomatically, though the disease can reactivate. Younger cats are more likely to experience severe symptoms from M. haemofelis infection. Subclinical infections can occur with all three feline haemoplasma species.

Diagnosis

A blood sample confirms a diagnosis of FIA. Infected cats should be screened for other illnesses like FeLV and FIV, which can complicate Haemoplasma infections. PCR is the best diagnostic method, identifying the infecting species. These infections typically cause regenerative macrocytic hypochromic anemia, although reticulocyte counts may vary. A positive Coombs’ test and autoagglutination can occur in acute cases, indicating erythrocyte-bound antibodies. Blood smears stained with Romanowsky-type stains can show haemoplasmas on red blood cells, but this method is unreliable for species differentiation. Haemoplasmas cannot be cultured, and antimicrobial sensitivity testing is not feasible.

Treatment

Doxycycline treatment for 2 weeks is generally effective for uncomplicated M. haemofelis-related clinical disease; and should be given with water or food to prevent esophagitis. Infection may not be fully cleared even if symptoms improve. If only partial improvement occurs, treatment can continue beyond 2 weeks. Fluoroquinolones for example Pradofloxacin at5-7.5mg/kg PO twice a day can serve as second-line treatments if doxycycline isn’t effective or if infection clearance is necessary.

Drugs and formulations available in India.

Drug and dose	Veterinary And Human Formulations
Doxycycline : Drug of choice 5 mg/kg PO BD for 28 days. 10 mg/kg PO OD for 28 days.	Veterinary Formulations: Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

*Pyoderma in cats — Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Pyoderma in cats is a definitive skin infection marked by the presence of pus, literally translating to “pus in the skin.” While it may not be the initial concern, it often arises as a consequence of other underlying issues that compromise the skin’s integrity, leaving it vulnerable to bacterial overgrowth. This condition is frequently spurred by irritants or damage to the skin, fostering an environment conducive to bacterial proliferation.

Pathogenesis

Common predisposing factors include: Allergies (flea allergies, food allergies, or environmental allergies induce inflammation and itching, paving the way for secondary bacterial infections), scratches obtained during fights, parasites (mites such as Demodex, fleas, or other parasites irritate the skin, enhancing the likelihood of pyoderma), and fungal infections. Conditions like feline acne, seborrhea, or autoimmune diseases further increase a cat’s predisposition to pyoderma. Disorders such as diabetes, hyperthyroidism, or feline immunodeficiency virus (FIV) compromise the immune system, elevating the risk of infections. Pyoderma is predominantly the result of an overgrowth of Staphylococcus pseudintermedius and Pasteurella multocida. Other bacteria, including S. aureus, S. felis, and secondary invaders such as Pseudomonas spp., Proteus spp., and Escherichia coli, can also play a significant role, especially in chronic or deep cases. There are two primary types of pyoderma: Deep Pyoderma: This severe form penetrates deeper into the skin, potentially reaching the dermis and leading to serious complications, such as cellulitis or bacteria entering the bloodstream. On the other hand, Superficial Pyoderma: This type affects the outer layers of the skin and hair follicles. It is predominantly caused by bacteria like Staphylococcus and occurs more frequently than deep pyoderma.

Clinical Symptoms

Symptoms of pyoderma vary depending on the infection’s depth and severity, with common signs including red, raised bumps (papules) or pustules (pus-filled bumps), crusting and scaling, hair loss (alopecia), itching (pruritus), ulcers or open sores, and draining tracts (in deep pyoderma).

Diagnosis

Diagnosis of pyoderma involves meticulous examination of skin lesions, often taking samples for microscopic analysis (cytology) to pinpoint bacteria and inflammatory cells. It is important to carry out bacterial culture and sensitivity tests to identify the specific bacteria involved and determine the most effective antibiotics. Furthermore, an investigation into potential underlying causes through various tests (e.g., allergy testing, blood work) is essential.

Treatment

Treatment involves the use of antibiotics: Oral or topical antibiotics are routinely prescribed to eliminate the bacterial infection, with the type and duration of therapy tailored to the severity and type of pyoderma. Topical treatments: Medicated shampoos, sprays, or creams containing antibacterial or antiseptic agents are utilized, particularly for superficial infections. Antiparasitic medications: Appropriate antiparasitic drugs are administered when parasites are involved. Addressing underlying conditions: Managing allergies, hormonal imbalances, or other diseases is crucial to avert recurrence. Supportive care: Treatment may include medications to alleviate itching, whirlpool baths for deep infections, and meticulous wound care. The prognosis for pyoderma in cats is generally very favorable, especially when the infection is identified early and treated appropriately. Superficial pyoderma typically resolves within a few weeks of treatment, while deep pyoderma may necessitate a longer treatment period.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Clindamycin: 10-12.50 mg /kg PO/SC OD for 4wks.	Clindapet 30ml( 25mg Clindamycin/ml ) inj vial( Offered by Vea Impex India loyal pet zone/ India loyal pet zone India). Clindapet 300(300mg Clindamycin) tab (offered by Vea Impex India/ loyal pet zone India). Clivet 150(150mg Clindamycin) tab( Corise India). Goclin 150 (150mg Clindamycin) tab (Veko India). Petclind 450 (450mg Clindamycin) tab (Pet care India). Petclind 600 (600mg Clindamycin) tab (Pet care India).
Amikacin: 10-14 mg/kg IM/IV/SC OD for 3-5days.	Kancin-vet 100ml( 250mg Amikacin/ml) inj vial( Morvel India). AmikaZep 100ml ( 250mg Amikacin/ml) inj vial (Rapid Life India). Amikin 30ml ( 250mg Amikacin/ml) inj vial ( Vets Pharma India).
Enrofloxacin: 2.5 mg-5mg/kg IM/IV OD for 5-10days. 5mg-20mg/kg PO OD for 5-10 days. NB: Avoid in young animals. Provide supportive treatment as per requirement.	Fortivir 30 ml (100mg Enrofloxacin/ml) inj vial( Verbac India). Floxidin 100ml (100mg Enrofloxacin/ml) inj vial (MSD india). Efx -LA 100ml (120mg Enrofloxacin/ml) inj vial(Parex India). Enolox-K 30ml (100mg Enrofloxacin and 60 mg Ketoprofen/ml)inj vial( Zenley Animal health). Enrovet 100ml (100mg Enrofloxacin/ml) inj vial ( Vets Pharma India). Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Cephalexin: 20-30mg/ kg PO BD .	Lexin 300mg cephalexin tab( Virbac India). Lexin 20g sachet( Virbac India). Lexin 30g powder( Virbac India). Vetalexin 300mg cephalexin tab ( Indian Immunological). Celex 250 oral dry syrup( Indian Genomix).
Cefpodoxime: 5mg/ kg PO BD or 10mg /kg PO OD X 7 days .	CefPetXL 100 (100mg ) tab( Intas India). CefPetX 200 ( 200mg cefpodoxime) tab( Intas India). CefPetXL 30ml (12.95g cefpodoxime) dry syrup( Intas India). Hatpod DS 30ml (100mg cefpodoxime/ml) syrup( Hatvet India). Cef DP- 100 (100mg cefpodoxime) tab ( SkyEc India). Cefvet-200( 200mg cefpodoxime) tab ( Malick Licenses Private Limited India)
Cefovecin: 8mg/ Kg Sc OD single injection.	Convenia 10ml(80mg Cefovecin/ml) inj vial (Zoetis India).
Amoxicillin+Clavulanate: 20mg/kg PO QID for 5-7 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg(400mg Amoxicillin and 100mg Clavulanate ) tab( Savavet India).
Marbofloxacin: 2.75- 5.5mg /Kg PO/ IM OD for 5- 10 days.	Marbidac 30ml(16% Marbofloxacin) Injection (Zydus India). Marbofloxacin 20 ml (10% Marbofloxacin) Injection Vial (Credence Remedies India). Marbofloxacin 50 ml (10% Marbofloxacin) Injection Vial (Credence Remedies India). Marbofloxacin 100 ml (10% Marbofloxacin) Injection Vial (Credence Remedies India). Marbomet 30ml(100 mg Marbofloxacin/ml ) injection Vial ( Intas Pharmaceutical India). Marbomet 50(50mg Marbofloxacin) tab ( Intas Pharmaceutical India).

---

*Salmonellosis in cats -— Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Salmonellosis in cats is an uncommon disease and healthy cats are carriers of the bacteria without showing any disease signs. Salmonella is a gram-negative bacterium, which is commonly found in the intestinal tract of cats but can also be found in the blood or other organs of the body. Salmonella is a foodborne pathogen that belongs to the family Enterobacteriaceae. Salmonella in cats can be transmitted to humans through contaminated food. In cats, it can cause many different types of infections, such as an acute or chronic intestinal infection/inflammation (enteritis), or more severe infections such as septicemia (sepsis), a bacterial blood infection. Salmonella can affect a cat of any age and any breed, but young or much older cats have an immature or weakened immune system that tends to be more susceptible. Antibiotic therapy can leave a cat more likely to get salmonella because the “good bacteria” is killed as well, causing them to be more vulnerable to infection. Other predisposing factors are underdeveloped GIT, inflammatory bowel disease, and cancer.

Pathogenesis

Under favorable conditions, Salmonella bacteria colonize the digestive tract, particularly the small and large intestines, where they invade enterocytes and lymphoid tissue, causing an inflammatory response that leads to symptoms like diarrhea. This invasion involves changes to the intestinal cellular structure, and in severe cases, can extend beyond the intestines to cause systemic infections such as septicemia, conjunctivitis, or pneumonia. The immune system typically responds to control the infection, but in cats with weakened immunity or chronic conditions, Salmonella can evade these defenses, resulting in more severe disease.

Clinical Symptoms

The clinical signs present with anorexia, fever, nausea, vomiting, and acute gastroenteritis, accompanied by abdominal pain and diarrhea. Additionally, dehydration, rapid or troubled breathing, yellowing of the skin and other white membranes such as the eyes (jaundice), drooling, and pale gums clearly indicate systemic involvement.

Diagnosis

A repeat positive culture is diagnostic of Salmonella infection in cats, particularly in those without clinical signs, as multiple positive tests can indicate an infection. A bacterial culture analyzes a sample of your cat’s feces to detect the presence of Salmonella. In cases where cats are suspected of being asymptomatic carriers, isolating the bacteria can prove challenging due to intermittent shedding and low bacterial counts in the stool, complicating capture efforts. If there is a suspicion of sepsis, a blood culture may be performed to identify Salmonella in the bloodstream. Following a positive diagnosis and treatment for Salmonella, it is advisable to repeat the bacterial culture after three to four weeks to ensure the infection has been resolved.

Treatment

Most cats can recover from salmonellosis on their own if diarrhea is the only symptom. More severely affected cats will need supportive care for additional symptoms. Intravenous fluids are crucial for maintaining hydration and blood pressure. Antibiotics are reserved for cats with life-threatening symptoms or signs of shock or sepsis, as they can lead to longer shedding of bacteria in stool. The preferred antibiotic choices include ampicillin, third-generation quinolones such as ciprofloxacin and levofloxacin, third generation cephalosporins like ceftriaxone, and macrolides. Other treatments include NSAIDs, anti-nausea medications and an appetite stimulant. In severe cases, a feeding tube may be necessary, and hospitalization might be required depending on your cat’s condition.

Drugs and formulations available in India.

Drug and Dose	Veterinary and Human nformulations
Ciprofloxacin: 20 to 25 mg/kg PO OD or 10-12.5mg/kg PO BD in dog and cat.	Human Formulations: Ciplox 250 ( ciprofloxacin 250mg)tab (Cipla India). Ciplox 50o( ciprofloxacin 500mg)tab (Cipla India). Cifran 250 ( ciprofloxacin 250mg)tab ( Sun India). Cifran 500 ( ciprofloxacin 500mg)tab ( Sun India). Cipribid 250 ( ciprofloxacin 250mg)tab ( Zydus India). Cipribid 500 ( ciprofloxacin 500mg)tab ( Zydus India). Alcipro 250 ( ciprofloxacin 250mg)tab (Alembic India). Alcipro 500 ( ciprofloxacin 500mg)tab (Alembic India). Zoxan 250 ( ciprofloxacin 250mg)tab (FDC India). Zoxan 500 ( ciprofloxacin 500mg)tab ( FDC India).
Ceftriaxone : 25 to 50 mg/kg IV/IM BD for 5-7days.	Vetrinary Formulatio0ns: Intacefpet 500 ( 500mg ceftriaxone ) inj ( Intas India). Logipet 500 ( 500mg ceftriaxone ) inj ( Medilogy Biotech India). Promicef 500 ( 500mg ceftriaxone ) inj ( ZSava Vet India).
Levofloxacin : 10mg/kg PO OD for 5days	Griptol-N 60ml(Levofloxacin 100 mg and Ornidazole 200 mg /5ml) oral solution( Intas India).

---

*Bordetellosis in cats- Disease description , Drugs and formulation in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease discription.

Etiology

Feline Bordetellosis in cats is caused by Bordetella bronchiseptica, a bacterium that significantly affects their health. This Gram-negative rod primarily targets the respiratory tracts of different animals, including dogs, cats, swine, and rabbits. It grows well in various environments, thriving on media like blood agar, MacConkey agar, and specifically designed media such as Smith-Baskerville and Regan-Lowe transport mediums. The optimal growth temperature is between 35 to 37 °C, which is similar to the body temperature of its hosts. Smith-Baskerville medium specifically aids in isolating B. bronchiseptica for study. It can also thrive on enriched media with cephalexin to limit competing bacteria or in Stainer-Scholte broth. The colonies are small, grayish-white, and shiny. The bacterium is sensitive to common disinfectants, making sanitation essential in outbreak-prone areas. Bordetella bronchiseptica spreads easily through direct contact or aerosol droplets from coughing or sneezing. Dogs with respiratory issues can infect vulnerable cats, emphasizing the need to monitor interactions between different species, especially in homes with multiple pets. Additionally, B. bronchiseptica can survive in the environment and within amoebae, which can help it spread, making control more challenging.

Pathogenesis

Pathogenesis of Bordetellosis – Bordetella bronchiseptica adheres to ciliated respiratory epithelium, producing adhesion and cytolytic toxins that lead to an inflammatory response, antiphagocytic activity, and dermonecrosis. This bacterium primarily targets the respiratory system, where it damages the respiratory lining by releasing various virulent factors that disrupt normal cellular function. These factors can promote a cascade of inflammatory reactions that further compromise the host’s defenses. Furthermore, the release of these toxins can potentially lead to ciliary dysfunction by paralyzing ciliary movement, which is crucial for clearing mucus and pathogens from the airways. As ciliary function diminishes, the clearance of respiratory secretions becomes increasingly inefficient, thereby increasing the risk of serious lower respiratory infections. In immunocompromised individuals or those with pre-existing respiratory conditions, the impact of Bordetella bronchiseptica can be particularly severe, resulting in prolonged illness and the potential for secondary complications, emphasizing the importance of understanding this pathogen’s mechanisms for effective prevention and treatment.

Clinical Symptoms

Bordetella bronchiseptica infection can manifest a wide range of symptoms, which vary greatly in severity—from mild illness characterized by fever, coughing, sneezing, ocular discharge, and swollen lymph nodes to severe pneumonia that results in shortness of breath, cyanosis, and potentially death if left untreated.

Diagnosis

Diagnosis is established through bacterial culture and PCR techniques. Samples for isolation can be obtained from the oropharynx (via swabs) or through methods such as transtracheal wash or bronchoalveolar lavage. Prompt antibacterial therapy is indicated, even in mild cases, to prevent progression. In instances where sensitivity data are unavailable, the effective treatment includes tetracyclines, with doxycycline often being the antimicrobial of choice due to its effectiveness against B. bronchiseptica. Cats diagnosed with severe B. bronchiseptica infection require not only antibacterial treatment but also supportive therapy and intensive nursing care to ensure recovery.

Treatment

For preventive measures, a modified-live vaccine product is licensed for use as a single vaccination with annual boosters. However, it is essential to note that routine vaccination against B. bronchiseptica in cats is generally not recommended (classified as non-core), since the infection typically leads to only mild disease, and over-vaccination can pose unnecessary risks. Thus, maintaining awareness of this infection within and around feline populations is crucial for optimal health management.

Drugs and formulations available in India.

Drug and Dose	Veterinary and Human nformulations
Tetracycline : 10mg-33mg/kg PO BD x 3-5 days in cats.	Vetrinary Formulatio0ns: Tetracycline WSP 100gm (50 mg Tetracycline hydrochloride /g) sachet( MSD India). Nucocin 500 mg Tetracycline Bolus( Nugen Pharma India).
Doxycycline : Drug of choice 5 mg-10 mg /kg PO BD for 28 days.	Vetrinary Formulatio0ns: Dclat 100 g (200mg Doxycycline/g) powder(IPPL India). Doxypet 300(200mg Doxycycline) tab(Sava Vet India). Doxymust 100 (100mg Doxycycline) tab(Sky-Ec India). Doxymust 300(300mg Doxycycline) tab(Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

*Pasteurella infection in Cats —Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description:

Etiology

Pasteurellosis in cats is a significant zoonotic disease, is attributable to Pasteurella multocida . Pasteurella are Gram-negative, encapsulated, non-hemolytic, non-spore-forming, coccobacilli and facultatively anaerobic bacteria. These bacteria are typically cultured on sheep blood agar or chocolate agar media. Pasteurella species are commonly isolated from subcutaneous abscesses and pyothorax in cats. While usually harmless, these organisms can become pathogenic, particularly when cats experience stress or immunocompromised states, leading to non-zoonotic respiratory and digestive diseases. They are commonly implicated in zoonotic bite wound infections in cats, with human infections arising from scratches and bites from dogs, or from exposure to cats wounds. The bacteria are transmitted through bites or by licking open wounds, posing a risk of zoonotic bite wound infections. Bacteria usually enter through skin wounds, but inhalation of secretion droplets from the upper respiratory tract is another possible source.

Clinical Symptoms

Clinical manifestations associated with P. canis infections include pyoderma, cutaneous abscesses in animals, and sometimes osteomyelitis, systemic bacteremia and septic arthritis. It is also one of the common bacteria producing pyothorax in cats. Pasteurella species may also cause secondary lower respiratory tract infection and have been associated with spinal empyema and meningoencephalomyelitis.

Diagnosis

Laboratory identification of Pasteurella species is achieved by culturing the bacteria (isolated from wounds) on sheep blood agar, resulting in pale gray mucoid non-hemolytic colonies that emit a “mousy odor” and exhibit a blue halo under oblique lighting. P. multocida is noted to be oxidase-positive, catalase-positive, ornithine decarboxylase positive, indole positive, mannitol positive, and urease negative, whereas P. canis is characterized as ornithine, indole, and mannitol negative.

Treatment

Pet owner must exercise caution when interacting with a cats mouth and prioritize the oral hygiene of their pet. Protective gloves and masks are essential when addressing a cats wounds. It is imperative to use sanitizers before and after handling any cat injuries. Scratches inflicted by pets should not be dismissed lightly; they must be thoroughly cleansed with antiseptic soap and appropriate germicides. Pasteurella species demonstrate susceptibility to a broad range of antibiotics, with penicillin derivatives such as potentiated amoxicillin, potentiated ampicillin and penicillin G, p being the most effective treatment options.  Quinolones, cephalosporins and modern macrolides are also indicated.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Amoxicillin+Clavulanate: 20mg/kg PO QID for 5-7 days.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate) tab( Savavet India).
Ampicillin: 20–40 mg/kg IM, SC, PO QID for 5-7 days.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).
Procaine Penicillin 100,000 IU/kg IM, SC TID	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).

---

Pyelonephritis in cats: —Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description

Etiology

Pyelonephritis in cats is a kidney infection primarily caused by bacteria that ascend the urinary tract from the bladder to the kidneys, with Escherichia coli and Staphylococcus being the most prevalent bacteria. Other bacteria such as Proteus, Streptococcus, Klebsiella, Enterobacter, and Pseudomonas can also invade the lower urinary tract and ascend to the upper urinary tract. While less common, anaerobic bacteria and fungal organisms can contribute to pyelonephritis as well. Developmental conditions like ectopic ureters, vesicoureteral reflux, and renal dysplasia significantly increase the risk of this kidney infection. Furthermore, medical conditions and procedures such as diabetes mellitus, kidney failure, urine retention, bladder and kidney stones, steroid medications, catheterization of the urethra, and urethrostomy increase the likelihood of urinary tract infections.

Pathogenesis

The urinary tract naturally defends against infections through mechanisms like mucosal barriers, valves, ureteral movement, and good blood supply. Any weakness in these defenses can lead to urinary tract infections (UTIs). Factors such as low urine concentration, changes in urine composition, vesicoureteral reflux (VUR), kidney stones, poor urine flow, and weak immune responses heighten the risk of UTIs. Normally, the vesicoureteral valve ensures urine flows one way, but VUR allows urine to flow back into the kidneys, particularly under pressure from obstructions like tumors or stones. Urine stasis from these issues or nerve problems can further increase UTI risk. Bacteria like E. coli can disrupt ureteral movement, worsening VUR, and structural problems in dogs may also lead to lower urinary tract disease. Kidney failure lowers urine concentration and changes urine composition, contributing to UTIs. The renal medulla can easily get infected due to low blood supply and high osmolality, which reduces immune response effectiveness. When bacteria grow in the renal pelvis, they can spread through the collecting ducts, causing damage and inflammation. Certain bacteria have virulence factors that help them attach and increase UTI risk, with E. coli being the most common cause in dogs and cats. Some conditions, like Cushing’s disease or immune-mediated diseases, can weaken the immune system and lead to higher chances of infections, including pyelonephritis. Other viruses like feline leukemia and immunodeficiency can also compromise immunity, making infections more likely.

Clinical Symptoms

Symptoms of pyelonephritis include polydipsia, polyuria, straining during urination, fever, pain and discomfort, hematuria, vomiting, and anorexia; however, not all symptoms may manifest in every affected cat, and some may show no signs of the disease at all.

Diagnosis

Diagnosis of pyelonephritis relies on clinical signs, urine examinations, kidney function tests, urine cultures, ultrasound, and X-ray findings. PM findings in acute feline pyelonephritis are large dark red firm kidneys with tubular necrosis whereas deep, irregular cortical depressions with fibrosis are seen in Chronic pyelonephritis. Other observations may include tubular dilation, leukocytic casts in the tubules, and eventual glomerular obliteration.

Treatment

Treatment of cats with pyelonephritis is based on diagnostic reports, if underlying kidney disease exists, treatment may include a specialized kidney support diet. Surgical intervention is employed for repositioning ectopic ureters to ensure proper urine drainage, while urinary tract obstructions caused by bladder stones are treated as medical emergencies, often requiring surgery. Antibiotics are selected based on urine testing for bacteria and antibiotic sensitivity, ensuring they are effective at killing bacteria, maintain appropriate levels in the blood and urine, and pose no toxicity to the kidneys. Generally, antibiotics are administered for 4–6 weeks. For cats with pyelonephritis, broad-spectrum antibiotics are typically given for 4–8 weeks, often at higher dosages than those prescribed for lower urinary tract infections. Amoxicillin-clavulanate or enrofloxacin are frequently utilized, with enrofloxacin sometimes being preferred due to its higher efficacy against feline uropathogens. Regular urinalyses and urine cultures are conducted during the antibiotic treatment phase, generally 5–7 days after treatment initiation and again 1–4 weeks post-therapy. Potential complications of pyelonephritis may include kidney failure, recurrent kidney infections, and the spread of infection to other body parts, such as the heart lining or joints. Fortunately, cats with sudden pyelonephritis often recover fully, unless they also suffer from kidney stones, chronic kidney disease, urinary tract obstructions, or urinary tract cancer. Conversely, cats experiencing chronic or recurrent pyelonephritis may face difficulties in treatment, resulting in a more serious prognosis. If pyelonephritis goes undiagnosed and untreated, it can lead to permanent kidney damage and chronic kidney disease, culminating in kidney failure.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Enrofloxacin : 5 mg/kg, PO, IV, or SC	Fortivir 30 ml(100mg Enrofloxacin/ml) inj vial( Verbac India). Floxidin 100ml(100mg Enrofloxacin/ml) inj vial( MSD india). Efx -LA 100ml(120mg Enrofloxacin/ml) inj vial( Parex India). Enolox-K 30ml (100mg Enrofloxacin and 60 mg Ketoprofen/ml)inj vial( Zenley Animal health). Enrovet 100ml (100mg Enrofloxacin/ml) inj vial ( Vets Pharma India). Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Amoxicillin+Clavulanate: 20mg/kg PO QID for 4-6 weeks.	Clavpet 500mg ( 400mg Amoxicillin and 100mg Clavulanate) tab( Veko India). Wigclav 250mg ( 200mg Amoxicillin and 50mg Clavulanate) tab(Wiggles India). Toxo-Mox ( 200mg Amoxicillin and 28.5mg Clavulanate/reconstituted 5ml)dry syrup ( Savavet India). Toxo-Mox 500mg (400mg Amoxicillin and 100mg Clavulanate) tab( Savavet India).

---

Coxiellosis (Q fever) in cats: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Coxiellosis (Q fever) in cats is caused by Coxiella (C.) burnetii, a small, Gram-negative bacterium in the family Coxielaceae and order Legionellales. It has two forms: a large-cell variant that replicates inside cells and a small-cell variant that acts as a resistant spore. The small-cell variant can survive in the environment for long periods and resists various chemical and physical inactivations.The most common reservoirs are cattle, sheep and goats.Cats can become infected via ingestion of contaminated carcasses or after aerosol exposure or via tick bites. Rodents are also considered natural reservoirs of C. burnetii and cats may become infected when they prey on rodents or become infected through contact with their faeces, urine and secretions. the bacterium has a tropism for the uterus and mammary gland; the placenta and foetal membranes may be heavily contaminated and  could be detected in the birth fluids of parturient queens.

Pathogenesis

After infection via the oral or respiratory route, C. burnetii enters mononuclear phagocytes where it replicates and subsequently spreads to different organs with a predilection for the uterus. C burnetii can localize in mammary glands, supramammary lymph nodes, placenta, and uterus, from which it may be shed in subsequent parturitions and lactations. Both acute and chronic signs of disease are observed.

Clinical Symptoms

In cats, the disease often shows no symptoms, but it can lead to stillbirth, abortion, and prolonged vaginal bleeding for three weeks before delivery.

Diagnosis

In humans, the diagnosis of Q fever is confidently achieved through antibody tests and organism identification. A range of tests, including the immunofluorescent antibody test (IFA), ELISA, and complement fixation test (CFT), effectively detect antibodies in both humans and animals. The IFA is the optimal method for human diagnosis, with a fourfold increase in paired serum samples serving as a clear diagnostic indicator. The organism exhibits phase variations during the infection, and the presence of antibodies against phase I and II antigens decisively determines the infection stage. During acute infection, phase II antibody levels are significantly elevated compared to phase I, typically becoming detectable in the second week of illness. Phase I antibodies emerge later, indicating ongoing exposure to the bacteria. A rise in phase II antibodies clearly signals an acute infection, while an increase in phase I antibodies suggests chronic Q fever. Culturing the organism is generally avoided due to safety concerns and the necessity for BSL3 conditions. Fortunately, conventional and real-time PCR, as well as immunohistochemistry, effectively detect C. burnetii DNA or antigens in a variety of samples such as blood, serum, and urine. While similar techniques may be utilized for cats, laboratory diagnosis remains uncommon.

Treatment

Doxycycline at 10 mg/kg is prescribed antibiotic given orally twice a day for 2 weeks. Doxycycline should be given with food or water to prevent esophagitis in cats.

Drugs and formulations available in India.

Drug and Dose	Veterinary formulations
Doxycycline: Drug of choice 5 mg-10 mg /kg PO BD for 28 days.	Dclat 100 g (200mg Doxycycline/g) powder (IPPL India). Doxypet 300(200mg Doxycycline) tab (Sava Vet India). Doxymust 100 (100mg Doxycycline) tab (Sky-Ec India). Doxymust 300(300mg Doxycycline) tab (Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

Tularemia in cats: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Tularemia is a disease caused by Francisella tularensis, affecting humans and various mammals like rabbits and mice. This bacterium is a gram-negative, nonmotile coccobacillus that requires oxygen to grow. It spreads through tick bites, contact with infected animals, eating contaminated food or water, and inhalation of bacteria. Cats usually get tularemia from ticks or by eating small rodents. Ticks can carry the infection to their offspring. Infected domestic cats can transmit tularemia to humans through bites, scratches, or direct contact with infected fluids on the skin.

Pathogenesis

Francisella tularens can live both inside and outside the cells of the animals it infects, which makes it a facultative intracellular bacterium. It mainly infects macrophages, a type of white blood cell, allowing it to escape the immune system. The disease spreads to various organs, including the lungs, liver, spleen, and lymphatic system.

Clinical Symptoms

Clinical findings vary depending upon the severity of the disease. The common symptoms are fever, anorexia, lethargy, and vomiting to marked depression. The other symptoms observed are oral/lingual ulceration, regional or generalized lymphadenomegaly, and hepatosplenomegaly.

Diagnosis

The most commonly reported laboratory findings include pancytopenia, toxic neutrophils, high band neutrophil counts, thrombocytopenia and hyperbilirubinemia. Tularemia should be suspected in febrile cats with a history of contact with wild animals or ticks. The high susceptibility of cats also poses a public health concern, given that cats can transmit this disease to people, usually through biting. Cats’ susceptibility makes them a sentinel species in tularemia-endemic areas. A definitive diagnosis is achieved by isolating the organism in culture or demonstrating a four-fold increase in antibody levels between acute and convalescent samples. Due to its highly infectious nature, isolating F tularensis necessitates special precautions, and antibodies may take up to 3 weeks to develop after infection; consequently, these methods are not ideal for rapid detection. In clinical environments where swift diagnosis is essential, PCR stands as the most effective method for diagnosing tularemia. A single positive titer (⩾1:160 in cats), coupled with consistent clinical signs, strongly indicates an active infection.

Treatment

Gentamicin is the preferred treatment, while doxycycline and fluoroquinolones are good alternatives for 2–4 weeks. Tetracyclines (like doxycycline) and fluoroquinolones (such as marbofloxacin and pradofloxacin) can treat cats but have a higher relapse risk.

Drugs and formulations available in India.

Drug and Dose	Veterinary formulations
Gentamicin: 5–8 mg/kg slow i.v. (over 30 min), i.m., or s.c. once a day for 2 weeks.	Gentamicin 100ml(40 mg Gentamicin/ml) inj vial(Zuche Pharmaceuticals India). Gentamicin 30ml(40 mg Gentamicin/ml) inj vial (Zuche Pharmaceuticals India). Genacyn LA 30ml(80 mg Gentamicin/ml) inj vial( Zenley Animal Health India). Gentamor Vet 100ml(40 mg Gentamicin/ml) inj vial( Morvel India)
Doxycycline: Drug of choice 5 mg-10 mg /kg PO BD for 2-3 weeks. Higher doses of doxycycline (50 mg once daily for 2-3 months) can yield good results.	Dclat 100 g (200mg Doxycycline/g) powder (IPPL India). Doxypet 300(200mg Doxycycline) tab (Sava Vet India). Doxymust 100 (100mg Doxycycline) tab (Sky-Ec India). Doxymust 300(300mg Doxycycline) tab (Sky-Ec India). Zedox 200(200mg Doxycycline) tab( Corise India).

---

Section C: Bacterial Diseases in Cattle

---

• Anthrax
• Actinomycosis
• Wooden tongue
• Contagious abortion( Brucellosis)
• Black quarter
• Colibacillosis
• Enterotoxaemia(Clostridium perfringens infection)
• Bovine foot rot
•  Diptheria( necrobacilosis)
• Cystitis and Pyelonephritis
• Haemorrhagic septicemia
• IBK(Pink eye)
• Johne’s disease( Paratuberculosis)
• Joint ill
• Navel ill
• Bovine Leptospirosis
• Bovine Salmonella infection
• Bovine Mycoplasmosis
• Bovine listeriosis
• Bovine genital Campylobacteriosis
• Contagious mastitis
• Environmental mastitis

---

Anthrax in Cattle: Disease description, drugs and formulations in India .

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Anthrax in cattle is a grave disease resulting from the bacterium Bacillus anthracis, known for its ability to form resilient spores when exposed to air. These spores persist in soil and are encased by a protective capsule that aids the bacteria in evading the immune response. The bacterium is Gram-positive, non-motile, requires oxygen, and often appears as “boxcar” chains under microscopic examination. PLET agar is utilized for culturing Bacillus anthracis; however, it contains the hazardous compound thallous acetate. The colonies manifest as small, white, and circular growths. Other media, such as LB broth, serve general growth purposes. Animals may ingest anthrax spores while grazing or through contaminated feed, and biting flies can facilitate the transfer of these spores. Infected animals may exhibit bleeding, which contributes to the dissemination of the bacteria.

Pathogenesis

Upon entering the body, spores of B.anthracis are swiftly absorbed by macrophages and transported to regional lymph nodes where they germinate into active bacteria, multiplying and spreading throughout the organism, often leading to severe septicemia. The Poly-γ-D-glutamic acid capsule (encoded by genes on the pXO2 plasmid) effectively hinders the immune system’s phagocytic cells from clearing the bacteria. Bacillus anthracis produces a potent toxin composed of three components: Protective Antigen (PA), Lethal Factor (LF), and Edema Factor (EF), all of which are capable of inducing significant tissue damage and edema. PA acts as the “B” component, adeptly attaching to cell surfaces and facilitating the entry of LF and EF into the cytoplasm of host cells. LF and EF represent the “A” or toxigenic components that cause cellular damage and dysfunction. EF sharply reduces neutrophil function and disrupts water homeostasis, leading to edema. LF amplifies the delivery of IL-1β factors and TNF-α, which are associated with septic shock and sudden mortality. Anthrax is an aggressive zoonotic disease that infects humans primarily through contact with infected animals, displaying symptoms such as fever and swelling.

Clinical Symptoms

Clinical progression of this disease can be categorized into peracute, acute, subacute, and chronic forms. In peracute instances, animals may die abruptly without exhibiting clinical symptoms, while in acute cases, mortality typically occurs within 48–72 hours. Infected animals become febrile (107°F/42°C), exhibit signs of excitement, and present with congested and hemorrhagic mucosa, followed by tachycardia, labored breathing leading to terminal convulsions, and eventual death. Abortion, decreased milk production, and discolored milk (blood-tinged or deep yellow) have been reported in dairy cattle. Generally, involvement of the alimentary tract occurs, characterized by dysentery and diarrhea, with blood potentially failing to clot and exuding from the nose, mouth, and anus. Dying animals are typically discovered bloated with either no rigor mortis or incomplete rigor mortis, and the lack of blood clotting stands out as a significant characteristic of anthrax.

Diagnosis

Diagnosis necessitates the testing of samples while maintaining contamination prevention. Detection of Bacillus anthracis generally requires culturing the bacteria from blood and identifying its genetic material through Polymerase Chain Reaction (PCR). Hematology and blood chemistry examinations are discouraged due to zoonotic risks. Should such examinations be performed, they must be conducted with utmost precaution. B. anthracis may be identified in stained smears from living animals utilizing Gram stain or polychrome methylene blue (M’Fadyean stain). Gram-stained smears typically reveal Gram-positive, thick, long, straight bacilli with square or truncated ends and parallel sides, usually arranged in single pairs or chains of three or four bacilli. M’Fadyean-stained smears demonstrate the capsulated bacilli (pink capsule surrounding dark blue bacilli, often square-ended, either singly or in short chains) when viewed under a microscope. The capsule appears pink upon poly-D-glutamic acid staining, surrounding purple-stained vegetative bacilli. During advanced decomposition, the detection of bacteria in the carcass becomes exceedingly difficult, with Ascoli’s thermoprecipitation test proving suitable for anthrax diagnosis. Mudusa head colonies are characteristic features of Bacillus anthracis and Bacillus cereus, with the former being non-hemolytic and the latter displaying hemolytic properties.

Treatment

Treatment includes antibiotics, vaccines, and ways to stop disease from spreading. The following measures should be taken to prevent the spread of disease.

• The dead animals are properly disposed.
• The carcass should not be opened, since exposure to oxygen will allow the bacteria to form spores.An unopened carcass over 72 h inhibits sporulation of the vegetative cells, resulting in the end of their life cycle.
• Premises are to be quarantined until all susceptible animals are vaccinated and all carcasses disposed of preferably by incineration or alternatively by deep burial with quick lime.
• Cleaning and disinfection are important as is control of insects and rodents.

The author has effectively treated a six-month-old calf with a strong suspicion of anthrax, exhibiting clear signs of fever (106°F), excitement, congested conjunctiva, tachycardia, respiratory distress, inability to stand, and bleeding from the nose and rectum. The calf received a precisely calculated loading dose of 80 lac IU procain penicillin, followed by 40 lac IU procain penicillin administered IM twice daily for five days. Additionally, a substantial dose of prednisolone and a large dose of deriphyllin human formulation were administered twice daily for five days to decisively alleviate symptoms of respiratory distress and edema. Meloxicam combined with paracetamol was given once a day for three days, acting as potent antipyretic and anti-inflammatory agents. Remarkably, the calf regained the ability to stand and suck milk the very next day and achieved a full recovery post-treatment.

Vaccination in endemic areas is crucial. The World Organisation for Animal Health (WOAH) sets forth stringent requirements for the manufacture and quality control of animal vaccines in the WOAH Manual of Diagnostic Tests and Vaccines. While vaccination is a vital preventive measure against outbreaks, Veterinary Services occasionally overlook vaccination efforts during prolonged periods without disease incidence. However, due to the remarkable resilience of anthrax spores, the threat remains ever-present. Although anthrax is susceptible to antibiotic treatment, the rapid progression of the disease often precludes timely intervention for affected animals. Therefore, early detection of outbreaks, strict quarantine of impacted premises, humane destruction of diseased animals and contaminated materials, along with the enforcement of rigorous sanitary protocols at abattoirs and dairy factories, are absolutely essential to ensure the safety of animal-origin products intended for human consumption.

Drugs and formulations available in India.

Drug and dose

Veterinary formulations

Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD or BD for 5- 7 days

Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).

---

*Actinomycosis in Cattle: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Actinomycosis (lumpy jaw) in cattle is a well-defined chronic infectious disease that significantly affects the facial bones, caused by Actinomyces bovis. This Gram-positive filamentous anaerobe naturally resides within the oral flora, as well as the upper respiratory and digestive tracts of most animals. Actinomyces bovis thrives in anaerobic conditions and requires enriched media, often blood-supplemented, for optimal growth, such as anaerobic blood agar (ABA), brain heart infusion (BHI) broth, or Brucella blood agar (BBA), maintained at temperatures ranging from 30°C to 37°C. Garrod’s medium, a complex organic formulation, is recommended for its isolation and maintenance, providing essential nutrients to this anaerobic bacterium. Specialized, semi-selective media effectively inhibit competing organisms, facilitating the isolation of Actinomyces. On culture, they distinctly appear as a network of branching filaments resembling a fungus, yet they are indeed bacteria. Within these colonies, particularly in exudates from infections, sulfur granules are present, formed by clumps of these filamentous bacteria.

Pathogenesis

Pathogenesis is initiated by wounds in the oral mucosa caused by sharp objects such as wires, hay, abrasive feed, or sharp branches. The organism penetrates soft tissues due to mucosal damage from these sharp objects or erupting teeth, leading to a marked proliferation of connective tissue, leukocyte invasion, and the formation of a tumor-like granulomatous mass. This mass invades the mandible or occasionally the maxilla, growing slowly and presenting as a firm, non-painful attachment to the mandible. Ulceration may occur, with or without purulent material draining from tracts.

Clinical Symptoms

Clinical signs of actinomycosis in cattle prominently feature osteomyelitis of the mandible or maxilla, aptly leading to the term “lumpy jaw,” characterized by suppurative granulation of the skull, particularly in the mandible and maxilla. Gross swelling, abscesses, fistulous tracts, and extensive fibrosis all contribute to the granulomatous lesion. Involvement of the alveoli of the cheek teeth often results in loose teeth, complicating the chewing process and leading to painful eating and noticeable weight loss.

Diagnosis

Diagnosis relies on clinical signs, while definitive identification requires a tissue core biopsy or fluid aspirate to isolate the causative organism, characterized by stained crushed yellow granules found in pus and demonstrating Gram-positive filamentous rods. Radiographic imaging confirms osteomyelitis, illustrating multiple radiolucent zones and periosteal bone proliferation. Fine-needle aspiration biopsy (FNAB) is an effective, less invasive procedure compared to histological biopsy and plays a crucial role in identifying microorganisms and sulfur granules, especially when bacteriological analyses yield negative results. FNAB is a reliable, safe, fast, and cost-effective diagnostic technique that can be employed prior to microbiological examination and antimicrobial therapy. Furthermore, FNAB is instrumental in distinguishing actinomycosis lesions from neoplastic bone disorders.

Treatment

Treatment for Actinomyces bovis infections, typically involves a decisive combination of surgical debridement (removing infected tissue), iodide therapy (oral potassium iodide or intravenous sodium iodide), and broad-spectrum antibiotics like penicillin, oxytetracycline and streptomycin. Treatment success can be limited in cases with severe bone involvement, yet less advanced lesions often respond, while advanced bony changes frequently prove irreversible.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD or BD for 5- 7 days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Streptopenicillin : 12.5 mg/Kg IM OD for 5-7 days.	Dicrysticine 5g(2.5g Streptomycin sulphate. 1500000IU procaine penicillin 500000 penicillin G sodium) inj vial( Zydus India). Xydocin 2.5 g (1.5g Streptomycin sulphate. 1500000IU procaine penicillin. 100000 penicillin G sodium) inj vial ( Sarabhai India).
Potassium Iodide at the rate of 6-10 gm/day orally for 7-10 days Note : Never give IV.

---

Wooden tongue in Cattle: Disease description, drugs and formulations in India .

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Wooden tongue in cattle represents a notable soft tissue infection instigated by Actinobacillus lignieresii. This bacterium is responsible for the formation of distinctive tumorlike lingual abscesses, aptly termed wooden tongue. The bacterium is also noted for causing pyogranulomatous lesions in soft tissues associated with the head, neck, limbs, and occasionally the lungs, pleura, udder, and subcutaneous tissue; significantly, many incidents do not involve the tongue. While it predominantly affects cattle, it can also impact sheep, horses, pigs, and dogs, and, though infrequently, chickens. Wooden tongue is acknowledged globally but tends to occur sporadically, posing challenges for effective prevention. Herd outbreaks can arise, commonly linked to the consumption of coarse and abrasive feeds that increase the risk of oral lesions. Actinobacillus lignieresii is a Gram-negative, rod-shaped, anaerobic, non-motile, and non-spore-forming bacterium typically residing in the upper GI tract of ruminants. Actinobacillus can be isolated on culture media, with blood agar and serum-containing media like TSBV agar routinely used for primary isolation. The colonies of Actinobacillus lignieresii are typically small (1-2 mm), sticky, raised, smooth, and grayish white. They display non-hemolytic characteristics on blood agar and can thrive on MacConkey agar, where they initially appear pale and transition to pink after 48 hours. The sticky appearance of the colonies is due to a slime layer enveloping the bacterial surface.

Pathogenesis

Pathogenesis begins with penetrating wounds, allowing A. lignieresii to infiltrate adjacent soft tissue, where it creates localized pyogranulomas that may resemble tumors, and it can spread through the lymphatics to other tissues. Its virulence factors, including adhesins, exotoxins, and lipopolysaccharides (LPS), incite inflammation and activate the immune system, leading to neutrophil infiltration that aids in abscess and granulomatous lesion formation.

Clinical Symptoms

Clinically, wooden tongue manifests as a very hard, diffusely swollen tongue, resulting in excessive salivation, difficulty in prehending feed normally, and sometimes a visibly enlarged tongue protruding from the mouth. On palpation, the tongue feels hard, and the animal exhibits pain; cows with wooden tongue often display firm or fluctuant swelling in the intermandibular space. Gastrointestinal (GI) and respiratory symptoms become apparent if the GI and respiratory tracts are involved. Additionally, if the mammary tissues are infected, a hard area will be palpated.

Diagnosis

Diagnosis of wooden tongue is established through ELSA, nested PCR, and quantitative real-time PCR (qPCR) of the sample. Gross examination and histopathology of body tissues or masses are also performed to accurately diagnose the disease.

Treatment

Treatment for wooden tongue entails a combination of medical therapy, supportive care, and preventive measures. Common antibiotics include tetracyclines, penicillin, and streptomycin, while sodium iodide proves highly effective in cases where granulomatous lesions are present. As an alternative to oral treatment, potassium iodide therapy is typically prescribed daily by a veterinarian. Severely affected animals may receive non-steroidal anti-inflammatory drugs (NSAIDs) to alleviate swelling and discomfort. Supportive care involves offering soft, digestible feeds to animals with oral or pharyngeal lesions, ensuring continuous access to clean water, and performing surgical removal of oral or pharyngeal lesions when necessary and severe.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD or BD for 5- 7 days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle,sheep, goat and pig.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India). Oxin 500mg (50omg oxytetracyclin) tab (Zoetis India). Oxytech 500mg (50omg oxytetracyclin) tab (Mediseller India). Himoxy 500mg (50omg oxytetracyclin) tab (Himal Bioscience India).
Streptopenicillin : 12.5 mg/Kg IM OD for 5-7 days.	Dicrysticine 5g(2.5g Streptomycin sulphate. 1500000IU procaine penicillin 500000 penicillin G sodium) inj vial( Zydus India). Xydocin 2.5 g (1.5g Streptomycin sulphate. 1500000IU procaine penicillin. 100000 penicillin G sodium) inj vial ( Sarabhai India).
Sodium iodide: 66 mg/kg slow IV, weekly.
Potassium Iodide at the rate of 6-10 gm/day orally for 7-10 days. Note : Never give IV.

---

Contagious abortion in Cattle: Disease description, drugs and formulations in India .

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Contagious abortion in cattle, commonly known as brucellosis or Bang’s disease, is a highly infectious disease caused by the bacteria Brucella abortus. Brucellosis has zoonotic implications and is transmitted to humans during handling contaminated material like placenta, fetus, uterine, or vulvar discharges. Milk from infected animals may also serve as a source of infection. Artificial insemination with contaminated semen is a potential source of infection in cattle, but the most common route of infection in cattle is the gastrointestinal tract. Aborted fetuses, as well as fetal membranes and uterine secretions eliminated after abortion or parturition, are the most important sources of infection. Brucella are Gram-negative, aerobic, small rod-shaped intracellular bacteria. The most important feature of Brucella is the ability to survive and multiply within both phagocytic and non-phagocytic cells. Bacterial cells are able to survive for a prolonged time in water, aborted fetuses, soil, dairy products, meat, dung, and dust. For the isolation of Brucella spp., the enrichment and selective media such as Thayer-Martin’s medium or Farrell’s medium are commonly used. For the culture of blood or body fluid, a biphase medium called Castaneda should be used.

Pathogenesis

Pathogenesis begins in the gastrointestinal tract, where Brucella spreads to local lymph nodes and replicates in phagocytes. B. abortus invades the intestinal mucosa mainly through M cells. The main targets for this bacterium are macrophages, dendritic cells, and trophoblast cells. Brucella abortus enters the bovine host, often via the gastrointestinal tract, then spreads via the lymphatic system and bloodstream to target specific organs, particularly the pregnant uterus and male genitalia. Intra-epithelial phagocytes in the intestinal wall assist in moving B. abortus to the lamina propria and submucosa. Some bacteria experience opsonization while some escape the opsonization phase. Opsonized B. abortus is taken up by phagocytes via complement or Fc receptors. The non-opsonized ones invade phagocytes by interacting with lectin and fibronectin receptors. Opsonized bacteria are typically killed inside phagocytes before they can replicate. The non-opsonized B. abortus survives intracellularly by resisting the acid environment and preventing the fusion of phagosomes and lysosomes. After invading lymphatic vessels, B. abortus causes bacteremia, leading to systemic infection, particularly affecting the pregnant uterus, male genital organs, and mammary glands. Brucella abortus has a strong preference for the uterus in late gestation due to high levels of erythritol (an energy source for bacteria) and steroid hormones, which support its survival. Erythrophagocytic cells at the chorionic villi base in ruminants are key sites for invading fetal placental tissues, allowing B. abortus to spread to trophoblasts. Brucella growth causes inflammation, tissue necrosis, and damage to the allantochorion, leading to compromised metabolic exchanges and potential abortion. Intracellular replication rates in trophoblasts are higher during late gestation, influenced by hormone secretion. B. abortus also modifies steroid synthesis and the metabolism of prostaglandin precursors, promoting its growth. The infected placenta undergoes hormonal changes, increasing prostaglandin F2a and cortisol and decreasing progesterone, resembling events during parturition and possibly contributing to abortion.

Clinical Symptoms

Clinical signs are abortion or stillbirths in the third trimester of gestation. The infected uterus discharges a foul yellowish exudate with necrotic debris. There is placentitis, and necrotic lesions are present unevenly on the placenta, with some placentomes being normal while others show severe damage.

Diagnosis

Diagnosis is based on abortion in late gestation with characteristic lesions on the placenta, identification of bacteria, blood and serological tests, and histopathology of tissue samples. Histologically, trophoblastic cells are swollen and filled with bacteria, with significant inflammatory infiltrates and signs of necrosis. The endometrium shows a heavy infiltration of immune cells and features erosions or ulcers in the lining. Necrotic debris contains many B. abortus bacilli, and weeks after abortion, the uterine inflammation remains prominent.

Treatment

Treatment of brucellosis with known antibiotics is not effective, although several Brucella vaccines are accessible for livestock. Live, attenuated vaccines such as the live B. abortus vaccine strain 19, live B. abortus vaccine strain RB51, and live B. melitensis vaccine strain Rev-1 are used in the field; however, these vaccines bear some virulent effects. Subunit vaccines are proven to be relatively safe and they raise fewer concerns compared to live vaccines. They do not cause infection, as they present purified proteins or DNA to stimulate an immune response.

Vaccines and formulations in India.

vaccine	Veterinary formulations
Strain 19 vaccine : 2ml s/c in female calves at age of 4-8 months.	Live attenuated Brucella vaccine containing NLT 40 x 109 viable organism/2ml reconstituted vaccine . A freeze dried (lyophilised) in glass vials. It is available in 1, 2 & 5 doses per vial with respective diluents( Hester Biosceince India). Bruvax 5 dose freeze dried (lyophilised)vial ( Indian Immunologicals).

---

Black quarter in Cattle: Disease description, drugs and formulations in India .

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Black quarter, also known as Blackleg, quarter evil, or quarter ill, is an infectious bacterial disease caused by Clostridium chauvoei. This disease primarily affects healthy, well-built muscular animals up to 2 years of age. C. chauvoei is a Gram-positive, rod-shaped, anaerobic, and motile pathogen that can be cultivated on various media, most effectively on blood agar supplemented with liver extract, or on specialized media like reinforced Clostridial medium (RCM). For optimal growth, the organism requires anaerobic conditions, a pH of 7.2-7.5, and an incubation temperature between 37-40°C. Blood agar with liver extract, in particular, promotes growth and yields hemolytic colonies, facilitating the identification of the organism. The bacterium can produce environmentally enduring spores that may linger in the soil for years, only to return to their infectious form when ingested by grazing livestock. Contaminated pastures are a primary source of these organisms.

Pathogenesis

Pathology of blackleg primarily manifests in the muscular tissues of infected animals, from where the pathogen is typically isolated. While the exact pathogenesis of blackleg remains incompletely understood, it is presumed to involve the ingestion of spores that are absorbed through the intestinal mucosa. Once in the bloodstream, spores disseminate to tissues, including skeletal and cardiac muscle, where they are engulfed by tissue macrophages. Remarkably, these organisms can survive for months to years within macrophages without harming the host. However, when oxygen levels decrease in muscle areas harboring spores—often due to blunt trauma and consequent tissue hemorrhage, degeneration, and necrosis—the spores germinate into vegetative form, proliferate, and produce toxins that lead to the hallmark clinical signs and lesions of blackleg. Due to this specific pathogenesis, blackleg is classified as an endogenous infection. C. chauvoei toxin A is recognized as the principal virulence factor of this microorganism, although the complete molecular Koch postulates have yet to be fulfilled, suggesting that other toxins could play a significant role in the disease’s pathogenesis. Typically, blackleg affects the large muscles of the pectoral and pelvic girdles, while other skeletal muscles are involved less frequently. Additionally, though lesions in the heart were once deemed uncommon, anecdotal evidence indicates that they occur more frequently than previously thought.

Clinical Symptoms

Clinical signs vary depending on the severity of the infection; onset is usually sudden, and affected animals may be found dead without preceding symptoms. Common symptoms include acute, severe lameness in the hind legs and pronounced depression. Initial signs feature fever, but as clinical symptoms become apparent, body temperature can normalize or drop below normal. Characteristic edematous and crepitant swellings develop in the hip, shoulder, chest, back, neck, or other areas, typically starting as focal, hot, and painful swellings. In rare instances, the tongue may become affected and protrude. As the disease rapidly advances, these swellings expand, crepitation occurs upon palpation, and the skin turns cold and insensitive with a reduced blood supply to the affected regions. General clinical signs include prostration and tremors, with death occurring within 12–48 hours. In certain cattle, lesions are confined to the myocardium and diaphragm, leading to abnormal breathing and a pericardial friction rub.

Diagnosis

Diagnosing BQ involves a combination of observed clinical signs and the identification of Clostridium chauvoei bacteria, the causative agent, in fluid samples taken from lesions or post-mortem tissues.

Treatment

Early treatment is effective, with antibiotics such as penicillin and oxytetracycline being the primary options, ideally used alongside hyperimmune serum (HIS). Nonetheless, vaccination with a combined vaccine against Clostridium chauvoei and Pasteurella multocida remains the most effective preventive strategy, with annual boosters recommended prior to the monsoon season in endemic areas.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD or BD for 5- 7 days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle,sheep, goat and pig.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

Colibacillosis in Calves: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Colibacillosis is primarily a disease of newborn calves and is caused by Escherichia coli (E. coli). E. coli is a rod-shaped gram-negative, facultative anaerobe, nonsporulating coliform bacterium. During the staining process, E. coli picks up the color of the counterstain safranin and stains pink. The outer membrane surrounding the cell wall provides a barrier to certain antibiotics, such that E. coli is not damaged by penicillin. E. coli grows in a variety of defined laboratory media, such as lysogeny broth, and the optimum temperature for growth is 37 degrees Celsius. There are several strains of E. coli, but only a few are pathogenic. Pathogenic E. coli is frequently seen in young calves. E. coli naturally exists in calves’ gastrointestinal tracts and can cause disease under certain conditions like poor hygiene, insufficient colostrum, and stress. Pathogenic E. coli can also cause serious infections beyond the intestines, including colisepticaemia and urinary tract issues. There are two main types of pathogenic E. coli: diarrhoeagenic and extra-intestinal. Notable diarrhoeagenic serotypes include Enteropathogenic E. coli (EPEC), Enterotoxigenic E. coli (ETEC), Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli (EIEC), Enteroaggregative E. coli (EAEC), and Diffusely Adherent E. coli (DAEC). Extra-intestinal strains include uropathogenic E. coli (UPEC) and neonatal meningitis E. coli (NMEC). The major E. coli types affecting newborn calves and causing severe illness are EPEC, ETEC, and EHEC.

Pathogenesis

Pathogenesis of E. coli is linked to plasmid-encoded factors that help it attach to intestinal cells. For instance, ETEC uses specific pili to adhere without damaging the intestines. After attaching, ETEC produces toxins that lead to diarrhea by causing the gut to secrete excess fluids. Additionally, Enteropathogenic E. coli can create lesions on intestinal cells, disrupting nutrient absorption and worsening calf health. Shiga toxin-producing E. coli (STEC) is another contributor to calf diarrhea but is less studied. E. coli serotypes 026 and 0111 have been noted for causing diarrhea in calves.

Clinical Symptoms

The clinical picture of E. coli in calves includes fever, depression, poor suckling, dehydration, and profuse diarrhea, which can be watery, yellowish, or even bloody. Depending on the affected E. coli type, signs can progress to severe symptoms like septic shock, organ damage, collapse, and death. Less common, but serious complications can include joint infections (arthritis), umbilical infections, and meningitis.

Diagnosis

Diagnosis of colibacillosis in calves, caused by E. coli, is based on history, clinical signs, and bacterial culture from the affected tissues. A differential diagnosis is essential for identifying the cause of diarrhea in young calves, but infections in the first week of life are mainly associated with E. coli.

Treatment

Effective treatment involves the administration of intravenous fluids for cases of severe dehydration and early systemic antibiotics like amoxicillin with clavulanic acid or oxytetracycline. Additionally, providing supportive care, which includes anti-inflammatory drugs (NSAIDs) and ensuring a warm, clean environment, is absolutely essential for recovery.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Ofloxacin : 5mg/kg PO BD for 3-4 days .	Diarest -O2(Ofloxacin 200mg and Ornidazole 500mg) tab( Med-Vet Biolinks Private Limited India) . Oflakind Oz- pet (50mgOfloxacin and 125mgOrnidazole/ml) syrup( Mankind India).
Oxytetracycline: 5-10mg/kg OD IM/IV	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

Enterotoxaemia in calves: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Enterotoxaemia in calves is a critical condition resulting from toxins produced by Clostridium perfringens in the intestinal tract. Although it can impact cattle of all ages, it predominantly causes disease in neonatal and young calves. The small intestine, the target organ of clostridial enterotoxaemia, typically has serosal and mucosal petechiae, ecchymoses, and paintbrush or diffuse hemorrhage similar in appearance to those of intestinal strangulation. Importantly, this disease may manifest in otherwise healthy calves, with risk factors including dietary changes, grazing on lush green pastures, and stress. C. perfringens are gram-positive, rod-shaped bacteria that normally reside in small numbers within the intestine. Optimal growth occurs on anaerobic blood agar, where it generates a distinct double zone of beta-hemolysis. The bacterial colonies are characterized as small to medium-sized, greyish, translucent, and can exhibit smooth, dome-shaped, rough, or filamentous forms with irregular margins. There are up to 30 identified toxins produced by various strains of C. perfringens, which are classified into five groups (A, B, C, D, and E) based on their primary toxins (α, β, ι, and ε). Additionally, these strains are discerned by the production of supplementary toxins: the enterotoxin (from the cpe gene) and the b2 toxin (from the cbp2 gene). C. perfringens type A generates the α toxin, leading to abomasitis, enterotoxaemia, and necrotic enteritis; type B produces α, β, and ε toxins, resulting in hemorrhagic enteritis; type C generates α and β toxins, causing necrotic or hemorrhagic enterotoxaemia; and type D produces α and ε toxins, which are responsible for enterotoxaemia.

Pathogenesis

Pathogenesis commences with sluggish or impaired intestinal motility, often triggered by multiple factors, with feed modifications and bloat from excessive lush grass consumption being common precursors. Sufficient carbohydrate or protein nutrients support bacterial growth. Efficient intestinal movement facilitates the elimination of bacterial toxins. Conversely, stasis allows for bacterial proliferation, culminating in the production of high concentrations of toxins that diffuse through the intestinal wall into the bloodstream, inducing toxemia. These toxins substantially disrupt the function of critical organs, resulting in severe damage.

Clinical Symptoms

Clinical manifestations are rarely observed, and severe cases may culminate in sudden death. Peracute instances may display no observable signs, although acute cases may present with abdominal pain, profuse diarrhea or dysentery, congested mucous membranes, restlessness, convulsions, respiratory distress, collapse, and syncope. The body temperature remains normal unless complications of systemic sepsis or peritonitis have developed, in which case their temperature can be decreased or increased. Mucous membranes in systemic shock may be pale with a prolonged capillary refill time. Rapid abdominal decomposition, accompanied by gas production and a putrid odor, is characteristic of clostridial infections. The most prevalent lesion observed is acute necrohemorrhagic jejunoileitis, featuring a significantly thickened, hemorrhagic, and necrotic intestinal wall with copious liquid hemorrhagic contents.

Diagnosis

Diagnosing cattle enterotoxemia requires a multifaceted approach. Sudden death without prior symptoms, when coupled with the presentation of acute hemorrhagic jejunoileitis and hemorrhagic intestinal contents during postmortem examination, strongly indicates the condition. A Gram-stained direct smear of intestinal content can effectively identify a substantial number of Gram-positive bacilli; however, quantitative anaerobic growth on blood agar remains the definitive benchmark for confirming field suspicion of enterotoxemia caused by C. perfringens. Timely sample collection is imperative, ideally within 1-3 hours of death, to mitigate the risk of false positive results. Multiplex polymerase chain reaction is also used to identify C. perfringens genotypes from anaerobic culture of samples.

Treatment

Treatment is not effective in peracute syndrome, with a case fatality rate nearing 100 percent. Consequently, the implementation of robust preventive strategies is paramount, particularly when specific risk factors are identified. The adoption of sound animal management practices is essential, with the objective of ensuring gradual dietary transitions and providing fiber-rich diets to maintain a balanced intestinal flora. Additionally, the provision of probiotics may act as a preventive measure by promoting the proliferation of beneficial bacteria and improving gut health. Although no vaccine currently exists for cattle in India, the MCC vaccine developed for sheep can be administered. Furthermore, the antibiotic penicillin may offer some potential in managing affected cases. Both oral penicillin and systemic or oral oxytetracycline, alone or in combination, may be clinically effective in treating acute cases of enterotoxaemia.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000IU/kg,PO OD or BD for 5- 7 days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 10mg/kg OD IM/IV .	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

Bovine foot rot: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Bovine foot rot (BFR), also called purchased disease as a purchased lame animal may act as a source of infection, is an infectious disease of the interdigital skin and subcutaneous tissues of cattle. It is caused by three main bacteria: Fusobacterium necrophorum, Dichelobacter nodosus (formerly Bacteroides nodosus), and Prevotella melaninogenica (formerly Bacteroides melaninogenicus). These are anaerobic, Gram-negative bacteria. Fusobacterium necrophorum is a normal inhabitant of the ruminant digestive tract and may survive in soil for up to ten months.

Pathogenesis

Pathogenesis is initiated by risk factors such as continuous exposure of the foot to wet, muddy environments and is aggravated by cuts and bruises. D. nodosus is identified as the primary invader of the epidermal matrix, initiating the process of hoof separation and creating a conducive environment for F. necrophorum to thrive. The infection results from the synergistic action of these two specific bacterial species, where D. nodosus serves as the causative agent and F. necrophorum is essential for the onset and progression of the disease. Fusobacterium necrophorum produces a leukocidal exotoxin that adversely affects white blood cells, inhibiting phagocytosis. The bacteria proliferate and cause suppurative necrosis. Bacteroides melaninogenicus produces proteases that inflict damage on the subcutaneous tissue and tendons. Dichelobacter nodosus produces an enzyme that digests the connective tissue between the hoof horn and the underlying flesh, facilitating migration to areas beneath the horn. If left uncontrolled, bacteria may invade deeper foot structures, including the joints, potentially leading to septic arthritis.

Clinical Symptoms

Clinical manifestations include the presence of swelling and erythema in the soft tissues of the interdigital space and the adjacent coronary band. Inflammation may extend to the pastern and fetlock regions. Typically, the claws exhibit marked separation, with inflammatory edema being uniformly distributed between the two digits. The onset of the condition is rapid, and the resultant pain leads to pronounced lameness. In severe instances, the animal demonstrates reluctance to bear weight on the affected foot. Accompanying symptoms such as fever and anorexia are commonly observed. Initially, the skin within the interdigital space may appear discolored; however, it subsequently progresses to fragmentation along with exudate production. As the necrosis of the skin advances, sloughing of tissue is likely to occur, leading to the generation of a characteristic foul odor.

Diagnosis

Diagnosis of foot rot is based on the observation of sudden, severe lameness, symmetrical swelling above the hoof, and a characteristic foul odor and discharge from the interdigital skin, which often shows splitting or necrosis.

Treatment

Treatment necessitates thorough cleaning, debridement, and disinfection of the infected tissues. Penicillin and oxytetracycline are typically used and considered effective antibiotics when administered early in the disease process at the recommended dosages. Additionally, intravenous administration of sulfonamides shows considerable efficacy against foot rot. Should animals fail to respond to treatment within a three-day period, it is crucial to acknowledge that this is not merely an instance of “just foot rot,” warranting further intervention. Delays in treatment may permit the infection to spread into deeper bone, synovial structures, or ligamentous systems, significantly impairing the prognosis for recovery.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD or BD for 5- 7 days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India)

---

Calf Diphtheria: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Calf diphtheria, actually known as necrobacillosis or **necrotic laryngitis, is a significant infectious disease that notably impacts the pharynx, larynx, and oral cavity, primarily caused by Fusobacterium necrophorum, a normal resident of the oral cavity. This pathogen initiates infection by exploiting traumatic injuries to the oral mucous membranes. Fusobacterium necrophorum is an anaerobic, Gram-negative, rod-shaped bacterium. While diphtheria typically manifests as necrotic stomatitis in calves under three months of age, it more commonly appears as necrotic laryngitis in older calves. It’s crucial to note that calf diphtheria can affect animals up to three years of age, despite the misleading name.

Pathogenesis Clini

Pathogenesis begins with injuries from sharp objects, such as grass awns. The bacterium invades soft tissue, producing a leukocidal exotoxin that undermines white blood cells and inhibits phagocytosis. The organism proliferates, leading to suppurative necrosis. Many affected animals may not respond adequately to treatment, and the diphtheritic area can detach, posing serious risks of sudden asphyxiation or lung infection.

Clinical Symptoms

Clinical signs of calf diphtheria include inappetence or anorexia, pyrexia (40.5°C, 105°F), stertor, varying degrees of dyspnea, and a moist, painful cough. Laryngeal palpation often provokes coughing, and a foul-smelling mouth is typically present. Calves with this condition frequently develop abscesses in the cheek area, show mild salivation, and may refuse solid feed.

Diagnosis

Diagnosis relies on clinical observations and bacterial culture. To confirm upper airway obstruction, a visual inspection of the larynx is necessary, using methods like laryngoscopy or endoscopy, while avoiding respiratory complications. A tracheostomy should be performed for cattle with severe inspiratory dyspnea prior to examinations. Differential diagnoses include pharyngeal trauma, viral laryngitis, actinobacillosis, abscesses, trauma, paralysis, or neoplasia.

Treatment

Treatment involves antibiotics, anti-inflammatory agents, and fluid therapy. Sulfonamides, oxytetracycline, or procaine penicillin G are the preferred medications. Flunixin meglumine or aspirin can be utilized to effectively alleviate fever and inflammation. Providing supportive care through oral or IV fluids, adequate shelter, ventilation, and easy access to food and water is essential. The prognosis remains highly favorable with early detection and aggressive treatment. To prevent the spread of this infectious disease, it is vital to thoroughly clean and disinfect all calf feeders, particularly in closely confined settings. Regular daily examinations of young calves facilitate the identification of early disease stages, ensuring prompt and effective management.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Sulfadimidine( Sulfamethazine) : Initial dose ( 150mg/kg PO/ IV / IM / SC ) followed by maintenance dose (75mg/kg PO/ IV / IM / SC BID) x 3-5 days.	Unodine 99ml (333mg Sulfadimidin/ml) injection vial ( Sarabhai India) SD-VET 100 ml (333mg Sulfadimidin/ml) injection vial ( Intracin pharmaceutical India). Vetsulfa 5g sulfadimidine bolus( Vet world India)
Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD or BD for 5- 7 days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

---

Cystitis and Pyelonephritis in cattle :: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Pyelonephritis and cystitis in cattle are definitive bacterial infections of the urinary tract, resulting from various pathogens, including Corynebacterium spp. (C. renale, C. pilosum, C. cystitidis), Escherichia coli (E. coli), Streptococcus spp., Proteus spp., and Staphylococcus spp. Notably, Mannheimia varigena is recognized for causing pyelonephritis in calves. Key risk factors include parturition, peak lactation, and a high-protein diet that elevates urine pH, promoting the colonization of Corynebacterium spp., alongside the use of nonsterile catheters for bladder catheterization. In young calves, pyelonephritis typically stems from an ascending umbilical infection, whereas in bulls and steers, it can occur due to urinary tract obstruction.

Pathogenesis

Pathogenesis of pyelonephritis begins with an infection ascending from the bladder. Crucially, cystitis can occur without affecting the ureters or kidneys until a factor compromises the defenses of the ureteral mucosa. Piliated forms of C. renale and E. coli attach more effectively to the urinary tract lining, making them more challenging for white blood cells to eliminate. This facilitates the spread of the organisms and sustains the initial infection. Pili are essential for these bacteria to colonize the urinary tract mucosa and drive the infection. These pathogens target the bladder and ureters, often following injuries such as calf birth or abnormalities in the vaginal tract.

Clinical Symptoms

Clinical signs vary, with some cows showing bloodstained or cloudy urine. Others may present with acute colic, characterized by tail swishing, foot treading, abdominal kicking, and straining to urinate; however, this typically resolves within hours. These episodes often result from a ureter or renal calyx obstruction caused by pus or debris, which can be mistaken for intestinal obstruction. More commonly, symptoms develop gradually, featuring fluctuating temperatures, poor appetite, weight loss, and a gradual decline in milk production over weeks. There is usually minimal systemic reaction, with symptoms primarily linked to the urinary tract. Key indicators encompass blood, pus, mucus, and tissue debris in the urine, especially towards the end of urination, which may appear dribbly and painful. In the early stages, the left kidney might be enlarged and tender, while the right kidney can also be palpable in small ruminants when enlarged.

Diagnosis

Diagnosing pyelonephritis is accomplished through urinalysis, serum biochemistry, and ultrasound (USG). Urinalysis usually reveals proteinuria and hematuria, with the latter often evident in many cases. Urine pH frequently exceeds 8.5, and specific gravity ranges from 1.008 to 1.021. Microscopic examination of urine may reveal pyuria. Detection of bacteria can be confirmed through culture, immunofluorescence, or direct microscopy. Blood tests typically indicate low albumin and elevated gamma globulin in advanced cases, while neutrophilia may be present but is not always evident. In severe cases, serum creatinine and BUN levels increase, although these remain unaltered in mild or early cases. Ultrasound may uncover cysts in the affected kidney, dilated renal sinuses and ureters, and a thickened echogenic bladder.

Treatment

Treatment involves administering specific antibiotics designed for particular bacteria. For instance, pyelonephritis caused by C. renale is most effectively addressed with daily penicillin administration for 2 to 3 weeks. In suspected or confirmed E. coli infections, broad-spectrum antimicrobials such as ampicillin, amoxicillin, tetracycline, trimethoprim-sulfamethoxazole, ceftiofur, and gentamicin are extensively utilized.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg, IM or SC OD for 2-3 weeks	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Ceftiofur: 1.1-2.2mg/kg IM ODfor 2-3 weeks.	Xnel 1g (1000mg Ceftiofur) Injection Vial (Zoetis India). Xfur 1g (1000mg Ceftiofur) Injection Vial (Vet Life Science India). Ceftio-4 1g (1000mg Ceftiofur) Injection Vial (Geevet Remedies India). Capoform 1g (1000mg Ceftiofur) Injection Vial (Carus Laboratories India). Xceft 1g (1000mg Ceftiofur) Injection Vial (Alembic India). Izafur 1g (1000mg Ceftiofur) Injection Vial (Izda Health Care India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

Haemorrhagic septicaemia in cattle:: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Haemorrhagic septicaemia (HS) is an acute septicemic disease experienced by cattle and buffaloes and is caused by a commensal organism P. multocida present in the nasopharynx or oropharynx of these animals. This disease is strongly associated with specific serotypes of P. multocida, a gram-negative coccobacillus that typically resides harmlessly in the nasopharynx. The Gram stain identifies it as a Gram-negative coccobacillus exhibiting a distinct bipolar staining pattern. P. multocida thrives on nutrient-rich media, such as blood agar and chocolate agar, where it forms small, shiny colonies emitting a characteristic mousy odor. The primary serotypes include Asian serotype B:2 and African serotype E:2, correlating with the 6:B and 6:E classifications. While the pathogen shows considerable resistance to physical and chemical treatments, it is susceptible to mild heat (55°C) and most hospital disinfectants. Environmental factors like high temperature and humidity, along with concurrent infections, poor nutrition, or work stress, significantly enhance the likelihood of HS infection, particularly during the rainy season. The organism demonstrates resilience, surviving for days in moist soil and water during monsoons. Oral or nasal secretions from both healthy and infected animals can contaminate feed and water, facilitating infection.

Pathogenesis

Pathogenesis initiates with infection in the tonsils and adjacent nasopharyngeal tissues. Critical biological features include a polysaccharide capsule that bolsters virulence and enables evasion of the host’s immune system, a crucial factor in infection severity. The bacteria colonize tissues, triggering a host cytokine response and endotoxin release, leading to a rapidly progressing systemic infection (endotoxemia), inflammation, and tissue damage. The endotoxin fraction, lipopolysaccharide (LPS), from the P. multocida cell membrane enters the bloodstream, inducing endotoxemia. This condition can provoke an excessive inflammatory immune response, a significant contributor to the pathogenesis of severe conditions like septic shock. Consequently, the clinical outcome includes high fever, respiratory distress, swelling, internal hemorrhages, and potentially rapid death.

Clinical Symptoms

Clinical signs typically manifest within 1–3 days after infection, with mortality possible within 8–24 hours of the first indication. These symptoms can present acutely or peracutely, often culminating in sudden death among affected animals. Buffaloes frequently endure a more severe and rapid progression of the disease, with low recovery prospects. Affected animals may exhibit fever, lethargy, and are soon followed by a watery nasal discharge and excessive drooling. Should the animal survive longer, a thicker nasal discharge may develop. Additional signs include swelling in the submandibular area and breathing difficulties, potentially leading to frothing at the mouth or nostrils. Occasionally, swelling may also occur in the front legs, neck, and chest. Some animals may experience hemorrhagic gastroenteritis, resulting in diarrhea and abdominal pain.

Diagnosis

Diagnosis of hemorrhagic septicemia in endemic areas relies on the typical clinical signs and lesions of the disease. The main lesion is swelling in the subcutis and muscles of the submandibular region, neck, and brisket, accompanied by clear to blood-tinged edema fluid. Serous to serofibrinous fluid might also be seen in the thorax, pericardium, and abdominal cavity. A lab diagnosis is made by isolating P. multocida serotype B:2 or E:2 from the blood and tissues of a patient showing classic symptoms. The passive mouse protection test with specific B:2 and E:2 rabbit sera has been used in Asia and Africa for identification. More accurate tests, such as indirect hemagglutination, coagglutination, counter immunoelectrophoresis, and immunodiffusion, are also employed in some labs. Recently, molecular methods like pulsed-field gel electrophoresis, Southern blots, loop-mediated isothermal amplification, and PCR have been utilized to differentiate between capsular and somatic serotypes. PCR array techniques are particularly suitable for use in endemic areas and can be applied to various samples, including blood, tissues, or bacteria from cultures.

Treatment

Treatment options include fluoroquinolones, tetracyclines, florfenicol, and cephalosporins, all proving effective against P. multocida. Other antibiotics such as penicillins, sulfonamides, and aminoglycosides also demonstrate efficacy against this bacterium. Flunixin can be utilized to manage inflammation, pain, endotoxic shock, and respiratory diseases. To effectively prevent HS, three vaccines are available: oil adjuvant vaccine (OAV), aluminum hydroxide vaccine (APV), and solid bacterin. Proper immunity requires repeated vaccinations. While a shock reaction may occur with the solid bacterin, it is highly unlikely with APV and OAV.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Enrofloxacin: 2.5mg-5mg/kg Parenteral OD for 3-5days.	Fortivir 30 ml(100mg Enrofloxacin/ml) inj vial( Verbac India). Floxidin 100ml(100mg Enrofloxacin/ml) inj vial( MSD india). Efx -LA 100ml(120mg Enrofloxacin/ml) inj vial( Parex India). Enolox-K 30ml (100mg Enrofloxacin and 60 mg Ketoprofen/ml)inj vial( Zenley Animal health). Enrovet 100ml (100mg Enrofloxacin/ml) inj vial ( Vets Pharma India). Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Ceftiofur: 1.1-2.2mg/kg IM OD for 3-5 days.	Xnel 1g (1000mg Ceftiofur) Injection Vial (Zoetis India). Xfur 1g (1000mg Ceftiofur) Injection Vial (Vet Life Science India). Ceftio-4 1g (1000mg Ceftiofur) Injection Vial (Geevet Remedies India). Capoform 1g (1000mg Ceftiofur) Injection Vial (Carus Laboratories India). Xceft 1g (1000mg Ceftiofur) Injection Vial (Alembic India). Izafur 1g (1000mg Ceftiofur) Injection Vial (Izda Health Care India).
Sulfadimidine( Sulfamethazine) : Initial dose ( 150mg/kg PO/ IV / IM / SC ) followed by maintenance dose (75mg/kg PO/ IV / IM / SC BID) for 3-5 days.	Unodine 99ml (333mg Sulfadimidin/ml) injection vial ( Sarabhai India) SD-VET 100 ml (333mg Sulfadimidin/ml) injection vial ( Intracin pharmaceutical India). Vetsulfa 5g sulfadimidine bolus( Vet world India)
	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Gentamicin: 6-12mg/kg IM/IV / SC OD for 3 -5days.	Gentamicin 100ml(40 mg Gentamicin/ml) inj vial(Zuche Pharmaceuticals India). Gentamicin 30ml(40 mg Gentamicin/ml) inj vial (Zuche Pharmaceuticals India). Genacyn LA 30ml(80 mg Gentamicin/ml) inj vial( Zenley Animal Health India). Gentamor Vet 100ml(40 mg Gentamicin/ml) inj vial( Morvel Indi
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

Infectious bovine keratoconjunctivitis (IBK): Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Infectious bovine keratoconjunctivitis (IBK), commonly referred to as pink eye complex or infectious ophthalmia, is a highly contagious disease in cattle caused by Moraxella bovis and Moraxella bovoculi. M. bovis is a Gram-negative, aerobic, oxidase-positive rod-shaped bacterium that exists in both piliated and non-piliated forms. It thrives on bovine blood agar, forming flat, rough colonies that can break down into smaller, convex, smooth, and non-corroding colonies upon further subculturing. The piliated form is responsible for causing the clinical disease. Flies are significant vectors in the transmission of IBK-related microbial agents among cattle, with outbreaks notably peaking during fly season.

Pathogenesis

Pathogenesis of infectious bovine keratoconjunctivitis is a systematic process—dust and flies inflict damage on the cornea, providing a surface for M. bovis to bind via its attachment pili. Subsequently, the bacteria release pore-forming cytotoxins that harm corneal epithelial cells, leading to inflammation, opacity, and ulceration. Additional factors such as UV light, host immunity, and the presence of other pathogens further influence this infection. Notably, M. bovis possesses enzymatic properties that contribute to corneal epithelial destruction. Other organisms capable of causing conjunctivitis in cattle—either independently or in conjunction with M. bovis—include Moraxella ovis (formerly Branhamella ovis), Mycoplasma spp., and Neisseria spp. Co-infection with infectious bovine rhinotracheitis (IBR) or other pathogens can exacerbate the severity of M. bovis infections. Environmental factors such as dry, dusty conditions, shipping stress, bright sunlight, and irritants like pollen and grasses also contribute to disease predisposition and exacerbation.

Clinical Symptoms

Clinical signs of IBK range from mild eye irritation with tears and small white ulcers to severe inflammation, ultimately leading to permanent scarring, corneal rupture, and vision loss. Additionally, elevated body temperature and significant pain can suppress appetite.

Diagnosis

Diagnosis is made through the identification of the Moraxella organism or by noting multiple affected animals within a herd exhibiting the same clinical symptoms when no other cause is present. A presumptive diagnosis of IBK or IKC typically relies on visible clinical signs in combination with general physical examination findings.

Treatment

Treatment for IBK includes both systemic and local application of antimicrobials, with oxytetracycline and tulathromycin being the preferred choices for M. bovis-associated IBK in cattle. Topical oxytetracycline, formulated as oxytetracycline hydrochloride and polymyxin B sulfate in an ophthalmic ointment, is approved for the treatment of pinkeye in cattle and sheep. Topical ointments or sprays must be applied at least every 8–12 hours for effectiveness, which may pose practical challenges in typical herd settings.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).
Oxytetracycline Eye Ointment	Human formulations: Teracin (Oxytetracycline) 3gm eye ointment( S3M Pharma India).

---

Johne’s disease (Paratuberculosis):: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Johne’s disease, also known as Paratuberculosis, is a significant infectious disease caused by the bacteria Mycobacterium avium subspecies paratuberculosis (Map), which primarily affects the intestines and nearby lymph nodes of ruminants such as cows. Initially, infections often go unnoticed, complicating detection efforts. Infected animals are the primary source of Johne’s disease, shedding the bacteria in their feces. Mycobacterium avium subspecies paratuberculosis is a fastidious, nonspore-forming, acid-fast, gram-positive rod bacterium. The most common route of infection is through fecal or manure contamination. Infection typically begins in the first few months of life; while older animals demonstrate better resistance, they remain susceptible if they ingest a sufficient quantity of the bacteria. In beef herds, manure can contaminate feed and soil quality, increasing the risk for younger animals. Young animals contract the infection by drinking contaminated milk, licking dirty surfaces in their environment, or coming into contact with areas with accessible adult manure. Additionally, water and feed contaminated with manure further pose infection risks. Furthermore, milk and colostrum from infected mothers can also be sources of infection. Although Map does not thrive outside the host, its resilient cell wall enables it to survive for over a year in various environments. Exposure to sunlight, heat, and dehydration can diminish the bacteria’s viability.

Pathogenesis

Pathogenesis initiates with the ingestion of contaminated feed and water; the bacteria (Map) are taken up by intestinal cells known as M cells. M cells present Map to macrophages, allowing the bacteria to multiply slowly, and if the infection establishes, it can destroy the macrophage and continue to proliferate. Macrophages fuse into large cells and, along with lymphocytes, infiltrate infected tissues in large numbers, leading to granulomatous thickening of the intestine. In later phases of the immune response, bacteria escape from macrophages into the intestinal lumen, and animals begin to shed Map in their feces. Notably, Map can evade the immune response, even when the immune system is activated. However, not all infections progress to disease; some animals’ immune responses can effectively halt the infection. An inadequate immune response to Map can lead to serious complications, including inflammation, nutrient absorption issues in the intestines, disturbances in various immune systems, and an eventual breakdown of the immune response, allowing unchecked infection growth.

Clinical Symptoms

Clinical signs appear late in life due to the gradual progression of the infection, with cattle remaining infected for years before showing any signs of disease. The primary manifestations include intermittent diarrhea that becomes chronic, weight loss, and a generally good appetite. Some infected animals may initially appear unthrifty, and affected cattle typically do not exhibit fever. The manifestations of this disease can easily be mistaken for other conditions and may coincide with stressful events such as calving, dietary changes, or relocation. Some studies indicate that subclinical stages may lead to decreased performance, particularly in milk production, during the final lactation before culling.

Diagnosis

Diagnosis relies on clinical symptoms and Map detection through culture and other validated methods. A key advantage of Map culture is that it allows for the storage of colonies or biomass at −80°C for further research. Map can be cultured from infected tissues, feces, or blood, as well as from soil, grass, water, and food samples like milk and cheese. Serological tests are quick and inexpensive for confirming clinical diagnoses; those employing ELISA technology offer the best sensitivity and specificity for determining herd infection rates. PCR has largely replaced culture for Map detection, being more sensitive and specific, in light of the slow growth rate (2–4 months) of the organism and the higher costs associated with culture.

Treatment

Treatment is not effective in curing Johne’s disease; the best approach is the culling of diseased and infected animals. Proper hygienic management practices in sheds and surrounding environments must be followed to ensure minimal exposure of young animals to Map infection.

Drugs and formulations available in India.

There is no treatment or formulation for paratuberculosis in cattle in India.

---

Joint ill: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Joint ill (infectious polyarthritis) is a serious bacterial disease commonly caused by E. coli and Strep. spp., resulting in infectious arthritis in calves. Bacteria enter the bloodstream from the gut. They also enter from the upper respiratory tract. This occurs particularly in calves born in unhygienic conditions such as dirty calving pens and wet bedding. Inadequate colostrum intake promotes bacterial growth in the body, and an untreated umbilicus serves as a portal for infection. Calves in their first few weeks are more vulnerable than older ones. The fetlock, carpal joints, hock, and stifle joints are the most frequently affected. Either a single joint or multiple joints can become involved, leading to polyarthritis.

Pathogenesis

Pathogenesis commences with bacteria entering and proliferating in the joints, triggering an inflammatory response that results in joint swelling. Pain arises from septic joints, synovial reactions, and erosion of articular cartilage. The synovial membrane, which lines the joint, becomes inflamed and proliferates, fostering a more favorable environment for bacteria. The infection causes the release of destructive enzymes. Inflammatory agents are also released into the joint fluid. This process leads to the degradation of the articular cartilage. Pus may accumulate, causing joint effusion, with the affected joints appearing swollen, hot, and painful. The draining lymph nodes (prescapular or popliteal) typically swell to two to four times their normal size. Infection leads to significant muscle wasting in the gluteal and shoulder regions. If untreated, the infection can become chronic, resulting in lasting consequences. Damage to the cartilage and underlying bone can lead to permanent arthritis, chronic pain, and severe lameness.

Clinical Symptoms

Clinical symptoms include swollen, painful joints and varying degrees of non-weight-bearing lameness. Calves with multiple limbs affected may adopt a “crab-like” stance, with rectal temperature often remaining within normal limits. The navel may appear thickened and painful.

Diagnosis

Diagnosis is achieved through clinical findings and examination of joint effusion obtained via needle aspiration.

Treatment

Treatment involves lavage of the infected joint, administration of broad-spectrum antibiotics, and NSAIDs. Flunixin meglumine can be given intramuscularly, twice daily for 3 days, acting as an analgesic, anti-inflammatory, and antipyretic agent. A combination of penicillin and dihydrostreptomycin is administered intramuscularly, once daily for 5 days. In severe, untreated cases, joint ill can be fatal. Polyarthritis represents a significant welfare concern; therefore, calves or animals with severe unresponsive lameness must be euthanized. Joint ill can effectively be prevented by implementing crucial measures. Provide at least 3 liters of high-quality colostrum. Do this within the first 6 hours of life. Ideally, it should be provided within the first two hours. An oesophageal feeder may be utilized to administer colostrum if the calf does not suck. Reduce the environmental bacterial challenge in calving boxes by cleaning thoroughly between each calving cow. Immerse the umbilicus (navel) in strong veterinary iodine BP within the first 15 minutes of life. If feasible, repeat the treatment 2 to 4 hours later. Promptly treat all infections after consulting veterinary advice.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg + Streptomycin 5 to 10 mg/kg IM OD 5-7 days.	Dicrysticine 5g(2.5g Streptomycin sulphate. 1500000IU procaine penicillin 500000 penicillin G sodium) inj vial( Zydus India). Xydocin 2.5 g (1.5g Streptomycin sulphate. 1500000IU procaine penicillin. 100000 penicillin G sodium) inj vial ( Sarabhai India)

---

Navel ill: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Navel ill is a condition involving an infection of the navel portion of the umbilical cord. Mixed bacteria infect it. The most commonly found bacteria are Staphylococcus aureus, Streptococcus bovis, and Escherichia coli. Navel ill may be in the form of omphalitis, omphalibitis, or omphaloarteritis. Calves born in dirty calving pens face a high risk of navel infection. This risk is most acute during the first few days after birth. The stressful conditions and inadequate feeding of colostrum exacerbate the condition. The omphalitis may lead to liver abscess, while omphaloarteritis can lead to internal iliac artery abscess. The infection of navel ill can also reach the blood, causing septicemia and affecting other organs including joints. Navel ill can also lead to thrift in calves.

Pathogenesis

Pathogenesis of naval ill begins with the contamination of the naval cord by dirt and manure that harbor pathogens. These pathogens thrive and multiply in the naval cord, triggering an inflammatory response that leads to swelling. This is followed by necrosis and the formation of an abscess. The infection can disseminate along the naval tracts, resulting in abscesses in the liver. It may enter the bloodstream, thereby affecting other organs, including the joints. Consequently, this progression results in septicemia, joint ill, other organ diseases, and overall ill thrift.

Clinical Symptoms

Clinical signs of infection are heat, swelling, purulent discharge, or pain. Concurrent signs of systemic infection, such as joint infection, pneumonia, diarrhea, meningitis, or uveitis.

Diagnosis

Diagnosis of navel infections is based on physical palpation and clinical signs. Swelling, pain on palpation, fever, and abscess formation in a neonatal calf are strong indications of navel ill.

Treatment

Treatment involves lavage of the infected joint, administration of broad-spectrum antibiotics, and NSAIDs. Flunixin meglumine can be given intramuscularly, twice daily for 3 days, acting as an analgesic, anti-inflammatory, and antipyretic agent. A combination of penicillin and dihydrostreptomycin is administered intramuscularly, once daily for 5 days. The best preventive measures focus on maintaining hygienic conditions in calving areas. After calving, ensure the calf stays in clean pens. Applying disinfectant to the umbilical stump immediately after parturition is crucial. Use 2% iodine or a chlorhexidine solution. Providing supportive care may help resolve the infection. This can prevent the development of abscess and distention in the urachus or the umbilical arteries and vein.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin 22,000–66,000 U/kg + Streptomycin 5 to 10 mg/kg IM OD 5-7 days.	Dicrysticine 5g(2.5g Streptomycin sulphate. 1500000IU procaine penicillin 500000 penicillin G sodium) inj vial( Zydus India). Xydocin 2.5 g (1.5g Streptomycin sulphate. 1500000IU procaine penicillin. 100000 penicillin G sodium) inj vial ( Sarabhai India)

---

Bovine leptospirosis: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Bovine leptospirosis is a significant reproductive disease affecting cattle, primarily caused by strains from the Sejroe serogroup, which are specific to cattle and transmitted directly among them. These strains are widely distributed globally and are commonly detected in serological studies. The key serovars in this group include Hardjoprajitno (L. interrogans) and Hardjobovis (L. borgpetersenii), while the serovar Guaricura (L. santarosai) is frequently found in South American cattle. Other strains, such as Icterohaemorrhagiae, Pomona, Australis, and Grippotyphosa (L. interrogans), can also infect cattle but are mainly adapted to different hosts. Leptospira is a Gram-negative bacterium with a spiral conformation. Cattle contract Leptospira infection through direct contact with the bodily fluids of infected animals or indirectly through contaminated environments like water or soil. The bacteria penetrate the body via mucous membranes (eyes, nose, mouth) or through skin abrasions. While incidental infections in bovines are less frequent than those caused by the Sejroe group, they can result in acute manifestations, particularly in calves, sometimes leading to abortion outbreaks. Numerous animal species, especially rodents, serve as reservoir hosts for serotypes other than Sejroe.

Pathogenesis

Pathogenesis includes direct infection of the embryo and inflammation of the uterus. Infection of the embryo leads to its non-viability and death. Inflammation of the endometrium due to leptospiral infection compromises the uterine environment and embryonic development.

Clinical Symptoms

Clinical signs of bovine leptospirosis encompass acute symptoms such as fever, reduced milk production (accompanied by blood-tinged or viscous milk), and in severe cases, anemia, jaundice, and hemoglobinuria. Reproductive symptoms, which often appear chronic and silent, consist of abortions, stillbirths, weak offspring, infertility, and repeated breeding cycles.

Diagnosis

Diagnosis involves the detection of leptospiral antibodies by the microscopic agglutination test (MAT), employing live cultures of Leptospira strains tested at various dilutions against serum from patients (animal or human). The enzyme-linked immunosorbent assay (ELISA) is also widely utilized for the serological diagnosis of leptospirosis. PCR-based techniques provide rapid results and exhibit high sensitivity and specificity for detecting Leptospira in urine, cerebrospinal fluid, or blood samples during the early stages of the disease, as well as in the urine, kidney, or genital tract of chronic animal carriers.

Treatment

Treatment protocol for leptospiral carriers is the administration of streptomycin at a dosage of 25 mg/kg for three consecutive days. Studies have shown that other antimicrobial drugs, such as enrofloxacin, oxytetracycline, and ceftiofur, can effectively treat renal carriers, although their efficacy for genital colonization remains untested. Vaccination of animals before their introduction into endemic areas is strongly advised. The available commercial vaccines are all composed of bacterins, i.e., whole inactivated bacterial cells. It is crucial that vaccines include representatives of the main serogroups present in the region, and ongoing epidemiological monitoring through serology is vital in this respect.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Streptomycin 25/kg IM OD for 3 days days.	Dicrysticine 5g(2.5g Streptomycin sulphate. 1500000IU procaine penicillin 500000 penicillin G sodium) inj vial( Zydus India). Xydocin 2.5 g (1.5g Streptomycin sulphate. 1500000IU procaine penicillin. 100000 penicillin G sodium) inj vial ( Sarabhai India)

---

Bovine Salmonella infection: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Salmonella infection in dairy calves often leads to enteritis in those under one month old. Infected calves are known to develop severe enteritis characterized by a significant presence of neutrophils. The most common Salmonella serotypes identified in cattle are Salmonella typhimurium and Salmonella dublin, both of which exhibit resistance to many antibiotics. Notably, Salmonella dublin is host-specific, contrasting with the non-host-specific nature of S. typhimurium, with both affecting calves aged six to twelve weeks. Members of the Salmonella genus are gram-negative, rod-shaped bacteria within the Enterobacteriaceae family, typically motile except for S. enterica ser. Pullorum and S. enterica ser. Gallinarum, which lack flagella. The presence of Salmonella in the environment plays a crucial role in calf salmonellosis, commonly found in farm waste and human sewage, which complicates its epidemiology in intensive animal husbandry. Contaminated environments and food supplies are significant risk factors, as infected animals and humans can spread the disease via feces, saliva, and milk, with fecal-oral transmission being the primary method. Additionally, Salmonella may be indirectly transmitted through contaminated feed and water, and by wildlife such as small mammals and birds.

Pathogenesis

Pathogenesis of Salmonella infection involves various virulence factors, such as type three secretion systems (T3SS), virulent plasmids, flagella, capsules, and adhesion systems. These systems, found in most serovars of Salmonella enterica, include adhesins, invasins, toxins, fimbriae, and hemagglutinins, allowing Salmonella to effectively colonize host cells and evade the body’s defenses.

Clinical Symptoms

Clinical manifestations can range from asymptomatic to clinically evident salmonellosis, with acute diarrheal disease being most common with S. typhimurium and systemic disease with S. dublin in cattle. The disease is predominantly found in dairy cattle rather than beef cattle and is closely linked to management practices. The infective dose, along with predisposing factors and host immunity status, plays a decisive role in determining the infection’s outcome. Salmonella infection presents in per acute (diarrhea and septicemia), acute (fever), and chronic (unthrifty, scruffy hair) forms.

Diagnosis

Diagnosis methods include cultural isolation, immunology-based assays, nucleic acid-based assays, miniaturized biochemical assays, and biosensors. Although cultural isolation is time-consuming, immunology-based assays leverage specific antibodies to detect Salmonella species, including techniques like ELISA, latex agglutination tests, immunodiffusion, and dipstick tests. While these assays can identify non-culturable Salmonella cells, they may exhibit cross-reactions, require longer processing times, and can be costly. Nonetheless, they effectively handle large samples and are easily automated. The ELISA test assesses the infection status of individual animals and herds, distinguishing between recently infected and convalescent calves, with carriers maintaining constant titers. Nucleic acid-based assays identify organisms directly from samples by targeting specific nucleic acid sequences. These techniques are known for their heightened sensitivity and specificity; the predominant methods are direct hybridization (DNA probe) and PCR. The PCR test amplifies specific DNA segments for the detection of Salmonella pathogens, focusing on the conserved Salmonella invasion gene (invA). This method significantly enhances the detection of low organism numbers, thus reducing enrichment time for reliable results compared to other approaches. A biosensor integrates a detector with a biological recognition system, transforming biological responses into measurable output signals. When an analyte binds to the recognition element, it generates a signal, which may manifest as changes in mass, oxygen consumption, voltage, refractive index, pH, and more. Biosensor diagnostics have the potential to replace existing immunology and nucleic acid-based methods, effectively identifying biological components such as enzymes and nucleic acids.

Treatment

Treatment of  Salmonella infection with antibiotics is controversial for several reasons. First, appropriate antimicrobial selection is challenging because most Salmonella strains are multidrug-resistant. Enrofloxacin, trimethoprim sulphonamides, oxytetracyclines, and ceftiofur are reasonable choices. Calves with systemic infection should be administered NSAIDs like flunixin meglumine or meloxicam to manage inflammation. Effective prevention and control of Salmonella hinge on Hazard Analysis Critical Control Point (HACCP) principles, stringent biosecurity measures, proper disinfection, stress avoidance, and routine immunization.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Enrofloxacin: 2.5mg-5mg/kg Parenteral OD for 3-5days.	Fortivir 30 ml(100mg Enrofloxacin/ml) inj vial( Verbac India). Floxidin 100ml(100mg Enrofloxacin/ml) inj vial( MSD india). Efx -LA 100ml(120mg Enrofloxacin/ml) inj vial( Parex India). Enolox-K 30ml (100mg Enrofloxacin and 60 mg Ketoprofen/ml)inj vial( Zenley Animal health). Enrovet 100ml (100mg Enrofloxacin/ml) inj vial ( Vets Pharma India). Fnoro-vet 250ml(100mg Enrofloxacin/ml) oral solution( Facemed Pharma India). Floxavet 100ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Floxavet 150ml(100mg Enrofloxacin/ml) oral solution( Geevet India). Meriquin 150mg (150mg Enrofloxacin)tab ( Vetoquinol India).
Ceftiofur: 1.1-2.2mg/kg IM OD for 3-5 days.	Xnel 1g (1000mg Ceftiofur) Injection Vial (Zoetis India). Xfur 1g (1000mg Ceftiofur) Injection Vial (Vet Life Science India). Ceftio-4 1g (1000mg Ceftiofur) Injection Vial (Geevet Remedies India). Capoform 1g (1000mg Ceftiofur) Injection Vial (Carus Laboratories India). Xceft 1g (1000mg Ceftiofur) Injection Vial (Alembic India). Izafur 1g (1000mg Ceftiofur) Injection Vial (Izda Health Care India).
Sulfadimidine( Sulfamethazine) : Initial dose ( 150mg/kg PO/ IV / IM / SC ) followed by maintenance dose (75mg/kg PO/ IV / IM / SC BID) for 3-5 days.	Unodine 99ml (333mg Sulfadimidin/ml) injection vial ( Sarabhai India) SD-VET 100 ml (333mg Sulfadimidin/ml) injection vial ( Intracin pharmaceutical India). Vetsulfa 5g sulfadimidine bolus( Vet world India)
	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

Bovine Mycoplasmosis : Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Bovine Mycoplasmosis is caused by Mycoplasma bovis (M. bovis), a gram-negative bacterium from the Mycoplasmataceae family. It has a small genome, no cell wall, and low G+C content. A Mycoplasma colony on a solid agar medium is known for its characteristic “fried egg” appearance. It has a central, spherical or hemispherical part that grows into the agar. It also has a flatter, peripheral zone that spreads across the agar’s surface. M. bovis is a major opportunistic pathogen in beef and dairy calves, causing pneumonia, ear infections, and arthritis in those under three months old. The disease is chronic and doesn’t respond well to treatment, persisting in herds for weeks to months, which raises animal welfare concerns due to severe suffering. In the dairy industry, it leads to economic losses from reduced milk production and increased death rates in calves. The bacteria spread directly through contact or aerosols and indirectly via contaminated tools or respiratory secretions. A key transmission method from cows to calves is through contaminated milk. The bacteria can survive well in humid, cool conditions and may be carried by healthy animals in their upper respiratory tracts, serving as a source of infection for others.

Pathogenesis

Pathogenesis is initiated with the growth and colonization of mycoplasma within the respiratory tract. Certain virulence factors (adhesin, CARDS toxins, H2O2, H2S, and other enzymes) of M. bovis favor adhesion, host cell invasion, modulation of the host immune system, production of secondary metabolites, and biofilm formation. The synergistic infections with other viral and/or bacterial microorganisms also enable mycoplasma to overcome the host immune system. Actinomyces pyogenes, Haemophilus somnus, and Pasteurella species may synergistically act with M. bovis to cause bovine pneumonic pasteurellosis, bovine enzootic bronchopneumonia, or bovine respiratory disease (BRD). Colonization of the respiratory tract occurs more often in calves fed milk infected with M. bovis compared to calves fed non-infected milk.

Clinical Symptoms

Clinical signs vary from animal to animal, and young calves may show signs of coughing, nasal discharge, fever, and otitis media. Polyarthritis, lameness, joint swelling, pain, and difficulty breathing are seen in adult animals, along with mastitis in dairy cows. In severe cases, calves may develop pneumonia and require intensive care. In some cases, the infection can spread to the central nervous system, leading to neurological signs such as incoordination and seizures.

Diagnosis

Diagnosis of M. bovis infection is challenging, as the clinical signs are not specific. Cultural isolation, serological tests, and molecular diagnostic approaches can be used to diagnose Mycoplasma bovis infections from nasal swabs, joint fluid, and blood samples. PCR is a molecular technique that can detect the DNA of Mycoplasma bovis in samples.

Treatment

Treatment with antibiotics can be difficult because Mycoplasma bovis is resistant to many common antibiotics like fluoroquinolones, macrolides, tetracyclines, and β-lactams due to overuse in the animal industry. However, macrolides can be effective against bovine mycoplasmosis. Antimicrobial susceptibility testing should be done to help choose the right antibiotic. Supportive care is also crucial, with calves facing respiratory issues possibly needing oxygen, nebulization, and bronchodilators, while those with arthritis may require pain relief and joint support. To prevent and control Mycoplasma bovis infections in dairy calves, a comprehensive strategy is necessary, including biosecurity, vaccination, and proper antibiotic use. Maintaining good hygiene by cleaning and disinfecting equipment and surfaces can lower transmission risks. Vaccines against Mycoplasma bovis can help reduce infection severity in calves, but no single vaccine offers complete protection against all strains.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Tylosin: 10–20mg/ kg IM OD for 5 days in cattle.	Tylosin tartrate 30ml ( 200mg Tylosin/ml) inj vial( Facemed Pharmaceutical India). Tylosin tartrate 100ml ( 200mg Tylosin/ml) inj vial( Facemed Pharmaceutical India). Tylo-200 – 99ml ( 200mg Tylosin/ml) inj vial ( Vet India). Tysin 100 / Tysin 200 – 100ml( 100mg / 200mg Tylosin/ml) inj vial ( Vet India). Tylo- Rd- Vet 100ml( 100mg / 200mg Tylosin/ml) inj vial ( TTK Health Care India). Trox 50g /120g Powder ( Verbac India ).
Tilmicosin: 10-20mg/kg S/C single Injection	Tilmotil 15ml (300mg Tilmicosin/ml) inj vial (Zenex AH India). Tilmotil 30ml (300mg Tilmicosin/ml) inj vial (Zenex AH India).

---

Bovine Listeriosis: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Bovine listeriosis in calves and dairy cows is caused by Listeria monocytogenes and L. ivanovii. The genus Listeria is an intracellular gram-positive bacterium that belongs to the family Listeriaceae. The bacteria of this genus are non-capsulated, coccoid to rod-shaped cells, facultative anaerobes, flagellated, and non-spore-forming organisms. L. monocytogenes is ubiquitous, thriving in diverse environments such as soil, mud, decaying plant matter, raw and treated sewage, water, and food processing facilities. Its remarkable ability to grow at refrigerator temperatures highlights its adaptability. As the causative agent of listeriosis, L. monocytogenes poses one of the most significant emerging and opportunistic foodborne threats to human health. Risk factors contributing to infection in animals include poor nutritional status, age, parity, abrupt weather changes, late pregnancy, parturition stress, transportation, and overcrowding. Listeria monocytogenes is transmitted through ingestion, inhalation, or direct contact with infected animals. Contaminated silage, feed, water, or bedding are the principal modes of transmission. Calves afflicted with septicemic L. monocytogenes disease may contract the infection from contaminated cow teats while consuming milk or from a cow exhibiting subclinical bacteremia, through environmental exposure via the navel, or even from congenital infection. The infection can lead to severe outcomes, including septicemia, meningitis, uterine infections (such as abortion and stillbirth), subclinical mastitis, and even death in dairy calves and cows. Listeriosis predominantly affects calves, pregnant cows, and immunocompromised cattle.

Pathogenesis

Pathogenesis of L. monocytogenes arises from several molecular determinants, including hemolysin (listeriolysin O), two phospholipases, protein (ActA), internalin A (InlA), internalin B (InlB), and various cytotoxins, all essential for the pathogen’s intracellular motility. The hemolysin toxin effectively lyses tissue and blood cells, while the cytotonic toxin boosts cyclic AMP production, akin to cholera toxin. All serotypes of L. monocytogenes possess the capability to provoke monocytosis.

Clinical Symptoms

Clinical manifestations of listeriosis in dairy cows include neonatal septicemia, encephalitis, and abortion during late pregnancy, alongside symptoms such as depression, fever, diarrhea, anorexia, meningitis, and neurological issues in calves. These neurological signs can manifest as circling, head pressing, and ataxia.

Diagnosis

Diagnosis of Listeria monocytogenes is established through bacterial culture, animal inoculation, immunological assays, and molecular tests performed on brain tissue, blood, and fecal samples.

Treatment

Treatment with preferred antibiotics for listeriosis involves penicillin G, aminoglycosides, trimethoprim, sulfamethoxazole, and tetracycline for dairy calves. Effective infection prevention strategies for dairy calves include diligent management practices, such as maintaining clean and hygienic facilities and equipment, ensuring proper colostrum management, and reducing stress. Vaccination also serves as an effective measure in preventing infections in calves.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Procaine Penicillin : 11000-22000IU/ kg IM OD×5-7days	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Ceftiofur: 1.1-2.2mg/kg IM OD for 3-5 days.	Xnel 1g (1000mg Ceftiofur) Injection Vial (Zoetis India). Xfur 1g (1000mg Ceftiofur) Injection Vial (Vet Life Science India). Ceftio-4 1g (1000mg Ceftiofur) Injection Vial (Geevet Remedies India). Capoform 1g (1000mg Ceftiofur) Injection Vial (Carus Laboratories India). Xceft 1g (1000mg Ceftiofur) Injection Vial (Alembic India). Izafur 1g (1000mg Ceftiofur) Injection Vial (Izda Health Care India).
Sulfadimidine( Sulfamethazine) : Initial dose ( 150mg/kg PO/ IV / IM / SC ) followed by maintenance dose (75mg/kg PO/ IV / IM / SC BID) for 3-5 days.	Unodine 99ml (333mg Sulfadimidin/ml) injection vial ( Sarabhai India) SD-VET 100 ml (333mg Sulfadimidin/ml) injection vial ( Intracin pharmaceutical India). Vetsulfa 5g sulfadimidine bolus( Vet world India)
	Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial (Zydus AH India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( IPPL India). Fortified Procaine Penicillin 20 lac IU Penicillin inj vial (White Swan Pharmaceuticals India). Fortified Procaine Penicillin 40 lac IU Penicillin inj vial ( White Swan Pharmaceuticals India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle.	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).

---

Contagious mastitis in Cattle: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Contagious mastitis in cattle is an inflammatory disease of mammary tissue in the udder and is transmitted from cow to cow, especially during milking. It is caused by Staphylococcus aureus and Streptococcus agalactiae, and less common species like Mycoplasma bovis and Corynebacterium. Contagious mastitis can be caused by these organisms that live on the cow’s udder and teat skin, colonizing and growing into the teat canal. These are capable of establishing subclinical infections, usually with an elevation in the Somatic Cell Count (SCC). The somatic cells consist of leukocytes (i.e., neutrophils, macrophages, lymphocytes, and erythrocytes) and epithelial cells. These cells present in significant numbers indicate marked mammary tissue infection. Genetic factors and dairy cow breeding affect the risk of mastitis. High-yielding breeds, especially Holstein-Friesians, are more prone to mastitis compared to medium-yielding breeds. Jersey cattle show lower mastitis rates than Holstein-Friesians. Cows with large teats or abnormal udder shapes and those with blind quarters after calving are at higher risk for subclinical mastitis. Additionally, teat size and the distance from teats to the floor can reduce the effectiveness of leukocytes in milk, increasing the likelihood of infections. Older cows are more susceptible due to wider teat canals from frequent milking and higher mammary epithelium permeability from past inflammation. The transition period, which is three weeks before and after calving, is when dairy cows are at greater risk for mastitis and other diseases.

Pathogenesis

Pathogenesis of contagious mastitis begins with the formation of biofilms by gram-positive bacteria. Staph. aureus creates a sugar structure called glycocalyx, which forms the biofilm’s matrix. This biofilm enables Staph. aureus to attach to mammary cells and obtain nutrients, helping it survive harsh environments and evade stressors such as antibiotics and immune responses. Once attached, the biofilm grows until it reaches a certain size, after which polysaccharide intercellular adhesin (PIA) is produced. Different biofilms may also produce extra slime that enhances bacterial adhesion. When the biofilm reaches a critical size, bacteria detach, spreading the infection. This is known as metastasis. After attaching to host cells, the bacteria release proteins that help them invade by breaking down host proteins. These factors contribute to a deep and lasting infection that intramammary antibiotics struggle to eliminate. Certain surface proteins on the bacterial cell wall are crucial for mastitis pathogenesis, including Staphylococcal protein A (SpA), coagulases, biofilm-associated protein (Bap), and invasins. SpA contributes in two ways: (1) it binds the Fcγ regions of IgG antibodies, helping S. aureus avoid detection and removal from the host, and (2) it binds to the Fab region of IgM, causing cross-links between B-cell receptors. This cross-linking alters host immune responses and can lead to the death of B lymphocytes as new cells are produced. Coagulases work in two ways: (1) they interact with prothrombin to create staphylothrombin, which changes fibrinogen into fibrin, resulting in blood clots that shield the bacteria from phagocytosis and immune responses, and (2) they increase the production of fibrinogen-binding proteins, which further aid in cell clumping and provide a protective fibrin coat against the host’s immune system. Biofilm-associated protein (Bap) plays a critical role in biofilm formation.

Clinical Symptoms

Clinical features of contagious mastitis are characterized by visual alterations in the udder. These include redness, swelling, and an increase in temperature. There may be elevated body temperature and anorexia in the cow. The affected milk exhibits abnormalities, becoming watery, discolored, and potentially containing flakes or clots. In severe cases, the cow becomes dull, depressed, and comatose and may die in the terminal stage.

Diagnosis

Diagnosing contagious mastitis in cattle requires observing clinical signs (like abnormal milk, swollen udder, fever, and reduced milk yield) and subclinical signs (high somatic cell count with normal milk), which can be confirmed through lab tests such as milk culture (to identify bacteria like Staph. aureus and Strep. agalactiae), PCR (for rapid pathogen detection), and the California Mastitis Test (CMT) for on-farm screening; these steps are essential for effective treatment and control of the infection.

Treatment

Treatment success depends on the stage of infection when antibiotics are started and the type and dosage used. Starting treatment early typically leads to better outcomes. An antibiotic sensitivity test (AST) is recommended to choose the most effective antibiotic. Without AST, various antibiotics are used; however, in the author’s experience, a combination of potentiated Ampicillin (Ampicillin + Cloxacillin) given twice daily with Gentamicin once daily for 3-5 days has proven effective. Cefoperazone and Telmicosin are also effective against Staphylococcus aureus and coagulase-negative staphylococci (CNS). Additional supportive treatments may include anti-inflammatory drugs, such as NSAIDs like Flunixin or steroids like prednisolone, taken daily for 5-7 days. Preventive measures include proper hygiene during and after milking, regularly cleaning the cow shed, and dusting the floor with lime each morning to keep infections at bay, as lime raises the pH to 12, which is harmful to most microbes, including fungi. During lactation, dairy cattle need more energy and nutrients to produce colostrum and milk. If their feed intake doesn’t meet these needs, they can experience a negative energy balance. This imbalance is linked to deficiencies in trace elements (like selenium, iron, copper, zinc, cobalt, and chromium), amino acids (such as lysine and L-histidine), and vitamins (including A, C, E, β-carotene, and lycopene), which can suppress the immune system at both the cellular and humoral levels during lactation, making them more prone to infections. Therefore, managing their diet during the transition period, such as by supplementing with vitamin E and zinc, is crucial to preventing mastitis and enhancing milk production.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Ampicilline + Colxacillin: 5-10mg/kg IM/IV/SC BD-TD for 3- 7days.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).
Cefparazone: 5-10mg /kg IM/IV BD for 3- 5 days.	Rampzone-4.5g (3g Cefparazone and 1.5 g Salbactum) inj vial (Iskon Remedies India). Pathocef 4.5 g inj vial (Zydus India). Pathocef 250 (250 mg Cefparazone) intra mammary suspension in a tube(Zydus India). Cefzone 4.5 g (3g and 1.5 g Salbactum)inj vial ( Gemtech India). Vet Sipzone-S 4500 (3g Cefparazone and 1.5 g Salbactum) inj vial ( Indian Genomix).
Tilmicosin: 10-20mg/kg S/C single Injection	Tilmotil 15ml (300mg Tilmicosin/ml) inj vial (Zenex AH India). Tilmotil 30ml (300mg Tilmicosin/ml) inj vial (Zenex AH India).

---

Environmental mastitis with special reference to E. coli in dairy Cattle: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Environmental mastitis in dairy cows arises from organisms residing in their surroundings, including Escherichia coli (E. coli), Klebsiella pneumoniae, Streptococcus uberis, Streptococcus dysgalactiae, and Enterobacter spp. Factors such as dirty and wet bedding, overcrowding, poor ventilation, inadequate manure management, ineffective pre-milking teat preparation, and seasonal variations—especially warm, humid conditions—greatly elevate the risk of mastitis. E. coli stands out as the most prevalent pathogen responsible for coliform mastitis in cattle, rapidly triggering an inflammatory response in the host. Genetic predispositions play a significant role; high-yielding breeds such as Holstein-Friesian show greater vulnerability to mastitis compared to those with medium yields, while Jersey cattle exhibit a lower incidence of the disease. Cows with large funnel-shaped teats or pendulous udders, as well as those with blind quarters post-calving, face an increased likelihood of subclinical mastitis. Additionally, the teat size and the distance from the teat to the floor may compromise the in vitro activity of leukocytes in milk, thereby amplifying the occurrence of intramammary infections (IMIs). Older cows are more susceptible to infections, likely due to a wider or permanently partially open teat canal resulting from frequent milking. The mammary epithelium of older cows also experiences heightened permeability due to irreversible damage from previous inflammations. The transition period, spanning three weeks before and after parturition, marks a time of heightened disease risk, including mastitis.

Pathogenesis

Pathogenesis of mastitis-related E. coli starts with its colonization of the udder, where adhesion factors like intimin, and Fimbriae present in E. coli are essential for effective adhesion to tissue surfaces. Firm adherence leads to cell aggregation via cell-to-cell interactions, generating an extracellular matrix that facilitates biofilm formation. Hemolysins produced by E. coli inflict cytotoxic damage on udder tissue through thrombotic microangiopathy, while Shiga toxins induce apoptosis in epithelial cells. Lipopolysaccharides (LPS), a primary virulent factor in the cell walls of gram-negative bacteria, bind to Toll-Like Receptor 4 on macrophages and dendritic cells, activating them. This activation initiates pathways (MyD88, TRIF) that spur the release of pro-inflammatory cytokines and interferons, which are crucial in launching inflammatory responses both locally and systemically. They also bolster the functions of leukocytes, including neutrophils and macrophages, guiding their migration to infection sites for effective clearance.

Clinical Symptoms

Clinical signs of coliform mastitis stem from endotoxin release and include udder swelling, watery milk with small flakes, reduced milk production, fever, and anorexia. In severe cases, symptoms may escalate to pyrexia, tachycardia, and shock due to endotoxemia. While typically affecting just one quarter, these infections can result in clinical mastitis in up to 90% of instances and are frequently linked to systemic illness. Although some cases of coliform mastitis can become chronic, typically over 50% resolve within ten days.

Diagnosis

Diagnosing coliform mastitis relies on clinical signs, culture of coliform organisms from milk, and elevated somatic cell counts. Often, culturing for coliform bacteria can yield limited results since host defenses may eliminate the bacteria from the gland within one or two milkings. To improve detection, streaking blood agar and MacConkey agar plates with 0.01 ml and 0.1 ml of milk, respectively, can facilitate observable growth for a conclusive diagnosis. If the cow succumbs to endotoxemia, bacteriology from chilled mammary tissue and regional lymph nodes, combined with histological evaluation of formalin-fixed mammary tissue, can confirm coliform mastitis. Clinical pathology in peracute coliform mastitis often shows hemoconcentration and significant leukopenia characterized by neutropenia with a degenerate left shift. Moderate lymphopenia, monocytopenia, and thrombocytopenia may also be present. Serum biochemistry in severe cases may reflect uremia, elevated aspartate aminotransferase levels, and metabolic acidosis. California Mastitis Test scores of +3 and a somatic cell count of 14-25,000,000 cells/ml of milk corroborate the diagnosis.

Treatment

Treatment of coliform mastitis necessitates addressing systemic endotoxemia. Severely affected cows are administered broad-spectrum intravenous antimicrobials to mitigate bacteremia, which can be present in up to 48% of coliform mastitis cases. Though intramammary infusions of antibiotics may not significantly alter the outcome of coliform mastitis cases, they can help reduce the presence of pathogenic gram-positive organisms within the mammary gland. Frequent stripping of the affected quarter, paired with oxytocin injections, has proven effective in reducing bacterial and endotoxin levels in the gland. Anti-inflammatory measures and fluid therapy are often essential to prevent shock and ensure overall hydration. Prevention of coliform mastitis poses challenges, as Escherichia coli, Klebsiella, and Enterobacter are omnipresent even in optimally managed dairies. Culturing individual milk samples is crucial for identifying the primary pathogens within the herd. Enhancing pre-milking hygiene and regularly assessing milking machine functionality can diminish bacterial load and teat-end alterations. Proper use of dry cow intramammary antimicrobials and teat sealants is essential for mitigating existing infections and preventing new ones during the dry period. Additionally, vaccination with a core lipopolysaccharide antigen vaccine can lessen the severity of coliform mastitis. During lactation, dairy cattle face heightened energy and nutrient demands for colostrum and milk production. A shortfall in feed intake relative to these demands leads to negative energy balance, which correlates with dietary deficiencies in trace elements (e.g., selenium, iron, copper, zinc, cobalt, and chromium), amino acids (e.g., lysine, L-histidine), and vitamins (e.g., A, C, E, β-carotene, lycopene). These deficiencies trigger cellular and humoral immunosuppression during lactation onset, increasing infection susceptibility. Thus, effective management of the diet during the transition period, including vitamin E and zinc supplementation, is vital to prevent mastitis infections and enhance lactation outcomes.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Amoxicillin: 4-10mg/kg IM BD or 10-20mg/kg PO BD X 3-7 days.	Amoxirum fort 3g inj vial ( Virbac India). Amoxirum fort 4.5 g inj vial ( Virbac India). Intamox-D 3.5g inj vial ( Intas India). Intamox-D 4.5 g inj vial ( Intas India). Moxel 3g (Amoxicillin 250mg and Cloxacillin 250 mg) inj vial( Alembic India).
Oxytetracycline: 5-10mg/kg OD IM/IV in cattle	OXIVIA 100ml(50mg Oxytetracycline/ml ) Inj vial ( Nicosia international India). Vetocyclin-DS 50ml (100mg Oxytetracycline/ml )inj vial( Vetoquinol India). Vetocyclin-DS 100ml (100mg Oxytetracycline/ml ) inj vial( Vetoquinol India) Teravet-LA 50ml (200mg Oxytetracycline/ml )inj vial ( Geevet Remidies India).
Ampicilline + Colxacillin: 5-10mg/kg IM/IV/SC BD-TD for 3- 7days.	Inj RC Fort D 4g ( 2gm Ampicillin Sodium and 2gm Dicloxacillin )Inj vial( Zenex AH India). Inj Nillin- vet 4.5 g (2.5gm Ampicillin Sodium and 2.5gm Colxacillin) Inj vial( Morvel India). Inj A C vet fort 3g (1.5gm Ampicillin Sodium and 1.5gm Colxacillin) Inj vial ( Intas India).
Cefparazone: 5-10mg /kg IM/IV BD for 3- 5 days.	Rampzone-4.5g (3g Cefparazone and 1.5 g Salbactum) inj vial (Iskon Remedies India). Pathocef 4.5 g inj vial (Zydus India). Pathocef 250 (250 mg Cefparazone) intra mammary suspension in a tube(Zydus India). Cefzone 4.5 g (3g and 1.5 g Salbactum)inj vial ( Gemtech India). Vet Sipzone-S 4500 (3g Cefparazone and 1.5 g Salbactum) inj vial ( Indian Genomix).
Tilmicosin: 10-20mg/kg S/C single Injection	Tilmotil 15ml (300mg Tilmicosin/ml) inj vial (Zenex AH India). Tilmotil 30ml (300mg Tilmicosin/ml) inj vial (Zenex AH India).

---

Bovine genital *Campylobacteriosis: Disease description, drugs and formulations in India.

By M. Younus, BVSc, MVSc, SKUAST-K

Disease description.

Etiology

Bovine genital campylobacteriosis is caused by Campylobacter fetus venerealis or C fetus fetus, which are motile, gram-negative bacteria. For a long time, C fetus fetus was seen mostly as a harmless intestinal bacterium, but it is now recognized as a significant cause of infertility, often confused with C fetus venerealis. To find out if a strain causes infertility, testing a potentially infected group of heifers is needed. Campylobacter spp. are fragile and can be quickly destroyed by heat, drying, or the environment. They must be cultured soon after collection under specific conditions to grow. C fetus is transmitted during mating, through contaminated instruments or bedding, or artificial insemination with contaminated semen. Bulls show different susceptibility; some are permanent carriers while others resist infection, likely due to the age-related development of preputial and penile crypts. Young bulls (< 3–4 years old) have less developed crypts, which means infections are usually temporary and depend on contact with uninfected cows after mating with infected ones. Young bulls can easily get reinfected as their clearance isn’t linked to immune responses. Older bulls (> 3–4 years old) have deeper crypts allowing for chronic infections. In cows, some clear the infection quickly, while others carry C fetus for more than 2 years. IgA is detected in cervical mucus in about half of the cows for months after infection and helps with diagnosis. Even if most of the genital tract is infection-free when a cow becomes pregnant, the vagina might remain infected throughout the pregnancy.

Pathogenesis

Pathogenesis confidently begins with the introduction of bacteria through the bull’s semen into the cervix of the cow or heifer, from which it swiftly moves to the uterus. In the uterus, C. fetus effectively employs flagella and adhesins (such as CadF) to firmly adhere to and invade endometrial and oviductal epithelial cells. This leads to successful colonization, followed by an inflammatory response that results in subacute mucopurulent endometritis, cervicitis, and salpingitis. Consequently, the uterine environment becomes hostile for a developing embryo, leading to early embryonic death between 15 and 80 days. This phenomenon results in “repeat breeding” and irregular estrous cycles. Occasionally, the fetus may survive until the third trimester, only to abort at 4–7 months of gestation. In most cows, the infection is self-limiting, and they clear the bacteria from the uterus within 3–6 months, developing temporary immunity. However, a small percentage can remain chronic vaginal carriers.

Clinical Symptoms

Clinical signs of campylobacteriosis range from repeat breeding to abortion. Cows may return to heat at irregular intervals, often between 30 and 90 days after service, due to early embryonic death. Sporadic abortions may occur, typically between the 4th and 7th months of gestation. A mild, mucopurulent (cloudy) vaginal discharge may be observed in some cases. No clinical symptoms are noticed in infected bulls.

Diagnosis

Diagnosing campylobacteriosis in cows involves checking for signs like infertility and abortion. It includes sampling vaginal mucus or preputial washings for lab tests such as bacterial culture, Direct Fluorescent Antibody Test (DFA), ELISA (especially for herd testing), PCR (quick and precise), Gram staining (which shows “seagull” shaped bacteria), and motility tests. Due to the slow growth of C. fetus, advanced PCR and ELISA methods are preferred, along with traditional culture for proper identification.

Treatment

Treatment is not generally given to cows for genital campylobacteriosis, but 2 doses of streptomycin at 20 mg/kg, SC, on consecutive days are given to infected bulls together with 5 g of streptomycin in an oil-based suspension applied to his penis for 3 consecutive days. Vaccinating infected cows approximately 4 weeks before breeding starts hastens the elimination of C fetus and improves the fertility rate.

Drugs and formulations available in India.

Drug and dose	Veterinary formulations
Streptomycin 25/kg IM OD for 3 days days.	Dicrysticine 5g(2.5g Streptomycin sulphate. 1500000IU procaine penicillin 500000 penicillin G sodium)inj vial( Zydus India). Xydocin 2.5 g (1.5g Streptomycin sulphate. 1500000IU procaine penicillin. 100000 penicillin G sodium) inj vial (Sarabhai India)