Drug information	Disease information
Amphotericin Fluconazole Flucytosine Griseofulvin Iodides Itraconazole Ketoconazole Miconazole Nystatin Terbinafine	Malassezia dermatitis (Dog and Cat). Dermatophytosis/Ringworm (Dog, Cat and Cattle). Aspergillosis (Dog, Cat and Cattle). Cryptococcosis (Dog, Cat and Cattle). Coccidioidomycosis (Dog and Cat). Histoplasmosis (Dog and Cat) Blastomycosis (Dog and Cat)

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Fungal diseases in Animal : Disease discriptrion , drugs and formulations in India.
Diseases:

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Malassezia/Yeast Dermatitis in dogs and cats : Disease discriptrion , drugs and formulations in India.

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

Disease discription.

Malassezia are dimorphic (yeast/mycelial), lipophilic fungi (yeasts) that live normaly on dogs and cats skin,and uses skin oils (lipids) for growth. Malassezia are characterized by bottle-shaped cells with a distinct collarette from monopolar budding. These organism overgrows under favourable conditions for example warm, moist, oily environments, often triggered by factors like hot weather, excessive sweating (hyperhidrosis), greasy skin (high sebum),bacterial infections, skin folds, and immune suppression. This overgrowth leads to inflammation of dog skin and is described as Yeast Dermatitis or Malassezial dermatitis. The affected sites include lip margins, ear canals, axillae, groin, ventral neck, interdigital skin, facial folds or tail folds, perivulvar skin, and perianal skin . Lesions may be localized or generalized.

Pathogenesis of Malassezia dermatitis begins with micro environmental changes in the skin. Anatomical factors, particularly skin folds, create optimal warm, moist niches. The zymogen( pro-enzyme ) present in the yeast cell wall actively triggers the complement system, leading to damage of keratinocyte integrity, resulting in epidermal spongiosis, inflammation, and pruritus. The yeast synthesizes a variety of enzymes, including lipases, phospholipases, and proteases. These enzymes effectively break down skin lipids into irritating fatty acids, compromising the epidermal barrier, and inciting inflammation. Malassezia maintains a mutually beneficial relationship with Staphylococcus bacteria. Staphylococci produce growth factors that bolster yeast proliferation, while Malassezia modifies the environment to favor bacterial colonization.

Clinical signs prominently include pruritus, an unpleasant odor, and either regional or generalized alopecia accompanied by erythema (exfoliative erythroderma). There is also seborrhea which is scaly, waxy, or greasy, displaying hues of yellow or slate gray. Lesions appear crusty or papulocrusty, resembling superficial staphylococcal infections. Additionally, lichenification and/or hyperpigmentation can develop, resulting in leathery or elephant-like skin. Paronychia develops in nails with dark brown nail bed discoloration, often linked to obsessive paw chewing in some cases. Lip margins exhibit hypotrichosis and/or crusting, while intertrigo (inflammatory skin rash) is commonly observed in skin folds.

Diagnosis of Malassezia dermatitis is based on clinical presenytation and cytologic examination . Samples collected using glass slide impression, acetate tape impression, superficial skin scraping, or cotton swab method are evaluated under the microscope to ascertain the numbers of Malassezia yeast, bacteria, and inflammatory cells present on superficial skin. Yeast organisms are often observed in clusters or adhered to keratinocytes. the diagnosis of Malassezia dermatitis should rely on the combination of clinical presentation and cutaneous cytology. Even low numbers of Malassezia organisms noted on cytology may indicate  Malassezia dermatitis if samples are collected from inflamed, pruritic skin. 

Treatment varies based on the severity of lesions. For mild or localized cases, frequent use of topical antifungal products like 2% ketoconazole, 2% miconazole, or 1% selenium sulfide is often effective. Shampoos with two active ingredients may work better. Medicated antifungal wipes or pads containing 0.3% chlorhexidine are also effective against M. pachydermatis. For generalized or multifocal lesions, a combination of oral and topical antifungal therapies is most effective. Oral drugs that work against Malassezia include ketoconazole, fluconazole, and terbinafine. Griseofulvin is not effective for Malassezia infections. Patient factors such as age, health history, and breed predisposition should be evaluated before using systemic medications, and blood tests are recommended for monitoring. If underlying issues aren’t managed, ongoing antifungal therapy may be necessary.

Drugs and Formulations in India.

Drug and dose	Veterinary formulations
Terbinafine: 30 mg/kg, PO BD till complete cure in dogs . 10-30 mg/kg, PO BD till complete cure in cats .	Cantinea 110g(Terbinafine 1%w/w ) powder( Veko India). Terbovet 250mg(Terbinafine 250 mg )/500mg tab( Vivaldis India). Terbovet 500mg(Terbinafine 500mg ) tab( Vivaldis India). Terbiraj 500mg(Terbinafine 500mg ) tab( Hatvey India).
Ketoconazole : 10 mg/kg/day PO for 6–8 weeks	Ketoheal 200mg (Ketoconazole 200 MG) tab( Health -Kare India). K-Pet 200mg (Ketoconazole 200 MG) Tab( SAVA Vet India).
Fluconazole : 2.5-5 mg/kg PO OD for 8-12 weeks in dog. 2.5-10 mg/kg PO BD in cat	Fluka-150 ( Fluconazole 150mg) tab(Cipla India). Af-150 ( Fluconazole 150mg) tab (Systopic India). Gocan 150 ( Fluconazole 150mg) tab( Hetero Drugs India). Fungid best 150 ( Fluconazole 150mg)tab (Hegde and Hegde Pharmaceuticals India).

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Dermatophytosis (Ring worm) in animals: Disease discriptrion , drugs and formulations in India.

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

Cat and Dog:

Disease discription.

Ringworm is a common name for dermatophytosis and is caused by fungi belonging to the genera Microsporum, Trichophyton, and Epidermophyton. In dogs and cats, Microsporum spp (M. canis) and Trichophyton spp (T. verrucosum and T. mentagrophytes) are common causes of ringworm. The colony of M. canis is cottony, white to buff in color; with increasing age, it becomes brownish yellow. The colony of Trichophyton spp is white, fluffy, with a central umbo and flat periphery. More than 90% of dermatophyte infections in cats are caused by M. canis. Predisposing factors affecting dermatophytosis include the number of infective spores, frequency of transmission, health conditions, and the physiological stress experienced by animals. The route of infection occurs through skin wounds, scars, or burns. This infection occurs either directly through contact with sick cats or indirectly through blankets, bed covers, toys, cages, clothes, and other objects contaminated with spores. Ringworm in pets may often be asymptomatic, resulting in a carrier condition that infects other pets. In some cases, the disease only appears when the animal develops an immunodeficiency condition.

Pathogenesis of ringworm begins with the attachment of dermatophytes to the keratin tissue in the nails or hair of the host. The arthroconidia (asexual fungal spores of dermatophytes) attach to keratin maximally at 6 hours after infection. These spores germinate into vegetative cells, which then invade the stratum corneum. The colonization process results in various immune system reactions in the host, including inflammation. Dermatophytes release serine proteinase (urokinase and tissue plasminogen activator), keratinase, which causes damage to the external proteins of the host and is facilitated by the process of injury to the skin.

Clinical signs are itchy, red, scaly patches, often forming a circular, ring-shaped rash with raised borders and clearer centers, but they vary by location, causing scalp bald spots, athlete’s foot between toes, jock itch in the groin, or thick, discolored nails (onychomycosis). Key signs are persistent itching, scaling, redness, and sometimes bumps or pus, especially on the skin, scalp, or nails, due to a common fungal infection.

Diagnosing ringworm in animals involves observing classic circular, scaly, hairless patches, but definitive confirmation needs lab tests like Wood’s lamp screening (for some species) and, most accurately, a fungal culture of hair/skin scrapings to identify the fungus. Microscopic exams and PCR are also used, but culture is key for confirming cure, as clinical signs can be misleading.

Treatment with itraconazole (5 mg/kg, PO, every 24 hours on a week on/week off schedule) for at least 3-4 cycles helps resolve lesions in cats and small dogs. Larger dogs can be treated with ketoconazole (5 mg/kg, every 24 hours) or terbinafine (30–40 mg/kg, every 24 hours) for 4–6 weeks. Ketoconazole is not suitable for cats due to the risk of anorexia. A whole-body rinse using lime sulfur (1:16) or enilconazole (1:100) should be done twice a week, as these have residual effects. A shampoo with 2% chlorhexidine/2% miconazole is effective and may be the only choice in locations where lime sulfur or enilconazole is unavailable; shampoo treatment has no residual activity and should occur 2–3 times a week.

Drugs and Formulations in India.

Drug and dose	Veterinary formulations
Itraconazole: Cats and small dogs (5 mg/kg, PO, every 24 hours on a week on/week off schedule) for at least 3-4 cycles	Itopet 60 ml( 10mg Itraconazole/ml) oral suspension( Medilogy Biotech india). Izopet 100ml ( 10mg Itraconazole/ml) oral solution ( Intas India). Vetconazole 100mg ( 100mg Itraconazole Capsule( Vetina India). Vetconazole 200mg ( 200mg Itraconazole Capsule( Vetina India). SUBAvet IT 50 (50mg Itraconazole Capsule( Vivaldis India). Itrpet 100ml ( 20mg Itraconazole/ml) oral solution ( PCD India).
Terbinafine: 30 mg/kg, PO BD till complete cure in dogs .	Cantinea 110g(Terbinafine 1%w/w ) powder( Veko India). Terbovet 250mg(Terbinafine 250 mg )/500mg tab( Vivaldis India). Terbovet 500mg(Terbinafine 500mg ) tab( Vivaldis India). Terbiraj 500mg(Terbinafine 500mg ) tab( Hatvey India).
Ketoconazole : 10 mg/kg/day PO for 6–8 weeks	Ketoheal 200mg (Ketoconazole 200 MG) tab( Health -Kare India). K-Pet 200mg (Ketoconazole 200 MG) Tab( SAVA Vet India).

Cattle:

Disease discription.

Ringworm in cattle is predominantly caused by Trichophyton verrucosum (95% of cases), with Trichophyton mentagrophytes being a less common culprit. The infection spreads primarily through direct contact among animals, making infected individuals the main source of transmission. Ringworm spores are incredibly resilient, capable of surviving for months or even years in the environment, and can be disseminated via contaminated items or asymptomatic carriers. Outbreaks are particularly likely during construction work, as this activity significantly increases spore release. Lesions commonly appear around the head and neck of cattle, as they often rub against fences and feeding barriers. While natural outbreaks typically impact younger animals, older animals lacking prior exposure can also be affected due to insufficient immunity. The disease is more prevalent in cooler regions and is influenced by humidity levels. The incubation period usually lasts about one week, although it can extend to four weeks in certain outbreaks. Factors contributing to susceptibility include the animal’s age, with younger ones being more vulnerable due to their lack of previous exposure and hence no immunity. Adult cattle may also experience infections. Crowding young animals escalates risk, along with factors such as poor nutrition, underlying diseases, and prior use of immunosuppressive drugs. Environmental conditions, like hot, humid climates or calves housed indoors with limited sunlight, can elevate incidence rates. Other species, such as horses, sheep, and even humans, can contract the infection, leading to severe skin lesions in people. The zoonotic risks are noteworthy, necessitating all precautions to prevent transmission to farm staff, especially children.

Pathogenesis of ringworm begins with the attachment of dermatophytes to the keratin tissue in the nails or hair of the host. These spores germinate into vegetative cells, which then invade the stratum corneum. The colonization process results in various immune system reactions in the host, including inflammation. Dermatophytes release serine proteinase (urokinase and tissue plasminogen activator) and keratinase, which causes damage to the external proteins of the host and is facilitated by the process of injury to the skin.

Clinical manifestation of the disease varies regarding the number and size of affected areas, with the head and neck being the most susceptible. Lesions are typically greyish-white, circular, and slightly raised due to the layering of scales and mild inflammation. Their size generally ranges from 3 to 5 cm in diameter, and in more severe cases, they can coalesce into larger infection zones. Pruritus is often mild or absent. Most cases of ringworm resolve independently within 1 to 4 months, thanks to the development of immunity. Lesions clear from the center outward, frequently leaving behind scar tissue and collagen deposits. Diagnosis relies on the clinical signs of classic ringworm lesions, which are characteristically asbestos-like in cattle.

Diagnosing ringworm in cattle requires a keen eye for the distinctive circular, gray-white, crusty, hairless patches, particularly around the head, neck, and eyes. This diagnosis is confirmed through microscopic examination (KOH prep) of skin scrapings or hair for fungal elements (spores/hyphae), alongside fungal culture (DTM) for definitive identification.

Treatment of ringworm in cattle with Enilconazole creams applied 2 to 3 times weekly has proved effective in resolving the lesions. Although this drug is unavailable in India, the human formulation containing Eberconazole can serve as an effective substitute. The author has successfully treated numerous cases of ringworm with a mixture of vegetable oil and sodium bicarbonate (1-2%), achieving a high success rate. Prior to applying any local treatment, it is crucial to thoroughly rub the lesions with a cloth brush to ensure maximum efficacy.

Drugs and formulation in India.

Drug and dose	Human formulations
Ebraconazole : Apply Ebraconazole 1% w/w cream 2- 3 times a day.	Ebernet 30gm/60 gm ( Ebraconazole 1% w/w) cream (Dr Reddys Lab India). Ebspor 30gm/50 gm ( Ebraconazole 1% w/w) cream (Intas Pharmaceuticals India). Crurix 30gm ( Ebraconazole 1% w/w) cream (Torrent Pharmaceuticals India). Eberwin 30gm ( Ebraconazole 1% w/w) cream (Sun Pharmaceuticals India). Ebermac 30gm ( Ebraconazole 1% w/w) cream (Macleods Pharmaceuticals India).

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Aspergillosis in animals: Disease description , drugs and formulations in India.

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

Cat and Dog:

Disease description:

Aspergillosis in dogs and cats is primarily attributed to the fungus Aspergillus fumigatus. Nasal aspergillosis is frequently observed in long-nosed dog breeds and short-nosed cat breeds. Although the disease is less prevalent in cats compared to dogs, felines can develop sino-orbital aspergillosis, which is caused by Aspergillus felis. Aspergillus species are ubiquitous in the environment, particularly in decomposed organic matter within the soil. In immunocompromised dogs and cats, aspergillosis may progress to a systemic (disseminated) form, affecting bones, eyes, and vital organs, with systemic disease notably occurring in German Shepherds. The transmission occurs through the inhalation of Aspergillus spores present in contaminated environments. These spores may remain in healthy animals’ bodies for extended periods without causing harm; however, favorable conditions, such as rhinitis, can promote the organism’s growth and colonization, ultimately leading to sinonasal aspergillosis.

Pathogenesis commences with the inhalation of Aspergillus spores present in contaminated environments, such as contaminated food or during soil sniffing. These spores are deposited in the sinonasal cavity, the primary site of infection. The fungus firmly adheres to the respiratory epithelium, penetrates it, destroys surrounding cells, and evades phagocytosis. Aspergillus species conidia bind to various cell surface proteins through specific adhesion molecules like hydrophobins. Notably, A. fumigatus produces an immunosuppressive toxin (gliotoxin) that effectively inhibits macrophage phagocytosis. Other metabolites hinder mucociliary action, prolonging the organism’s epithelial resistance, while enzymes (e.g., proteases) facilitate tissue invasion.

Clinical signs of sinonasal aspergillosis (SNA) are primarily characterized by localized manifestations of chronic nasal infection, which include sneezing, unilateral or bilateral serous to mucopurulent nasal discharge, and/or epistaxis. Other less common, findings may include stertorous breathing, granuloma formation, soft tissue masses protruding from the nares, and bone lysis. The mucosa of the nasal and paranasal sinuses may exhibit a layer of necrotic material accompanied by gray-white fungal growth. Furthermore, the mucosa and the underlying bone may present necrosis, resulting in a loss of bone definition observable on radiographs or CT scans. Sino-orbital aspergillosis (SOA) in felines represents a progression of SNA, extending into orbital and subcutaneous tissues, presenting with signs of orbital invasion, including swelling of the orbital area, unilateral or bilateral exophthalmos, third eyelid prolapse, conjunctival hyperemia, miosis, retrobulbar fungal granulomas, orbital bone lysis, and keratitis. Additionally, involvement of the central nervous system can occur, leading to neurological signs such as peripheral vestibular signs and blindness, along with regional lymphadenopathy and fever. The clinical manifestations of disseminated aspergillosis may encompass lethargy, lameness, anorexia, weight loss, muscle wasting, pyrexia, hematuria, urinary incontinence, generalized lymphadenopathy, and neurologic deficits, including head tilt, ataxia, and proprioceptive deficits.

Diagnosing nasal aspergillosis only with culture results is insufficient, since aspergilli can exist in healthy animals. Positive cultures must be confirmed by identifying branching hyphae in lesions. X-rays can show dark areas in the nasal cavity due to turbinate damage, with bone infections present in up to 80% of cases. CT or MRI scans offer clearer details than standard X-rays for lesion assessment. Diagnosis often requires rhinoscopy to find fungal plaques and needs mycological or radiographic evidence. A history of poor response to long-term antimicrobial therapy is also common. Systemic disease is usually diagnosed by culturing the organism from urine. A galactomannan assay in urine or serum can suggest disseminated aspergillosis, but it may also react with other fungi. Ultrasound may reveal enlarged abdominal lymph nodes and kidney lesions. Speciation of Aspergillus often requires PCR amplification and sequencing of several genes to ensure appropriate treatment and prognosis.

Treatment of choice is topical application of the anti-fungal agent 1% Clotrimazole. It is administered for one hour under general anaesthetic via indwelling catheters placed in the frontal sinus. Several treatments may be required. For cases that are non-responsive to Clotrimazole, treatment with Enilconazole, 10 mg/kg, instilled every 12 hours for 7–14 days via tubes implanted surgically into the frontal sinuses, has also been used with a similar success rate but this is associated with a higher complication rate. Ketoconazole can be administered orally for 6-8 weeks in dogs. Itraconazole posaconazole, and/or amphotericin B has also been used in dogs and cats.

Drugs and formulation in India.

Drug and dose	Veterinary and Human formulations
Clotrimazole 1% intranasal for several treatments.	Human formulations: Canesten 15 ml (Clotrimazole 1%) Topical Solution (Bayer Pharmaceuticals India). Surfaz  10 ml (Clotrimazole 1%) Topical Solution (Franco-Indian Pharmaceuticals India).
Itraconazole: Cats and small dogs (5 mg/kg, PO, every 24 hours on a week on/week off schedule) for at least 3-4 cycles	Veterinary formulations: Itopet 60 ml (10mg Itraconazole/ml) oral suspension( Medilogy Biotech india). Izopet 100ml ( 10mg Itraconazole/ml) oral solution ( Intas India). Vetconazole 100mg ( 100mg Itraconazole Capsule( Vetina India). Vetconazole 200mg ( 200mg Itraconazole Capsule( Vetina India). SUBAvet IT 50 (50mg Itraconazole Capsule( Vivaldis India). Itrpet 100ml ( 20mg Itraconazole/ml) oral solution ( PCD India).
Terbinafine: 30 mg/kg, PO BD till complete cure in dogs .	Cantinea 110g(Terbinafine 1%w/w ) powder( Veko India). Terbovet 250mg(Terbinafine 250 mg )/500mg tab( Vivaldis India). Terbovet 500mg(Terbinafine 500mg ) tab( Vivaldis India). Terbiraj 500mg(Terbinafine 500mg ) tab( Hatvey India).
Ketoconazole : Not given in cats 10 mg/kg/day PO for 6–8 weeks in dogs.	Ketoheal 200mg (Ketoconazole 200 MG) tab( Health -Kare India). K-Pet 200mg (Ketoconazole 200 MG) Tab( SAVA Vet India).

Cattle:

Disease description:

Aspergillosis in cattle is primarily attributed to the fungus Aspergillus fumigatus. This infection may present in a subclinical form, manifest as bronchopulmonary disease, or lead to mastitis, placentitis, and abortion. Mycotic pneumonia is often rapidly fatal, particularly among older or immunocompromised animals.

Clinical manifestations include pyrexia; rapid, shallow, and stertorous respiration; nasal discharge; and a moist cough, which, if not addressed with urgency, can result in serious complications. The lungs characteristically remain firm, heavy, and mottled, failing to collapse—this distinct feature serves as a critical diagnostic indicator. In cases of subacute to chronic mycotic pneumonia, the lungs are marked by multiple discrete granulomas, prompting considerations of differential diagnoses such as tuberculosis and highlighting the necessity for accurate identification and management of the condition. In instances where pneumonia is absent, infected cows may display no obvious clinical signs aside from abortion; a deceased fetus may be expelled as early as 6–9 months of gestation, with retained fetal membranes posing further complications for the herd’s overall health. Pathological lesions are typically observed in the uterus, fetal membranes, and often the skin of the aborted fetuses, threatening the health of affected animals. Within the uterus, intercaruncular areas are markedly thickened, leathery, and display dark red to tan coloration, indicative of chronic infection. These regions can exhibit elevated or eroded foci, covered by a yellow-gray adherent pseudomembrane, making recovery particularly arduous. Maternal caruncles may appear dark red to brown, while the adherent fetal cotyledons often show significant thickening, suggesting persistent inflammation and infection. Additionally, cutaneous lesions in aborted fetuses typically manifest as soft, red to gray, elevated, circumscribed areas resembling ringworm, which underscores the extensive ramifications of Aspergillus infection in affected populations and the critical need for vigilant monitoring of cattle to identify early signs of this severe disease.

Diagnosis is based on clinical signs, lesions on aborted fetus and placenta, culture of mastitis milk, and uterine secretion.  identification of hyphae on histopathology of placenta or fetal skin is diagnostic. Postmortem examination may demonstrate fungal granulomas or firm lungs that fail to collapse; hyphae will be evident on histopathologic examination.

Treatment of pulmonary aspergillosis is rarely done due to its fast progression. It is important to assess feed and the environment to find contamination sources in areas with pulmonary cases or mycotic abortion. Bovine mastitis has seldom been successfully treated with a mix of intra-arterial and intramammary miconazole injections, though this is outside standard use; most cases do not respond to treatment.

Drugs and formulation in India.

Drug and dose	Human formulations
Miconazole: Combined intra- arterial and intramammary injection on three successive days Intramammary application. 100 mg of miconazole (diluted in 10 ml water) is injected into the right external pudendal artery. Miconazole diluted with 50-ml saline is infused into the affected udder. Costly treatment with variable results. Reserved for heavy lactating animals.	Micona (50mg miconazole) Injection (Glenmark Pharmaceuticals Ltd)

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Cryptococcosis in animals: Disease description, drugs and formulations in India.

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

Cat and Dog:

Disease description.

Cryptococcosis, caused by C. neoformans and C. gattii, is a notable local and systemic fungal disease found in Cat and Dogs. While sporadic cases of Cryptococcosis are frequently reported in cats, instances in dogs are considerably rarer. This condition manifests in four distinct forms: nasal form, nervous form, cutaneous form, and systemic form. The nasal form is more prevalent among cats, whereas Cryptococcal meningitis is more frequently observed in dogs. Notably, immunocompromised animals are vulnerable to C. neoformans, but C. gattii affects both immunosuppressed and immunocompetent hosts. Factors such as malnutrition and immunosuppression significantly contribute to the disease’s spread within the body. C. neoformans is ubiquitous, often isolated from bird droppings, particularly pigeons (Columba livia), as well as soil and decaying organic matter. Animals typically contract the infection through contaminated organic material, inhaling the airborne spores, specifically the blastoconidia of Cryptococcus spp. The nasal cavity serves as the primary infection site, with potential extensions to the lungs or the entire system.

Pathogenesis depends on the host’s immune status, strain virulence, and fungal load. The incubation period is long. The spores germinate into yeast form under favorable conditions, followed by proliferation and colonization. Fungal invasion of epithelial tissue triggers an inflammatory response, with yeast cells surviving within phagocytic cells like macrophages, dendritic cells, and neutrophils, replicating both extracellularly and intracellularly. Host cells also fall victim to infections through direct cell-to-cell transfer. Chronic inflammation culminates in granulomatous lesions. In the brain, the yeast triggers nerve cells to produce cytokines and chemokines, resulting in inflammation of the brain tissue. The virulence of C. neoformans is largely associated with the antiphagocytic and immunosuppressive capsule and a unique enzyme diphenol oxidase.

Clinical signs of Nasal cryptococcosis are observed as breathing difficulties, weight loss, decreased appetite, or issues with balance and ears. Central nervous system (CNS) cryptococcosis typically arises when the nasal form infiltrates the brain. The CNS form can lead to sudden blindness, seizures, behavioral changes, and pain in the head or spine. Cats with cutaneous cryptococcosis develop single or multiple non-painful, non-itchy nodules on or beneath their skin and may show lymph node enlargement. Systemic cryptococcosis occurs as the infection disseminates through the bloodstream, potentially affecting the eyes, bones, causing joint inflammation, and leading to multi-organ system disease. Animals suffering from prolonged systemic cryptococcosis exhibit lethargy and anorexia. About 50% of dogs present with lesions primarily in the respiratory tract, often in the lungs, with many exhibiting granulomas across multiple systems. The most frequently involved structures, in order, include the CNS, respiratory tract, skin, kidneys, lymph nodes, spleen, liver, thyroid, adrenals, pancreas, bone, GI tract, muscle, myocardium, prostate, heart valves, and tonsils.

Diagnosing cryptococcosis is grounded in clinical observations, confirmed via cytologic evaluation of nasal and skin exudates, CSF, or samples obtained through paracentesis of the aqueous or vitreous chambers of the eye, or by impression smears of nasal or cutaneous masses. The Gram stain proves most beneficial; the organism retains crystal violet, while the capsule lightly stains red with safranin. Culturing the organism from exudate, CSF, urine, joint fluid, and tissue samples is feasible if sample volume is sufficient. To address bacterial contamination risks, Sabouraud agar with antibiotics is employed. C. neoformans will grow well on blood agar or on SDA (without cycloheximide). The colonies are smooth, moist, shiny, white and become wrinkled, cream to brownish granular colonies on further incubation. Bird seed agar (which contain Guizotia abyssinica seeds) is the selective medium.
for C. neoformans.

Feline cryptococcosis is often diagnosed through the Latex Agglutination Test (LAT), assessing antigen presence in blood, urine, or cerebrospinal fluid. In localized cases, such as nasal or cutaneous disease, blood tests may yield negative results despite suspected cryptococcosis.

Treatment necessitates prolonged oral antifungal therapy lasting several months, alongside surgical excision of any skin lesions. Continuation of treatment is essential until the LAT returns negative or for 2-4 months following the resolution of clinical signs. Fluconazole (10 mg/kg, PO, every 12 hours) and itraconazole (5–10 mg/kg every 24 hours) are the preferred treatments. Amphotericin B may be incorporated for dogs, particularly those with disseminated disease.

Drugs and formulation in India.

Drug and dose	Veterinary and Human formulations
Fluconazole: Cats and dogs (10 mg/kg, PO, every 12 hours)2-4 months past the resolution of any clinical signs.	Human formulations: Fluka-150 ( Fluconazole 150mg) tab(Cipla India). Af-150 ( Fluconazole 150mg) tab (Systopic India). Gocan 150 ( Fluconazole 150mg) tab( Hetero Drugs India). Fungid best 150 ( Fluconazole 150mg)tab (Hegde and Hegde Pharmaceuticals India).
Itraconazole: Cats and dogs (5 mg- 10 mg /kg, PO, every 24 hours on a week on/week off schedule) for 2-4 months past the resolution of any clinical signs.	Veterinary formulations: Itopet 60 ml (10mg Itraconazole/ml) oral suspension( Medilogy Biotech india). Izopet 100ml ( 10mg Itraconazole/ml) oral solution ( Intas India). Vetconazole 100mg ( 100mg Itraconazole Capsule( Vetina India). Vetconazole 200mg ( 200mg Itraconazole Capsule( Vetina India). SUBAvet IT 50 (50mg Itraconazole Capsule( Vivaldis India). Itrpet 100ml ( 20mg Itraconazole/ml) oral solution ( PCD India).

Cattle :

Disease description.

Bovine cryptococcosis is definitively caused by C. neoformans and is linked to cases of mastitis in dairy cows, where multiple animals within a herd can be infected. The transmission occurs either through the teat canal or via the bloodstream. The incubation period typically spans 2–13 months. Lesions associated with cryptococcosis can range from gelatinous masses filled with numerous organisms and minimal inflammation to distinct granuloma formation. These lesions are primarily composed of aggregates of encapsulated organisms within a connective tissue framework, accompanied by a cellular response dominated by macrophages and giant cells, with a few plasma cells and lymphocytes. While epithelioid giant cells and areas of caseous necrosis are less common compared to other systemic mycoses, in cases of cryptococcal mastitis, cows with mild infections may show no clinical signs beyond the swelling of affected glands. However, in severe infections, animals exhibit clear clinical signs of bacterial mastitis, including fever, swelling, and firmness of the udder, with a gradual decrease in milk secretion. The milk will appear gray, white, and highly viscid. Diagnosis in clinical cases is confirmed by culturing a milk sample on blood agar or SDA. The resulting colonies are smooth, moist, shiny, and white, eventually becoming wrinkled and transforming into cream to brownish granular colonies with further incubation. Bird seed agar, which contains Guizotia abyssinica seeds, serves as the selective medium for C. neoformans. This medium is rich in di and polyphenolic compounds, allowing Cryptococcus species to utilize creatinine and produce melanin-pigmented (brown) colonies. The dark brown pigment colonies develop after the plates are incubated at 37°C for at least a week. Direct microscopy reveals budding yeast with a large capsule using India ink, Nigrosin, and LPCB staining methods. Treating cryptococcal mastitis is very difficult, and currently, there is no treatment available in India.

Treatment for Bovine cryptococcosis is not available. For cryptococcal mastitis, administer Fluconazole injection (5 mg/kg body weight, slow IV) for three days after performing a hypersensitivity test, and do not mix with other drugs. Other treatments are DNS (500ml, IV for two days), Maxxitol injection (2ml, IM for three days), and chlorpheniramine maleate injection (1.5ml, IM for three days) to alleviate symptoms. Prevention includes maintaining hygiene, balanced nutrition, and effective management of bovine cryptococcal mastitis.

Drugs and formulation in India.

Drug and dose	Veterinary and Human formulations
Fluconazole. 5 mg/kg body weight, slow IV for three days.	Human formulations: Forcan 100ml (2mg fluconazole /ml) inj vial (Cipla India). Fluconal 100ml (2mg fluconazole /ml) inj vial (Vernal Bioptech India).

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Coccidioidomycosis in Dogs and Cats: Disease description, drugs and formulations in India.

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

Disease description.

Coccidioidomycosis, known as valley fever, is a significant fungal disease affecting dogs and cats, predominantly caused by Coccidioides immitis and Coccidioides posadasii . Dogs are more susceptible than cats. These dimorphic fungi exist in a mycelium or spherule form, flourishing as a soil saprophyte in semiarid environments. In nature, C. immitis manifests as a mycelium with robust, barrel-shaped arthroconidia. Upon inhalation, these arthroconidia transition into spherules. Infections typically occur through the respiratory route, with inhaled arthrospores traversing the pleural tissue to reach the subpleural space. The incubation period for dogs varies from 1 to 3 weeks, during which a vigorous inflammatory response arises, often presenting clinical respiratory symptoms. Should the infection disseminate, it may affect various organ systems, including bones, eyes, heart, pericardium, testicles, brain, spinal cord, and visceral organs. Young adult, large breed outdoor dogs are particularly vulnerable to these infections.

Pathogenesis initiates when inhaled arthroconidia settle in the terminal bronchiole, transforming into spherules. A single inhaled arthroconidia is sufficient to cause an infection. Within these spherules, numerous endospores develop and are subsequently released, amplifying the disease burden. A T-cell immune response can effectively contain the infection within the lungs, leading to either mild symptoms or none at all. Possible outcomes range from a pulmonary nodule to a cavity, yet most infections resolve entirely. The severity and dissemination of the disease depend on the robustness of innate and adaptive immune responses. Initial defensive measures involve neutrophils, macrophages, and dendritic cells, while cellular immunity from T-helper cells plays a pivotal role in managing the infection in the lungs and staving off its spread. Dogs exhibiting T-cell deficiencies face heightened risk for disseminating the infection beyond the lungs. Conversely, animals with low levels of complement fixation antibodies and a robust T-cell response generally fare better, posing a minimal risk of spreading the infection.

Clinical signs are primarily respiratory and may often go unnoticed post-exposure. In animals with inadequate immune responses, symptoms become pronounced. Chronic cough ranks as the most common initial complaint, with fever, weight loss, and anorexia frequently accompanying it. Bone involvement occurs in 65% of dogs, sometimes leading to draining skin nodules over bone lesions. Myocardial or pericardial infections may result in cardiac arrhythmias or restrictive pericarditis. CNS signs can include seizures, behavioral changes, or coma, while ocular involvement is less prevalent in coccidioidomycosis compared to other systemic fungal infections. Cats exhibit greater resistance to coccidioidomycosis than dogs, with no apparent age, breed, or gender predilection. Skin lesions are common (~50%) in cats and they are not often associated with adjacent bone involvement. Lesions reported include subcutaneous nodules, abscesses, and draining lesions. Affected cats commonly experience fever, inappetence, and weight loss, with respiratory signs observed in only 25% of cases.

Diagnosing coccidioidomycosis necessitates astute clinical suspicion and corroborating laboratory findings, which may include positive serology, cultures, and/or histopathological results. CBC changes may reveal normocytic, normochromic, nonregenerative anemia, neutrophilia (with or without a left shift), and monocytosis. Common serum biochemical findings include hypoalbuminemia, hyperglobulinemia, increased hepatic transaminases, and azotemia, with hypercalcemia also a possibility. Thoracic radiographs often display a diffuse interstitial or peribronchial pattern, frequently accompanied by hilar lymphadenopathy, and alveolar infiltrate may also occur. Pleural involvement can manifest as pleural thickening, effusion, and fibrosis. Instances of hypertrophic osteopathy linked to pulmonary involvement have been documented. Definitive diagnosis of coccidioidomycosis requires the demonstration of the organism, though locating them can be challenging due to their relatively low numbers and the difficulty of sampling inaccessible sites. Fungal culture lacks clinical utility, as definitive identification mandates inoculation into animals to trigger spherule formation. Serologic testing frequently becomes the method of choice when organisms are undetectable. Various serologic tests can be employed to identify immunoglobulin M and immunoglobulin G antibodies, and results should always align with clinical signs indicative of active infection for diagnosis confirmation. It is feasible to obtain negative serology results in affected animals, so repeat testing in 2 to 4 weeks to ascertain increasing titers is advised in ambiguous cases.

Coccidioidomycosis treatment is challenging and harder to eliminate than other systemic fungal infections. Localized respiratory infections may clear up on their own and usually have a good outcome. However, untreated disseminated infections can be fatal. Ketoconazole therapy shows a recovery rate of 60%, but multiple bone or CNS involvement leads to a worse prognosis. Fluconazole (5–10 mg/kg every 24 hours) is the most commonly prescribed medication. Itraconazole (10 mg/kg every 24 hours) is also often used for treating dogs with coccidioidomycosis.

Drugs and formulation in India.

Drug and dose	Veterinary and Human formulations
Fluconazole: Cats and dogs (10 mg/kg, PO, every 12 hours)2-4 months past the resolution of any clinical signs.	Human formulations: Fluka-150 (Fluconazole 150mg) tab (Cipla India). Af-150 (Fluconazole 150mg) tab (Systopic India). Gocan 150 (Fluconazole 150mg) tab (Hetero Drugs India). Fungid best 150 (Fluconazole 150tabs (Hegde and Hegde Pharmaceuticals India).
Itraconazole: Cats and dogs (5 mg- 10 mg /kg, PO, every 24 hours on a week on/week off schedule) for 2-4 months past the resolution of any clinical signs.	Veterinary formulations: Itopet 60 ml (10mg Itraconazole/ml) oral suspension( Medilogy Biotech india). Izopet 100ml ( 10mg Itraconazole/ml) oral solution ( Intas India). Vetconazole 100mg ( 100mg Itraconazole Capsule( Vetina India). Vetconazole 200mg ( 200mg Itraconazole Capsule( Vetina India). SUBAvet IT 50 (50mg Itraconazole Capsule( Vivaldis India). Itrpet 100ml (20mg Itraconazole/ml) oral solution ( PCD India).
Terbinafine: Synergistic effect with azoles. Increase the effect of azoles. Dogs: 35-50 mg/kg q 24h. Cats: half of 500 mg tablet (i.e. 250 mg q 24h).	Veterinary formulations: Cantinea 110g (Terbinafine 1%w/w) powder( Veko India). Terbovet 250mg (Terbinafine 250 mg)/500mg tab( Vivaldis India). Terbovet 500mg (Terbinafine 500mg) tab( Vivaldis India). Terbiraj 500mg(Terbinafine 500mg ) tab( Hatvey India).

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Histoplasmosis in Dogs and Cats: Disease description, drugs and formulations in India.

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

Disease description.

Histoplasmosis is a common systemic infection caused by the fungus Histoplasma capsulatum, which can grow as hyphae with spores at room temperature and as yeast at body temperature (thermal dimorphic fungus). It frequently affects dogs, cats, and horses, leading to granulomatous pulmonary disease that may look like tuberculosis or coccidioidomycosis. The infection usually occurs when contaminated dust is ingested or inhaled, often from areas with pigeon, chicken, or bat feces. Histoplasma acts as an intracellular parasite within the monocyte-macrophage system and can spread throughout the body.

Pathogenesis is linked to cellular immunity. A strong immune system can stop disease progression at the infection point. Environmental microconidia are inhaled, leading to initial infections in the lungs and thoracic lymph nodes. In the lungs, these microconidia attract dendritic cells, neutrophils, and macrophages, which engulf the organism that then transforms into yeasts and multiplies uncontrollably in individuals with weak immune systems. In the first two weeks, the infection spreads throughout the reticuloendothelial system. By day 14, specific T cell immunity develops, stopping yeast proliferation and infection progression. Evidence of self-limited spread includes calcified granulomas in the spleen and liver of healthy individuals in endemic areas, containing inactive organisms and occasional isolation of H. capsulatum from other samples in patients with acute pulmonary histoplasmosis. Key cytokines in immunity to H. capsulatum are IL-12, IL-18, TNF-α, and interferon-γ. A successful T cell response relies on dendritic cells, CD4 and CD8 T lymphocytes, and activated macrophages. T cells produce interferon-γ and tumor necrosis factor-γ to activate macrophages to kill Histoplasma yeast. The role of TNF-α is emphasized by the recognition of histoplasmosis as a significant opportunistic infection in patients receiving TNF inhibitors.

Clinical signs of illness include pneumonia, fever, difficulty breathing (dyspnea), coughing, and tiredness (lethargy). X-rays typically show widespread nodules known as “cotton tuft” lesions or diffuse lung changes, often with swollen lymph nodes in the chest area (hilar lymphadenopathy). Enlarged lymph nodes can press on the airways, causing coughing and trouble breathing. Common signs in cats are fever, weight loss, lower activity, anemia, and lung disease. In dogs, diarrhea, blood loss in the intestines, anemia, and lower activity are more common. Cats often have bone problems, and issues in the brain and eyes can occur in all types of animals.

Diagnosis is obtained by detection of Histoplasma antigen in the urine and/or serum or demonstration of yeast in the body fluids or tissues. A galactomannan antigen in the cell wall of proliferating Histoplasma yeasts is released into the tissues and blood and excreted in the urine. The antigen found in histoplasmosis cross-reacts with that found in blastomycosis. Antibody detection may be useful in cases in which antigen tests and/or pathology are negative or specimens are not available for pathology. Complement fixation (CF) and agar gel immunodiffusion (AGID) methods are used for antibody detection, but the sensitivity of these tests varies widely. Sensitivity may be improved using an enzyme immunoassay. As per reports, IgG antibodies were detected by the MVista Histoplasma antibody EIA in 88% of human patients with acute pulmonary histoplasmosis, and the specificity was 95%. Combining antigen and antibody detection, the sensitivity was 96%.

Treatment of choice is long-term use of Itraconazole at 10 mg/kg every 24 hours. Fluconazole at 10 mg/kg/day works well for central nervous system, eye, or prostate cases due to its smaller size and fat solubility. Ketoconazole at 10–15 mg/kg every 12 hours for 4–6 months may help in early or mild histoplasmosis cases in dogs, but resistance can occur. For severe cases, it is recommended to use amphotericin B or its lipid complex alongside. Treatment duration varies with disease severity, with a minimum of 4- 6 months suggested, though many may need over 12 months. Treatment should be stopped based on the resolution of symptoms and urine antigen levels. Relapses happen in 10%–40% of patients.

Drugs and formulation in India.

Drug and dose	Veterinary and Human formulations
Itraconazole: Cats and dogs (5 mg- 10 mg /kg, PO, every 24 hours) for 4-6 months.	Veterinary formulations: Itopet 60 ml (10mg Itraconazole/ml) oral suspension( Medilogy Biotech india). Izopet 100ml ( 10mg Itraconazole/ml) oral solution ( Intas India). Vetconazole 100mg ( 100mg Itraconazole Capsule( Vetina India). Vetconazole 200mg ( 200mg Itraconazole Capsule( Vetina India). SUBAvet IT 50 (50mg Itraconazole Capsule( Vivaldis India). Itrpet 100ml (20mg Itraconazole/ml) oral solution ( PCD India).
Fluconazole: Cats and dogs (10 mg/kg, PO, every 12 hours) 4-6 months	Human formulations: Fluka-150 (Fluconazole 150mg) tab (Cipla India). Af-150 (Fluconazole 150mg) tab (Systopic India). Gocan 150 (Fluconazole 150mg) tab (Hetero Drugs India). Fungid best 150 (Fluconazole 150tabs (Hegde and Hegde Pharmaceuticals India).

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Blastomycosis in Dogs: Disease description, drugs and formulations in India.

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

Disease description.

Blastomycosis is a serious fungal infection in dogs caused by Blastomyces dermatitidis. It starts when spores are inhaled and change into yeast-like cells, leading to local and widespread disease. Young, large sporting dogs and hounds like coonhounds, pointers, Weimaraners, golden retrievers, Labrador retrievers, and Doberman pinschers are most affected. By the time it’s diagnosed, the disease is often found beyond the lungs. Chest X-rays may show either localized air space issues or a “snowstorm” pattern of disease. Ocular problems are more common in dogs than in humans, seen in up to half of cases, with half of those being bilateral. Eye issues can affect the front, back, or both parts of the eyes. Skin involvement is also frequent in infected dogs, seen in about half. Other common areas for disease include lymphatic and bone structures. Central nervous system involvement is less frequent, occurring in 6% of cases, while cardiovascular blastomycosis has been noted in nine dogs.

Pathogenesis starts when conidia from the mycelial phase in soil or decaying matter are inhaled into the lungs. The body’s temperature triggers the conversion from spores to large, budding yeast cells. Phagocytes serve as the first line of defense, and complement helps B. dermatitidis adhere. In healthy, immunocompetent dogs, the condition is self-limiting. However, in weak or immunocompromised dogs, the budding becomes uncontrolled and spreads from the lungs to other body organs through the bloodstream. In the lungs and other organs, this leads to an inflammatory reaction and the formation of pyogranulomatous lesions.

Clinical symptoms of blastomycosis can vary based on severity and location. Common symptoms include weight loss, lack of appetite, slowness, fever, breathing difficulties, and swollen lymph nodes. Key eye issues are red eyes, discharge, blindness, uveitis, glaucoma, and retinal detachment. Skin infections show up as lesions that can include granulomas and abscesses, which may ulcerate and drain a bloody discharge. These skin lesions are often small and multiple, primarily affecting the planum nasale, face, and nail beds. Central nervous system signs can involve circling and confusion. Lameness from fungal osteomyelitis or severe nail infections occurs in about 25% of dogs. Hematuria and dysuria might also be found in cases of urogenital blastomycosis.

Diagnosis of blastomycosis includes clinical signs, chest X-rays, cultures, microscopic exams, and antigen detection in urine. X-rays may reveal non-calcified nodules or consolidations and swollen bronchial and mediastinal lymph nodes. Common patterns on thoracic X-rays show diffuse nodular interstitial and peribronchial densities, with enlarged bronchial lymph nodes appearing as dense masses. The main method for diagnosis is culturing Blastomyces spp. from samples on Sabouraud’s dextrose agar at 25–30 °C. The colonies turning white to buff in 10–14 days, possibly up to 6 weeks. Microscopically, B. dermatitidis shows conidiophores standing out from hyphae, with single conidia looking like “lollipops.” Diagnostic methods include wet smears, cytopathology, and histopathology, showing large (8–15 μm), round yeast-like cells with thick walls. Stains like Papanicolaou and Wright help identify the organism in respiratory samples. There is an enzyme immunoassay (EIA) for detecting B. dermatitidis galactomannan in humans and animals, which is highly sensitive for antigen detection in urine and blood of dogs.

Treatment of blastomycosis is performed by using Itraconazole (5 mg/kg every 24 hours) for a minimum of 3 months. the drug should be continued until active disease is not apparent. Clinical cure can be expected in ~70% of dogs, with recurrence months or years after treatment noted in ~20% of treated d

Disease description.

Drug and dose

Veterinary and Human formulations

Itraconazole: (5 mg- 10 mg /kg, PO, every 24 hours) for 3 months.

Veterinary formulations: Itopet 60 ml (10mg Itraconazole/ml) oral suspension( Medilogy Biotech india). Izopet 100ml ( 10mg Itraconazole/ml) oral solution ( Intas India). Vetconazole 100mg ( 100mg Itraconazole Capsule( Vetina India). Vetconazole 200mg ( 200mg Itraconazole Capsule( Vetina India). SUBAvet IT 50 (50mg Itraconazole Capsule( Vivaldis India). Itrpet 100ml (20mg Itraconazole/ml) oral solution ( PCD India).