Indian Journal of Comparative Microbiology, Immunology and Infectious Diseases
Year : 2003, Volume : 24, Issue : 2
First page : ( 115) Last page : ( 123)
Print ISSN : 0970-9320.

Yeasts as animal pathogens

Jand S.K., Kaur Paviter, Sharma N.S.

Department of Veterinary Microbiology, College of Veterinary Science, PAU, Ludhiana–141 003 (Punjab)

Received:  27  March,  2004.

Abstract

Yeasts are oval, spherical, elongated or rectangular unicellular fungal cells of about 3-5 µm diameter. However sometimes they adhere in chains, forming pseudomycelium and reproducing through budding. These form moist colonies that are usually larger, but not unlike bacterial colonies. Yeasts have been known to man since ages–ever since the use of wine and baked bread. Not even a single day passes during which all of us are not benefited or harmed directly or indirectly by these organisms. These are involved in number of industrial processes of fermentation, such as the making of bread, wines, beers, and the fermentation of the coaca beans and the preparation of certain cheeses. These have been found to be associated with number of disease manifestations, both in animals and human beings. The yeasts are mainly opportunistic organisms producing disease conditions both in animals and man. Excessive and erratic use of antibiotics, corticosteroides, immunosuppressive drugs and chronic diseases are the major contributing factors in increasing incidence of diseases due to yeasts. Yeasts in different hosts produce multifarious clinical manifestations e.g. thrush, disseminated candidiasis, cryptococcosis, mastitis, etc.

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Candida albicans

Disease (Candidiasis/Moniliasis/Thrush/Candidosis)

Candidiasis is a general term covering diseases caused by yeasts of the genus Candida. There are more than 150 species of Candida but only C. albicans is commonly associated with diseases in animals (Quinn et al., 1994). It is capable of causing both superficial and deep infections. The infection is associated with unhygienic surroundings and secondary to other debilitating conditions. Increased virulence of the fungus plays an important role in causing the disease. C. albicans is an asporogenous, pseudomycelial, fermenting yeast. Surface growth on agar media is largely composed of oval budding cells. C. albicans grows on ordinary media over a wide range of pH and temperature. It can utilize ammonium (but not nitrate), as well as, nitrogen and most (but not all) strains need to be supplied with growth factor biotin.

Epidemiology and Pathogenesis

Candida species are so commonly present in the gastrointestinal tract and have been found so frequently in nature that it seems proper to consider the disease they cause as endogenous in origin. In certain circumstances in man, individual-to-individual transmission occurs. Balanoposthitis has resulted from vaginal contact, and there is mother to child transmission through the vagina. The possibility that fecal contamination of meat at slaughter serves as a source of transmission to man has also been observed. Fecal contamination of feed undoubtedly accounts for the spread of candidiasis.

C. albicans possesses a number of putative virulent factors (Cutler, 1991). Candida possesses adhesins consisting of fibrillar, peptide mannans which have an affinity for the fibronectin on the surface of cells. The yeast forms are responsible for tissue damage and inhibition of yeast cell division results in hyphal elements that invade tissues. Phospholipase concentrated in hyphal tips, may enhance invasiveness. Although as a saprophyte, the organism is found in the spore form, it was demonstrated that the mycelial phase of C. albicans facilitates penetration of the fungus into tissues (Gresham and Burns, 1960). Haematogenous spread may occur following vascular invasion by hyphae or pseudohyphae, producing systemic lesions. Neuraminidase and proteases may play a role in virulence and cell wall glycoprotein has an endotoxin like activity. Other virulence factors are chitin, mannoprotein and lipids. Inflammatory responses are predominantly neutrophils and granulomatous lesions are rare. Phenotypic switching, which has been demonstrated in C. albicans may facilitate evasion of host defense mechanisms. C. albicans has a worldwide distribution and is frequently found associated with apparently normal individuals. It is a normal inhabitant of the mucocutaneous areas of digestive tract, oral cavity and urogenital tract of many animal species and humans. Candida albicans has been isolated from environmental sources less frequently than other Candida species suggesting adaptation towards a parasitic rather than saprophytic existence.

Oral and alimentary candidiasis

Localized mucocutaneous form of candidiasis is associated with overgrowth of resident C. albicans in the oral cavity or gastrointestinal and urogenital tract. Overgrowth of commensal Candida species may result in localized mucosal damage in parts of the digestive or urogenital tracts. Dorko et al. (1996) revealed that the Candida albicans strain isolated from a cat with oral candidiasis when inoculated experimentally in rats demonstrated the ability to induce a grossly evident lesion of the midline posterior dorsal tongue mucosa of rats. Chronic episods of diarrhoea have been seen associated with apparent colonization of intestines by Candida famata in a dog and there are reports of involvement of Candida glabrata in neonatal calf diarrhoea (Milner et al., 1997; Elad et al., 1998).

The infection is initiated due to endogenous and predisposing causes. Predisposing factors include defects in the cell mediated immunity, concurrent disease, disturbance of the normal flora by prolonged use of antimicrobial drugs and damage to the mucosa from indwelling catheters with affected mucosa being thickened and often hyperaemic. Intestinal candidiasis was observed in a wild captive black buck (Antilope cervicapra) and one sambar (Cervus unicolor) by Chakraborty and Chaudhary (1994). They suggested that as captive animals are always in the stress of confinement, the animals develop ulcer in the duodenum and the opportunistic Candida aggravates the lesions. A case of gastrointestinal candidiasis was diagnosed in a 16-year-old Himalayan black bear and C. albicans was isolated from the oesophagus and nasal sinus by (Chakraborty 1998). Secondary Candia albicans associated gingivitis and oesophagitis were noted in outbreak of natural measles virus infections in Japanese macaques in Korea by Choi et al. (1999). The young ones are especially susceptible. Candida infections of the alimentary tract especially in the fore stomach have been reported in calves (Cross et al., 1970). Clinical signs include watery diarrhoea, melena, subsequent anorexia, dehydration, prostration and death. Mycotic stomatitis has been reported in pups, kittens and foals (McClure et al., 1985). C. albicans has been implicated in gastro-oesophageal ulceration in pigs and foals (Kadel et al., 1969; Gross and Mayhew, 1985). C. albicans was isolated from stomachs of pigs having recognizable ulcers and subacute to chronic inflammatory reactions. A triad was found for the occurrence of altered keratinization with a change in the cysteine and cystine content of epithelium of stomach which had grossly abnormal keratin and increased glycogen content in epithelium of stomach with dyskeratotic changes, ulceration and C. albicans was observed in the stomach of swine by Kadel et al. (1969). Isolation rates of C. albicans increased with the increased severity of the ulcers.

Infection of birds with C. albicans is associated with unhygienic surroundings and it is secondary to other debilitating conditions like malnutrition, Vit. D deficiency. Candida albicans was demonstrated in pigeon faecal droppings by Martins et al. (1997). Sampurnanand et al. (1990) identified C. albicans in intestinal culture of peacocks that had died due to candidiasis. C. albicans were found to be pathogenic for quails by Naveen and Arun (1992). Das et al. (1993) isolated C. albicans from various pathological samples of crops, gizzards, lungs and livers from fowls, which had died of various diseases in Bhubaneshwar. Faecal contamination of feed also accounts for spread of infection.

Mastitis

Candida spp. has been isolated from apparently healthy animals having subclinical mastitis and from clinically ill mastitic animals (Sharma et al., 1977; Chhabra et al., 1996; Langoni et al., 1997; Tweyongyere and Kasirye, 1998). C. albicans was found to be the predominant yeast species (47.9%) followed by C.krusei (20.8%), C. parapsilosis (18.8%) and C. guillermondii (2.1%) (Chabbra et al., 1998). C. parapsilosis, C.krusei and C. guillermondii were isolated from mastitic milk samples of cattle and buffaloes by Kumar (1988) and Bansal et al. (1990). Monga and Kalra (1971) isolated C. albicans, C. krusai, C. parapsilosis, C. tropicalis, C. stelatoidea, C. pseudotropicalis and C. guillermondi from both apparently healthy and clinically affected quarters of cows, buffaloes and goats. C. albicans has been isolated from milk samples of buffaloes suffering from mastitis (Chhabra et al., 1998; Sharma, 1983; Sarma and Boro, 1980; Rahman and Baxi, 1980; Kumar and Thakur, 2000; Misra et al., 1993) and in dairy cows by Kaya et al. (1998). A greater susceptibility of cows to C. albicans than buffaloes in causing mycotic mastitis was found by Singh et al. (1989). Candida species were isolated from both normal as well as mastitic cattle by Simaria and Dholakia (1986). Jand and Dhillon (1975a) isolated C. albicans, C. guillermondii, C. tropicalis, C. parapsilosis and C. stellatoidea from clinical and sub clinical cases of mastitis of cows and buffaloes. Mycotic mastitis occurs sporadically either as a consequence of contaminated intramammary preparations or from heavy environmental contamination (Elad et al., 1995). Usually one quarter is involved and spontaneous elimination of the infection frequently occurs. Rarely yeast cells may be shed for upto 12 months. The higher incidence of mastitis due to yeast could be attributed to the ability of yeast to produce small budding cells which can establish themselves in the ducts and acini of the udder like those of bacteria (Ainsworth and Austwick, 1973). Thilagar et al. (2000) did clinical studies on obstructive theilitis in buffaloes and isolated C. albicans from culture of affected tissues in 3 of the 20 cases. C. albicans was isolated from quarters and milk samples of dairy goats suffering from subclinical mastitis by Mishra et al. (1996) and Moshi et al. (1998) and from mastitic cases of one humped she camel by El-Jakee (1998). Experimental mastitis was induced in healthy goats by infusing isolates of C. albicans and the fungi were isolated from milk samples throughout the disease (Jand and Dhillon, 1975b). C. albicans was highly pathogenic to the lactating goat mammary gland even without immunosupression or antibiotic treatment resulting in severe irreversible tissue damage and nearly complete agalactia (Singh et al., 1998).

Reproductive Disorder

In cattle they have been found associated with chronic pneumonia and have been found in pathogenic vaginal discharges and aborted fetuses. Six cows failed to conceive after insemination with semen contaminated with C. albicans (Misra et al., 1984). C. albicans was isolated from cervical mucus samples of infertile cows and buffaloes many of which had experienced difficulty at the last parturition and returned to heat several times but failed to conceive inspite of repeated insemination. Genus Candida was reported from repeater cows and buffaloes by Singh et al. (1992). Candida albicans was isolated from neat and chilled buffalo bull semen by Bindra et al. (1993). Jand et al. (1978) isolated C. albicans from swabs taken from the anterior vagina and cervix of sheep and goats. C. albicans was cultured from vagina and vulva of mares suffering from vulvo vaginal candidiasis by Montes et al. (2001).

Systematic candidiasis

Disseminated candidiasis has been reported occasionally in immunocompromised animals and those undergoing prolonged chemotherapy. Systemic candidiasis in association with repeated antibiotic therapy was observed in two young 18 and 22 days old calves by Mills and Hirth (1967). Possible damage to the tissues by the offending antibiotics, conversion of Candida to a more invasive form, toxic products elaborated by Candida and depression of host responses to the infection are the possible mechanisms whereby antibiotics enhance candidiasis. Tissue destruction by antibiotics may enhance candidiasis, invasion by Candida (Seligman, 1953) and destruction of alimentary flora by broad-spectrum antibiotics may cause a vitamin deficiency thereby lowering resistance of tissues to invasion by C. albicans (Harris, 1950).

Systemic candidiasis in foals with isolation of C. albicans was reported by Laura and Jonathan (1994). They further suggested that neonatal foals with complex problems are at risk to develop systemic Candida spp. infections with factors like use of i/v catheters, urinary catheters or endotracheal tubes, and treatment with multiple antibiotics increasing the risk of contracting candidiasis in foals. C. albicans was observed histopathologically in the heart, kidneys, brain and aorta of dogs by Kim et al. (1998). C. albicans was isolated from the lungs of rodents showing no evidence of infection by Gugnani (1972), whereas it was isolated from porcine pneumonic lung by Baruah et al. (1984).

Cutaneous candidiasis

C. albicans was isolated from skin scrapings of dogs suffering from dermatitis though the involvement of this organism in canine dermatitis is rare (Chittawar and Rao, 1982). C. albicans was identified in the skin scrapings of dogs suffering from dermatomycoses by Vishwakarma et al. (1997). They further revealed that Dermocept ointment (an Indian herbal preparation), oral griseofulvin or both resulted in 85.7, 16.6 and 85.7 per cent clinical cure, respectively, whereas the combined therapy acted more rapidly. Ahmed (2000) isolated Candida frequently from bull terrier dogs with LAD (Lethal acro dermatitis) and C. albicans was detected in samples collected from the nails and footpads of dogs with LAD by McEwan (2001). He concluded that C. albicans infection might, in part, be responsible for the pathogenic changes of the nails and footpads commonly seen in cases of LAD.

Diagnosis

Direct examination of clinical material for the demonstration of yeast cells may include scrapings from lesions, centrifuged milk samples. Organisms can frequently be seen in wet mounts (20% KOH and Lacto phenol Cotton Blue) and in smears stained with Gram's stain (gram positive) where they appear as oval, thin walled, budding cells and/or in the form of pseudohyphae. Germ tube test-is based on production of a filamentous outgrowth by cells of this organism when inoculated in serum and incubated at 37°C for 2-3 h. Small tubes will be seen projecting from some of yeast cells when observed under microscope. Isolation and cultivation of organisms can be done on blood agar and SDA with chloramphenicol at 25°C and at 37°C. Soft, white, shiny, high convex, creamy colonies appear in 24-48 h and have diameter of 4-5 mm. On corn meal agar or on special chlamydospore agar thick walled resting cells known as chlamydospores are produced. Carbohydrate assimilation and fermentation tests allow definitive species identification. Conventional biochemical tests can be used for definite identification of C. albicans. Biopsy of tissue samples in 10 per cent formalin can be used for diagnosis of candidiasis by histopathological examination. Tissue sections stained with PAS or methenamine silver methods may reveal budding yeast cells or hyphae. DNA probes are also available for identification of important species of Candida. Animal inoculation–Rabbits, mice and other laboratory animals are susceptible to infection. The pathogenicity of C. albicans in rabbits was determined by Jand and Dhillon (1975c) and was observed that C. albicans when inoculated experimentally in rabbits caused death of the rabbits after 4 days with large abscesses in the kidneys. Serological tests used in humans are not used routinely in veterinary medicine to detect Candida antigens (Carter et al., 1995).

Prevention and control

The majority of candidiasis cases are associated with predisposing diseases, unsanitary conditions or with prolonged use of antibiotics. So all these factors should be corrected. Oral and cutaneous infection may respond favourably to nystatin ointment, 1% iodine or application of amphotericin B. Copper sulphate at 1:200 dilution in drinking water is effective both as prophylactic as well as therapeutically in enteric infections. Affected birds can be fed with grains treated with Nystatin 10-100 mg/kg in feed and 200-1000 mg/l in drinking water. Ketoconazole and clotrimazole have been effective in treatment of mucocutaneous candidiasis in human beings (Carter et al., 1995). Intravaginal treatment with clotrimazole resulted in complete treatment of thoroughbred mares suffering from vulvo vaginal candidiasis (Montes et al., 2001). Mycostatin (nystatin) in all dilutions and thiobendazole (only in higher concentration) was found sensitive to C. albicans and thus could be used as the drug of choice against these organisms (Jand et al., 1978b; Shah et al., 1986). Mycostatin twice daily for 5 days was found to be effective in treatment of C. albicans in buffaloes suffering from mastitis by Kumar and Thakur (2000). Clotrimazole, ketoconazole, miconazole and nystatin were used effectively for treatment of mycotic mastitis due to Candida species with clotrimazole being the drug of choice (Bansal et al., 1989). Treatment with amphotericin B is indicated for animals with disseminated candidiasis; however, fluconazole may prove to be as effective as amphotericin B and is less toxic, less expensive and easier to administer (Laura and Jonathan, 1994). Fluconazole treatment may be especially useful in the prevention or early treatment of fungal infections of horses. Santolina oil, a volatile oil distillate of S. chamaecyparissus, was effective against C. albicans and had a synergistic effect on clotrimazole in vitro and this significantly controlled experimental vaginal candidiasis and systemic candidiasis in mice and superficial cutaneous mycoses in Guinea pigs (Suresh et al., 1997).

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Cryptococcus neoformans

Disease (Cryptococcosis/Torulosis/European blastomycosis/Buse Buschk's disease.)

Cryptococcosis, is a subacute or chronic disease of man and different species of animals. The disease in dogs and cats is characterized by pulmonary and central nervous system involvement and/or by localized lesions of the oral and nasal mucosa. The infection in cattle usually involves mammary tissue and respiratory distress with nasal granulomata. There are atleast 37 species in genus Cryptococcus but only C. neoformans is potentially pathogenic. It is a nonmycelial, non-fermenting, yeast multiply by single buds. It is characterized by thin walled spherical to oval cells that vary greatly in diameter (2.5–20.0 µm). When recovered directly from affected animals, a hyaline gelatinous capsule of polysaccharide material surrounds each cell. The yeast grows well on malt or beer wort agar to give a moist brownish growth, which runs down the slope and collects at the bottom of the tube. Apart from an inability to use nitrate and a need for thiamine, the nutrient requirements are not very exacting. Yeast like structures on corn meal agar are formed. Terminal chlamydospores are not produced. The ability to grow at 37°C distinguishes C. neoformans from other Cryptococcus species. On basis of capsular antigens, four serotypes of C. neoformans are recognized. Serotypes A and D are designated as C. neoformans var neoformans while B and C as C. neoformans var gattii.

Epidemiology and pathogenesis

Cryptococcus neoformans produces disease in humans and animals by inhalation of the organisms from exogenous source, principally pigeon droplets or soil contamination with it. It can survive in pigeon droppings for more than a year due to their high content of creatinine. Creatinine inhibits many other organisms but can be utilized by C. neoformans (Quinn et al., 1994). Cryptococcosis is not known to be transmitted from human to human, animal to animal or animal to human. Virulence of C. neoformans is largely associated with the antiphagocytic and immuno suppressive capsule, the ability to grow at mammalian body temperature and the production of phenol oxidase. The virulence arising from phenol oxidase activity may relate to the degradation of catecholamine, which results in the accumulation of melanin in the yeast cell walls protecting against the toxic effects of free radicals (Jacobson and Emery, 1991). Cryptococcus neoformans var neoformans has a worldwide distribution. It has been isolated from the skin, mucous membrane and intestinal tract of normal animals and birds. Cryptococcosis is not a contagious disease. Cryptococcus was isolated from clinically healthy pigeons as well as birds with clinical illness at Calcutta Zoo by Chakraboraty et al. (1991). Cryptococcus neoformans var gattii isolated from forest red gum trees (Eucalyptus species) in Australia has been spread in timber products. Cryptococcus neoformans can act as primary pathogen and cause infection in apparently normal host. Localization of organism occurs in nasal cavity or para nasal sinuses and later extends to brain and meninges while others are deposited in the lungs. Dissemination from the respiratory tract to brain, meninges, skin and bones is usually associated with defective cell mediated immunity. Fatal disseminated cryptococcosis with involvement of the skin, eyes and lymph nodes was diagnosed in a four-year-old dog by Pal et al. (1996). Extension to optic nerve may result in blindness. The disease in dogs, which is less common than in cats, is often disseminated with neurological and ocular signs. C. neoformans has been identified in bone marrow and lymph node of a dog suffering from neurological symptoms and bilateral lymphadenitis respectively (Acosta et al., 1999). Pal and Merhotra (1985) isolated C. neoformans from the brains of dogs, which had clinical signs of meningoencephalitis. Cryptococcal infection in a 1.5-year-old German shepherd dog characterized by intermittent fever, blood in faeces, mild nasal discharge and anorexia was reported by Kamboj et al. (1993). In cats, nasal, ocular, cutaneous and neural form of cryptococcois can be seen. Predominant is nasal form, which is characterized by flesh coloured, polyp like granulomas in the nasal cavity. Cutaneous lesions affect the face, head and neck. Peripheral lymph adenopathy is common. Chorioretinitis may be seen in some instances in neurological signs. Pal and Mehrotra (1983) isolated C. neoformans from a chronic ulcerated wound on the left tibio tarsal joint of a four-year-old female cat with a history of prolonged treatment with broad-spectrum antibiotics and corticosteroids. C. neoformas was ascertained as the prime cause of fatal meningitis in young adult female domestic short haired cat suspected of rabies by Pal (1991a). C. neoformans was identified in lymph nodes of a five-year-old female siamese cat with history of bronchopneumonia by Cabanes et al. (1995). In experimental cryptococcosis induced in young male calves, cryptococcal organisms could be demonstrated in nasal discharge and various tissue sections by Sood et al. (1996). They found that except for greater involvement of respiratory tract in immuno suppressed animals, immuno suppression did not appear to play much role in modulating the disease pattern. Cryptococcosis has been recorded infrequently in horses. Clinical signs include nasal granulomas and sinusitis (Scott et al., 1974), pneumonia (Hilbert et al., 1980), meningoencephalitis and abortions (Blanchard and Filkins 1992). Pneumonia due to C. neoformans var neoformans was recorded in sheep by Pal (1989). Cryptococcus species was isolated from cows and buffaloes suffering from mastitis (Monga et al., 1970; Sharma, 1983; Sharma et al., 1977). Infection of mammary gland occurs through teat canal. Pal (1991b) detected C. neoformans in samples of mastitic milk obtained from a seven year old indigenous female water buffalo that had clinical signs of acute mastitis. Intramammary inoculation of C. neoformans in goats leads to sever mastitis with sharp fall in milk yield (Singh et al., 1994). C. neoformans was implicated as the etiological agent of caprine mastitis by Pal and Randhawa (1976). Singh et al. (1994) did unilateral intramammary inoculation of goats with C. neoformans and concluded that intramammary inoculation leads to severe mastitis with sharp fall in milk yield. Pal et al. (1984) isolated C. neoformans from the lungs of a five year old male monkey that was under going treatment for bacterial pneumonia and presenting with low grade fever, dyspnoea and cough. Grossly cryptococcal lesions consist of capsular slime, yeast cells, some inflammatory cells and later histiocytes, epitheloid and giant cells. Subcutaneous granulomas occasionally occur often in the cervical or pedal region

Diagnosis

Direct microscopic examination of clinical material i.e. cerebro-spinal fluid, lesions or exudates, mastitic milk, biopsies and tissues etc. in wet mounts may be done. Care must be taken while handling clinical material because of the risk of acquired infection. The large capsules can be seen if clinical material is mixed with India ink or nigrosin. Histological sections on biopsies of tissues from lesions stained by PAS-HE stain. In PAS-HE stain, spherical budding yeast cells, 2-15 µm diameter can be demonstrated. C. neoformans stains poorly by Gram's stain. In Mayer's mucicarmine stain the wall of yeast and capsule are stained red in tissue sections, which is diagnostic for C. neoformans. Melanin can be detected in cell walls of C. neoformans by the Fontana Masson technique. Isolation of and cultivation of the organisms can be made on blood agar and SDA at 37°C. Wrinkled whitish granular colonies appear usually within a week. They become slimy, mucoid and cream to brown in colour on further incubation. Growth of organism is inhibited by cycloheximide. C. neoformans produces brown colonies on birdseed agar as a result of phenol oxidase production. Most Cryptococcus species produce urease, rapidly hydrolyzing urea to ammonia. Differentiation of species is possible using carbohydrate assimilation test on commercially available biochemical kits. C. neoformans can not utilize glycine as a sole source of nitrogen and is susceptible to canavanine. FAT can be done to identify culture in the clinical material. Latex agglutination test, which detects soluble capsular material of C. neoformans within three weeks of infection, can be used on samples of cerebro spinal fluid, serum and urine. Inoculation of organisms in saline suspension in mice intracerebrally 0.02-0.03 ml results in death of mice in 4 days to 2 weeks.

Prevention and control

Education of public regarding exposure to pigeon droppings. Disinfectants–3% formalin can be used for elimination of organisms from site. Drug of choice for this is amphotericin B (Jand and Singh, 1994). There may a favourable response to amphotericin B with flucytosine or to ketaconazole, itraconazole or fluconazole. Therapy should continue for atleast two months. C. neoformans was found to be sensitive to amphotericin B, fluconazole, itraconazole and ketoconazole and resistant to 5 fluorocytosine (flucytosine) by Cabanes et al. (1995).

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Malassezia (Pityrosporum)

Diagnosis

Presumptive diagnosis can be made by demonstration of yeast cells by Gram's method of staining or methylene blue stained smears or 10% KOH preparation of exudates from dogs with otitis externa and seborrhoeic dermatitis. On SDA containing chloramphenicol, small smooth colonies are produced after incubation at 25°C for up to 2 weeks and often have an odour not unlike a wet dog. Stained smears from cultures often reveal typical bottle shaped yeast cells. Growth is increased if sterile coconut oil is applied to the surface of the medium. On blood agar greenish discolouration is produced at site of inoculation.

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Geotrichum candidum

Disease (Geotrichosis)

G. candidum is ubiquitous yeast like organism. Two cultural forms occur (a) the glabrous or yeast like form and (b) the fluffy form or oospore. The glabrous form of G. candidum is the one usually associated with disease and is usually recovered from otitis externa in dog. The yeast doesn't produce conidiophores but the hyaline septate hyphae fragment into rectangular one celled arthrospores that tend to remain in chains.

Epidemiology and pathogenesis

Organisms occur in milk, soil, tomato or other fruits. It produces minor secondary type of infection including oral, intestinal and infection of pulmonary mucosa both in man and animals. In animals, cattle and dogs are involved. The disease is usually mild and is characterized by the formation of granulomas that may suppurate. There is doubt regarding its ability to invade animal tissues, however, it may be associated with bovine mastitis or intestinal infections especially if the animals have been on a prolonged antibiotic therapy. G. candidum has been identified in cases of mastitis (Misra and Panda, 1986). G. candidum was isolated from cow suffering from clinical mastitis by Jand and Dhillon (1975a). G. candidum was isolated from cows aged 2.5 to greater than 6 years clinically affected by acute mastitis by Seddek (1997). It can be isolated from faeces of clincially normal animals. The fungus has been occasionally implicated in diarrhoea in dogs, lymphadenitis in pigs and disseminated geotrichosis in dogs (Rhyan et al., 1990). G. candidum was isolated from 14-month Labrador dog and an attendant with dermatitic lesions on ears and around eyes by Sidhu et al. (1993). A case of G. candidum infection was diagnosed in a five-month-old male Rottweiler in Australia by Reppas and Snoeck (1999). Gugnani (1972) isolated G. candidum from lungs of rodents showing no evidence of infection. Singh and Uppal (1982) isolated geotrichum from body and horn of uteri of buffaloes having lesions in the genitalia or which showed discharge or had history of repeat breeding. Dermatophytosis of green iguanas (Iguana iguana) due to G. candidum was reported by Wissman and Parsons (1993).

Diagnosis

Disease is diagnosed by postmortem where in, the lungs, bronchi, udder and other mucous membranes are involved. In wet mounts, organisms appear as rectangular or spherical arthrospores (non budding, thick walled, gram positive). On SDA, organisms grow at 25°C. Colonies are membranous with radial furrows and soft with a dry granular surface. Organisms don't grow well on blood agar at 37°C. G. candidum produces soft, yeast like colony at room temperature and doesn't form blastospores.

Treatment

No specific treatment is advised but organisms are susceptible to amphotericin-B and 5-flucytosine (Carter et al., 1995). In dogs with dermatitic lesions on ears and around eyes, miconazole lotion and savlon bath were found to be effective by Sidhu et al. (1993).

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Trichosporon beigelii

Disease (Trichosporonosis)

It is an imperfect fungus within the family Cryptococcaceae. T. beigelii produces yeast cells (Blastoconidia) pseudohyphae, true hyphae and arthrospores. After inoculation on SDA, colonies appear in about one week. Yeast is non fermentative and urease positive. This yeast is occasionally a contaminant in clinical specimens. Pal et al. (1991) demonstrated T. beigelii in the chronic, ulcerated burn wound of a 3 month old jersey cow and suggested that the aetiological significance of T. beigelii should be considered when the organism is isolated from animals that are immuno suppressed due to some underlying disease or due to the prolonged use of cytotoxic drugs. Sharma et al. (1977) isolated Trichosporon species from clinical and sub clinical cases of cows and buffaloes suffering from mastitis. T. beigelii was isolated from normal clinical and subclinical mastitic quarters of dairy herds by Costa et al. (1993) and Kuo and Chang (1993). It has been recovered from a nasal granuloma and a bladder infection in cats, skin infection in horse and monkeys and mastitis in cattle and sheep. Nasal granuloma, mycotic cystitis and disseminated trichosporonosis have been described in cats infected with feline leukaemia virus (Doster et al., 1987). A survey of mycotic otitis externa in dogs aged three months to 15 years from Portugal of different breeds revealed the presence of T. beigelii and M. pachydermatis (Bernado et al., 1998). T. beigelii was cultured from a case of white piedra in 11-year-old cocker spaniel by Pereiro et al. (1987). Systemic trichosporonosis caused by T. beigelii in a white-handed gibbon (Hylobates lar) has been reported by Vicek et al. (1995). T. beigelii was isolated from liver and spleen of free tailed bats (Rhinopoma hardwickii hardwickii) by Oyeka (1994). Soderhall et al. (1993) isolated T. beigelii from cuticle of several cray fishes. T. beigelli was isolated from lesions of oral mucosa of Paleosuchus palpebrosus and P. trigonalus by Ladzianska et al. (1989). Taylor (1988) isolated T. beigelli from granulomatus foci and skin of the vent margin from mature Green winged macaw (Ara chloroptera).

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Torulopsis glabrata

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Rhodotorula minuta and R. rubra

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