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| May 1998 |
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| COCCIDIOIDOMYCOSIS |
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| Background |
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Coccidioidomycosis is typically caused by inhalation of infectious arthrospores of the soil dwelling fungus,
Coccidioides immitis. The disease was first reported in animals in 1940 and is endemic in the southwestern
United States.
Endemic areas for C. immitis include California, Nevada, Utah, Arizona, New Mexico and Texas as well as
Mexico, Central and South America. Humans and animals can be infected, especially when hot, dry conditions exist
and favor inhalation of arthrospores spread by wind or physical disturbance of infected soil. Individuals travelling
in infected areas are also at risk for contracting the disease, so travel history is important as weeks to even years
can pass before clinical signs appear. Many animal infections are subclinical and depend on the competency of host
cell-mediated immunity to remain in check. Cats appear more resistant to the clinical disease, whereas humans and dogs
can develop severe disseminated disease, especially if immunocompromised (neoplasia, pregnancy, immune-mediated disease,
viral infection, prolonged or severe stress). Burial of infected animals in endemic areas is ill-advised, because soil
contamination can last many years. Infection cannot be spread directly between animals or from animals to humans.
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| Demographics of Infection |
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A review of 218 canine cases at University of Calif., Davis found 43 breeds and mixed breeds represented,
predominantly young adult males of medium and large breeds (62% < 4 years, 63% males, and 78% medium to
large size), and 76% were primarily outdoor dogs kept in backyards or for hunting and herding. Breeds stated
to be at apparent increased risk include boxer, pointer, Australian shepherd, beagle, Doberman pinscher, and
Scottish terrier.
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| Clinical Signs |
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Primary cutaneous disease is relatively uncommon and exhibits painless, firm, indurated nodules with central
ulceration, occasional draining tracts, and regional lymphadenitis and lymphadenopathy. All cutaneous lesions
should be assumed to result from disseminated disease unless proven otherwise. The classical acute, primary
pulmonary disease (80% of cases) causes a severe productive cough from widespread lung involvement (nodules,
consolidation) and tracheobronchial lymphadenopathy seen radiographically. Other systemic signs occur in 20%
of cases and can include antibiotic non-responsive low-grade fever, depression, exercise intolerance, weakness,
anorexia, and lameness with soft tissue swelling and bone pain. Bone is a common site for disseminated infection
which can occur without pulmonary signs or lesions. It should be considered in greyhounds, along with their
relatively high risk of long bone trauma and neoplasia, during workup for painful lameness (serology, location
or exposure to endemic region, x-ray, bone biopsy). While early clinical signs are often self-limiting, some
cases progress to systemic infection including CNS, GI, ocular, cardiac, liver, splenic, prostatic and renal
involvement.
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| Diagnosis |
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Hematologic and biochemical findings are variable and nonspecific. A definitive diagnosis is made by direct observation
of C. immitis by cytology of tracheobronchial lavage, draining skin lesions, and lung, lymph node or tissue aspirates.
Multiple site bone specimens should be taken as finding organisms can be difficult in some cases. Radiographs reveal varied
changes with the pulmonary disease. The fungus grows readily in culture in 3-10 days. Serology yields a positive IgM precipitin
test in 2-5 weeks with subsequent positive IgG complement fixation (CF) test in 8-10 weeks. High titers usually reflect
disseminated disease. During recuperation CF titers can persist at low levels (1:4).
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| Treatment |
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Systemic fungal chemotherapy is recommended for all forms except for the primary cutaneous disease, to prevent dissemination of
infection. The azoles, ketoconazole (Nizoral®, 5-15 mg/kg PO q 12 hr) and itraconazole (Sporanox®, 5-10 mg/kg, PO q 12-24 hr),
both given with food, are the drugs most widely used for dogs and cats. The former is less expensive but has more side effects.
Fluconazole (Diflucan®, 2.5-5 mg/kg PO or IV q 24 hr) is also used but is very costly. Amphotericin B in liposome form (Abelcet®,
1 mg/kg IV QOD for up to 12 mg/kg) is used for serious disseminated disease and is less nephrotoxic. Nikkomycin and lufenuron are newer
drugs under study. Treatment with azoles should continue for at least 2 months following resolution of clinical signs (a total of 6-12
months for disseminated disease). Relapses can occur. Azoles are mutagenic and cannot be used during pregnancy. The extremely high cost
of treatment is a major deterrent. Asymptomatic dogs with positive CF titers do not need to be treated but should be monitored for signs
of disease..
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| Coccidioidomycosis Serology |
| Test codes |
| Specimen requirement |
Serum |
| Turnaround time |
24 days |
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