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Coccidioidomycosis (Valley Fever)

Coccidioidomycosis (Valley Fever) is a benign fungal disease affecting cattle and dogs. It creates a major public health problems in human.

Coccidioidomycosis (Valley Fever) is a non contagious infection.

Etiology

Coccidioides immitis cause Coccidioidomycosis (Valley Fever).
C. immitis is a dimorphic, saprophytic organism develops as a mycelium in the soil and produces a spherules within the host.
Arthroconidia (arthrospores) produced by the hyphae are the infectious units of the organism.
The spores are known as arthroconidia (Barrel shaped).
C. immitis colonies grow rapidly. It produce white, cottony colonies and in old culture it turn to tan to brown color.
It is dormant during long dry period and develops as a mold with long filaments that break off into airborne spores following rainfall.

It is enzootic in South West US and up to 20% of cattle reared under feed lot condition.
It is a fungal disease and is sporadic in distribution.
Coccidioides spp. is endemic in hot and semi-arid zones.
The organism is detected in humans or animals present in endemic areas.

Coccidioides spp. grows in the soil as mycelia with lateral growing “barrel” shaped arthroconidia.
Coccidioides lies dormant in the mycelial phase during the times of draught, but heavy rain causes germination of the arthroconidia and production of more mycelia.
Infection occurs most often during dry weather disperse the conidia more easily following periods of heavy rain and wind.
Soil also promote exposure.

The disease spread by means of inhalation of spores which are saprophytic in nature.
Infection may also occur through cutaneous abrasions.
The disease is not transmitted from person to person.

Cattle, deer, dogs, elk, fish, mules, apes, kangaroos, wallabies, tigers, bears, badgers, otters and marine mammals are affected.
The disease also affects lesser extent the species such as pigs, sheep and horses.
Pulmonary coccidioidomycosis recorded in adult foal.
Human beings are affected.

Following inhalation of the arthroconidia, few conidia can produce infection.
Arthroconidia are distributed through the alveoli phagocytosed and develops to spherules, which then enlarge and undergo endosporulation.
The spherules rupture and release endospores into surrounding tissues, and spread locally or disseminate hematogenously to extra pulmonary sites.
The endospores develop into spherules and continue the cycle until host develop resistance.
Reactivation of latent infection is thought to occur in immunosuppressed patients.
T lymphocytes recognizing coccidioides antigens in the first four to six weeks of infection and activate macrophages to halt progression of infection.
In humans, those with impaired cell mediated immunity suffer from severe form of progressive coccidioidomycosis.
If conidia inhaled, they produce spherules, thus propagating the infection.
The hematogenous spread of the pathogen in the host’s bloodstream results in infection of skin, bones, joints, lymph nodes, adrenal glands and central nervous system.
Once the arthroconidia are inhaled, the fungus develops into 30-60 micron diameter spherules that are filled with 3-5 micron diameter endospores.
The large spherules then release the endospores that continue the infection.

Weight loss, severe emaciation, fluctuation of body temperature, persistent cough, muscle pain, superficial abscesses with frequent recurrence.
Muscle pain and development of superficial abscess in pectoral area is most common.
Increased lung sounds, wheezing, dullness are audible over the vertical chest area.
Other signs includes edema of legs, anaemia, intermittent colic due to internal abscesses and peritoneal adhesions.
Death due to rupture of liver occurs.

Cattle and pigs develops granulomatous lesion which contains a creamy coloured pus, calcified materials in bronchial, mediastinal, rarely in mesentric, pharyngeal, submaxillary and supramammary lymphnodes.
Lungs of neonatal foal contains diffusely infiltrated miliary pattern of multiple, coalescing, pale tan to red irregular shaped slightly raised firm foci 0.1-0.5 cm in diameter.

Based on clinical signs and necropsy findings.
Isolation and identification of organism.
An extract of fungal antigen, coccidioidin used in an intradermal sensitivity test.
CFT and Immuno diffusion test in humans.

Oral antifungal agents such as ketoconazole, itraconazole, and fluconazole are given.
The role of newer agents, such as voriconazole, posaconazole and caspofungin are still being tried.
It is often a self-limiting chronic respiratory or multisystemic disease and it requires a long term antifungal therapy.
For disseminated infection, treatment of at least 6-12 months is required.
Ketoconazole (10-30 mg/kg/day) or itraconazole (10 mg/kg/day) is commonly used to treat dogs.
Amphotericin-B may be used in animals not responding to azole antifungals.
Fluconazole also be effective. The use of long term fluconazole (2-3 mg/kg/day) resulted in a 55% success rate in monkeys with coccidioidomycosis.
Coccidioidomycotic osteomyelitis in a horse has been successfully treated with itraconazole 2.6 mg/kg body weight twice a day for 6 months.

Eradication of spores from soil is not feasible.
Halogens (such as iodine, and chlorine in the form of hypochlorite [bleach]), phenolics and quaternary ammonium compounds are proven effective against Coccidioides spp.
Arthroconidia are resistant to dry heat, but they can be inactivated by moist heat (121°C for a minimum of 15 minutes).