Coccidioidomycosis may occur initially as a mild acute diseases referred to as “Valley fever” but can later progress into a more serious form of the disease that may be in chronic or disseminated form. The symptomatology of coccidioidomycosis and its presentation vary considerably depending on the stage of the disease. These signs and symptoms of coccidioidomycosis are seen in the following stages of the disease:
The initial form of coccidioidomycosis appears to be mild with a few signs and symptoms. Onset of symptomatology often occurs one to three weeks after the spore exposure. Complains of flu-like symptoms like: fever, chills, cough, headache, arthralgia, and fatigue. Cutaneous spotty rashes may occur in the thorax and the extremities. Severe constricting chest pain may also occur resembling that of a heart attack.
This condition progresses from acute form when symptoms fail to resolve during the acute phase of the disease. Chronicity of coccidioidomycosis most of the time progress to pneumonia which are commonly seen in immunocompromised hosts. The following signs and symptoms are commonly seen in chronic coccidioidomycosis: Weight loss, low grade fever, recurrent cough, persistent chest pain, blood tinged expectorations, and nodules in the lungs.
This condition is the most severe form of coccidioidomycosis, where the infection has already gone beyond the lungs to infect other organs like the skin, bones, liver, brain, meninges and the heart. Symptomatology depends on the organ where the infection affects and commonly presents as: Nodules and ulcers of the skin, painful lesions of the skull, bones and spine, swollen ankle and knee joints, and meningitis which is the most deadly among its complications.
The diagnosis of coccidioidomycosis is very difficult to ascertain clinically because this fungal infection may mimic common viral infections. Chest X-ray may not even give a specific diagnosis inferring to Coccidioidomycosis. The definitive diagnosis of coccidioidomycosis falls on the demonstration of the fungus in the tissues, blood, secretions and washings from bronchoalveolar lavage .
The following test are done to diagnose coccidioidomycosis:
Coccidioidomycosis is often mild and may not require any treatment. In severe cases, symptoms are treated with increased fluid intake and adequate rest. For patients with persistent symptoms with high risk medical profile, antifungal medications like fluconazole and itraconazole in serious cases of coccidioidomycosis are used. The most serious disseminated forms of coccidioidomycosis are treated with intravenous amphotericin B .
Majority of cases of coccidioidomycosis is self-limiting and resolves completely within a few months. The use of antifungal therapy is associated with excellent prognosis. Patients who progress to chronic inflammatory phase of coccidioidomycosis with deficient cellular immunity has higher risk for intrapulmonary cavitations and extrapulmonary spread of the coccidioides infection to other organs. Poor prognosis is associated with the disseminated type of spread of coccidioides spherules which only represents 1% of all cases.
A majority of patients who inhales the coccidioides spores develop mild to moderate symptoms that may resolve spontaneously without medications. However, certain races like Filipinos, Hispanic and Asians may be at risk to develop the severe disseminated form of the infection. The following clinical conditions are common complications of coccidioidomycosis in an immune deficient hosts:
Coccidioidomycosis is caused by two genetically distinct organisms but morphologically identical soil fungus. These fungus are Coccidioides immitis and Coccidioides posadasii respectively. Both fungus are found to be endemic in the arid regions of the western hemisphere. Coccidiodes soil fungi abound regions with low elevation, scant rainfall, mild winters, hot summers, sandy alkaline soil with increase in salinity . The Coccidioides immitisis is largely limited to the San Joaquin Valley; thus, coined the “valley fever”. There has been reports of zooanthropologic transmission from coccidioidomycosis infected cats to humans .
Coccidioides are found to be endemic in the soil of the western hemisphere regions located between latitude 40 degrees north and 40 degrees south . In the United States, the occurrence of C. immitis dominates the San Joaquin Valley of California while C. posadasii abounds in the desert of the southwest which includes regions of Arizona, Utah, Nevada, New Mexico and Texas.
Archeologists, farmers and construction workers are potentially at risk to coccidioidomycosis because of their frequent contact to the infected soil . There is an estimated 150,000 coccidioides infections per year in the United States. The death rate approaches 75 cases per year in the US alone due to coccidioides infection.
The prevalence rate of the disease reaches 30 to 40% of the population in endemic areas like California and Arizona . There are no known racial predilection for coccidioidomycosis. Older males are more prone to the infection due to occupational exposure. Coccidioides infection of the neonate rarely occurs .
The pathophysiology of coccidioidomycosis begin with the inhalation of the coccidioides spores from the soil where it is lodged in the terminal bronchioles as a C. immitis or a C. posadasii arthroconidia. Spherules are formed within the bronchioles as the arthroconidia enlarges. Hundreds to thousands of endospore offspring within the spherules rapidly divides within 48-72 hours until it is fully filled. The rupture of the endospore offspring within the bronchioles gives rise to new spherules in the pulmonary mucosa .
The transformation of the arthroconidia into a coccidioides spherule results into a local inflammatory process within the bronchioles causing suppuration and tissue necrosis. C. immitis has been found to trigger the complement system and release mediators of chemotaxis for neutrophils. Macrophages engulfs endospores that initiates the acute phase of the inflammation.
Chronic unabated infection with the coccidioides endospores harbors more histiocytes and lymphocytes forming a granuloma or giant cells marking the initiation of the chronic phase of inflammation in coccidioidomycosis.
Those who are living near coccidioidomycosis endemic areas must take extra precaution especially during the summer months. One may use protective mask to prevent spore inhalation. Staying inside the house during dust storms, wetting the soil before digging, and keeping doors and windows tightly closed can prevent the fungal spores from being inhaled to the lungs.
Coccidioidomycosis or valley fever is a fungal infection characterized by coughing, fever, shortness of breath, and chest pain caused by a fungus called Coccidioides. The fungi are commonly found in the soil where it can be agitated to the air by anything that disrupts the soil such as the wind, farming, excavation, and construction.
The spores can easily be inhaled into the lungs and cause coccidioidomycosis. Mild fungal infection may spontaneously resolve without treatment while more serious infections may require antifungal medications for its resolution.
The soil fungi Coccidioides immitis and Coccidioides posadasii cause the disease.
Flu-like symptoms and rashes occur in acute phase, persistent symptoms may be joint pains and pneumonia in the chronic phase. Extrapulmonary involvement in disseminated coccidioidomycosis is possible.
Sputum smear and culture and blood tests (fungal antibodies) are used to diagnose the condition.
Treatment and follow-up
Rest, oral antifungal and intravenous amphotericin B are the treatment options for coccidioidomycosis.