Coccidioidomycosis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]
Overview
Coccidioidomycosis is a fungal disease caused by Coccidioides immitis or C. posadasii. It can be caused by breathing coccidioides spores in the air, especially after a soil disturbance. As per CDC [3] about 30-60 % people living in endemic areas are exposed to the infection sometimes in their lives.[1]
Historical Perspective
Coccidioidomycosis was first discovered in 1892 by, Alejandro Posadas (a medical student) along with his mentor. They grouped coccidioidomycosis under parasitic family. Emmet Rixford and T. Caspar Gilchrist coined the term coccidioidomycosis (resembling coccidia) in 1896. William Ophüls and Herbert C. Moffitt described its dimorphic nature and defined it as a fungal etiology in 1900. C. immitis was investigated by the United States during the 1950s and 1960s as a potential biological weapon. It was never standardized, around beyond a few field trials, it was never weaponized.
Pathophysiology
Coccidioidomycosis is a fungal infection, that is acquired through inhalation of the spores from the environment. Following inhalation, the spores gets deposited into terminal bronchioles and enlarge, become rounded and develop internal septations to form what are known as the spherules. It then disseminates through the lymphatics and blood stream to gain access to any organ of the body.[2][3][4][5]
Causes
Coccidioidomycosis is caused by an infection with Coccidioides immitis or Coccidioides posadasii
Epidemiology and Demographics
California state prisons have been particularly affected by Coccidioidomycosis, as far back as 1919. In 2005 and 2006, the Pleasant Valley State Prison near Coalinga and Avenal State Prison near Avenal on the western side of the San Joaquin Valley had the highest incidence rate in 2005, of at least 3,000 per 100,000. It is endemic in certain parts of Arizona, California, Nevada, New Mexico, Texas, Utah and northwestern Mexico.
Differentiating Coccidioidomycosis from other Diseases
Coccidioidomycosis presents as a mild flu-like illness that needs to be differentiated from a number of other fungal/bacterial disorders. These disorders have overlapping signs & symptoms such as fever, muscle pain along with rash that often needs detailed history, physical examination, and serological tests to pinpoint the diagnosis. Blastomycosis, Histoplasmosis, Aspergillosis, Pneumocystis pneumonia, Sporotrichosis.
Risk Factors
On occasion, those particularly susceptible, including pregnant women, people with weakened immune systems, and those of Asian, Hispanic and African descent, may develop a serious or even fatal illness from valley fever.
Natural History, Complications and Prognosis
Natural History
Symptomatic infection (40% of cases) usually presents as an influenza-like illness with fever, cough, headaches, rash, and myalgia. Some patients fail to recover and develop chronic pulmonary infection or widespread disseminated infection (affecting meninges, soft tissues, joints, and bone). Severe pulmonary disease may develop in HIV-infected persons.[6][7]
Complications
Serious complications include severe pneumonia, lung nodules, and disseminated disease, where the fungus spreads throughout the body. The disseminated form of valley fever can devastate the body, causing skin ulcers and abscesses to bone lesions, severe joint pain, pericarditis, prostatitis,urinary tract infection, meningitis, and death.
Prognosis
The prognosis of Coccidioidomycosis is good in immunocompetent patients. It is self-limited in most of the patients and recovery is without any complications. The mortality rate is currently <0.07%. Approximately less than 1 % of patients develop disseminated coccidioidomycosis.
Diagnosis
Symptoms
A positive history of fever, arthralgia and erythema nodosum are suggestive of coccidioidomycosis. The most common symptoms of coccidioidomycosis include fever with chills, cough, and pleuritic chest pain.
Physical Examination
The physical manifestations of the disease depends on the organ of involvement. In the order of incidence the most commonly involved organs are lungs, skin, bones, genitourinary system, central nervous system and other organs.
Laboratory Findings
The fungal infection can be demonstrated by microscopic detection of diagnostic cells in body fluids, exudates, sputum and biopsy-tissue. With specific nucleotide primers C.immitis DNA can be amplified by PCR. It can also be detected in culture by morphological identification or by using molecular probes that hybridize with C.immitis RNA. An indirect demonstration of fungal infection can be achieved also by serologic analysis detecting fungal antigen or host antibody produced against the fungus.
Chest Xray
Every patient suspected of coccidioides infection needs a chest X-ray. The findings can be variable ranging from infiltrates, nodules, cavities to mediastinal adenopathy and pleural effusions. Nodules in the upper part of the lung is a usual finding, they are rarely calcified if at all. The nodules are better visualized on CT scan and after contrast enhancement
Treatment
Antifungals are the mainstay of treatment. The drug therapy is guided by the severity of symptoms and the immune status of the patient. Since most patients are asymptomatic or mildly affected, no treatment or a single drug azole therapy (fluconazole or itraconazole) may be sufficient in these cases. More recently resistant cases are being treated with voriconazole or posaconazole.[1]. However, patients with HIV, immunocompromised, those on steroids or pregnant females need much more aggressive approach. More severe cases may require intravenous amphotericin B, with or without simultaneous oral azole therapy. Meningitis or vasculitis often need initial in-patient treatment with oral azoles plus intravenous amphotericin B with or without intrathecal amphotericin B. Untreated cases may sometimes be fatal.
References
- ↑ Walsh TJ, Dixon DM (1996). Spectrum of Mycoses. In: Baron's Medical Microbiology (Baron S et al, eds.) (4th ed. ed.). Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1.
- ↑ Stockamp NW, Thompson GR (2016). "Coccidioidomycosis". Infect. Dis. Clin. North Am. 30 (1): 229–46. doi:10.1016/j.idc.2015.10.008. PMID 26739609.
- ↑ Twarog M, Thompson GR (2015). "Coccidioidomycosis: Recent Updates". Semin Respir Crit Care Med. 36 (5): 746–55. doi:10.1055/s-0035-1562900. PMID 26398540.
- ↑ DiCaudo DJ (2014). "Coccidioidomycosis". Semin Cutan Med Surg. 33 (3): 140–5. PMID 25577855.
- ↑ Malo J, Luraschi-Monjagatta C, Wolk DM, Thompson R, Hage CA, Knox KS (2014). "Update on the diagnosis of pulmonary coccidioidomycosis". Ann Am Thorac Soc. 11 (2): 243–53. doi:10.1513/AnnalsATS.201308-286FR. PMID 24575994.
- ↑ Ampel N (2005). "Coccidioidomycosis in persons infected with HIV type 1". Clin Infect Dis. 41 (8): 1174–8. PMID 16163637.
- ↑ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. pp. pp. 680-83. ISBN 0838585299.