Coccidioidomycosis Clinical Presentation

  • Author: Duane R Hospenthal, MD, PhD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Dec 8, 2011
 

History

The incubation period of coccidioidomycosis averages 10-16 days, with a range of less than 7 days to 30 days.[2] . The natural history of Coccidoides infection is usually one of a self-limited respiratory tract infection. In most cases, symptoms do not occur or are so mild that the infected individual does not seek medical attention.[10, 37] Approximately 30-40% of patients develop symptomatic disease, ranging from a mild influenzalike illness, to subacute pneumonia, to, rarely, respiratory failure.

Common symptoms of primary infection are nonspecific and include fever, cough, chest pain, fatigue, dyspnea, headache, arthralgias, and/or myalgias. Skin manifestations are also seen in a small percentage of cases. In addition to the above symptoms, infection can progress to various presentations. The constellation of fever, arthralgias, erythema nodosum or erythema multiforme, and chest pain is commonly referred to as San Joaquin Valley fever (or simply Valley fever) or desert rheumatism.

A study by Johnson and colleagues reported the following frequency of symptoms[38] :

  • Fever (76%)
  • Cough (73%)
  • Chest pain (44%)
  • Fatigue (39%)
  • Shortness of breath (32%)
  • Chills (29%)
  • Erythema nodosum (26%)

Other symptoms included the following:

  • Night sweats
  • Weight loss
  • Urticaria
  • Arthralgias

Primary pulmonary infection may progress to overt pneumonia and chronic lung infections; hematogenous spread may occur, leading to disseminated disease, with focal involvement such as arthritis, osteomyelitis, and meningitis. Patients who have disseminated disease present with dramatic sweats, dyspnea at rest, fever, and weight loss.

Exposure history

In patients with suspected coccidioidomycosis, a history of travel to, or residence in, an endemic area is very important in establishing the risk of exposure. The exposure may be as limited as driving through an endemic area.[6, 2, 3, 7, 4, 8, 9] The clinician should inquire about activities that involve increased exposure to dust or soil (eg, farming, construction work, archaeological digs). Rare cases of infection from contaminated fomites (eg, contaminated plaster cast, dusty clothing) have been reported.[4]

Coccidioidomycosis is considered to be an occupational hazard in endemic regions, and it is a compensable illness in such cases.

Severe disease

Dissemination usually occurs weeks to months after the initial infection but may occur after 1 year in a host who is immunocompromised. In addition, reactivation of treated primary disease may occur at any time in a host who is immunosuppressed. Some patients may have no radiographic evidence of previous pulmonary disease, as well as no history of a preceding respiratory illness.

Factors associated with increased risk of more severe coccidioidal disease include the following:

  • HIV disease, especially when CD4+ cell counts are < 250/mL[31]
  • Pregnancy; the risk increases slightly with each progressive trimester
  • Lymphoma
  • Immunosuppressive therapy in solid organ transplant recipients (especially during first year after transplantation)
  • Long-term corticosteroid treatment (>20 mg prednisone)
  • Treatment with tumor necrosis factor (TNF)-alpha inhibitors[35]
  • Chemotherapy for solid tumors
  • Diabetes mellitus
  • Preexisting cardiopulmonary conditions
  • Thymectomy

The male-to-female ratio in disseminated disease is 5:1, but this disparity reverses in pregnant women.

Next

Physical Examination

No physical findings are pathognomonic for coccidioidal infection. However, in endemic areas, coccidioidal infection should be a strong consideration for patients who present with an influenzalike illness and a lower-extremity rash. Suggestive signs of disseminated disease include dramatic sweats, dyspnea at rest, fever, and weight loss.

In addition to nonspecific systemic signs (eg, fever), findings on physical examination reflect the organ system or systems involved.

Respiratory manifestations

Pulmonary coccidioidomycosis may be difficult to differentiate from other acute or subacute respiratory infections with fever. Most symptomatic primary infections are not easily diagnosed as coccidioidomycosis unless classic findings (eg, erythema nodosum) are present in an endemic area.

Respiratory symptoms are related to the severity of lung involvement and destruction, and they range from cough, to mild respiratory distress, to respiratory failure and acute respiratory distress syndrome.

Pulmonary involvement may manifest as the following:

  • Bronchial breath sounds
  • Rales
  • Rhonchi
  • Dullness to percussion
  • Increased tactile and vocal fremitus
  • Decreased breath sounds from effusions

Less commonly, diffuse coccidioidal pneumonia in immunocompetent hosts manifests as respiratory failure. This is due to either inoculation with a large number of spores or to hematogenous seeding of the lung at several sites.

Approximately 5% of pulmonary infections result in the formation of nodules. These typically cause no symptoms but may be indistinguishable from a neoplasm on radiologic studies. without histologic examination.

Approximately half of these nodules resolve spontaneously. However, persistent nodules can eventually degenerate into thin-walled cavitations, which may erode into adjacent small airways or the pleural space, resulting in hemoptysis or pneumothorax. Rupture of a peripheral coccidioidal cavity into the pleural space is a complication that is most common in young male patients.

Patients with diabetes mellitus or preexisting pulmonary fibrosis (eg, from cigarette smoking) may develop a chronic fibrotic pneumonia process. These patients may present with chronic cough and systemic symptoms such as fever, night sweats, and weight loss, as well as local symptoms.

Skin manifestations

Cutaneous hypersensitivity reactions are common in primary coccidioidomycosis. More than 50% of affected children, and 25% of infected individuals overall, develop diffuse, evanescent, maculopapular rashes or urticaria that may progress to erythema nodosum or erythema multiforme after 3-21 days. Erythema multiforme is more common in children, but erythema nodosum is the classic presentation in an endemic area.

Erythema nodosum presents as tender, erythematous nodules, 1-2 cm in diameter, on the anterior lower extremities (see the image below), although they may develop virtually anywhere. Erythema multiforme consists of relatively symmetric erythematous, expanding macules or papules that evolve into classic iris or target lesions with bright-red borders. Central vesicle formation is common.

Erythema nodosum can be observed in coccidioidomycErythema nodosum can be observed in coccidioidomycosis, tuberculosis, histoplasmosis, drug reactions, and streptococcal infections.

Ocular hypersensitivity reactions frequently accompany erythema nodosum. These include phlyctenular conjunctivitis, episcleritis, scleritis, and keratoconjunctivitis.

These cutaneous hypersensitivity reactions are a favorable prognostic sign; they suggest a low risk of dissemination because they correlate with development of cell-mediated immunity. Erythema nodosum occurs less often in persons outside of endemic areas and occurs infrequently in blacks, Hispanics, and Filipinos. Among adults, women experience erythema nodosum much more frequently than men.

Cutaneous hypersensitivity reactions must be distinguished from cutaneous Coccidioides infection, in which the organism is present in the lesion. The skin eventually is involved in most types of disseminated disease. Cutaneous infection usually results from hematogenous seeding, but direct inoculation may occur, evidenced by lymphangitis.

Cutaneous coccidioidal infection has a variable appearance; papules, plaques, and verrucous lesions are the most common. The classic skin manifestation of coccidioidomycosis is a verrucous granuloma at the nasolabial fold. Other typical lesions include granulomatous papules, nodules, and plaques, especially on the head. These lesions can progress to subcutaneous involvement, sinus tracts, abscesses, and chronic ulcers (see the image below).

Abscess formation may be associated with underlying bone or organ involvement. Facial involvement is associated with a 10-fold increase in the probability of coccidioidal meningitis.

Disseminated infection can also result in ulceration and fistulas from underlying infection.

Soft tissue abscess due to cocci. Soft tissue abscess due to cocci.

Musculoskeletal manifestations

Musculoskeletal involvement occurs in one third of patients with dissemination and include the following:

  • Unifocal bone lesions (lytic or sclerotic in 60% of cases)
  • Unifocal joint lesions (monoarticular arthritis in 90% of cases,)
  • Rarely, infected tendon sheaths demonstrating a villonodular synovitis

Although arthritis is usually monoarticular, it can be migratory in nature. Knees are the most common joints involved, followed by ankles and wrists. Physical findings are not helpful in differentiating coccidioidomycosis from other causes of monoarthritis or oligoarthritis.

Arthrocentesis samples typically reveal an exudative effusion. The presence of organisms varies, and reports suggest that direct visualization of organisms is rare but can occur in up to half of cases.

Coccidioidomycosis also affects joints, causing synovitis. Infection of the bone typically causes a chronic osteomyelitis, often draining to soft tissue and creating fistulae. Long bones, as well as bones of the hands, feet, pelvis, and skull, may be involved. Approximately 60% of incidents of coccidioidomycosis are limited to a single bone, with 20% involving 2 bones and 10% involving 3 bones. Vertebral osteomyelitis can affect any part of the vertebra, sparing the disc, but putting the patient at risk of meningitis.[39]

Although osteomyelitis can occur from direct inoculation of bone from contaminated penetrating objects, it is more commonly due to hematogenous spread and disproportionately affects the vertebra; paraspinal abscesses are a possible complication. Local pain and tenderness may be evident with vertebral osteomyelitis or paraspinous abscesses. Progressive bony destruction in the vertebrae can lead to spinal cord compression that may require urgent surgical intervention.

Other common sites of involvement include the tibia, femur, skull, and bones of the hands and feet. Other complications of osteomyelitis include contiguous joint arthritis, draining sinus formation, and subcutaneous abscess formation in adjacent soft tissue.

Other organ involvement

Coccidioides infection can involve virtually any organ system. At autopsy, involvement of the liver, spleen, kidney, adrenal glands, psoas muscle, heart, thyroid, and prostate has been noted. These infected sites rarely are responsible for the presenting signs or symptoms. Infection of the thyroid gland has been reported to result in a thyroid abscess and thyrotoxicosis.

Lymph node involvement can be prominent; occasionally, such cases lead to a mistaken diagnosis of lymphatic malignancy. Supraclavicular and cervical lymphadenopathy are common and probably result from lymphatic drainage from the pulmonary infection site. Lymphadenopathy may be generalized, and associated drainage from contiguous lesions is not unusual.

In a minority of patients, splenic enlargement is clinically apparent. Hepatic involvement with prominently elevated alkaline phosphatase levels is common in the context of widespread disease. Hepatic infection is usually asymptomatic but can be part of a hepatic-pulmonary syndrome with a brief hepatitis-like illness, hepatic granulomas, and eosinophilia.

Coccidioidal infection of the biliary tree is uncommon but has been reported to present as abdominal pain and obstructive jaundice. Intestinal obstruction and peritonitis have also been reported to be secondary to coccidioidal infection.[40]

Cardiovascular complications account for an extremely small percentage of clinical presentations. In the rare cases in which they do occur, however, they can be devastating. Pericardial effusions and can produce cardiovascular compromise and tamponade in extreme cases.[41] Myocardial involvement is most often discovered at autopsy.

Urinary tract involvement is rare (with the exception of asymptomatic coccidiuria) and is usually found in the setting of widely disseminated disease. The prostate may serve as a nidus of infection and has been implicated as a source of urinary cultures that are positive for the Coccidioides organism. Involvement of the ovaries and testicles is very uncommon.

Ocular coccidioidomycosis is rare but is probably underappreciated. Ocular involvement usually occurs in the context of disseminated disease. Ocular coccidioidomycosis can present as a lacrimal gland fossa mass or with eye pain, photophobia, and other symptoms of chorioretinitis or iridocyclitis. Anterior uveitis and posterior uveitis (choroiditis and chorioretinitis) are uncommon, and endophthalmitis is rare and can occur without systemic involvement.[42]

Meningitis

Approximately 50% of patients with disseminated coccidioidomycosis acquire CNS disease. It can occur acutely with primary infection or later with dissemination. The meninges can be the only site of dissemination, in which case the patients is at increased risk of complications and death.[43]

Coccidioidal meningitis can present as an acute process but it is usually chronic with insidious onset, in contrast to meningitis from bacterial causes. Persistent headaches should be evaluated thoroughly upon worsening, especially in cases of unusual severity, associated nausea and vomiting, blurry vision, or a change in mental status (eg, drowsiness and confusion). Other common manifestations include nuchal rigidity and photophobia.

Symptoms related to increased intracranial pressure (eg, nausea, vomiting, altered mental status) are relatively common. Less-common presentations include focal neurologic deficits, cranial nerve palsies, tremulousness, intention tremor, papilledema, gait abnormalities, seizure, and coma.[44]

Typically a granulomatous and suppurative basilar process, coccidioidal meningitis can also involve the brain parenchyma and spinal cord with granulomas and abscesses. Hydrocephalus is a common sequela and is often present at initial diagnosis in children.

Septic shock

Septic shock generally develops in older individuals or immune-compromised patients. For example, patients with advanced HIV disease may present with a fulminant picture of respiratory failure, diffuse pneumonia, fungemia, and septic shock that resembles a gram-negative infection.

This condition is diagnosed on the basis of established criteria and hemodynamic monitoring. Cytokine assays reveal elevated levels of tumor necrosis factor (TNF) and interleukin-6, as in bacterial sepsis.

Coccidioidal fungemia

This is a very rare, fulminant complication of disseminated coccidioidomycosis. Coccidioidal fungemia seems to be more common in patients with comorbidities and immunosuppressive states. The literature notes 113 cases, with about 38% associated with HIV; 18% with corticosteroids; 10% with solid organ transplants; and 4% with pregnancy. Dissemination occurred to the liver, spleen, and meninges/CNS, but endocarditis was not found. Serologic tests were positive in 87% patients. Overall mortality at 30 days was 62%, with a mean survival of 11.4 days. Survival is poorest in immunocompromised patients or those not receiving antifungal therapy.[45]

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Contributor Information and Disclosures
Author

Duane R Hospenthal, MD, PhD  Professor of Medicine, Uniformed Services University of the Health Sciences; Physician, Infectious Disease Service, San Antonio Military Medical Center (formerly Brooke Army Medical Center)

Duane R Hospenthal, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Society for Human and Animal Mycology, International Society for Infectious Diseases, International Society of Travel Medicine, and Medical Mycology Society of the Americas

Disclosure: Nothing to disclose.

Coauthor(s)

Kelley Struble, DO  Fellow, Department of Infectious Diseases, University of Oklahoma College of Medicine

Disclosure: Nothing to disclose.

Ana Paula Oppenheimer, MD, MPH  Fellow, Section of Infectious Diseases, Wake Forest University Baptist Medical Center

Disclosure: Nothing to disclose.

Edward L Arsura, MD  Chair, Department of Medicine, Chief Medical Officer, Richmond University Medical Center

Edward L Arsura, MD is a member of the following medical societies: American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Heart Association, American Medical Association, California Medical Association, Society of General Internal Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases,Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Ear, Nose and Throat Advances in Children, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, and Surgical Infection Society

Disclosure: Nothing to disclose.

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Archana Chatterjee, MD, PhD Professor of Pediatrics, Medical Microbiology and Immunology, and Pharmacy, Division of Pediatric Infectious Diseases, Chief of Division of Pediatric Infectious Diseases, Creighton University School of Medicine; Hospital Epidemiologist and Medical Director of Infection Control, Children's Hospital

Archana Chatterjee, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, International Society for Infectious Diseases, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Michele M Cheung, MD Consulting Staff, Department of Pediatrics, Division of Pediatric Infectious Diseases, University of California, San Francisco, School of Medicine

Michele M Cheung, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

John E Cho, MD Staff Physician, Providence Tarzana Medical Center

John E Cho, MD is a member of the following medical societies: American College of Chest Physicians, California Medical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

James de la Torre, MD Resident Physician, Department of Emergency Medicine, LAC+USC Medical Center

Disclosure: Nothing to disclose.

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of America, and Infectious Diseases Society of Ohio

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Joseph Kim, MD Chairman, Department of Emergency Medicine, Western Medical Center; Clinical Instructor, University of California, Irvine, School of Medicine

Disclosure: Nothing to disclose.

Zab Mosenifar, MD Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

Catherine O'Keefe, DNP, APRN Assistant Professor of Nursing and Pediatric Nurse Practitioner, Pediatric Infectious Diseases, Creighton University Medical Center

Catherine O'Keefe, DNP, APRN is a member of the following medical societies: American Academy of Nurse Practitioners, National Association of Pediatric Nurse Practitioners, and Nebraska Nurse Practitioners

Disclosure: Nothing to disclose.

Michael Peterson, MD Chief of Medicine, Vice-Chair of Medicine, University of California, San Francisco, School of Medicine; Endowed Professor of Medicine, University of California, San Francisco-Fresno, School of Medicine

Michael Peterson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Allison J Richard, MD Assistant Professor of Emergency Medicine, Keck School of Medicine of the University of Southern California; Associate Director, Division of International Medicine, Attending Physician, Department of Emergency Medicine, LAC+USC Medical Center

Disclosure: Nothing to disclose.

Mark R Schleiss, MD American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Guy W Soo Hoo, MD, MPH Clinical Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Medical Intensive Care Unit, Pulmonary and Critical Care Section, West Los Angeles Healthcare Center, Veteran Affairs Greater Los Angeles Healthcare System

Guy W Soo Hoo, MD, MPH is a member of the following medical societies: American Association for Respiratory Care, American College of Chest Physicians, American College of Physicians, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Peggy Weintrub, MD Chief, Division of Pediatric Infectious Diseases, Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine

Peggy Weintrub, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

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Soft tissue abscess due to cocci.
Pulmonary cocci spherule (Hematoxylin-eosin stain).
Pulmonary cocci spherule, periodic acid-Schiff stain.
Erythema nodosum can be observed in coccidioidomycosis, tuberculosis, histoplasmosis, drug reactions, and streptococcal infections.
A Coccidioides immitis spherule containing daughter cysts. Courtesy of Thomas Matthew.
Arthroconidia become airborne and infect the human host to begin the parasitic phase of its life cycle. The arthroconidia develop into spherules containing endospores, which propagate infection in human tissues. Courtesy of Thomas Matthew.
A granuloma with coccidioides immitis spherule (pretracheal lymph node biopsy).
A ruptured Coccidioides immitis spherule (pretracheal lymph node biopsy).
Gomori methenamine silver stain of Coccidioides immitis spherule (pretracheal lymph node biopsy).
Periodic acid-Schiff stain of Coccidioides immitis spherule (pretracheal lymph node biopsy).
Coccidioidal spherules rupturing and releasing endospores. Gomori methenamine silver (GMS) stain. Photograph by Joseph Rabban, MD.
 
 
 
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