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Letter
Disseminated Coccidioidomycosis
Cheng-Yi Wang,* Jih-Shuin Jerng,* Jen-Chung Ko,† Ming-Feng Lin,† Cheng-Hsiang
Hsiao,* Li-Na Lee,* Po-Ren Hsueh,*
and Sow-Hsong Kuo*
*National Taiwan University Hospital, Taipei, Taiwan; and †Hsin-Chu General
Hospital, Hsinchu, Taiwan
Suggested
citation for this article
To the Editor: Coccidioidomycosis, an infection caused by the
dimorphic fungus Coccidioides immitis, is endemic in the southwestern
United States, parts of Mexico, and Central and South America (1).
Patients with C. immitis infection may have chronic pneumonia,
fungemia, and extrapulmonary dissemination to skin, bones, meninges, and
other body sites. The clinical features of coccidioidomycosis may mimic
those of melioidosis, penicilliosis marneffei, and tuberculosis, which
are commonly seen in some southeastern Asian countries, including Taiwan.
A previously healthy, 71-year-old retired gynecologist from Taiwan, visited
Los Angeles in August 2003 and traveled to the San Joaquin Valley in November
2003. He had smoked 1 package of cigarettes daily for 50 years. He noted
fever 5 days before returning to Taiwan on December 1, 2003. He came to
a local hospital on December 4 with a temperature of 39°C and a history
of 1 month of night sweats, productive cough, and weight loss of 10 kg.
Chest radiograph showed diffuse nodular lung lesions bilaterally (Figure,
panel A). His leukocyte count was 16.65 x 109/L (neutrophils
85.6%, lymphocytes 6.2%), and C-reactive protein was 21.5 mg/dL (reference
value, <0.8 mg/dL). Empiric antimicrobial drugs (amoxicillin/clavulanic
acid and ciprofloxacin) and antituberculosis therapy (isoniazid, rifampin,
ethambutol, and pyrazinamide) were administered. Blood and sputum specimens
were negative for bacteria; HIV antibody test results were negative, but
the fever persisted. A follow-up chest film showed a left pleural effusion.
The pleural effusion aspirate was exudative with 3.6 x 109/L
leukocytes (73% neutrophils). Computed tomographic scan of the patient's
chest showed collapse of the left lower lung with central necrosis, bilateral
pleural effusions, and mediastinal lymphadenopathy. Pleural biopsy by
video-assisted thoracoscopic surgery showed no evidence of malignancy,
but heavy lymphoplasmacytic infiltration and chronic necrotizing granulomatous
inflammation were found (Figure, panel C). On December
17, 2003, 30 mg/day prednisolone orally was prescribed for intermittent
fever. Biopsy material and cultures of blood samples taken at admission
grew an unidentified mold, which was also isolated from the biopsy wound.
The patient was discharged afebrile from the hospital on January 20, 2004.
The fever recurred, with a disturbance in consciousness on January 25,
2004. Computed tomographic scan of the brain revealed no obvious organic
lesions. He was referred to our hospital on January 26, 2004.
After the patient was admitted, fever persisted and respiratory distress
worsened rapidly. He developed severe headache, seizures, and loss of
consciousness. He was transferred to the intensive care unit for aggressive
management of acute respiratory distress syndrome and deterioration of
renal function. Chest radiograph showed coalescence of nodular shadows
and almost complete white-out of bilateral lung fields (Figure,
panel B). Meropenem, antituberculosis agents, and intravenous voriconazole,
200 mg every 12 hours, were administered.
Both the unidentified mold, which was sent to our hospital for further
identification, and a mold cultured from the previous biopsy wound at
our hospital were identified as C. immitis by their characteristic
gross and microscopic morphotypes in standard slide cultures incubated
at 28°C for 10 days. Hematoxylin and eosin staining of the biopsied
tissue showed many spherules.
Lumbar puncture was performed on January 30, 2004, and showed an elevated
opening pressure of 380 cm H2O and a few destructed large spherules
in the cerebrospinal fluid (CSF). However, cultures of CSF were negative
for bacteria and fungi. After the diagnosis of disseminated coccidioidomycosis
(pneumonia, fungemia, and meningitis), voriconazole was replaced by intravenous
fluconazole, 400 mg/day. The patient's intensive care course was complicated
by Pseudomonas pneumonia and repeated episodes of upper gastrointestinal
bleeding. A second lumbar puncture was conducted on February 13, 2004,
and also showed an elevated opening pressure (290 cm H2O).
Uncontrolled coccidioidomycosis meningitis was suspected, and intrathecal
amphotericin B treatment was planned. Refractory shock with bradycardia
developed when an intrathecal catheter was implanted. The patient did
not respond to therapy and died on February 16, 2004. The MIC of fluconzole
for the C. immitis isolate was 48 μg/mL, and the MIC of amphotericin
B was found to be 1 μg/mL for by using the Etest (ABiodisk, Solna,
Sweden) according to manufacturer's information.
This case is the first to be reported of disseminated coccidioidomycosis
with fulminant pneumonia, fungemia, and meningitis reported from Taiwan
(2). Review of the patient's travel history and clinical
course indicated that the C. immitis was acquired in California
and that the initial manifestations had begun before the patient returned
to Taiwan. Coccidioidomycosis is commonly diagnosed in disease-endemic
areas but frequently overlooked in disease-nonendemic areas because of
a low index of suspicion among physicians. The interval from onset of
symptoms to disease diagnosis was relatively long (3).
Our patient had chills, productive cough, weight loss, and night sweats
followed by fever as the initial manifestations of this infection. These
symptoms had been most frequently reported in previous coccidioidomycosis
cases (4). Radiographic scans of the patient initially
showed diffuse reticular lesions, followed by pleural effusion and consolidation.
This clinical course was also fully compatible with those of previously
reported cases (4). However, the clinical manifestations
of chronic pneumonia with pleural effusion, the initial partial response
to steroid treatment, and the delay in recognizing the mold contributed
to delayed diagnosis of this disease.
The isolate was not susceptible to fluconazole (MIC 48 μg/mL). Although
the National Committee for Clinical Laboratory Standards does not have
a standard susceptibility method and MIC breakpoint of fluconazole for
defining susceptibility against C. immitis. Fluconazole has been
recommended as a drug of choice for treating meningal coccidioidomycosis,
particularly in patients with underlying renal disease or with disease-associated
renal function deterioration (4,5). Immunocompromise
secondary to steroid use, as well as resistance of the isolate to fluconazole,
may have contributed to treatment failure in this patient.
With increasing international travel, physicians should consider those
diseases that are endemic in regions where their patients have traveled.
In addition to tuberculosis, melioidosis, and penicilliosis marneffii,
coccidioidomycosis should be included in the differential diagnosis of
chronic pneumonia in Taiwan, considering the number of residents who travel.
Only then can prompt microbial investigations be conducted to accurately
diagnosis and determine the appropriate antifungal treatment.
References
- Kirkland TN, Fierer J. Coccidioidomycosis:
a reemerging infectious disease. Emerg Infect Dis. 1996;2:192–9.
- Chen CH, Shih JF, Hsu YT, Perng RP. Disseminated
coccidioidomycosis with lung, skin and lymph node involvement: report
of a case. J Formos Med Assoc. 1991;90:788–92.
- Desai SA, Minai OA, Gordon SM, Neil BO, Wiedemann HP, Arroliga AC.
Coccidioidomycosis
in non-endemic areas: a case series. Respir Med. 2001;95:305–9.
- Am. 2003;17:41–57.
- Galgiani JN, Ampel NM, Catanzaro A, Johnson RH, Stevens DA, Williams
PL. Practice
guideline for the treatment of coccidioidomycosis. Clin Infect Dis.
2000;30:658–61.
Suggested citation
for this article:
Wang C-Y, Jerng J-S,
Ko J-C, Lin M-F, Hsiao C-H, Lee L-N, et al. Disseminated coccidioidomycosis
[letter]. Emerg Infect Dis [serial on the Internet]. 2005 Jan [date
cited]. Available from http://www.cdc.gov/ncidod/EID/vol11no01/04-0613.htm
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