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Abstract

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

We report a case of pulmonary coccidioidomycosis imported from the United States to Italy. This disease should enter in the differential diagnosis of any febrile patient (especially if presenting with pulmonary symptoms, with or without hypereosinophilia) coming from Coccidioides immitis endemic areas.


Case Report

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

Coccidioidomycosis is a primitive mycosis, endemic in well-defined geographical areas of the Americas. In view of the increasing frequency of travels and of the continuing migration flows, it is very important to consider this possibility in the differential diagnosis of pneumonia also outside endemic countries, and carefully ascertain the patients' travel history.

On January 2, 2008, a 28-year-old Italian man presented at our Clinic. The patient's medical history was unremarkable, except for a recurrent sinusitis.

From July 15 to December 15, 2007, he had been in Tucson (Arizona, USA) for study purposes. During this period he had briefly visited California and Nevada; he had also gone hiking in the Sonora Desert and climbing Mt. Lemon and other local mountains (mid-November 2007). In the last week of November he started complaining of dizziness, vertigo, increasing weakness, and dry coughing fits. On December 7, joint and muscle pain, night sweats, and fever (39°C) appeared.

On December 15, he came back to Italy. General conditions worsened, so he started an unspecified antibiotic therapy for 4 days without any improvement. On December 28, he consulted his GP, who prescribed levofloxacin 500 mg qd for 4 days. Blood tests showed leukocytosis (WBC 20,500/mm3) with hypereosinophilia (11,200/mm3), erythrocyte sedimentation rate 26 mm/h, C-reactive protein 80 mg/L. Chest X-ray and abdominal ultrasound resulted negative.

On January 2, 2008, he was admitted to our Clinic with fever, cough, and chest pain. Iatrogenic and allergic causes were ruled out. Results of serial stool examinations and serologic tests for human immunodeficiency virus (HIV), Strongyloides, and Toxocara were all negative. Autoantibodies (ANA, ANCA, and LKM) and neoplastic markers resulted negative. Sputum microscopy and culture resulted negative for tuberculosis. Blood cultures were also negative.

A chest and abdomen computed tomography scan revealed in both lungs multiple nodules with ground glass areas, the bigger one of 3 cm diameter (Figure 1); the spleen was enlarged, with small areas of reduced density.

image

Figure 1. Coronal and sagittal high definition computed tomography scan showing multiple nodules (white arrows) with ground glass borders: the biggest one, diameter 3 cm, in apical left pulmonary region (black arrow).

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The radiological findings led to the suspicion of mycotic infection. Therefore, a serum sample was sent to “S. Carlo Borromeo Hospital” in Milan, to test the presence of antibodies against Hystoplasma capsulatum and Coccidioides immitis using the double diffusion test according with the Oudin and Outcherlony technique.

On January 11, after performing a bronchoscopy with BAL, spherules with endoconidia were observed at the Gram staining (Figure 2A), and itraconazole was immediately started (200 mg bid). In the following days the therapy gradually led to full recovery. In the meantime anti-coccidioidin but not anti-H capsulatum antibodies were detected in serum, and the fungus was isolated from BAL. Expanding, felty, whitish to grayish colonies yielded at room temperature (Figure 2B). At microscopy, fertile hyphae arose at right angles, and hyaline, one-celled, cylindrical arthroconidia were seen. The isolate was identified as C immitis, presenting all its typical characteristics.

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Figure 2. (A) Coccidioides immitis sphaerula in the sputum (Gram stain, ×100). (B) Coccidioides immitis arthroconidia with typical alternance of empty disjunctor cells, obtained from sputum culture in Agar Sabouraud (Gram stain, ×100).

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On January 18, the patient was discharged under treatment with itraconazole, that was stopped after 6 months. No other therapies were prescribed. The patient showed complete clinical recovery, radiological findings resulted negative, and eosinophilia gradually disappeared.

Discussion

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

Coccidioidomycosis is caused by C immitis, a dimorphic fungus living as mould in mycelial form in the soil of desert areas of the Western hemisphere, mainly the United States (California, Arizona, and Texas), Northern Mexico, some Central and South American countries.1 The Coccidiodes lifecycle consists of a mycelial and a spherule phase. The mycelial phase is a mould in the soil growing in hyphae, that develop into arthroconidia. The latter, becoming airborne when disturbed by wind (dust storms and earthquakes) or soil excavation, remain viable for long periods of time. When inhaled, arthroconidia convert in the lung into spherules filled with endospores. Once released, each endospore can start the development of a new spherule and extend the infection. Coccidioidomycosis is not transmitted from person to person. Risk of infection is highest in dry summer. The incidence of the infection has dramatically increased in the last 10 years.2 Approximately 60% of infected persons are asymptomatic. Otherwise, the primary infection may present with fever, weight loss, sweating, cough, and chest pain. Other symptoms may include arthalgias and cutaneous manifestations, such as erythema nodosum and erythema multiforme.1 Laboratory findings may include marked hypereosinophilia.3 Overall, less than 5% of infected persons has progressive pulmonary infection or extrapulmonary dissemination of the disease. Extrapulmonary spread of the infection tends to occur more commonly in pregnant women, in infants, in non-Caucasians, and in the immunocompromised host, such as patients with HIV infection, organ transplant recipients, and patients receiving high-dose corticosteroids.1

The mainstays of the diagnosis are culture of clinical specimens and serologic testing. Colonies grow in 3–4 days. Mature cultures are very infectious and should be handled only by experienced personnel at laboratories with appropriate safety equipment.1 Most patients with primary C immitis infection recover without therapy. Nevertheless, management should include a follow-up to document resolution or identify complications. On the other hand, patients with extensive spread of infection or who are at high risk of complications require a variety of treatment strategies that may include antifungal drug therapy and/or surgical debridement. Both fluconazole and itraconazole are appropriate as first line therapy for most chronic pulmonary or disseminated infections.4

We found in the literature some cases of coccidioidomycosis imported to Europe: one case each in The Netherlands, Sweden, Hungary, and two cases in France.5–9 The areas visited by these patients were California (two cases), Arizona (two cases), and Mexico (one case). A concomitant diagnosis of histoplasmosis was made in a HIV-positive patient.9 The serology for C immitis was positive in all but the HIV-positive patient, while the culture resulted positive in every case. Two patients (including the HIV-positive patient) received itraconazole, one posaconazole, one ketoconazole, and one no antifungal treatment. Every patient fully recovered.

To our knowledge, this is the first case reported in Italy. In recent years, mycotic diseases have been described with increasing frequency outside their respective endemic areas, both as isolated cases and outbreaks.10 Because the incubation period usually ranges from 1 to 4 weeks, persons may well get sick only after return to home countries, where clinicians may not be familiar with this infection. Coccidioidomycosis should enter in the differential diagnosis of any febrile patient (especially if presenting with pulmonary symptoms) upon return from C immitis endemic areas;11 hypereosinophilia is also a useful clue for the diagnosis.3

Declaration of Interests

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

The authors state they have no conflicts of interest to declare.

References

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References