Hantavirus Pulmonary Syndrome, French Guiana

A systematic serological survey of patients suffering from symptoms suggestive of Hantavirus pulmonary syndrome allowed us to identify a native case in French Guiana. Partial molecular characterization of the implicated hantavirus revealed its close relationship with the Bolivian Rio Mamore virus. We tentatively named it Maripa virus.

A study of 224 patients with Buruli ulcer in Benin that evaluated the WHO-recommended regimen of 8 weeks of treatment with rifampin/ streptomycin showed promising results (9). Chemotherapy alone was successful in achieving a cure rate of 47% of patients and was effective against ulcers <5 cm in diameter (9). However, HIV testing was not performed in this study. In Spain, an HIVpositive patient with aggressive, multifocal Buruli ulcer and osteomyelitis was cured by surgery, broad-spectrum antimicrobial drugs (not rifampin/ streptomycin), and antiretroviral drugs (10). Relapse was not reported in this study at 6-months follow-up.
For control of Buruli ulcer in HIV-positive patients, patients should be treated with rifampin/streptomycin and antiretroviral therapy to stimulate their immunity. Our report emphasizes the urgent need to evaluate treatment of HIV-positive patients infected with Buruli ulcer with rifampin/streptomycin and antiretroviral drugs.  (1), different viruses belonging to this genus have been reported in the Americas (2-5). These New World viruses are responsible for a disease called hantavirus pulmonary syndrome (HPS), a respiratory illness caused by the inhalation of dust contaminated by rodent feces or urine containing the virus (6)(7)(8).
Until recently, no information was available concerning the presence of hantaviruses in French Guiana, a French overseas department (administrative unit) in South America. Nevertheless, the description of atypical pneumonia cases not related to any known etiologic agent and the identifi cation of hantavirus reservoirs in neighboring countries led us to con-LETTERS duct a serologic study in a selected population of patients with compatible symptoms. The prevalence of immunoglobulin (Ig) G antibodies to hantavirus in this population was 1.42% (9). Subsequently, we systematically screened patients who had suggestive pathologies for hantavirus serology, which led us to the characterization of a divergent hantavirus.
On August 4, 2008, a 38-year-old man sought medical attention at the emergency department of Cayenne Hospital. He had had persistent symptoms of fever (>38.5°C), myalgia, diarrhea with melena, cough for 8 days, recurrent vomiting for 4 days, and dyspnea for 2 days. At consultation, tachypnea (respiratory rate 28/min) and oxygen desaturation (SaO 2 83%) were observed. Chest radiograph showed bilateral diffuse interstitial infi ltrates causing respiratory distress; mechanical ventilation was required. The patient was admitted to the intensive care unit for treatment of acute respiratory distress syndrome. Results of laboratory investigations performed when the patient was admitted showed thrombocytopenia (50,000 cells/mm 3 ), leucocytosis (22,500 cells/mm 3 ) associated with a high neutrophil count (20,300 cells/mm 3 ), moderate hepatonephritis (alanine aminotransferase 17 IU/L, aspartate aminotransferase 31 IU/L, gamma-glutanyl transferase 44 IU/L; alkaline phosphatase 44 IU/L; creatinine 192 μmol/L and urea 9.3 mmol/L); and an elevated C-reactive protein concentration (>192 mg/L). Laboratory tests for infectious agents ruled out malaria, dengue, leptospirosis, Chagas disease, Q fever, cytomegalovirus, and HIV, and blood cultures were negative for bacterial growth. The patient remained under respiratory assistance for 25 days in the intensive care unit and was discharged from hospital 47 days after admission with a complete clinical recovery.
With no etiologic agent identifi ed, 2 factors led to the suspicion of han-tavirus infection: clinical symptoms compatible with HPS and the patient's exposure to potential reservoirs. Indeed, a month before the onset of symptoms, he had moved to a rural municipality located near agricultural lands and forest.
Retrospective serologic investigations were performed with the 3 available serum samples obtained during the hospitalization. These samples were tested by IgM capture with inactivated Sin Nombre virus antigens and by indirect ELISA with recombinant antigens to detect IgG antibodies to Sin Nombre virus (10). IgM to Sin Nombre virus were present in the samples collected 8 and 9 days, respectively, after onset of the disease, confi rming hantavirus infection. Furthermore, IgG to Sin Nombre virus were only detected in the convalescent-phase serum samples obtained on day 41 of the disease. These serologic results suggested a recent infection with hantavirus.
Molecular investigations were performed to characterize and identify the virus. Viral RNA was extracted from the 2 acute serum samples. Reverse transcription-PCR was performed with consensus primers targeting the S segment of the hantavirus genome as described in Johnson et al. (4). Amplifi cation products of the expected size (434 bp of the nucleoprotein N-encoding region) were obtained from both samples. Cloning and sequencing of these products allowed obtaining a consensus sequence, which was deposited with GenBank (GQ179973  deaths. Serologic evidence has demonstrated that WNV is present throughout Mexico, Central America, South America, and the Caribbean region (2)(3)(4)(5)(6)(7)(8). However, WNV illness in humans and vertebrate animals in these regions has been only sparsely reported. For instance, 7 human cases of WNV infection have occurred in Mexico (excluding the case described here), 3 of which were severe. All patients survived. To our knowledge, no fatal human cases of WNV infection have occurred in Central America, South America, or the Caribbean region.
We describe a fatal case of WNV infection in a human in Central America. The patient, a man 40 years of age, lived in Monterrey, Nuevo León State, in northern Mexico. He had not traveled outside of the metropolitan area in the 6 months before illness onset. On June 11, 2009, infl uenza-like signs and symptoms (i.e., fever, malaise, fatigue, arthralgia, headache, and dizziness) developed in the patient. On June 26, the signs and symptoms had not resolved, and the man was admitted to University Hospital "Dr. José E. Gonzalez" at the Universidad Autonoma de Nuevo León (UANL). At the time of admission, cerebrospinal fl uid (CSF) was collected, and laboratory analysis indicated a markedly elevated leukocyte count (182 cells/ mm 3 ; reference range 0-5 cells/mm 3 ) and slightly elevated protein and glucose levels.