Between 1993 and 1998, 10 cases of clinical hantavirus infection were diagnosed in Brazil. Hantavirus-specific IgM, or positive immunohistochemical analysis for hantavirus antigen, or positive reverse transcription-polymerase chain reaction results for hantavirus RNA were used to confirm nine of these cases; eight were hantavirus pulmonary syndrome (HPS), and one was mild hantavirus disease. The remaining clinical case of hantavirus infection was fatal, and no tissue was available to confirm the diagnosis. During the first 7 months of 1998, five fatal HPS cases caused by a Sin Nombre-like virus were reported from three different regions in the State of São Paulo, Brazil: two in March (Presidente Prudente Region), two in May (Ribeirão Preto Region), and one in July (Itapecerica da Serra Region). Epidemiologic, ecologic, and serologic surveys were conducted among case contacts, area residents, and captured rodents in five locations within the State of São Paulo in June of 1998. Six (4.8%) of 125 case contacts and six (5.2%) of 116 area residents had IgG antibody to Sin Nombre virus (SNV) antigen. No case contacts had a history of HPS-compatible illness, and only one area resident reported a previous acute respiratory illness. A total of 403 rodents were captured during 9 nights of trapping (1969 trap nights). All 27 rodents that were found to be positive for IgG antibody to SNV antigen were captured in crop border and extensively deforested agricultural areas where four of the 1998 HPS case-patients had recently worked. The IgG antibody prevalence data for rodents suggest that Bolomys lasiurus and perhaps Akodon sp. are potential hantavirus reservoirs in this state of Brazil.

Following an elective transphenoidal resection of a pituitary tumor, a 66-year-old Hispanic male acutely developed fulminant hepatic failure and severe coagulopathy. He received parenteral corticosteroids the day prior to surgery, and was first noted to have significant coagulopathy intraoperatively. Despite aggressive workup and treatment for fulminant hepatic failure, the patient developed multiorgan failure by post-operative day 2, and expired on post-operative day 3. On post-mortem examination, hemorrhagic necrosis of the liver was noted and microscopic examination revealed Cowdry type A inclusions, consistent with Herpes Simplex Virus (HSV) infection. This diagnosis was subsequently confirmed by immunehistochemistry. Fulminant hepatic failure due to HSV is a rare but highly fatal disease if untreated. Most case reports include only immunocompromised or pregnant patients. However, the lack of clinical suspicion in this previously healthy patient may have delayed prompt treatment with antiviral agents. It is important to raise the awareness of this rare and life-threatening, but potentially treatable, etiology when clinicians are faced with acute idiopathic fulminant hepatic failure.