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During 2 consecutive influenza seasons we investigated the presence of influenza virus, human herpesvirus (HHV) type 6, and HHV-7 in cerebrospinal fluid samples from 9 white children suffering from influenza-associated encephalopathy. We conclude that it is unlikely that neuroinvasion by influenza virus or reactivation of either HHV-6 or HHV-7 is involved.

Enterovirus infections have been implicated in the development of type I diabetes mellitus. They may cause beta cell destruction either by cytolytic infection in the pancreas or indirectly by contributing to autoimmune reactivity. We sought evidence for these 2 mechanisms in a case of acute-onset diabetes mellitus that occurred during severe echovirus 9 infection. The virus was isolated and administered to cultured human beta cells. No viral proliferation was observed, and no beta cell death was induced, while parallel exposure to Coxsackie B virus serotype 3 resulted in viral proliferation and massive beta cell death. Although the viral protein 2C exhibited a sequence similar to that of the beta cell autoantigen glutamic acid decarboxylase (GAD(65)), no cross-reactive T cell responses were detected. The patient did not develop antibodies to GAD(65) either. Absence of evidence for direct cytolytic action or an indirect effect through molecular mimicry with GAD(65) in the present case raises the possibility of another indirect pathway through which enteroviruses can cause diabetes mellitus.

Microbial persistence may be involved in the pathogenesis of idiopathic dilated cardiomyopathy (IDC). Therefore, we evaluated the role of various cardiopathogenic microorganisms in patients with end-stage IDC. In a previous study, we did not find evidence for the persistence of enterovirus RNA in end-stage IDC. In the present study, we looked for other microorganisms that are frequently associated with heart disease, including cytomegalovirus, hepatitis B virus, hepatitis C virus, Borrelia burgdorferi, Chlamydia species, mycoplasmata, and Toxoplasma gondii. Serology, polymerase chain reaction (PCR) analysis specific for detection of microbial genomic sequences, or both investigations were performed on myocardial samples from 37 patients with end-stage IDC. PCR analysis was performed on multiple myocardial samples per patient. Thirty-nine patients with end-stage heart disease of known cause were included as controls. On the basis of our serological data and PCR analyses, we did not find any evidence that microbial persistence in the heart is involved in the end-stage disease process of IDC.

We described a patient who developed heart failure and pericarditis after bone marrow transplantation for a hematologic malignancy. The patient died of heart failure complicated by pneumonia. Despite extensive surveillance, an infectious cause for the heart failure was not found while he was alive. In addition, cultures of specimens obtained at autopsy did not reveal a cause for the heart failure. Enterovirus was detected by the polymerase chain reaction (PCR) in two samples of pleural fluid that were obtained 21 days apart while he was alive. After the patient died, enteroviral RNA was also detected in his lungs, liver, and spleen, indicating a generalized infection. Analysis of the PCR products revealed sequences sharing close homology with the coxsackie B-like group of enteroviruses. In addition to reporting this case, we review the literature regarding enteroviral infections after transplantation.

The etiology of chronic fatigue syndrome (CFS) is unknown. Some patients have high antibody titers to viral capsid antigen (VCA) and early antigen (EA) of Epstein-Barr virus (EBV), suggesting that reactivation of EBV is involved. We investigated virus load (spontaneous transformation) and immunologic regression of EBV-induced transformation in peripheral blood mononuclear cells (PBMCs) from 10 selected patients with CFS who had high antibody titers to VCA and EA. The outcome was compared with that for nine healthy controls and one patient with severe chronic active EBV infection (SCAEBV). There were no significant differences in viral load between patients and healthy controls. Immunologic regression of in vitro-transformed PBMCs was also equally efficient in patients and controls. The SCAEBV-infected patient and two controls, who were all seronegative for EBV, showed impaired regression. In conclusion, we were unable to demonstrate a role for reactivation of EBV in CFS, even in selected patients with high titers of antibody to VCA and EA of EBV.

Severe respiratory failure is an uncommon manifestation of psittacosis. We describe a patient with psittacosis who developed severe respiratory failure and required artificial ventilation. We also review 11 cases reported in the English-language literature over the past 30 years. A history of exposure to birds was reported in 10 of 12 cases and remains the most significant risk factor. Severe hypoxemia or renal impairment was associated with a poor prognosis. Eight patients died of psittacosis or related complications of the infection. Diagnostic aspects, clinical manifestations, and management options are discussed.

The possible role of enteroviral persistence in the etiology of the chronic fatigue syndrome (CFS) was investigated by serological testing, VP-1 antigen testing, and polymerase chain reaction (PCR) analysis of stool specimens as well as by viral cultures of stool--both direct and after acid treatment. No differences between 76 patients with disabling unexplained fatigue and 76 matched controls were found by serological or antigen testing. Furthermore, no enteroviruses were isolated from any stool culture. Enterovirus was detected by PCR in one stool specimen from a patient with CFS but was not detectable in a second sample obtained from the same patient 3 months later. All stool specimens from controls were PCR-negative. These results argue against the hypothesis that enteroviruses persist in patients with CFS and that their persistence plays a role in the pathogenesis of this syndrome.