Enterobacter sakazakii can cause serious infections especially among the very young and the elderly. It continues to be more common among neonates and infants than adults. Its tropism for the central nervous system in neonates and infants remains a mystery. Among neonates and infants, E. sakazakii has a propensity to cause meningitis resulting in ventriculitis, brain abscess or cyst formation, and development of hydrocephalus requiring ventricular-peritoneal shunt. Computed tomography of the head is therefore useful in following patients with E. sakazakii meningitis. Mortality and morbidity of E. sakazakii meningitis is high, and virtually all patients recovering from the central nervous system infection suffered mental and physical developmental delays. The case-fatality rate decreased among patients with meningitis treated with the third-generation cephalosporins. Most adults with E. sakazakii infection had serious underlying diseases and 50% of the adults with the infection had malignancies. However there has never been a known case of meningitis. Increasing antibiotic resistance among Enterobacter species should lead one to consider using the carbapenems or the newer cephalosporins in combination with a second agent such as an aminoglycoside. Limited data suggest that trimethoprim-sulfamethoxazole may be a useful agent in the treatment of infections caused by the Enterobacter species, especially in view of the production of extended-spectrum beta-lactamases capable of inactivating the cephalosporins and extended-spectrum penicillin.

Treatment of HIV-1-infected individuals with a combination of anti-retroviral agents results in sustained suppression of HIV-1 replication, as evidenced by a reduction in plasma viral RNA to levels below the limit of detection of available assays. However, even in patients whose plasma viral RNA levels have been suppressed to below detectable levels for up to 30 months, replication-competent virus can routinely be recovered from patient peripheral blood mononuclear cells and from semen. A reservoir of latently infected cells established early in infection may be involved in the maintenance of viral persistence despite highly active anti-retroviral therapy. However, whether virus replication persists in such patients is unknown. HIV-1 cDNA episomes are labile products of virus infection and indicative of recent infection events. Using episome-specific PCR, we demonstrate here ongoing virus replication in a large percentage of infected individuals on highly active anti-retroviral therapy, despite sustained undetectable levels of plasma viral RNA. The presence of a reservoir of 'covert' virus replication in patients on highly active anti-retroviral therapy has important implications for the clinical management of HIV-1-infected individuals and for the development of virus eradication strategies.

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