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Aging cohort of perinatally human immunodeficiency virus-infected children in New York City. New York City Pediatric Surveillance of Disease Consortium.

BACKGROUND: New York City (NYC) pediatricians are now caring for fewer HIV-infected infants and more school age children and adolescents than earlier in the epidemic. METHODS: Clinical, laboratory and demographic data were abstracted from medical records at 10 NYC centers participating in the CDC Pediatric Spectrum of HIV Disease project. Pediatric AIDS cases and HIV-related deaths reported to the NYC Department of Health were examined. RESULTS: Median age of HIV-infected children in care increased from 3 years in 1989 to 1991 to 6 years in 1995 to 1998. The number of HIV-infected women giving birth in NYC declined 50% from 1990 to 1997 (1630 to 831); increasing numbers were identified prenatally (14% in 1989; 78% after 1995); and most received prenatal zidovudine prophylaxis (73% in 1997). Estimated perinatal transmission decreased to 10% by 1997. Improved identification of seropositive status in infants was associated with an increased proportion of infected infants receiving Pneumocystis carinii pneumonia (PCP) prophylaxis, 84% in 1997. AIDS free survival was longer for children born 1995 to 1998 than for those born before 1995, P = 0.004. In 1998 among children with advanced immunosuppression (CDC category 3), 66% were prescribed 3 or more antiretroviral medicines and 88% received PCP prophylaxis. Citywide AIDS cases and HIV-related deaths fell precipitously beginning in 1996. CONCLUSIONS: Based on the observations of this study, the cohort of NYC HIV-infected children in care is aging, associated with a decline in new HIV infections, high rates of PCP prophylaxis and increased time to AIDS. Falling HIV-related deaths citywide support these observations.

Aging↗

Pathology of fatal West Nile virus infections in native and exotic birds during the 1999 outbreak in New York City, New York.

West Nile fever caused fatal disease in humans, horses, and birds in the northeastern United States during 1999. We studied birds from two wildlife facilities in New York City, New York, that died or were euthanatized and were suspected to have West Nile virus infections. Using standard histologic and ultrastructural methods, virus isolation, immunohistochemistry, in situ hybridization and reverse-transcriptase polymerase chain reaction, we identified West Nile virus as the cause of clinical disease, severe pathologic changes, and death in 27 birds representing eight orders and 14 species. Virus was detected in 23/26 brains (88%), 24/ 25 hearts (96%), 15/18 spleens (83%), 14/20 livers (70%), 20/20 kidneys (100%), 10/13 adrenals (77%), 13/ 14 intestines (93%), 10/12 pancreata (83%), 5/12 lungs (42%), and 4/8 ovaries (50%) by one or more methods. Cellular targets included neurons and glial cells in the brain, spinal cord, and peripheral ganglia; myocardial fibers; macrophages and blood monocytes; renal tubular epithelium; adrenal cortical cells; pancreatic acinar cells and islet cells; intestinal crypt epithelium; oocytes; and fibroblasts and smooth muscle cells. Purkinje cells were especially targeted, except in crows and magpies. Gross hemorrhage of the brain, splenomegaly, meningoencephalitis, and myocarditis were the most prominent lesions. Immunohistochemistry was an efficient and reliable method for identifying infected cases, but the polyclonal antibody cross-reacted with St. Louis encephalitis virus and other flaviviruses. In contrast, the in situ hybridization probe pWNV-E (WN-USAMRIID99) reacted only with West Nile virus. These methods should aid diagnosticians faced with the emergence of West Nile virus in the United States.

Animals↗