Denis Nash

The outbreak of West Nile virus infection in the New York City area in 1999.

BACKGROUNDnIn late August 1999, an unusual cluster of cases of meningoencephalitis associated with muscle weakness was reported to the New York City Department of Health. The initial epidemiologic and environmental investigations suggested an arboviral cause.nnnMETHODSnActive surveillance was implemented to identify patients hospitalized with viral encephalitis and meningitis. Cerebrospinal fluid, serum, and tissue specimens from patients with suspected cases underwent serologic and viral testing for evidence of arboviral infection.nnnRESULTSnOutbreak surveillance identified 59 patients who were hospitalized with West Nile virus infection in the New York City area during August and September of 1999. The median age of these patients was 71 years (range, 5 to 95). The overall attack rate of clinical West Nile virus infection was at least 6.5 cases per million population, and it increased sharply with age. Most of the patients (63 percent) had clinical signs of encephalitis; seven patients died (12 percent). Muscle weakness was documented in 27 percent of the patients and flaccid paralysis in 10 percent; in all of the latter, nerve conduction studies indicated an axonal polyneuropathy in 14 percent. An age of 75 years or older was an independent risk factor for death (relative risk adjusted for the presence or absence of diabetes mellitus, 8.5; 95 percent confidence interval, 1.2 to 59.1), as was the presence of diabetes mellitus (age-adjusted relative risk, 5.1; 95 percent confidence interval, 1.5 to 17.3).nnnCONCLUSIONSnThis outbreak of West Nile meningoencephalitis in the New York City metropolitan area represents the first time this virus has been detected in the Western Hemisphere. Given the subsequent rapid spread of the virus, physicians along the eastern seaboard of the United States should consider West Nile virus infection in the differential diagnosis of encephalitis and viral meningitis during the summer months, especially in older patients and in those with muscle weakness.

The Guillain–Barré Syndrome and the 1992–1993 and 1993–1994 Influenza Vaccines

BACKGROUNDnThe number of reports of influenza-vaccine-associated Guillain-Barré syndrome to the national Vaccine Adverse Event Reporting System increased from 37 in 1992-1993 to 74 in 1993-1994, arousing concern about a possible increase in vaccine-associated risk.nnnMETHODSnPatients given a diagnosis of the Guillain-Barré syndrome in the 1992-1993 and 1993-1994 influenza-vaccination seasons were identified in the hospital-discharge data bases of four states. Vaccination histories were obtained by telephone interviews during 1995-1996 and were confirmed by the vaccine providers. Disease with an onset within six weeks after vaccination was defined as vaccine-associated. Vaccine coverage in the population was measured through a random-digit-dialing telephone survey.nnnRESULTSnWe interviewed 180 of 273 adults with the Guillain-Barré syndrome; 15 declined to participate, and the remaining 78 could not be contacted. The vaccine providers confirmed influenza vaccination in the six weeks before the onset of Guillain-Barré syndrome for 19 patients. The relative risk of the Guillain-Barré syndrome associated with vaccination, adjusted for age, sex, and vaccine season, was 1.7 (95 percent confidence interval, 1.0 to 2.8; P=0.04). The adjusted relative risks were 2.0 for the 1992-1993 season (95 percent confidence interval, 1.0 to 4.3) and 1.5 for the 1993-1994 season (95 percent confidence interval, 0.8 to 2.9). In 9 of the 19 vaccine-associated cases, the onset was in the second week after vaccination, all between day 9 and day 12.nnnCONCLUSIONSnThere was no increase in the risk of vaccine-associated Guillain-Barré syndrome from 1992-1993 to 1993-1994. For the two seasons combined, the adjusted relative risk of 1.7 suggests slightly more than one additional case of Guillain-Barré syndrome per million persons vaccinated against influenza.

Long-Term Prognosis for Clinical West Nile Virus Infection

Patients recovering from West Nile virus infection may experience sequelae for months.

Trends in predictors of death due to HIV-related causes among persons living with AIDS in New York City: 1993–2001

To examine trends in predictors of HIV-related mortality among cohorts of persons living with AIDS (PLWA) in New York City (NYC), nine calendar year-specific cohorts of PLWA were created from 1993 to 2001. Cohorts were defined as persons who had been alive at any time during that year and had been diagnosed with AIDS before the end of that year. Predictors of death because of HIV-related causes of death were assessed by examinnng year-specific, stratified death rates per 1,000 PLWA and adjusted relative risks (RRs) from proportional hazards models. We conducted an analysis of AIDS surveillance data PLWA in NYC between 1993 and 2001. Univariate and multivariate Cox proportional hazards models were constructed for each calendar year cohort to evaluate trends in the RR of HIV-related death over the subsequent 5 years, adjusting for sex, reace/ethnicity, age, transmission risk borough of residence, category of AIDS diagnosis [opportunistic illness (OI) or CD4 count <200 cells/μL], time since AIDS diagnosis, and CD4 count at time of AIDS diagnosis. Death rates due to all causes and HIV-related causes declined substantially during 1993–1997 and then stabilized in all subgroups of PLWA between 1998 and 2001. Beginning in 1995, differences in survival emerged in some subgroups, such that by 2001 (1) injecting drug users (IDUs) had poorer survival compared with men who have sex with men (MSM) [RR2001=2.1, 95% confidence intervals (95% CI)=1.8–2.4]; (2) black and Hispanic PLWA had a significantly higher risk of death than white PLWA (RR2001=1.4, 95% CI=1.2–1.6, RR2001=1.2, 95% CI=1.1–1.4, respectively, and (3) PLWA aged 60 and above had poorer survival compared with younger persons (RR2001=2.4, 95% CI=1.9–3.0), after adjustment for other factors. The observed disparities that began to emerge in 1995 may be attributable to differential effects of, access to, or usage of highly active antiretroviral therapy (HAART). More targeted studies are needed to determine why such disparities have emerged.