After an epidemic of West Nile (WN) virus neurologic infections in southeastern Romania in 1996, human and animal surveillance were established to monitor continued transmission of the virus. During 1997 and 1998, neurologic infections were diagnosed serologically as WN encephalitis in 12 of 322 patients in 19 southeastern districts and in 1 of 75 Bucharest patients. In addition, amid a countrywide epidemic of measles, the etiology of the febrile exanthem in 2 of 180 investigated cases was determined serologically to be WN fever; 1 case was complicated by hepatitis. Sentinel chickens placed in Bucharest seroconverted to WN virus during the summer months, indicating their potential value in monitoring transmission. The continued occurrence of sporadic WN infections in southeastern Romania in consecutive years after the 1996 epidemic is consistent with local enzootic transmission of the virus.

A unique urban encephalitis epidemic in Romania signaled the emergence of neurological infection due to West Nile (WN) virus as a novel public health threat in Eastern Europe and provided an opportunity to evaluate patterns of immunoglobulin G (IgG) and IgM reactivity in IgM capture and IgG enzyme-linked immunosorbent assays (ELISAs). WN virus infection was diagnosed serologically in 236 of 290 patients from whom acute serum or cerebrospinal fluid (CSF) samples were available. In 37% of serum samples and in 25% of CSF samples collected in the first week of illness, anti-WN virus IgM antibody was detected in the absence of virus-specific IgG. The switch to an IgG antibody response occurred after 4 to 5 days of illness and earlier in CSF than in serum. A specific humoral immune response was detected in the CSF before the serum in some patients for whom paired CSF and serum samples from the same day were available. IgM antibody in convalescent serum samples persisted beyond 2 months after the onset of illness in more than 50% of patients. ELISA optical density values and antibody concentrations were well correlated for both IgM and IgG immunoassays. Anti-WN virus IgM antibody in acute-phase samples did not cross-react significantly with flaviviruses in other antigenic groups.

Background During the late 1980s and early 1990s, an estimated 10,000 Romanian children were infected with HIV-1 subtype F nosocomially through contaminated needles and blood transfusions. However, the geographic source and origins of this epidemic remain unclear. Methods Here we used phylogenetic inference and “relaxed” molecular clock dating analysis to further characterize the Romanian HIV-1 subtype F epidemic. Results These analyses revealed a major lineage of Romanian HIV sequences consisting nearly entirely of virus sampled from adolescents and children and a distinct cluster that included a much higher ratio of adult sequences. Divergence time estimates inferred the time of most recent common ancestor of subtype F1 sequences to be 1973 (1966–1980) and for all Angolan sequences to 1975 (1968–1980). The most common ancestor of the Romanian sequences was dated to 1978 (1972–1983) with pediatric and adolescent sequences interspersed throughout the lineage. The phylogenetic structure of the entire subtype F epidemic suggests that multiple introductions of subtype F into Romania occurred either from the Angolan epidemic or from more distant ancestors. Since the historical records note that the Romanian pediatric epidemic did not begin until the late 1980s, the inferred time of most recent common ancestor of the Romanian lineage of 1978 suggests that there were multiple introductions of subtype F occurred into the pediatric population from HIV already circulating in Romania. Conclusions Analysis of the subtype F HIV-1 epidemic in an historical context allows for a deeper appreciation of how the HIV pandemic has been influenced by socio-political events.

In response to the 1996 West Nile (WN) fever epidemic that occurred in Bucharest and southeastern Romania, a surveillance program was established. The surveillance system detected 39 clinical human WN fever cases during the period 1997-2000: 14 cases in 1997, 5 cases in 1998, 7 cases in 1999, and 13 cases in 2000. Thirty-eight of the 39 case-patients lived in the greater Danube Valley of southern Romania, and 1 case-patient resided in the district of Vaslui, located on the Moldavian plateau. The estimated annual case incidence rate for the surveillance area during the period 1997-2000 was 0.95 cases per million residents. Thirty-four cases were serologically confirmed, and 5 cases were classified as probable. Twenty-four case-patients presented with clinical symptoms of meningitis (62%), 12 with meningoencephalitis (31%), 1 with encephalitis (3%), and 2 with febrile exanthema (5%). Five of the 39 cases were fatal (13%). Fourteen case-patients resided in rural areas, and 25 in urban and suburban areas, including 7 case-patients who resided in Bucharest. The ages of case-patients ranged from 8 to 76 years with a median age of 45 years. Twenty-four case-patients were males and 15 were females. Dates of onset of illness occurred from May 24 through September 25, with 82% of onset dates occurring in August and September. Limited entomological surveillance failed to detect WN virus. Retrospective sampling of domestic fowl in the vicinity of case-patient residences during the years 1997-2000 demonstrated seroprevalence rates of 7.8%-29%. Limited wild bird surveillance demonstrated seroprevalence rates of 5%-8%. The surveillance data suggest that WN virus persists focally for several years in poorly understood transmission cycles after sporadic introductions or that WN virus is introduced into Romania at relatively high rates, and persists seasonally in small foci.

The occurrence of Q fever endocarditis likely involves some alterations in the responses of monocytes, the in vivo targets of Coxiella burnetii. To test this hypothesis, the production of the inflammatory cytokines tumor necrosis factor alpha, interleukin-1␤, and interleukin-6 was assessed in monocytes from patients with Q fever endocarditis. Spontaneous transcription and secretion of tumor necrosis factor and interleukin-1 were significantly higher in patient monocytes than in healthy controls. The interleukin-6 transcripts were also upregulated in patient cells. Moreover, in patients with recent endocarditis exhibiting high titers of immunoglobulin G directed to C. burnetii in phase I, monocytes released significantly higher levels of tumor necrosis factor and interleukin-1 than in patients with stabilized endocarditis. Immunoglobulin G titers and the overproduction of tumor necrosis factor and interleukin-1 were significantly correlated. Hence, the overproduction of inflammatory cytokines might be a marker of disease activity.