共查询到20条相似文献,搜索用时 31 毫秒
1.
In early 1976, the novel A/New Jersey/76 (Hsw1N1) influenza virus caused severe respiratory illness in 13 soldiers with 1 death at Fort Dix, New Jersey. Since A/New Jersey was similar to the 1918–1919 pandemic virus, rapid outbreak assessment and enhanced surveillance were initiated. A/New Jersey virus was detected only from January 19 to February 9 and did not spread beyond Fort Dix. A/Victoria/75 (H3N2) spread simultaneously, also caused illness, and persisted until March. Up to 230 soldiers were infected with the A/New Jersey virus. Rapid recognition of A/New Jersey, swift outbreak assessment, and enhanced surveillance resulted from excellent collaboration between Fort Dix, New Jersey Department of Health, Walter Reed Army Institute of Research, and Center for Disease Control personnel. Despite efforts to define the events at Fort Dix, many questions remain unanswered, including the following: Where did A/New Jersey come from? Why did transmission stop?Key words: Influenza, military, respiratory disease, swine, perspectiveRevisiting events surrounding the 1976 swine influenza A (H1N1) outbreak may assist those planning for the rapid identification and characterization of threatening contemporary viruses, like avian influenza A (H5N1) (1). The severity of the 1918 influenza A (H1N1) pandemic and evidence for a cycle of pandemics aroused concern that the 1918 disaster could recur (2,3). Following the 1918 pandemic, H1N1 strains circulated until the "Asian" influenza A (H2N2) pandemic in 1957 (3). When in early 1976, cases of influenza in soldiers, mostly recruits, at Fort Dix, New Jersey, were associated with isolation of influenza A (H1N1) serotypes (which in 1976 were labeled Hsw1N1), an intense investigation followed (4).Of 19,000 people at Fort Dix in January 1976, ≈32% were recruits (basic trainees) (4). Recruits reported to Fort Dix for 7 weeks of initial training through the basic training reception center, where they lived and were processed into the Army during an intense 3 days of examinations, administrative procedures, and indoctrination. At the reception center, training unit cohorts were formed. Recruits were grouped into 50-member units (platoons) and organized into companies of 4 platoons each. Units formed by week''s end moved from the reception center to the basic training quarters. To prevent respiratory illnesses, recruits were isolated in their company areas for 2 weeks and restricted to the military post for 4 weeks (4). Platoon members had close contact with other platoon members, less contact with other platoons in their company, and even less contact with other companies.On arrival, recruits received the 1975–1976 influenza vaccine (A/Port Chalmers/1/73 [H3N2], A/Scotland/840/74 [H3N2], and B/Hong Kong/15/72) (4). Other soldiers reported directly to advanced training programs of 4 to 12 weeks at Fort Dix immediately after basic training at Fort Dix or elsewhere. These soldiers received influenza vaccinations in basic training. Civilian employees and soldiers'' families were offered vaccine, but only an estimated <40% accepted (4).Training stopped over the Christmas–New Year''s holidays and resumed on January 5, 1976, with an influx of new trainees. The weather was cold (wind chill factors of 0° to –43°F), and the reception center was crowded (4). Resumption of training was associated with an explosive febrile respiratory disease outbreak involving new arrivals and others. Throat swabs were collected from a sample of hospitalized soldiers with this syndrome. On January 23, the Fort Dix preventive medicine physician learned of 2 isolations of adenovirus type 21 and suspected an adenovirus outbreak (4). He notified the county health department and the New Jersey (NJ) Department of Health of the outbreak (4). On January 28, an NJ Department of Health official consulted with the military physician and suggested that the explosive, widespread outbreak could be influenza (4). Over the next 2 days, 19 specimens were delivered to the state laboratory and 7 A/Victoria-like viruses and 3 unknown hemagglutinating agents were identified (4). Specimens were flown to the Center for Disease Control (CDC), Atlanta, Georgia, on February 6, where a fourth unknown agent was found (4).On February 2, Fort Dix and NJ Department of Health personnel arranged for virologic studies of deaths possibly caused by influenza (4). Tracheal swabs taken on February 5 from a recruit who died on February 4 yielded a fifth unknown agent on February 9. By February 10, laboratory evidence had confirmed that a novel influenza strain was circulating at Fort Dix and that 2 different influenza strains were causing disease. By February 13, all 5 unknown strains were identified as swine influenza A (Hsw1N1). The possibility of laboratory contamination was evaluated (4). No known swine influenza A strains were present in the NJ Department of Health Virus Laboratory before the Fort Dix outbreak. Additionally, all unknown Fort Dix viruses were independently isolated from original specimens at CDC and the Walter Reed Army Institute of Research (WRAIR), Washington, DC. Also, 2 patients with novel virus isolates had convalescent-phase, homologous, hemagglutination-inhibition (HAI) antibody titers of 1:40–1:80, consistent with recent infections. The new influenza strain had been independently identified in 3 different laboratories and supporting serologic evidence developed within 15 days after the original specimens were collected (4).
Open in a separate window 相似文献
Table
Key events in the swine influenza A (Hsw1N1) outbreak, Fort Dix, NJDate (1976) | Event |
---|---|
January 5 | After the holidays, basic training resumed at Fort Dix, NJ; a sudden, dramatic outbreak of acute respiratory disease followed the influx of new recruit trainees (4). |
January 19 | Earliest hospitalization of a Fort Dix soldier with acute respiratory disease attributed to swine influenza A (Hsw1N1) (identified retrospectively by serologic tests) (7,14) |
January 21 | Influenza A/Victoria (H3N2) identified away from Fort Dix in NJ civilians (4) |
January 23 | Fort Dix received reports of adenovirus type 21 isolations from soldiers ill with respiratory disease and reported the outbreak to the local and state health departments (4) |
January 28 | A NJ Department of Health official suggested the Fort Dix outbreak may be due to influenza and offered to process specimens for virus isolation (4) |
January 29–30 | 19 specimens sent to NJ Department of Health in 2 shipments (4) |
February 2–3 | NJ Department of Health identified 4 isolates of H3N2-like viruses and 2 unknown hemagglutinating agents in 8 specimens sent on January 29. Fort Dix and NJ Department of Health arranged for the study of deaths possibly due to influenza. NJ Department of Health identified 3 H3N2-like viruses and a third unknown hemagglutinating agent in 11 specimens sent on January 30 (4). |
February 4 | Fort Dix soldier died with acute respiratory disease (4). |
February 5 | Tracheal specimens from the soldier who died on February 4 were sent to NJ Department of Health (4). |
February 6 | NJ Department of Health sent the Fort Dix specimens to Center for Disease Control (CDC), Atlanta, GA; CDC identified a fourth unknown hemagglutinating agent in the Fort Dix specimens (4). |
February 9 | Specimens from the soldier who died on February 4 yielded a fifth unknown hemagglutinating agent (4). Last hospitalization of an identified Fort Dix soldier with febrile, acute respiratory disease attributed to swine influenza A (Hsw1N1) (identified retrospectively by serologic tests) (7,14). |
February 10 | Laboratory evidence supported 2 influenza type A strains circulating on Fort Dix; 1 was a radically new strain. Prospective surveillance for cases in the areas around Fort Dix was initiated; only cases of H3N2 were found (4). |
February 13 | Review of laboratory data and information found that all 5 unknown agents were swine influenza A strains (later named A/New Jersey [Hsw1N1]); 3 laboratories independently identified the swine virus from original specimens (serologic data supporting swine influenza A virus infection was later obtained from 2 survivors with A/New Jersey isolates) (4). |
February 14–16 | Initial planning meeting between CDC, NJ Department of Health, Fort Dix, and the Walter Reed Army Institute of Research personnel was held in Atlanta, GA. Prospective case finding was initiated at Fort Dix; H3N2 was isolated; Hsw1N1 was not isolated (7). Retrospective case finding was initiated by serologic study of stored serum specimens from Fort Dix soldiers who had been hospitalized for acute respiratory disease; 8 new cases of disease due to Hsw1N1 were identified with hospitalization dates between January 19 and February 9 (7,14). |
February 22–24 | Prospective case finding was again conducted at Fort Dix; H3N2 virus was isolated but not Hsw1N1 (7). |
February 27 | Thirty-nine new recruits entering Fort Dix February 21–27 gave blood samples after arrival and 5 weeks later; serologic studies were consistent with influenza immunization but not spread of H3N2 virus. None had a titer rise to Hsw1N1 (11). |
March 19 | Prospective surveillance identified the last case of influenza in the areas around Fort Dix; only H3N2 viruses were identified outside of Fort Dix (4). |
2.
Neisseria meningitidis carriage was compared in swab specimens of nasopharynx, tonsils, and saliva taken from 258 students. We found a higher yield in nasopharyngeal than in tonsillar swabs (32% vs. 19%, p<0.001). Low prevalence of carriage in saliva swabs (one swab [0.4%]) suggests that low levels of salivary contact are unlikely to transmit meningococci.Invasive meningococcal disease has a high case-fatality rate and an immediate risk of further cases among household contacts. Public health measures therefore include prompt identification of contacts for chemoprophylaxis (1). One question that commonly arises is whether salivary contact through sharing cups or glasses is an indication for prophylaxis, but the evidence base to inform an answer is weak, and national guidelines are inconsistent (1,2). Although saliva is thought to inhibit meningococcal growth (3), carriage rates in saliva are not known, and swabs to detect carriage are usually taken from tonsils or nasopharynx (4–6). We compared meningococcal isolation rates in swabs of saliva (front of mouth), tonsils, and nasopharynx.We recruited volunteers among students from two colleges in Hereford, England. After giving written consent, students completed a short questionnaire on age, sex, smoking, recent antimicrobial drug use, and meningococcal vaccine status. Three sterile, dry, cotton-tipped swabs were used to take samples from each volunteer: one from the nasopharynx (through the mouth and swept up behind the uvula), one from both tonsils, and one swab of saliva between the lower gum and lips. Swabs were plated directly onto a selective culture medium primarily designed for the isolation of pathogenic Neisseria species (modified New York City base containing vancomycin, colistin, and trimethoprim), prepared by Taunton Media Services, UK (7). The plates were transported to Hereford Public Health Laboratory, where they were spread once from the primary inoculum and incubated in 7% CO2 at 37°C for 48 h. Putative Neisseria species isolated were sent to the Meningococcal Reference Unit, Manchester Public Health Laboratory, for Neisseria meningitidis confirmation and serologic phenotypic characterization. Data were entered into the computer using Excel (Microsoft Corp., Redmond, WA). Carriage rates by site were compared with McNemar’s test and by risk factor using chi-square tests. Ethical approval was obtained from the Public Health Laboratory Service Ethics Committee and Herefordshire District Ethics Committee.Of the 258 participants, 90 (35%) were identified as carrying Neisseria meningitidis from one or more sites. The site with the highest yield was the nasopharynx (32.2%), whereas tonsillar carriage was 19.4% (Site of swab One site positive Two sites positive Three sites positive Total positive Overall carriage % Nasopharynx
39
44
0
83
32.2
Tonsils
6
44
0
50
19.4
Saliva 1 0 0 1 0.4