Two clustered cases of confirmed influenza A(H5N1) virus infection, Cambodia, 2011.

In February 2011, a mother and her child from Banteay Meanchey Province, Cambodia, were diagnosed, postmortem, with avian influenza A(H5N1) virus infection. A field investigation was conducted by teams from the Cambodian Ministry of Health, the World Health Organization and the Institut Pasteur in Cambodia. Nasopharyngeal, throat and serum specimens collected from 11 household or three neighbour contacts including two suspect cases tested negative by reverse transcriptase-polymerase chain reaction (RT-PCR) for A(H5N1). Follow-up sera from the 11 household contacts also tested negative for A(H5N1) antibodies. Twenty-six HCW who were exposed to the cases without taking adequate personal protective measures self-monitored and none developed symptoms within the two following weeks. An unknown number of passengers travelling with the cases on a minibus while they were symptomatic could not be traced but no clusters of severe respiratory illnesses were detected through the Cambodian surveillance systems in the two weeks after that. The likely cause of the fatal infection in the mother and the child was common-source exposure in Preah Sdach District, Prey Veng Province. Human-to-human transmission of A(H5N1) virus was unlikely but genetic susceptibility is suspected. Clusters of A(H5N1) virus infection should be systematically investigated to rule out any human-to-human transmission.

International foodborne outbreak of Shigella sonnei infection in airline passengers.

During 22-24 August 2004, an outbreak of Shigella sonnei infection affected air travellers who departed from Hawaii. Forty-seven passengers with culture-confirmed shigellosis and 116 probable cases who travelled on 12 flights dispersed to Japan, Australia, 22 US states, and American Samoa. All flights were served by one caterer. Pulsed-field gel electrophoresis of all 29 S. sonnei isolates yielded patterns that matched within one band. Food histories and menu reviews identified raw carrot served onboard as the likely vehicle of infection. Attack rates for diarrhoea on three surveyed flights with confirmed cases were 54% (110/204), 32% (20/63), and 12% (8/67). A total of 2700 meals were served on flights with confirmed cases; using attack rates observed on surveyed flights, we estimated that 300-1500 passengers were infected. This outbreak illustrates the risk of rapid, global spread of illness from a point-source at a major airline hub.

Molecular epidemiology of dengue in the Pacific: introduction of two distinct strains of dengue virus type-1 [corrected] into Hawaii.

In 2000, a major dengue epidemic, caused by the type-1 virus (DENV-1), began in the Pacific and Asia, with cases still being reported in 2006. The phylogenetic analysis of full-length sequences of the envelope-protein gene of DENV-1 isolates recovered during outbreaks in Hawaii and Tahiti in 2001-2002 indicated that most Hawaiian isolates were Tahitian in origin. All the Hawaiian and Tahitian isolates were identified as the Pacific subtype (i.e. subtype IV) of DENV-1. A Hawaiian isolate, collected from a resident who had travelled to Samoa, differed significantly at the nucleotide level, however, from all the other Hawaiian strains, clustering, in the phylogenetic analysis, with a virus previously isolated from another visitor to Samoa. These results not only indicate that two distinct strains of DENV-1 were introduced into Hawaii in 2001 but also illustrate the ease with which dengue can be carried across distances of many thousands of miles.

Epidemic West Nile encephalitis, New York, 1999: results of a household-based seroepidemiological survey.

BACKGROUND: In the summer of 1999, West Nile virus was recognised in the western hemisphere for the first time when it caused an epidemic of encephalitis and meningitis in the metropolitan area of New York City, NY, USA. Intensive hospital-based surveillance identified 59 cases, including seven deaths in the region. We did a household-based seroepidemiological survey to assess more clearly the public-health impact of the epidemic, its range of illness, and risk factors associated with infection. METHODS: We used cluster sampling to select a representative sample of households in an area of about 7.3 km(2) at the outbreak epicentre. All individuals aged 5 years or older were eligible for interviews and phlebotomy. Serum samples were tested for IgM and IgG antibodies specific for West Nile virus. FINDINGS: 677 individuals from 459 households participated. 19 were seropositive (weighted seroprevalence 2.6% [95% CI 1.2-4.1). Six (32%) of the seropositive individuals reported a recent febrile illness compared with 70 of 648 (11%) seronegative participants (difference 21% [0-47]). A febrile syndrome with fatigue, headache, myalgia, and arthralgia was highly associated with seropositivity (prevalence ratio 7.4 [1.5-36.6]). By extrapolation from the 59 diagnosed meningoencephalitis cases, we conservatively estimated that the New York outbreak consisted of 8200 (range 3500-13000) West Nile viral infections, including about 1700 febrile infections. INTERPRETATION: During the 1999 West Nile virus outbreak, thousands of symptomless and symptomatic West Nile viral infections probably occurred, with fewer than 1% resulting in severe neurological disease.

Risk factors for Nipah virus transmission, Port Dickson, Negeri Sembilan, Malaysia: results from a hospital-based case-control study.

A hospital-based case-control study of viral encephalitis was carried out at Port Dickson Hospital, in the state of Negeri Sembilan, Malaysia. Between March and May 1999, 69 clinically diagnosed viral encephalitis cases and 31 controls were interviewed. Job histories on pig farming activities were assessed by a group of epidemiologists and veterinary surgeons. Results show that among clinical cases of viral encephalitis, 52 (75.4%) cases were diagnosed to have Nipah virus infection based on positive serology for antibodies to the cross-reacting Hendra virus antigen. The Nipah virus encephalitis was significantly associated with a history of working in pig farms (p < 0.001, OR = 196.0, 95% CI = 20.4-4741.6), history of contact with animals (p < 0.001, OR = 38.3, 95% CI = 8.2-209.0) and with history of direct contact with pigs (p = 0.002, OR = 34.4, 95% CI = 2.6-1,024.4). The Nipah virus infection was also significantly associated with history of feeding/cleaning pigs (p < 0.001, OR = 102, 95% CI = 11.9-2,271.5). These results provide evidence that involvement in pig farming activities is significantly associated with the risk of getting Nipah virus infection. They are potential risk factors for Nipah virus transmission in the major pig-producing area of Bukit Pelandok, Port Dickson Negeri Sembilan.

Hantavirus pulmonary syndrome in Panama: identification of novel hantaviruses and their likely reservoirs.

Hantavirus pulmonary syndrome (HPS), a severe respiratory disease with high mortality caused by rodent-borne hantaviruses, has previously been identified in the United States and Canada as well as central and southern South America. In late 1999 and early 2000, an outbreak of acute illness compatible with HPS was reported in Los Santos, Panama, with the death of 3 of the 12 (25%) suspected cases. Hantavirus-specific antibodies were detected in patient sera, and virus RNA was detected by reverse transcriptase-polymerase chain reaction. Sequence analysis of virus genome N-, G1-, and G2-encoding fragments showed this to be a novel hantavirus, Choclo virus. Serologic and virus genetic analyses of rodents trapped in the area showed Oligoryzomys fulvescens to be the likely reservoir for the HPS-associated Choclo virus. In addition, Zygodontomys brevicauda rodents were shown to harbor another genetically unique hantavirus, Calabazo virus.

Case-control study of risk factors for human infection with a new zoonotic paramyxovirus, Nipah virus, during a 1998-1999 outbreak of severe encephalitis in Malaysia.

An outbreak of encephalitis affecting 265 patients (105 fatally) occurred during 1998-1999 in Malaysia and was linked to a new paramyxovirus, Nipah, that infected pigs, humans, dogs, and cats. Most patients were pig farmers. Clinically undetected Nipah infection was noted in 10 (6%) of 166 community-farm controls (persons from farms without reported encephalitis patients) and 20 (11%) of 178 case-farm controls (persons from farms with encephalitis patients). Case patients (persons with Nipah infection) were more likely than community-farm controls to report increased numbers of sick/dying pigs on the farm (59% vs. 24%, P=.001) and were more likely than case-farm controls to perform activities requiring direct contact with pigs (86% vs. 50%, P=.005). Only 8% of case patients reported no contact with pigs. The outbreak stopped after pigs in the affected areas were slaughtered and buried. Direct, close contact with pigs was the primary source of human Nipah infection, but other sources, such as infected dogs and cats, cannot be excluded.

Hantavirus pulmonary syndrome in the Americas: the early years.

The initial recognition of hantavirus pulmonary syndrome (HPS) as a new disease associated with a cluster of acute respiratory deaths among American Indians in the southwestern United States in 1993 bears little resemblance to the current understanding of this syndrome. HPS is now recognized as a zoonotic disease that has been endemic throughout the Americas for at least 40 years and that is closely linked to population densities and virus dynamics among a specific subfamily of rodents. The classic disease description has also been markedly broadened to include a spectrum of illness that ranges from asymptomatic infection to fulminate cardiorespiratory failure. Clinical variants with hemorrhagic or prominent renal manifestations have also been recognized. Prevention efforts have been targeted at minimizing peri-domestic contact with rodents and their excreta and improving clinical recognition of infection. This paper describes the pathogenesis underlying the profound cardiorespiratory compromise, person-to-person transmission reported in South America, and viable treatment modalities.

Acute Sin Nombre hantavirus infection without pulmonary syndrome, United States.

Hantavirus pulmonary syndrome (HPS) occurs in most infections with Sin Nombre virus and other North American hantaviruses. We report five cases of acute hantavirus infection that did not fit the HPS case definition. The patients had characteristic prodromal symptoms without severe pulmonary involvement. These cases suggest that surveillance for HPS may need to be expanded.