Nipah virus outbreak with person-to-person transmission in a district of Bangladesh, 2007.

In February 2007 an outbreak of Nipah virus (NiV) encephalitis in Thakurgaon District of northwest Bangladesh affected seven people, three of whom died. All subsequent cases developed illness 7-14 days after close physical contact with the index case while he was ill. Cases were more likely than controls to have been in the same room (100% vs. 9.5%, OR undefined, P<0.001) and to have touched him (83% vs. 0%, OR undefined, P<0.001). Although the source of infection for the index case was not identified, 50% of Pteropus bats sampled from near the outbreak area 1 month after the outbreak had antibodies to NiV confirming the presence of the virus in the area. The outbreak was spread by person-to-person transmission. Risk of NiV infection in family caregivers highlights the need for infection control practices to limit transmission of potentially infectious body secretions.

Antibodies to Bartonella species in inner-city intravenous drug users in Baltimore, Md.

BACKGROUND: Bartonella quintana has recently been associated with homeless alcoholic men. Both B quintana and Bartonella henselae have been shown to be opportunistic pathogens of people with acquired immunodeficiency syndrome. The reservoirs and modes of transmission of these infections are incompletely known. OBJECTIVES: To examine serum samples that were taken from inner-city intravenous (IV) drug users for antibodies to Bartonella organisms to determine whether there is an urban transmission cycle for Bartonella species and to examine the demographic and behavioral characteristics of IV drug users to identify possible risk factors for infection with any of these agents. MATERIALS AND METHODS: A serologic survey was conducted, using a convenience sample of serum specimens collected during a study of IV drug use and human immunodeficiency virus infection among 630 inner-city residents in Baltimore, Md. A detailed questionnaire was administered at the initial collection of serum, and additional serum collections and questionnaire updates were made at 6-month intervals. The most recent available serum sample was tested for Bartonella antibody titer by using the indirect immunofluorescent antibody test with 3 antigens: Bartonella elizabethae, B henselae, and B quintana. Univariate and multivariate analyses of selected potential demographic and behavioral risk factors were conducted. RESULTS: Antibodies to Bartonella were highly prevalent in this group; more than 37% of all samples reacted with at least 1 antigen. Overall seroprevalence of antibodies to B elizabethae, B henselae, and B quintana was 33%, 11%, and 10%, respectively. Current IV drug use, frequency of injection, and seronegative human immunodeficiency virus status were significantly associated with Bartonella antibody presence, but these associations varied by analysis. There was a significant inverse association of antibody prevalence to B henselae and B quintana by using CD4+ cell counts among human immunodeficiency virus-seropositive individuals. CONCLUSIONS: Intravenous drug users have an elevated prevalence of antibodies to Bartonella organisms and may be at significant risk of becoming infected. Current IV drug use, high frequency of injection, and seronegative human immunodeficiency virus status are significant risk factors for an increased prevalence of Bartonella antibodies. The current natural histories of Bartonella species are rapidly changing, and mechanisms of transmission remain unknown.

Disseminated infection with Bartonella henselae as a cause of spontaneous splenic rupture.

A 65-year-old man developed massive hemoperitoneum secondary to spontaneous splenic rupture. Histopathological analysis of the spleen demonstrated necrotizing granulomas. Results of serological tests indicated infection with a species of Bartonella, and immunohistochemical staining established Bartonella henselae as the cause of splenitis. To our knowledge, this represents the first reported case of spontaneous splenic rupture caused by infection with a species of Bartonella.

Serologic evidence of rickettsialpox (Rickettsia akari) infection among intravenous drug users in inner-city Baltimore, Maryland.

We tested single serum samples from 631 intravenous (i.v.) drug users from inner-city Baltimore, Maryland for serologic evidence of exposure to spotted fever group rickettsiae. A total of 102 (16%) individuals had titers > or = 64 to Rickettsia rickettsii by an indirect immunofluorescence assay. Confirmation that infection was caused by R. akari was obtained by cross-adsorption studies on a subset of serum samples that consistently resulted in higher titers to R. akari than to R. rickettsii. Current i.v. drug use, increased frequency of injection, and shooting gallery use were significant risk factors for presence of group-specific antibodies reactive with R. rickettsii. There was a significant inverse association with the presence of antibodies reactive to R. rickettsii and antibodies reactive to the human immunodeficiency virus. This study suggests that i.v. drug users are at an increased risk for R. akari infections. Clinicians should be aware of rickettsialpox, as well as other zoonotic diseases of the urban environment, when treating i.v. drug users for any acute febrile illness of undetermined etiology.

Vesicular stomatitis virus, New Jersey serotype: replication in and transmission by Lutzomyia shannoni (Diptera: Psychodidae).

Laboratory-reared female sand flies (Lutzomyia shannoni) were experimentally infected, orally and by intrathoracic inoculation, with the New Jersey serotype of vesicular stomatitis (VSNJ) virus. Virus replication occurred in the insects following infection by both routes. Virus titers greater than 10(4) plaque forming units of VSNJ virus were present in heads of orally infected sand flies 12 days after virus ingestion, confirming that a persistent disseminated infection had occurred. Both orally and parenterally infected Lu. shannoni transmitted VSNJ virus by bite to susceptible rodents and by transovarial transmission to a small percentage of their F1 progeny. The significance of these findings in the epizootiology of VSNJ virus on Ossabaw Island, Georgia, an enzootic focus of this virus, is discussed.

Isolation of vesicular stomatitis virus New Jersey serotype from phlebotomine sand flies in Georgia.

Vesicular stomatitis virus New Jersey serotype (VSNJ virus) was isolated from 6 of 610 pools of phlebotomine sand flies (Lutzomyia shannoni) collected on Ossabaw Island, GA. All isolates were from non-blooded females. Infected sand flies were collected at 6 sites at 5 separate times from 3 June through 25 July 1988. Thirty-five pools of Culicoides ssp. and 48 pools of mosquitoes obtained in conjunction with the infected sand flies also were evaluated for VSNJ virus; all were negative. Concomitant serologic monitoring of sentinel swine indicated that VSNJ virus transmission began in late April and continued through the completion of this study in August. The incidence of seroconversion among the sentinel wild swine was 50%. Domestic sentinel swine did not seroconvert at 2 sentinel sites, 1 of 2 seroconverted at 1 site, and 2 of 2 seroconverted at the fourth site. Vesicular lesions were seen on 10 sentinel wild swine during the summer. Vesicular stomatitis virus (NJ) was isolated from 4 of these swine and was diagnosed in 1 additional swine by direct complement-fixation assay. The time period within which VSNJ virus was isolated from sand flies preceded detection of vesicular lesions but corresponded with the period of seroconversion in sentinel swine. Site specific data indicated that VSNJ virus activity was widespread within the study area.

Evidence of rodent-associated Bartonella and Rickettsia infections among intravenous drug users from Central and East Harlem, New York City.

We tested serum samples collected in 1997 and 1998 from a cohort of 204 injection drug users (IDUs) recruited from Central and East Harlem, New York City, New York, for antibodies reactive with seven rickettsial or Bartonella spp. antigens. Rodent-associated Bartonella elizabethae and Rickettsia akari were the primary etiologic agents of interest. The testing panel also included Bartonella henselae, Bartonella quintana, Rickettsia prowazekii, Rickettsia rickettsii, and Rickettsia typhi. The highest prevalence of seroreactive serum samples (46%) was found with B. elizabethae antigens; 10% of the samples reacted with B. henselae antigens, while 2% reacted with B. quintana antigens. Reactivity to the latter two antigens was likely due to cross-reactivity with B. elizabethae antigens in most instances. Among the spotted fever group rickettsiae, 18 (9%) samples reacted with R. akari, including 10 samples (5%) that also reacted with R. rickettsii. Cross-adsorption studies demonstrated that most of the spotted fever group rickettsiae antibodies were due to R. akari infections. Among the typhus group rickettsiae, 5 samples reacted weakly to R. prowazekii antigens, and no samples reacted with R. typhi antigens. These findings suggest that Harlem IDUs are commonly exposed to two rodent-associated zoonotic agents. Further study of IDU populations may help elucidate transmission cycles of these agents in inner cities where higher levels of transmission occur.

Urban zoonoses caused by Bartonella, Coxiella, Ehrlichia, and Rickettsia species.

The last half of the 20th Century witnessed an increase in the occurrence and recognition of urban zoonoses caused by members of the genera Bartonella, Coxiella, Ehrlichia, and Rickettsia, all traditionally considered to be members of the family Rickettsiaceae. In recent years, new human pathogens (Bartonella elizabethae, Bartonella henselae, and Rickettsia felis) have been recognized in urban environments. Other newly recognized pathogens (Ehrlichia chaffeensis and Ehrlichia phagocytophila in the United States) have sylvan zoonotic cycles but are present in urban areas because their vertebrate hosts and associated ectoparasitic arthropod vectors are able to survive in cities. Still other agents, which were primarily of historical importance (Bartonella quintana) or have not traditionally been associated with urban environments (Rickettsia rickettsii), have been recognized as causes of human disease in urban areas. Some diseases that have traditionally been associated with urban environments, such as rickettsialpox (caused by Rickettsia akari) and murine typhus (caused by Rickettsia typhi), still occur in large cities at low or undetermined frequencies and often go undetected, despite the availability of effective measures to diagnose and control them. In addition, alternate transmission cycles have been discovered for Coxiella burnetii, Rickettsia prowazekii, and R. typhi that differ substantially from their established, classic cycles, indicating that the epidemiology of these agents is more complex than originally thought and may be changing. Factors leading to an increase in the incidence of illnesses caused by these bacteria in urban areas include societal changes as well as intrinsic components of the natural history of these organisms that favor their survival in cities. Transovarial and transstadial transmission of many of the agents in their arthropod hosts contributes to the highly focal nature of many of the diseases they cause by allowing the pathogens to persist in areas during adverse times when vertebrate amplifying hosts may be scarce or absent. Domesticated animals (primarily cats, dogs, and livestock) or commensal rodents [primarily Norway rats (Rattus norvegicus) and house mice (Mus musculus)] can serve as vertebrate amplifying hosts and bring these agents and their ectoparasitic arthropod vectors into direct association with humans and help maintain transmission cycles in densely populated urban areas. The reasons for the increase in these urban zoonoses are complex. Increasing population density worldwide, shifts in populations from rural areas to cities, increased domestic and international mobility, an increase in homelessness, the decline of inner-city neighborhoods, and an increase in the population of immunosuppressed individuals all contribute to the emergence and recognition of human diseases caused by these groups of agents. Due to the focal nature of infections in urban areas, control or prevention of these diseases is possible. Increased physician awareness and public health surveillance support will be required to detect and treat existing urban infections caused by these agents, to determine the disease burden caused by them, to design and implement control programs to combat and prevent their spread, and to recognize emerging or resurging infections caused by members of these genera as they occur.

Fort Chaffee revisited: the epidemiology of tick-borne rickettsial and ehrlichial diseases at a natural focus.

A retrospective cohort study was conducted among troops training at Fort Chaffee, Arkansas, from May through June 1997, to identify infections caused by tick-borne pathogens. Serum samples were tested by IFAs for antibodies to selected Rickettsia and Ehrlichia species and by an investigational EIA for spotted fever group Rickettsia lipopolysaccharide antigens. Of 1,067 guardsmen tested, 162 (15.2%) had antibodies to one or more pathogens. Of 93 guardsmen with paired serum samples, 33 seroconverted to Rickettsia rickettsii or spotted fever group rickettsiae (SFGR) and five to Ehrlichia species. Most (84.8%) of the personnel who seroconverted to SFGR were detected only by EIA, and seropositivity was significantly associated with an illness compatible with a tick-borne disease. In addition, 34 (27%) of 126 subjects with detectable antibody titers reported a compatible illness. The primary risk factor for confirmed or probable disease was finding > 10 ticks on the body. Doxycycline use and rolling up of long sleeves were protective against seropositivity. The risk of transmission of tick-borne pathogens at Fort Chaffee remains high, and use of the broadly reactive EIA suggests that previous investigations may have underestimated the risk for infection by SFGR. Measures to prevent tick bite and associated disease may require reevaluation.

Funnel trap for the capture of phlebotomine sand flies (Diptera: Psychodidae) from tree holes.

A funnel trap that fitted over holes leading into hollow trees was used to capture adult phlebotomine sand flies, Lutzomyia shannoni Dyar, on Ossabaw Island, Chatham County, Ga. These insects rested in hollow trees during the day and were collected by funnel traps as they egressed from the tree holes at night. The trap is lightweight, durable, inexpensive, waterproof, and selective. Using this trap, greater than 100 healthy L. shannoni ++were captured per night by a single investigator during July and August 1988 when adult flies were abundant on the island.

Incompetence of white-tailed deer as amplifying hosts of vesicular stomatitis virus for Lutzomyia shannoni (Diptera: Psychodidae).

Sand flies, Lutzomyia shannoni Dyar, were allowed to feed on 3 white-tailed deer, Odocoileus virginiana Zimmermann, that previously had been infected with the New Jersey serotype of vesicular stomatitis (VSNJ) virus. Flies fed in the lower abdominal area of each deer on days 1-5 postinfection. A blood sample, nasal swab, and throat swab were taken during each feeding trial and examined for virus. Blood-fed flies were held for 4-5 d following the bloodmeal and tested for VSNJ virus infection. VSNJ virus was never detected in blood or from swabs taken from infected deer nor from any of the sand flies that fed on deer. The findings suggest that white-tailed deer do not fulfill the traditional concept of amplifying hosts of VSNJ virus.

Incompetence of domestic pigs as amplifying hosts of vesicular stomatitis virus for Lutzomyia shannoni (Diptera: Psychodidae).

Seven domestic pigs, Sus scrofa L., were infected by intradermal inoculation at 3 different sites with the New Jersey serotype of vesicular stomatitis (VSNJ) virus. Laboratory-reared Lutzomyia shannoni Dyar sand flies, a suspected biological vector of VSNJ virus, were allowed to feed on pigs at the lower abdomen or at sites of their own selection on days 1-7 and on day 10 postinfection. Blood samples were taken from infected swine concomitant with most feeding trials and tested for the presence of virus. Sand flies were held for up to 5 d following ingestion of blood and tested for VSNJ virus infection. Virus was not recovered from the blood of infected pigs or from any of the flies that fed on these pigs. The findings suggest that domestic pigs do not fulfill the traditional concept of amplifying hosts of VSNJ virus.

Population dynamics of Lutzomyia shannoni (Diptera: Psychodidae) in relation to the epizootiology of vesicular stomatitis virus on Ossabaw Island, Georgia.

Population dynamics of Lutzomyia shannoni Dyar were studied on Ossabaw Island, GA, to define further the role of this species in the epizootiology of the New Jersey serotype of vesicular stomatitis (VSNJ) virus. Bimonthly collections of sand flies egressing from hollow trees from April to November 1991 indicated that there were three generations of sand flies. Data from light trap collections from 1986 through 1989 indicated that similar seasonal cycles occurred during previous years. At this site, we hypothesize that L. shannoni undergoes facultative diapause. Two isolates of VSNJ virus were obtained from female sand flies collected in May and June of 1991. We believe that the virus overwinters in immature L. shannoni and that transovarially infected sand flies emerging each spring initiate a summer amplification cycle in swine on Ossabaw Island.

Seasonal abundance of Lutzomyia shannoni (Diptera: Psychodidae) on Ossabaw Island, Georgia.

Population dynamics of Lutzomyia shannoni were monitored from April 1986 through December 1987 on Ossabaw Island, Ga. Most (99%) of the 19,788 adult sand flies were collected in light traps supplemented with dry ice; less than or equal to 1% were aspirated from diurnal resting sites. Adult sand flies first appeared in April and were followed by peaks of abundance during May 1986, and May and July 1987. Numbers of adults captured fell rapidly in October and November 1986 and in September and October 1987. No specimens were collected in December 1986 or in March, November, and December 1987. Light trap catch was affected positively by mean nightly air temperature and negatively by rainfall 14 d before collection, but not by wind speed or moon phase. Vesicular stomatitis viral activity, as measured by antibodies in feral and domestic swine, roughly corresponded to the seasonal appearance of adult L. shannoni during 1986 and 1987. Significantly more adults (72%) were collected in light traps at ground level (0.5m) than at heights of 4 and 8m. Most resting adults were collected from dark, moist tree holes and cavities of various hardwoods.

Titers of vesicular stomatitis virus, New Jersey serotype, in naturally infected male and female Lutzomyia shannoni (Diptera: Psychodidae) in Georgia.

Seven isolates of the New Jersey serotype of vesicular stomatitis (VSNJ) virus were obtained from pooled specimens of phlebotomine sand flies, Lutzomyia shannoni Dyar, collected on Ossabaw Island, Chatham County, Ga., in 1989 and 1990. Three isolates, including two from males, were obtained from light-trapped sand flies in 1989. Four isolates were obtained from pools of sand flies collected from hollow trees in 1990. Three of the latter pools contained from 4.0 to 4.7 log10 of plaque-forming units of virus per ml, suggesting that the positive flies in these pools had supported VSNJ virus replication. One of these high-titered isolates was obtained from a pool of male sand flies. These data provide further support for the hypotheses that L. shannoni is a biological vector of VSNJ virus at this enzootic focus and that transovarial transmission of the virus occurs in nature.

Effect of forest type on the distribution of Lutzomyia shannoni (Diptera: Psychodidae) and vesicular stomatitis virus on Ossabaw Island, Georgia.

We studied the effects of three forest types on multiple factors that are believed to influence the transmission of the New Jersey serotype of vesicular stomatitis (VSNJ) virus on Ossabaw Island, GA. These factors included availability of tree hole diurnal resting habitat for the presumed sand fly vector, Lutzomyia shannoni Dyar; relative abundance of L. shannoni; prevalence of VSNJ virus infection in sand flies; and prevalence of VSNJ virus antibodies in wild swine. Tree hole availability, sand fly abundance, and antibody prevalence in swine were significantly greater in maritime live oak forest than in other forest types. A single isolate of VSNJ virus was obtained from sand flies collected in maritime live oak forest. These data indicate that the relative abundance of adult L. shannoni is influenced significantly by the availability of tree holes and that VSNJ virus infection in wild swine is linked to forest type and is greatest in areas capable of supporting abundant populations of L. shannoni.

Phlebotomine sand flies as vectors of vesiculoviruses: a review.

Phlebotomine sand flies appear to be involved in the epizootiology of 10 of the 16 currently recognized vesiculoviruses. Evidence in support of this includes isolation of viruses from wild-caught male and female sand flies; demonstration of oral infection, replication, and bite transmission of viruses by sand flies; the temporal and/or spatial association between infected sand flies and infected vertebrates; and demonstration of transovarial virus transmission. The present review summarizes the known sand fly-vesiculovirus relationships.

Lutzomyia shannoni (Diptera: Psychodidae): a biological vector of the New Jersey serotype of vesicular stomatitis virus on Ossabaw Island, Georgia.

The New Jersey serotype of vesicular stomatitis virus (VSNJ) is enzootic on Ossabaw Island, Georgia. Lutzomyia shannoni is the only phlebotomine sand fly present on the island and there is strong evidence that it is a vector of the virus at this site. This overview summarizes the studies that have been done on the island, reviews the evidence which confirms that L. shannoni is a biological vector of VSNJ, and discusses remaining unknown aspects of the epizootiology of VSNJ.

An update on the distribution of Parelaphostrongylus tenuis in the southeastern United States.

An update is presented on the distribution of the meningeal worm (Parelaphostrongylus tenuis) of white-tailed deer (Odocoileus virginianus) in the southeastern United States. The parasite is widely distributed and common in all or much of Arkansas, Kentucky, Louisiana, Maryland, North Carolina, Tennessee, Virginia and West Virginia. It is also common in the northern half of Alabama and Georgia. In contrast, it is rare or absent along the Atlantic and Gulf coastal plains of Alabama, Georgia, Mississippi and South Carolina. It has been collected from a single deer in Florida.

Detection of antibodies reactive with Ehrlichia chaffeensis in the raccoon.

Antibodies reactive with Ehrlichia chaffeensis were detected in raccoon (Procyon lotor) serum samples by using an indirect immunofluorescence assay. Samples from 411 raccoons trapped in the southeastern United States from 1977 to 1999 were tested. Serologically reactive samples with reciprocal titers of > or =16 were detected from 83 raccoons (20%) from 13 of 16 counties in eight states, indicating that raccoons are commonly exposed to E. chaffeensis. Samples collected as early as 1977 were positive. A polymerase chain reaction assay specific for E. chaffeensis failed to detect the presence of ehrlichial DNA in serum samples from 20 representative seroreactive raccoons. Because of serologic cross-reactivity among antigens derived from different Ehrlichia spp., additional immunologic, molecular, or culture-based studies will be required to confirm E. chaffeensis infections of raccoons in the southeastern United States.