This article presents a model and decision criteria for evaluating a person’s risk of pre- or postexposure smallpox vaccination in light of serious vaccine-related adverse events (death, postvaccine encephalitis and progressive vaccinia). Even at a 1-in-10 risk of 1,000 initial smallpox cases, a person in a population of 280 million has a greater risk for serious vaccine-related adverse events than a risk for smallpox. For a healthcare worker to accept preexposure vaccination, the risk for contact with an infectious smallpox case-patient must be >1 in 100, and the probability of 1,000 initial cases must be >1 in 1,000. A member of an investigation team would accept preexposure vaccination if his or her anticipated risk of contact is 1 in 2.5 and the risk of attack is assumed to be >1 in 16,000. The only circumstances in which postexposure vaccination would not be accepted are the following: if vaccine efficacy were <1%, the risk of transmission were <1%, and (simultaneously) the risk for serious vaccine-related adverse events were >1 in 5,000.

Infection with Toxoplasma gondii can lead to congenital and acquired disease, resulting in loss of vision and neurologic illness. We tested sera collected in the National Health and Examination Survey (NHANES) from 1999–2000 for T. gondii–specific immunoglobulin G antibodies and compared these results with results from sera obtained in the NHANES III survey (1988–1994). NHANES collects data on a nationally representative sample of the U.S. civilian population. Of 4,234 persons 12–49 years of age in NHANES 1999–2000, 15.8% (age-adjusted, 95% confidence limits [CL] 13.5, 18.1) were antibody positive; among women (n=2,221) 14.9% (age-adjusted, 95% CL 12.5, 17.4) were antibody positive. T. gondii antibody prevalence was higher among non-Hispanic black persons than among non-Hispanic white persons (age-adjusted prevalence 19.2% vs. 12.1%, p=0.003) and increased with age. No statistically significant differences were found between T. gondii antibody prevalence in NHANES 1999–2000, and NHANES III. T. gondii antibody prevalence has remained stable over the past 10 years in the United States.

Recent epidemiologic studies indicate that infectious agents may contribute to some cases of schizophrenia. In animals, infection with Toxoplasma gondii can alter behavior and neurotransmitter function. In humans, acute infection with T. gondii can produce psychotic symptoms similar to those displayed by persons with schizophrenia. Since 1953, a total of 19 studies of T. gondii antibodies in persons with schizophrenia and other severe psychiatric disorders and in controls have been reported; 18 reported a higher percentage of antibodies in the affected persons; in 11 studies the difference was statistically significant. Two other studies found that exposure to cats in childhood was a risk factor for the development of schizophrenia. Some medications used to treat schizophrenia inhibit the replication of T. gondii in cell culture. Establishing the role of T. gondii in the etiopathogenesis of schizophrenia might lead to new medications for its prevention and treatment.

Severe acute respiratory syndrome (SARS) has caused a major epidemic worldwide. A novel coronavirus is deemed to be the causative agent. Early diagnosis can be made with reverse transcriptase-polymerase chain reaction (RT-PCR) of nasopharyngeal aspirate samples. We compared symptoms of 156 SARS-positive and 62 SARS-negative patients in Hong Kong; SARS was confirmed by RT-PCR. The RT-PCR–positive patients had significantly more shortness of breath, a lower lymphocyte count, and a lower lactate dehydrogenase level; they were also more likely to have bilateral and multifocal chest radiograph involvement, to be admitted to intensive care, to need mechanical ventilation, and to have higher mortality rates. By multivariate analysis, positive RT-PCR on nasopharyngeal aspirate samples was an independent predictor of death within 30 days.

During the summer of 2002, an epidemic of West Nile meningoencephalitis occurred in southern Louisiana. Following the outbreak, blood samples were collected from 1,692 captive rhesus monkeys (Macaca mulatta), pigtail macaques (M. nemestrina), and baboons (Papio spp.) that were permanently housed outdoors at a nonhuman primate breeding facility in St. Tammany Parish, Louisiana. The serum samples were examined for antibodies to West Nile virus (WNV). Overall, 36% of the captive nonhuman primates had WNV antibodies; comparison of these samples with banked serum samples from previous blood collections indicated that the animals were infected subclinically from February to August 2002. WNV activity was demonstrated in surveillance at the nonhuman primate-breeding colony and in the neighboring community during this same period. The high infection rate in this captive nonhuman primate population illustrates the intensity of WNV transmission that can occur silently in nature among other susceptible vertebrates during epidemic periods.

The prevalent human hantavirus disease in Sweden is nephropathia epidemica, which is caused by Puumala virus and shed by infected bank voles (Clethrionomys glareolus). To evaluate temporal and spatial patterns of this disease, we studied 2,468 reported cases from a highly disease-endemic region in northern Sweden. We found that, in particular, middle-aged men living in rural dwellings near coastal areas were overrepresented. The case-patients were most often infected in late autumn, when engaged in activities near or within manmade rodent refuges. Of 862 case-patients confident about the site of virus exposure, 50% were concentrated within 5% of the study area. The incidence of nephropathia epidemica was significantly correlated with bank vole numbers within monitored rodent populations in part of the region. Understanding this relationship may help forestall future human hantavirus outbreaks.

The emergence and reemergence of a serious infectious disease are often associated with a high case-fatality rate because of misdiagnosis and inappropriate or delayed treatment. The current reemergence of spotted fever rickettsiosis caused by Rickettsia rickettsii in Brazil has resulted in a high proportion of fatal cases. We describe two familial clusters of Brazilian spotted fever in the state of Minas Gerais, involving six children 9 months to 15 years of age; five died. Immunohistochemical investigation of tissues obtained at necropsy of a child in each location, Novo Cruzeiro and Coronel Fabriciano municipalities, established the diagnosis by demonstration of disseminated endothelial infection with spotted fever group rickettsiae. The diagnosis in the two fatal cases from Coronel Fabriciano and the surviving patient from Novo Cruzeiro was further supported by immunofluorescence serologic tests.

The utility of the VecTest antigen-capture assay to detect West Nile virus (WNV) in field-collected dead corvids was evaluated in Manitoba and Ontario, Canada, in 2001 and 2002. Swabs were taken from the oropharynx, cloaca, or both of 109 American Crows, 31 Blue Jays, 6 Common Ravens, and 4 Black-billed Magpies from Manitoba, and 255 American Crows and 28 Blue Jays from Ontario. The sensitivity and specificity of the antigen-capture assay were greatest for samples from American Crows; oropharyngeal swabs were more sensitive than cloacal swabs, and interlaboratory variation in the results was minimal. The sensitivity and specificity of the VecTest using oropharyngeal swabs from crows were 83.9% and 93.6%, respectively, for Manitoba samples and 83.3% and 95.8%, respectively, for Ontario birds. The VecTest antigen-capture assay on oropharyngeal secretions from crows is a reliable and rapid diagnostic test that appears suitable for incorporation into a WNV surveillance program.

Dengue fever emerged in Bangladesh in 2000. We tested 225 serum and plasma samples from febrile patients and 184 blood donors in 1996 and 1997 for dengue antibodies; 55 (24.4%) febrile patients had dengue antibodies (65.5% with secondary infection pattern), compared with one (0.54%) donor (p < 0.001), suggesting that dengue transmission was ongoing well before 1996.

To determine whether fluoroquinolone exposure is a risk factor for the isolation of Staphylococcus aureus and whether the effect is different for methicillin-resistant S. aureus (MRSA) versus methicillin-susceptible S. aureus (MSSA), we studied two case groups. The first case group included 222 patients with nosocomially acquired MRSA. The second case group included 163 patients with nosocomially acquired MSSA. A total of 343 patients admitted concurrently served as controls. Outcome measures were the adjusted odds ratio (OR) for isolation of MRSA and MSSA after fluoroquinolone exposure. Exposure to both levofloxacin (OR 5.4; p < 0.0001) and ciprofloxacin (OR 2.2; p < 0.003) was associated with isolation of MRSA but not MSSA. After adjustment for multiple variables, both drugs remained risk factors for MRSA (levofloxacin OR 3.4; p < 0.0001; ciprofloxacin OR 2.5; p = 0.005) but not MSSA. Exposure to levofloxacin or ciprofloxacin is a significant risk factor for the isolation of MRSA, but not MSSA.

Analysis of partial nucleotide sequences of 22 West Nile virus (WNV) isolates collected during the summer and fall of 2001 and 2002 indicated genetic variation among strains circulating in geographically distinct regions of the United States and continued divergence from isolates collected in the northeastern United States during 1999 and 2000. Sequence analysis of a 2,004-nucleotide region showed that 14 isolates shared two nucleotide mutations and one amino acid substitution when they were compared with the prototype WN-NY99 strain, with 10 of these isolates sharing an additional nucleotide mutation. In comparison, isolates collected from coastal regions of southeast Texas shared the following differences from WN-NY99: five nucleotide mutations and one amino acid substitution. The maximum nucleotide divergence of the 22 isolates from WN-NY99 was 0.35% (mean = 0.18%). These results show the geographic clustering of genetically similar WNV isolates and the possible emergence of a dominant variant circulating across much of the United States during 2002.

From August 2000 through January 2001, a large epidemic of Ebola hemorrhagic fever occurred in Uganda, with 425 cases and 224 deaths. Starting from three laboratory-confirmed cases, we traced the chains of transmission for three generations, until we reached the primary case-patients (i.e., persons with an unidentified source of infection). We then prospectively identified the other contacts in whom the disease had developed. To identify the risk factors associated with transmission, we interviewed both healthy and ill contacts (or their proxies) who had been reported by the case-patients (or their proxies) and who met the criteria set for contact tracing during surveillance. The patterns of exposure of 24 case-patients and 65 healthy contacts were defined, and crude and adjusted prevalence proportion ratios (PPR) were estimated for different types of exposure. Contact with the patient’s body fluids (PPR = 4.61%, 95% confidence interval 1.73 to 12.29) was the strongest risk factor, although transmission through fomites also seems possible.

We analyzed data from 25 consecutive patients with hantavirus pulmonary syndrome (HPS) admitted to the Puerto Montt and Osorno Regional Hospitals, southern Chile, from 1997 to 2001, emphasizing epidemiologic, clinical, radiographic, treatment, and laboratory aspects. Hemorrhage was frequent (64%), and 48% of patients showed alterations in renal function. Ten patients died (40%). We identified three groups of patients, which included the following: 1) those with the least severe form who had prodromic symptoms without pulmonary involvement; 2) those with moderate illness who had interstitial pulmonary infiltrates, usually needed supplemental nasal oxygen, were hemodynamically stable, and had an APACHE II <12 (none of whom died); and 3) those with the severe form who required mechanical ventilation, frequently had hemodynamic instability (93%), experienced a high mortality rate (77%), and had an APACHE II >12. Mild forms of HPS also exist, which are poorly known; the symptoms could be confounded with those of other viral diseases, leading to underdiagnosis.

To address the source of infection in humans and public health importance of Giardia duodenalis parasites from animals, nucleotide sequences of the triosephosphate isomerase (TPI) gene were generated for 37 human isolates, 15 dog isolates, 8 muskrat isolates, 7 isolates each from cattle and beavers, and 1 isolate each from a rat and a rabbit. Distinct genotypes were found in humans, cattle, beavers, dogs, muskrats, and rats. TPI and small subunit ribosomal RNA (SSU rRNA) gene sequences of G. microti from muskrats were also generated and analyzed. Phylogenetic analysis on the TPI sequences confirmed the formation of distinct groups. Nevertheless, a major group (assemblage B) contained most of the human and muskrat isolates, all beaver isolates, and the rabbit isolate. These data confirm that G. duodenalis from certain animals can potentially infect humans and should be useful in the detection, differentiation, and taxonomy of Giardia spp.

Whether severe acute respiratory syndrome–associated coronavirus (SARS-CoV) infection can be asymptomatic is unclear. We examined the seroprevalence of SARS-CoV among 674 healthcare workers from a hospital in which a SARS outbreak had occurred. A total of 353 (52%) experienced mild self-limiting illnesses, and 321 (48%) were asymptomatic throughout the course of these observations. None of these healthcare workers had antibody to SARS CoV, indicating that subclinical or mild infection attributable to SARS CoV in adults is rare.

We report two cases of infection with clonally unrelated, high-level ciprofloxacin-resistant, β-lactamase–producing strains of Salmonella enterica Typhimurium. Resistance was caused by four topoisomerase mutations, in GyrA, GyrB, and ParC and increased drug efflux. Ciprofloxacin treatment failed in one case. In the second case, reduced susceptibility to third-generation cephalosporins occurred after initial treatment with these drugs and may explain the treatment failure with ceftriaxone.

Cowpox with a severe, generalized eruption was diagnosed in an atopic 4-year-old girl by electron microscopy, virus isolation, polymerase chain reaction, and immunoglobulin (Ig) M and low-avidity IgG antibodies. The hemagglutinin gene of the isolate clustered with a Russian cowpox virus strain, and more distantly, with other cowpox and vaccinia virus strains. The patient’s dog had orthopoxvirus-specific antibodies, indicating a possible transmission route.

We report the first case of pulmonary tuberculosis caused by Mycobacterium bovis subsp. caprae in a captive Siberian tiger, an endangered feline. The pathogen was isolated from a tracheal aspirate obtained by bronchoscopy. This procedure provided a reliable in vivo diagnostic method in conjunction with conventional and molecular tests for the detection of mycobacteria.

Dengue virus was detected for the first time in Chile, in an outbreak of dengue fever on Easter Island. The virus was isolated in tissue culture and characterized by reverse transcription–polymerase chain reaction as being dengue type 1.

Orthopoxvirus zoonosis or smallpox as result of bioterrorism or biological warfare represents a risk for epidemic spread. By monitoring T-cell responses by flow cytometry, we observed a recall response after recent vaccination against smallpox. When the high similarity between the orthopoxviruses is considered, this rapid assay that uses vaccinia antigens could identify recently exposures.

Since July 2002, bacteriologically confirmed shigellosis cases have increased, and multidrug-resistant Shigella dysenteriae serotype 1 strains have reemerged in patients hospitalized with diarrhea in Kolkata, India. The isolated strains of S. dysenteriae 1 showed resistance to chloramphenicol (80%), ampicillin (100%), tetracycline (100%), co-trimoxazole (100%), nalidixic acid (100%), norfloxacin (100%), and ciprofloxacin (100%). Emergence of fluoroquinolone resistance in S. dysenteriae 1 strains complicated treatment of shigellosis patients. Six strains belonging to provisional serovars of S. dysenteriae were also identified for the first time in patients hospitalized with diarrhea in Kolkata, India.

We describe the first case of failure of oral levofloxacin treatment of community-acquired pneumonia caused by Haemophilus influenzae. The strain showed cross-resistance to fluoroquinolones and carried four mutations in quinolone resistance–determining regions of DNA gyrase and topoisomerase IV genes.

To assess fluoroquinolone susceptibility of Campylobacter strains in Senegal, skin samples were collected from 250 chicken carcasses from January 2001 to October 2002. Among 205 isolated Campylobacter strains, 59% and 41% were identified as Campylobacter jejuni and C. coli, respectively; the overall ciprofloxacin-resistance rate was 34%.

Fluoroquinolone resistance was detected in 12 of 370 Australian human Campylobacter isolates; 10 of these were travel-associated, and for 2 isolates travel status was unknown. No resistance was found in isolates known to be locally acquired. In Australia, fluoroquinolones have not been licensed for use in food production animals, a policy that may have relevance for countries with fluoroquinolone-resistant Campylobacter.

In areas where melioidosis is endemic, stress on the healthcare system is substantial. Because clinical manifestations are protean, the illness is difficult to diagnose, and cutaneous Burkholderia pseudomallei infections can progress to necrotizing fasciitis. While it is an uncommon complication of cutaneous melioidosis, necrotizing fasciitis is potentially fatal and requires successful management, including early diagnosis, appropriate antibiotics selection, and operative débridement.

To compensate for the lack of laboratories in remote areas, the national reference laboratory for meningitis in Niger used polymerase chain reaction (PCR) to enhance the surveillance of meningitis caused by Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae. PCR effectively documented the wide geographic spread of N. meningitidis serogroup W135.