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Issue Cover for Volume 10, Number 9—September 2004

Volume 10, Number 9—September 2004

[PDF - 5.68 MB - 195 pages]

Perspective

New Measurable Indicator for Tuberculosis Case Detection [PDF - 285 KB - 6 pages]
M. W. Borgdorff

The World Health Organization’s goal for tuberculosis (TB) control is to detect 70% of cases with a new, smear-positive TB test and cure 85% of these cases. The case detection rate is the number of reported cases per 100,000 persons per year divided by the estimated incidence rate per 100,000 per year. TB incidence is uncertain and not measured but estimated; therefore, the case detection rate is uncertain. This article proposes a new indicator to assess case detection: the patient diagnostic rate. The patient diagnostic rate is the rate at which prevalent cases are detected by control programs and can be measured as the number of reported cases per 100,000 persons per year divided by the prevalence per 100,000. Prevalence can be measured directly through national prevalence surveys. Conducting prevalence surveys at 5- to 10-year intervals would allow countries with high rates of disease to determine their case detection performance by using the patient diagnostic rate and determine the effect of control measures.

EID Borgdorff MW. New Measurable Indicator for Tuberculosis Case Detection. Emerg Infect Dis. 2004;10(9):1523-1528. https://dx.doi.org/10.3201/eid1009.040349
AMA Borgdorff MW. New Measurable Indicator for Tuberculosis Case Detection. Emerging Infectious Diseases. 2004;10(9):1523-1528. doi:10.3201/eid1009.040349.
APA Borgdorff, M. W. (2004). New Measurable Indicator for Tuberculosis Case Detection. Emerging Infectious Diseases, 10(9), 1523-1528. https://dx.doi.org/10.3201/eid1009.040349.

Potential Public Health Impact of New Tuberculosis Vaccines [PDF - 358 KB - 7 pages]
E. Ziv et al.

Developing effective tuberculosis (TB) vaccines is a high priority. We use mathematical models to predict the potential public health impact of new TB vaccines in high-incidence countries. We show that preexposure vaccines would be almost twice as effective as postexposure vaccines in reducing the number of new infections. Postexposure vaccines would initially have a substantially greater impact, compared to preexposure vaccines, on reducing the number of new cases of disease. However, the effectiveness of postexposure vaccines would diminish over time, whereas the effectiveness of preexposure vaccines would increase. Thus, after 20 to 30 years, post- or preexposure vaccination campaigns would be almost equally effective in terms of cumulative TB cases prevented. Even widely deployed and highly effective (50%–90% efficacy) pre- or postexposure vaccines would only be able to reduce the number of TB cases by one third. We discuss the health policy implications of our analyses.

EID Ziv E, Daley CL, Blower S. Potential Public Health Impact of New Tuberculosis Vaccines. Emerg Infect Dis. 2004;10(9):1529-1535. https://dx.doi.org/10.3201/eid1009.030921
AMA Ziv E, Daley CL, Blower S. Potential Public Health Impact of New Tuberculosis Vaccines. Emerging Infectious Diseases. 2004;10(9):1529-1535. doi:10.3201/eid1009.030921.
APA Ziv, E., Daley, C. L., & Blower, S. (2004). Potential Public Health Impact of New Tuberculosis Vaccines. Emerging Infectious Diseases, 10(9), 1529-1535. https://dx.doi.org/10.3201/eid1009.030921.

Deaths due to Unknown Foodborne Agents [PDF - 119 KB - 8 pages]
P. D. Frenzen

This study reviews the available evidence on unknown pathogenic agents transmitted in food and examines the methods that have been used to estimate that such agents cause 3,400 annual U.S. deaths per year in the United States. The estimate of deaths was derived from hospital discharge and death certificate data on deaths attributed to gastroenteritis of unknown cause. Fatal illnesses due to unknown foodborne agents do not always involve gastroenteritis, and gastroenteritis may not be accurately diagnosed or reported on hospital charts or death certificates. The death estimate consequently omitted deaths from unknown foodborne agents that do not cause gastroenteritis and likely overstated the number of deaths from agents that cause gastroenteritis. Although the number of deaths from unknown foodborne agents is uncertain, the possible economic cost of these deaths is so large that increased efforts to identify the causal agents are warranted.

EID Frenzen PD. Deaths due to Unknown Foodborne Agents. Emerg Infect Dis. 2004;10(9):1536-1543. https://dx.doi.org/10.3201/eid1009.030403
AMA Frenzen PD. Deaths due to Unknown Foodborne Agents. Emerging Infectious Diseases. 2004;10(9):1536-1543. doi:10.3201/eid1009.030403.
APA Frenzen, P. D. (2004). Deaths due to Unknown Foodborne Agents. Emerging Infectious Diseases, 10(9), 1536-1543. https://dx.doi.org/10.3201/eid1009.030403.
Synopses

Laboratory Exposures to Staphylococcal Enterotoxin B [PDF - 175 KB - 6 pages]
J. M. Rusnak et al.

Staphylococcal enterotoxins are 23- to 29-kDa polypeptides in the bacterial superantigen protein family. Clinical symptoms from intoxication with staphylococcal enterotoxins vary by exposure route. Ingestion results in gastrointestinal symptoms, and inhalation results in fever as well as pulmonary and gastrointestinal symptoms. Review of occupational exposures at the U.S. Army Medical Research Institute of Infectious Diseases from 1989 to 2002 showed that three laboratory workers had symptoms after ocular exposure to staphylococcal enterotoxin B (SEB). Conjunctivitis with localized cutaneous swelling occurred in three persons within 1 to 6 hours after exposure to SEB; two of these persons also had gastrointestinal symptoms, which suggests that such symptoms occurred as a result of exposure by an indirect cutaneous or ocular route. Ocular exposures from SEB resulting in conjunctivitis and localized swelling have not previously been reported. Symptoms from these patients and review of clinical symptoms of 16 laboratory-acquired inhalational SEB intoxications may help healthcare workers evaluate and identify SEB exposures in laboratory personnel at risk.

EID Rusnak JM, Kortepeter MG, Ulrich R, Poli M, Boudreau E. Laboratory Exposures to Staphylococcal Enterotoxin B. Emerg Infect Dis. 2004;10(9):1544-1549. https://dx.doi.org/10.3201/eid1009.040250
AMA Rusnak JM, Kortepeter MG, Ulrich R, et al. Laboratory Exposures to Staphylococcal Enterotoxin B. Emerging Infectious Diseases. 2004;10(9):1544-1549. doi:10.3201/eid1009.040250.
APA Rusnak, J. M., Kortepeter, M. G., Ulrich, R., Poli, M., & Boudreau, E. (2004). Laboratory Exposures to Staphylococcal Enterotoxin B. Emerging Infectious Diseases, 10(9), 1544-1549. https://dx.doi.org/10.3201/eid1009.040250.
Research

Viral Loads in Clinical Specimens and SARS Manifestations [PDF - 195 KB - 8 pages]
I. Hung et al.

A retrospective viral load study was performed on clinical specimens from154 patients with laboratory-confirmed severe acute respiratory syndrome (SARS), prospectively collected during patients’ illness. Viral load in nasopharyngeal aspirates (n = 142) from day 10 to day 15 after onset of symptoms was associated with oxygen desaturation, mechanical ventilation, diarrhea, hepatic dysfunction, and death. Serum viral load (n = 53) was associated with oxygen desaturation, mechanical ventilation, and death. Stool viral load (n = 94) was associated with diarrhea, and urine viral load (n = 111) was associated with abnormal urinalysis results. Viral replications at different sites are important in the pathogenesis of clinical and laboratory abnormalities of SARS.

EID Hung I, Cheng V, Wu A, Tang B, Chan K, Chu C, et al. Viral Loads in Clinical Specimens and SARS Manifestations. Emerg Infect Dis. 2004;10(9):1550-1557. https://dx.doi.org/10.3201/eid1009.040058
AMA Hung I, Cheng V, Wu A, et al. Viral Loads in Clinical Specimens and SARS Manifestations. Emerging Infectious Diseases. 2004;10(9):1550-1557. doi:10.3201/eid1009.040058.
APA Hung, I., Cheng, V., Wu, A., Tang, B., Chan, K., Chu, C....Yuen, K. (2004). Viral Loads in Clinical Specimens and SARS Manifestations. Emerging Infectious Diseases, 10(9), 1550-1557. https://dx.doi.org/10.3201/eid1009.040058.

SARS Antibody Test for Serosurveillance [PDF - 100 KB - 5 pages]
P. Hsueh et al.

A peptide-based enzyme-linked immunosorbent assay (ELISA) can be used for retrospective serosurveillance of severe acute respiratory syndrome (SARS) by helping identify undetected chains of disease transmission. The assay was developed by epitope mapping, using synthetic peptides from the spike, membrane, and nucleocapsid protein sequences of SARS-associated coronavirus. The new peptide ELISA consistently detected seroconversion by week 2 of onset of fever, and seropositivity remained through day 100. Specificity was 100% on normal blood donor samples, on serum samples associated with infection by other pathogens, and on an interference panel. The peptide-based test has advantages of safety, standardization, and automation over previous immunoassays for SARS. The assay was used for a retrospective survey of healthy healthcare workers in Taiwan who treated SARS patients. Asymptomatic seroconversions were detected in two hospitals that had nosocomial disease.

EID Hsueh P, Kao C, Lee C, Chen L, Ho M, Sia C, et al. SARS Antibody Test for Serosurveillance. Emerg Infect Dis. 2004;10(9):1558-1562. https://dx.doi.org/10.3201/eid1009.040101
AMA Hsueh P, Kao C, Lee C, et al. SARS Antibody Test for Serosurveillance. Emerging Infectious Diseases. 2004;10(9):1558-1562. doi:10.3201/eid1009.040101.
APA Hsueh, P., Kao, C., Lee, C., Chen, L., Ho, M., Sia, C....Wang, C. Y. (2004). SARS Antibody Test for Serosurveillance. Emerging Infectious Diseases, 10(9), 1558-1562. https://dx.doi.org/10.3201/eid1009.040101.

Experimental Infection of Ground Squirrels (Spermophilus tridecemlineatus) with Monkeypox Virus [PDF - 294 KB - 5 pages]
R. B. Tesh et al.

A proposed new small-animal (rodent) model for studying the pathogenesis and treatment of severe orthopoxvirus infections is described. Thirteen-lined ground squirrels (Spermophilus tridecemlineatus) were infected intraperitoneally and intranasally with monkeypox virus (MPXV). A fulminant illness developed in all animals, and they died 6–9 days after infection. Virus was cultured from the blood and oropharynx several days before death; at necropsy, all of the organs tested contained relatively high titers of MPXV. The major pathologic findings were in the liver, which showed centrilobular necrosis, steatosis, and basophilic inclusion bodies in hepatocytes. Splenic necrosis was also observed, as well as interstitial inflammation in the lungs. The pathologic features of MPXV in ground squirrels is similar to that described with MPXV in macaques and severe variola (smallpox) virus infection in humans.

EID Tesh RB, Watts DM, Sbrana E, Siirin M, Popov VL, Xiao S. Experimental Infection of Ground Squirrels (Spermophilus tridecemlineatus) with Monkeypox Virus. Emerg Infect Dis. 2004;10(9):1563-1567. https://dx.doi.org/10.3201/eid1009.040310
AMA Tesh RB, Watts DM, Sbrana E, et al. Experimental Infection of Ground Squirrels (Spermophilus tridecemlineatus) with Monkeypox Virus. Emerging Infectious Diseases. 2004;10(9):1563-1567. doi:10.3201/eid1009.040310.
APA Tesh, R. B., Watts, D. M., Sbrana, E., Siirin, M., Popov, V. L., & Xiao, S. (2004). Experimental Infection of Ground Squirrels (Spermophilus tridecemlineatus) with Monkeypox Virus. Emerging Infectious Diseases, 10(9), 1563-1567. https://dx.doi.org/10.3201/eid1009.040310.

Silent Nucleotide Polymorphisms and a Phylogeny for Mycobacterium tuberculosis [PDF - 309 KB - 10 pages]
L. Baker et al.

Much remains unknown of the phylogeny and evolution of Mycobacterium tuberculosis, an organism that kills 2 million people annually. Using a population-based approach that analyzes multiple loci around the chromosome, we demonstrate that neutral genetic variation in genes associated with antimicrobial drug resistance has sufficient variation to construct a robust phylogenetic tree for M. tuberculosis. The data describe a clonal population with a minimum of four distinct M. tuberculosis lineages, closely related to M. bovis. The lineages are strongly geographically associated. Nucleotide substitutions proven to cause drug resistance are distributed throughout the tree, whereas nonsynonymous base substitutions unrelated to drug resistance have a restricted distribution. The phylogenetic structure is concordant with all the previously described genotypic and phenotypic groupings of M. tuberculosis strains and provides a unifying framework for both epidemiologic and evolutionary analysis of M. tuberculosis populations.

EID Baker L, Brown T, Maiden M, Drobniewski F. Silent Nucleotide Polymorphisms and a Phylogeny for Mycobacterium tuberculosis. Emerg Infect Dis. 2004;10(9):1568-1577. https://dx.doi.org/10.3201/eid1009.040046
AMA Baker L, Brown T, Maiden M, et al. Silent Nucleotide Polymorphisms and a Phylogeny for Mycobacterium tuberculosis. Emerging Infectious Diseases. 2004;10(9):1568-1577. doi:10.3201/eid1009.040046.
APA Baker, L., Brown, T., Maiden, M., & Drobniewski, F. (2004). Silent Nucleotide Polymorphisms and a Phylogeny for Mycobacterium tuberculosis. Emerging Infectious Diseases, 10(9), 1568-1577. https://dx.doi.org/10.3201/eid1009.040046.

Genetic Divergence and Dispersal of Yellow Fever Virus, Brazil [PDF - 349 KB - 7 pages]
P. Vasconcelos et al.

An analysis of 79 yellow fever virus (YFV) isolates collected from 1935 to 2001 in Brazil showed a single genotype (South America I) circulating in the country, with the exception of a single strain from Rondônia, which represented South America genotype II. Brazilian YFV strains have diverged into two clades; an older clade appears to have become extinct and another has become the dominant lineage in recent years. Pairwise nucleotide diversity between strains ranged from 0% to 7.4%, while amino acid divergence ranged from 0% to 4.6%. Phylogenetic analysis indicated traffic of virus variants through large geographic areas and suggested that migration of infected people may be an important mechanism of virus dispersal. Isolation of vaccine virus from a patient with a fatal case suggests that vaccine-related illness may have been misdiagnosed in the past.

EID Vasconcelos P, Bryant JE, Travassos da Rosa A, Tesh RB, Rodrigues SG, Barrett A. Genetic Divergence and Dispersal of Yellow Fever Virus, Brazil. Emerg Infect Dis. 2004;10(9):1578-1584. https://dx.doi.org/10.3201/eid1009.040197
AMA Vasconcelos P, Bryant JE, Travassos da Rosa A, et al. Genetic Divergence and Dispersal of Yellow Fever Virus, Brazil. Emerging Infectious Diseases. 2004;10(9):1578-1584. doi:10.3201/eid1009.040197.
APA Vasconcelos, P., Bryant, J. E., Travassos da Rosa, A., Tesh, R. B., Rodrigues, S. G., & Barrett, A. (2004). Genetic Divergence and Dispersal of Yellow Fever Virus, Brazil. Emerging Infectious Diseases, 10(9), 1578-1584. https://dx.doi.org/10.3201/eid1009.040197.

Rotavirus Serotype G9P[8] and Acute Gastroenteritis Outbreak in Children, Northern Australia [PDF - 168 KB - 8 pages]
C. D. Kirkwood et al.

During 2001, an outbreak of severe acute gastroenteritis swept through Central and northern Australia and caused serious disruption to health services. We tracked and characterized the rotavirus strain implicated in the outbreak. Comparison of the electropherotypes of outbreak samples suggested that one G9P[8] strain was likely responsible for the outbreak. Samples were obtained from geographically distinct regions of Australia where the epidemic had occurred. The outbreak strains showed identical nucleotide sequences in genes encoding three rotavirus proteins, VP7, VP8, and NSP4, but they were distinct from G9P[8] strains isolated in previous years. Several of the amino acid substitutions on the VP7 and NSP4 proteins were identified in regions known to influence function and may have contributed to the emergence and increased dominance of the outbreak strains. Rotavirus serotype surveillance should continue with methods capable of identifying new and emerging types.

EID Kirkwood CD, Bogdanovic-Sakran N, Barnes G, Bishop R. Rotavirus Serotype G9P[8] and Acute Gastroenteritis Outbreak in Children, Northern Australia. Emerg Infect Dis. 2004;10(9):1593-1600. https://dx.doi.org/10.3201/eid1009.040040
AMA Kirkwood CD, Bogdanovic-Sakran N, Barnes G, et al. Rotavirus Serotype G9P[8] and Acute Gastroenteritis Outbreak in Children, Northern Australia. Emerging Infectious Diseases. 2004;10(9):1593-1600. doi:10.3201/eid1009.040040.
APA Kirkwood, C. D., Bogdanovic-Sakran, N., Barnes, G., & Bishop, R. (2004). Rotavirus Serotype G9P[8] and Acute Gastroenteritis Outbreak in Children, Northern Australia. Emerging Infectious Diseases, 10(9), 1593-1600. https://dx.doi.org/10.3201/eid1009.040040.

Foodborne Botulism in the Republic of Georgia [PDF - 182 KB - 5 pages]
J. K. Varma et al.

Foodborne botulism is a potentially fatal, paralytic illness that can cause large outbreaks. A possible increase in botulism incidence during 2001 in Georgia prompted this study. We reviewed surveillance data and abstracted records of patients with botulism who were hospitalized from 1980 to 2002. During this period, 879 botulism cases were detected. The median annual incidence increased from 0.3 per 100,000 during 1980 to 1990 to 0.9 per 100,000 during 1991 to 2002. For 706 botulism patients hospitalized from 1980 to 2002, 80% of their cases were attributed to home-preserved vegetables. Surveillance evaluation verified that botulism incidence varied greatly by region. Georgia has the highest nationally reported rate of foodborne botulism in the world. A strategy addressing individual behaviors in the home is needed to improve food safety; developing this strategy requires a deeper understanding of why botulism has increased and varies by region.

EID Varma JK, Katsitadze G, Moiscrafishvili M, Zardiashvili T, Chokheli M, Tarkhashvili N, et al. Foodborne Botulism in the Republic of Georgia. Emerg Infect Dis. 2004;10(9):1601-1605. https://dx.doi.org/10.3201/eid1009.030806
AMA Varma JK, Katsitadze G, Moiscrafishvili M, et al. Foodborne Botulism in the Republic of Georgia. Emerging Infectious Diseases. 2004;10(9):1601-1605. doi:10.3201/eid1009.030806.
APA Varma, J. K., Katsitadze, G., Moiscrafishvili, M., Zardiashvili, T., Chokheli, M., Tarkhashvili, N....Sobel, J. (2004). Foodborne Botulism in the Republic of Georgia. Emerging Infectious Diseases, 10(9), 1601-1605. https://dx.doi.org/10.3201/eid1009.030806.

Foodborne Botulism in the United States, 1990–2000 [PDF - 67 KB - 6 pages]
J. Sobel et al.

Foodborne botulism, a potentially lethal neuroparalytic disease, is caused by ingesting preformed Clostridium botulinum neurotoxin. We reviewed surveillance data and reports from 1990 to 2000. Of 263 cases from 160 foodborne botulism events (episode of one or more related cases) in the United States, 103 (39%) cases and 58 events occurred in Alaska. Patients’ median age was 48 years; 154 (59%) were female; the case-fatality rate was 4%. The median number of cases per event was 1 (range 1–17). Toxin type A caused 51% of all cases; toxin type E caused 90% of Alaska cases. A particular food was implicated in 126 (79%) events. In the lower 49 states, a noncommercial food item was implicated in 70 (91%) events, most commonly, home-canned vegetables (44%). Two restaurant-associated outbreaks affected 25 persons. All Alaska cases were attributable to traditional Alaska Native foods. Botulism prevention efforts should be focused on those who preserve food at home, Alaska Natives, and restaurant workers.

EID Sobel J, Tucker N, Sulka A, McLaughlin J, Maslanka S. Foodborne Botulism in the United States, 1990–2000. Emerg Infect Dis. 2004;10(9):1606-1611. https://dx.doi.org/10.3201/eid1009.030745
AMA Sobel J, Tucker N, Sulka A, et al. Foodborne Botulism in the United States, 1990–2000. Emerging Infectious Diseases. 2004;10(9):1606-1611. doi:10.3201/eid1009.030745.
APA Sobel, J., Tucker, N., Sulka, A., McLaughlin, J., & Maslanka, S. (2004). Foodborne Botulism in the United States, 1990–2000. Emerging Infectious Diseases, 10(9), 1606-1611. https://dx.doi.org/10.3201/eid1009.030745.

Computer Algorithms To Detect Bloodstream Infections [PDF - 285 KB - 9 pages]
W. E. Trick et al.

We compared manual and computer-assisted bloodstream infection surveillance for adult inpatients at two hospitals. We identified hospital-acquired, primary, central-venous catheter (CVC)-associated bloodstream infections by using five methods: retrospective, manual record review by investigators; prospective, manual review by infection control professionals; positive blood culture plus manual CVC determination; computer algorithms; and computer algorithms and manual CVC determination. We calculated sensitivity, specificity, predictive values, plus the kappa statistic (κ) between investigator review and other methods, and we correlated infection rates for seven units. The κ value was 0.37 for infection control review, 0.48 for positive blood culture plus manual CVC determination, 0.49 for computer algorithm, and 0.73 for computer algorithm plus manual CVC determination. Unit-specific infection rates, per 1,000 patient days, were 1.0–12.5 by investigator review and 1.4–10.2 by computer algorithm (correlation r = 0.91, p = 0.004). Automated bloodstream infection surveillance with electronic data is an accurate alternative to surveillance with manually collected data.

EID Trick WE, Zagorski BM, Tokars JI, Vernon MO, Welbel SF, Wisniewski MF, et al. Computer Algorithms To Detect Bloodstream Infections. Emerg Infect Dis. 2004;10(9):1612-1620. https://dx.doi.org/10.3201/eid1009.030978
AMA Trick WE, Zagorski BM, Tokars JI, et al. Computer Algorithms To Detect Bloodstream Infections. Emerging Infectious Diseases. 2004;10(9):1612-1620. doi:10.3201/eid1009.030978.
APA Trick, W. E., Zagorski, B. M., Tokars, J. I., Vernon, M. O., Welbel, S. F., Wisniewski, M. F....Weinstein, R. A. (2004). Computer Algorithms To Detect Bloodstream Infections. Emerging Infectious Diseases, 10(9), 1612-1620. https://dx.doi.org/10.3201/eid1009.030978.

Space-Time Cluster Analysis of Invasive Meningococcal Disease [PDF - 98 KB - 6 pages]
C. J. Hoebe et al.

Clusters are recognized when meningococcal cases of the same phenotypic strain (markers: serogroup, serotype, and subtype) occur in spatial and temporal proximity. The incidence of such clusters was compared to the incidence that would be expected by chance by using space-time nearest-neighbor analysis of 4,887 confirmed invasive meningococcal cases identified in the 9-year surveillance period 1993–2001 in the Netherlands. Clustering beyond chance only occurred among the closest neighboring cases (comparable to secondary cases) and was small (3.1%, 95% confidence interval 2.1%–4.1%).

EID Hoebe CJ, de Melker HE, Spanjaard L, Dankert J, Nagelkerke N. Space-Time Cluster Analysis of Invasive Meningococcal Disease. Emerg Infect Dis. 2004;10(9):1621-1626. https://dx.doi.org/10.3201/eid1009.030992
AMA Hoebe CJ, de Melker HE, Spanjaard L, et al. Space-Time Cluster Analysis of Invasive Meningococcal Disease. Emerging Infectious Diseases. 2004;10(9):1621-1626. doi:10.3201/eid1009.030992.
APA Hoebe, C. J., de Melker, H. E., Spanjaard, L., Dankert, J., & Nagelkerke, N. (2004). Space-Time Cluster Analysis of Invasive Meningococcal Disease. Emerging Infectious Diseases, 10(9), 1621-1626. https://dx.doi.org/10.3201/eid1009.030992.

Methicillin-resistant Staphylococcus aureus in Europe, 1999–2002 [PDF - 158 KB - 8 pages]
E. W. Tiemersma et al.

We explored the variation in proportions of methicillin-resistant Staphylococcus aureus (MRSA) between and within countries participating in the European Antimicrobial Resistance Surveillance System and temporal trends in its occurrence. This system collects routine antimicrobial susceptibility tests for S. aureus. We examined data collected from January 1999 through December 2002 (50,759 isolates from 495 hospitals in 26 countries). MRSA prevalence varied almost 100-fold, from <1% in northern Europe to >40% in southern and western Europe. MRSA proportions significantly increased in Belgium, Germany, Ireland, the Netherlands, and the United Kingdom, and decreased in Slovenia. Within countries, MRSA proportions varied between hospitals with highest variance in countries with a prevalence of 5% to 20%. The observed trends should stimulate initiatives to control MRSA at national, regional, and hospital levels. The large differences between hospitals indicate that efforts may be most effective at regional and hospital levels.

EID Tiemersma EW, Bronzwaer SL, Lyytikäinen O, Degener JE, Schrijnemakers P, Bruinsma N, et al. Methicillin-resistant Staphylococcus aureus in Europe, 1999–2002. Emerg Infect Dis. 2004;10(9):1627-1634. https://dx.doi.org/10.3201/eid1009.040069
AMA Tiemersma EW, Bronzwaer SL, Lyytikäinen O, et al. Methicillin-resistant Staphylococcus aureus in Europe, 1999–2002. Emerging Infectious Diseases. 2004;10(9):1627-1634. doi:10.3201/eid1009.040069.
APA Tiemersma, E. W., Bronzwaer, S. L., Lyytikäinen, O., Degener, J. E., Schrijnemakers, P., Bruinsma, N....Grundmann, H. (2004). Methicillin-resistant Staphylococcus aureus in Europe, 1999–2002. Emerging Infectious Diseases, 10(9), 1627-1634. https://dx.doi.org/10.3201/eid1009.040069.

Outbreak of Hantavirus Pulmonary Syndrome, Los Santos, Panama, 1999–2000 [PDF - 118 KB - 8 pages]
V. Bayard et al.

An outbreak of hantavirus pulmonary syndrome occurred in the province of Los Santos, Panama, in late 1999 and early 2000. Eleven cases were identified; 9 were confirmed by serology. Three cases were fatal; however, no confirmed case-patient died. Case-neighborhood serologic surveys resulted in an overall hantavirus antibody prevalence of 13% among household and neighborhood members from the outbreak foci. Epidemiologic investigations did not suggest person-to-person transmission of hantavirus infection. By use of Sin Nombre virus antigen, hantavirus antibodies were detected in Oligoryzomys fulvescens and Zygodontomys brevicauda cherriei. This outbreak resulted in the first documented cases of human hantavirus infections in Central America.

EID Bayard V, Kitsutani PT, Barria EO, Ruedas LA, Tinnin DS, Muñoz C, et al. Outbreak of Hantavirus Pulmonary Syndrome, Los Santos, Panama, 1999–2000. Emerg Infect Dis. 2004;10(9):1635-1642. https://dx.doi.org/10.3201/eid1009.040143
AMA Bayard V, Kitsutani PT, Barria EO, et al. Outbreak of Hantavirus Pulmonary Syndrome, Los Santos, Panama, 1999–2000. Emerging Infectious Diseases. 2004;10(9):1635-1642. doi:10.3201/eid1009.040143.
APA Bayard, V., Kitsutani, P. T., Barria, E. O., Ruedas, L. A., Tinnin, D. S., Muñoz, C....Peters, C. J. (2004). Outbreak of Hantavirus Pulmonary Syndrome, Los Santos, Panama, 1999–2000. Emerging Infectious Diseases, 10(9), 1635-1642. https://dx.doi.org/10.3201/eid1009.040143.

Detection of Anaplasma phagocytophilum DNA in Ixodes Ticks (Acari: Ixodidae) from Madeira Island and Setúbal District, Mainland Portugal [PDF - 203 KB - 6 pages]
A. S. Santos et al.

A total of 278 Ixodes ticks, collected from Madeira Island and Setúbal District, mainland Portugal, were examined by polymerase chain reaction (PCR) for the presence of Anaplasma phagocytophilum. Six (4%) of 142 Ixodes ricinus nymphs collected in Madeira Island, and 1 nymph and 1 male (2%) of 93 I. ventalloi collected in Setúbal District tested positive for A. phagocytophilum msp2 genes or rrs. Infection was not detected among 43 I. ricinus on mainland Portugal. All PCR products were confirmed by nucleotide sequencing to be identical or to be most closely related to A. phagocytophilum. To our knowledge, this is the first evidence of A. phagocytophilum in ticks from Setúbal District, mainland Portugal, and the first documentation of Anaplasma infection in I. ventalloi. Moreover, these findings confirm the persistence of A. phagocytophilum in Madeira Island’s I. ricinus.

EID Santos AS, Santos-Silva MM, Almeida VC, Bacellar F, Dumler JS. Detection of Anaplasma phagocytophilum DNA in Ixodes Ticks (Acari: Ixodidae) from Madeira Island and Setúbal District, Mainland Portugal. Emerg Infect Dis. 2004;10(9):1643-1648. https://dx.doi.org/10.3201/eid1009.040276
AMA Santos AS, Santos-Silva MM, Almeida VC, et al. Detection of Anaplasma phagocytophilum DNA in Ixodes Ticks (Acari: Ixodidae) from Madeira Island and Setúbal District, Mainland Portugal. Emerging Infectious Diseases. 2004;10(9):1643-1648. doi:10.3201/eid1009.040276.
APA Santos, A. S., Santos-Silva, M. M., Almeida, V. C., Bacellar, F., & Dumler, J. S. (2004). Detection of Anaplasma phagocytophilum DNA in Ixodes Ticks (Acari: Ixodidae) from Madeira Island and Setúbal District, Mainland Portugal. Emerging Infectious Diseases, 10(9), 1643-1648. https://dx.doi.org/10.3201/eid1009.040276.

Genotyping, Orientalis-like Yersinia pestis, and Plague Pandemics [PDF - 176 KB - 8 pages]
M. Drancourt et al.

Three pandemics have been attributed to plague in the last 1,500 years. Yersinia pestis caused the third, and its DNA was found in human remains from the second. The Antiqua biovar of Y. pestis may have caused the first pandemic; the other two biovars, Medievalis and Orientalis, may have caused the second and third pandemics, respectively. To test this hypothesis, we designed an original genotyping system based on intergenic spacer sequencing called multiple spacer typing (MST). We found that MST differentiated every biovar in a collection of 36 Y. pestis isolates representative of the three biovars. When MST was applied to dental pulp collected from remains of eight persons who likely died in the first and second pandemics, this system identified original sequences that matched those of Y. pestis Orientalis. These data indicate that Y. pestis caused cases of Justinian plague. The two historical plague pandemics were likely caused by Orientalis-like strains.

EID Drancourt M, Roux V, Dang L, Tran-Hung L, Castex D, Chenal-Francisque V, et al. Genotyping, Orientalis-like Yersinia pestis, and Plague Pandemics. Emerg Infect Dis. 2004;10(9):1585-1592. https://dx.doi.org/10.3201/eid1009.030933
AMA Drancourt M, Roux V, Dang L, et al. Genotyping, Orientalis-like Yersinia pestis, and Plague Pandemics. Emerging Infectious Diseases. 2004;10(9):1585-1592. doi:10.3201/eid1009.030933.
APA Drancourt, M., Roux, V., Dang, L., Tran-Hung, L., Castex, D., Chenal-Francisque, V....Raoult, D. (2004). Genotyping, Orientalis-like Yersinia pestis, and Plague Pandemics. Emerging Infectious Diseases, 10(9), 1585-1592. https://dx.doi.org/10.3201/eid1009.030933.
Dispatches

Year-round West Nile Virus Activity, Gulf Coast Region, Texas and Louisiana [PDF - 99 KB - 4 pages]
R. B. Tesh et al.

West Nile virus (WNV) was detected in 11 dead birds and two mosquito pools collected in east Texas and southern Louisiana during surveillance studies in the winter of 2003 to 2004. These findings suggest that WNV is active throughout the year in this region of the United States.

EID Tesh RB, Parsons R, Siirin M, Randle Y, Sargent C, Guzman H, et al. Year-round West Nile Virus Activity, Gulf Coast Region, Texas and Louisiana. Emerg Infect Dis. 2004;10(9):1649-1652. https://dx.doi.org/10.3201/eid1009.040203
AMA Tesh RB, Parsons R, Siirin M, et al. Year-round West Nile Virus Activity, Gulf Coast Region, Texas and Louisiana. Emerging Infectious Diseases. 2004;10(9):1649-1652. doi:10.3201/eid1009.040203.
APA Tesh, R. B., Parsons, R., Siirin, M., Randle, Y., Sargent, C., Guzman, H....Zerinque, B. (2004). Year-round West Nile Virus Activity, Gulf Coast Region, Texas and Louisiana. Emerging Infectious Diseases, 10(9), 1649-1652. https://dx.doi.org/10.3201/eid1009.040203.

SARS-CoV Antibody Prevalence in All Hong Kong Patient Contacts [PDF - 139 KB - 4 pages]
G. M. Leung et al.

A total of 1,068 asymptomatic close contacts of patients with severe acute respiratory (SARS) from the 2003 epidemic in Hong Kong were serologically tested, and 2 (0.19%) were positive for SARS coronavirus immunoglobulin G antibody. SARS rarely manifests as a subclinical infection, and at present, wild animal species are the only important natural reservoirs of the virus.

EID Leung GM, Chung P, Tsang T, Lim W, Chan SK, Chau P, et al. SARS-CoV Antibody Prevalence in All Hong Kong Patient Contacts. Emerg Infect Dis. 2004;10(9):1653-1656. https://dx.doi.org/10.3201/eid1009.040155
AMA Leung GM, Chung P, Tsang T, et al. SARS-CoV Antibody Prevalence in All Hong Kong Patient Contacts. Emerging Infectious Diseases. 2004;10(9):1653-1656. doi:10.3201/eid1009.040155.
APA Leung, G. M., Chung, P., Tsang, T., Lim, W., Chan, S. K., Chau, P....Hedley, A. J. (2004). SARS-CoV Antibody Prevalence in All Hong Kong Patient Contacts. Emerging Infectious Diseases, 10(9), 1653-1656. https://dx.doi.org/10.3201/eid1009.040155.

Yellow Fever Virus Infectivity for Bolivian Aedes aegypti Mosquitoes [PDF - 148 KB - 4 pages]
J. Mutebi et al.

The absence of urban yellow fever virus (YFV) in Bolivian cities has been attributed to the lack of competent urban mosquito vectors. Experiments with Aedes aegypti from Santa Cruz, Bolivia, demonstrated infection (100%), dissemination (20%), and transmission of a Bolivian YVF strain (CENETROP-322).

EID Mutebi J, Gianella A, Travassos da Rosa A, Tesh RB, Barrett AD, Higgs S. Yellow Fever Virus Infectivity for Bolivian Aedes aegypti Mosquitoes. Emerg Infect Dis. 2004;10(9):1657-1660. https://dx.doi.org/10.3201/eid1009.031124
AMA Mutebi J, Gianella A, Travassos da Rosa A, et al. Yellow Fever Virus Infectivity for Bolivian Aedes aegypti Mosquitoes. Emerging Infectious Diseases. 2004;10(9):1657-1660. doi:10.3201/eid1009.031124.
APA Mutebi, J., Gianella, A., Travassos da Rosa, A., Tesh, R. B., Barrett, A. D., & Higgs, S. (2004). Yellow Fever Virus Infectivity for Bolivian Aedes aegypti Mosquitoes. Emerging Infectious Diseases, 10(9), 1657-1660. https://dx.doi.org/10.3201/eid1009.031124.

Typing of Borrelia Relapsing Fever Group Strains [PDF - 110 KB - 4 pages]
J. Bunikis et al.

Partial sequencing of the 16S-23S rDNA intergenic spacer showed two to four genotypes each for Borrelia hermsii and B. turicatae, both relapsing fever agents transmitted by argasid ticks, and for B. miyamotoi and B. lonestari, transmitted by ixodid ticks. Field surveys of Ixodes ticks in Connecticut and Sweden showed limited local diversity for B. miyamotoi.

EID Bunikis J, Tsao JI, Garpmo U, Berglund J, Fish D, Barbour AG. Typing of Borrelia Relapsing Fever Group Strains. Emerg Infect Dis. 2004;10(9):1661-1664. https://dx.doi.org/10.3201/eid1009.040236
AMA Bunikis J, Tsao JI, Garpmo U, et al. Typing of Borrelia Relapsing Fever Group Strains. Emerging Infectious Diseases. 2004;10(9):1661-1664. doi:10.3201/eid1009.040236.
APA Bunikis, J., Tsao, J. I., Garpmo, U., Berglund, J., Fish, D., & Barbour, A. G. (2004). Typing of Borrelia Relapsing Fever Group Strains. Emerging Infectious Diseases, 10(9), 1661-1664. https://dx.doi.org/10.3201/eid1009.040236.

Salmonella enterica Serotype Uganda Infection in New York City and Chicago [PDF - 94 KB - 3 pages]
R. C. Jones et al.

Outbreaks associated with distinct strains of Salmonella enterica serotype Uganda, a rare serotype, occurred in New York City and Chicago during the summer of 2001. Both outbreaks were linked to eating ready-to-eat pork products. This serotype may emerge as a more frequent cause of human infections.

EID Jones RC, Reddy V, Kornstein L, Fernandez JR, Stavinsky F, Agasan A, et al. Salmonella enterica Serotype Uganda Infection in New York City and Chicago. Emerg Infect Dis. 2004;10(9):1665-1667. https://dx.doi.org/10.3201/eid1009.030713
AMA Jones RC, Reddy V, Kornstein L, et al. Salmonella enterica Serotype Uganda Infection in New York City and Chicago. Emerging Infectious Diseases. 2004;10(9):1665-1667. doi:10.3201/eid1009.030713.
APA Jones, R. C., Reddy, V., Kornstein, L., Fernandez, J. R., Stavinsky, F., Agasan, A....Gerber, S. I. (2004). Salmonella enterica Serotype Uganda Infection in New York City and Chicago. Emerging Infectious Diseases, 10(9), 1665-1667. https://dx.doi.org/10.3201/eid1009.030713.

Yellow Fever Outbreak, Southern Sudan, 2003 [PDF - 75 KB - 3 pages]
C. O. Onyango et al.

In May 2003, an outbreak of fatal hemorrhagic fever, caused by yellow fever virus, occurred in southern Sudan. Phylogenetic analysis showed that the virus belonged to the East African genotype, which supports the contention that yellow fever is endemic in East Africa with the potential to cause large outbreaks in humans.

EID Onyango CO, Grobbelaar AA, Gibson GV, Sang RC, Sow A, Swanepoel R, et al. Yellow Fever Outbreak, Southern Sudan, 2003. Emerg Infect Dis. 2004;10(9):1668-1670. https://dx.doi.org/10.3201/eid1009.030727
AMA Onyango CO, Grobbelaar AA, Gibson GV, et al. Yellow Fever Outbreak, Southern Sudan, 2003. Emerging Infectious Diseases. 2004;10(9):1668-1670. doi:10.3201/eid1009.030727.
APA Onyango, C. O., Grobbelaar, A. A., Gibson, G. V., Sang, R. C., Sow, A., Swanepoel, R....Burt, F. J. (2004). Yellow Fever Outbreak, Southern Sudan, 2003. Emerging Infectious Diseases, 10(9), 1668-1670. https://dx.doi.org/10.3201/eid1009.030727.

Acinetobacter baumannii in Human Body Louse [PDF - 99 KB - 3 pages]
B. La Scola and D. Raoult

While we were isolating Bartonella quintana from body lice, 40 Acinetobacter baumannii strains were also isolated and genotyped. One clone was unique and the other was ampicillin susceptible. A. baumannii DNA was later detected in 21% of 622 lice collected worldwide. These findings show an A. baumannii epidemic in human body lice.

EID La Scola B, Raoult D. Acinetobacter baumannii in Human Body Louse. Emerg Infect Dis. 2004;10(9):1671-1673. https://dx.doi.org/10.3201/eid1009.040242
AMA La Scola B, Raoult D. Acinetobacter baumannii in Human Body Louse. Emerging Infectious Diseases. 2004;10(9):1671-1673. doi:10.3201/eid1009.040242.
APA La Scola, B., & Raoult, D. (2004). Acinetobacter baumannii in Human Body Louse. Emerging Infectious Diseases, 10(9), 1671-1673. https://dx.doi.org/10.3201/eid1009.040242.

Fluoroquinolone Resistance in Salmonella enterica Serotype Choleraesuis, Taiwan, 2000–2003 [PDF - 119 KB - 3 pages]
C. Chiu et al.

Salmonella enterica serotype Choleraesuis is a highly invasive pathogen that infects humans and causes systemic infections that require antimicrobial therapy. Surveillance in Taiwan showed that fluoroquinolone resistance in S. Choleraesuis markedly increased from 2000 to 2003, reaching approximately 70% in 2003.

EID Chiu C, Wu T, Su L, Liu J, Chu C. Fluoroquinolone Resistance in Salmonella enterica Serotype Choleraesuis, Taiwan, 2000–2003. Emerg Infect Dis. 2004;10(9):1674-1676. https://dx.doi.org/10.3201/eid1009.030596
AMA Chiu C, Wu T, Su L, et al. Fluoroquinolone Resistance in Salmonella enterica Serotype Choleraesuis, Taiwan, 2000–2003. Emerging Infectious Diseases. 2004;10(9):1674-1676. doi:10.3201/eid1009.030596.
APA Chiu, C., Wu, T., Su, L., Liu, J., & Chu, C. (2004). Fluoroquinolone Resistance in Salmonella enterica Serotype Choleraesuis, Taiwan, 2000–2003. Emerging Infectious Diseases, 10(9), 1674-1676. https://dx.doi.org/10.3201/eid1009.030596.

Barriers to Creutzfeldt-Jakob Disease Autopsies, California [PDF - 160 KB - 4 pages]
J. K. Louie et al.

Creutzfeldt-Jakob disease (CJD) surveillance relies on autopsy and neuropathologic evaluation. The 1990–2000 CJD autopsy rate in California was 21%. Most neurologists were comfortable diagnosing CJD (83%), but few pathologists felt comfortable diagnosing CJD (35%) or performing autopsy (29%). Addressing obstacles to autopsy is necessary to improve CJD surveillance.

EID Louie JK, Gavali SS, Belay ED, Trevejo R, Hammond LH, Schonberger LB, et al. Barriers to Creutzfeldt-Jakob Disease Autopsies, California. Emerg Infect Dis. 2004;10(9):1677-1680. https://dx.doi.org/10.3201/eid1009.040066
AMA Louie JK, Gavali SS, Belay ED, et al. Barriers to Creutzfeldt-Jakob Disease Autopsies, California. Emerging Infectious Diseases. 2004;10(9):1677-1680. doi:10.3201/eid1009.040066.
APA Louie, J. K., Gavali, S. S., Belay, E. D., Trevejo, R., Hammond, L. H., Schonberger, L. B....Vugia, D. J. (2004). Barriers to Creutzfeldt-Jakob Disease Autopsies, California. Emerging Infectious Diseases, 10(9), 1677-1680. https://dx.doi.org/10.3201/eid1009.040066.

Leishmaniasis in Refugee and Local Pakistani Populations [PDF - 95 KB - 4 pages]
S. Brooker et al.

The epidemiology of anthroponotic cutaneous leishmaniasis was investigated in northwest Pakistan. Results suggested similar patterns of endemicity in both Afghan refugee and Pakistani populations and highlighted risk factors and household clustering of disease.

EID Brooker S, Mohammed N, Adil K, Agha S, Reithinger R, Rowland M, et al. Leishmaniasis in Refugee and Local Pakistani Populations. Emerg Infect Dis. 2004;10(9):1681-1684. https://dx.doi.org/10.3201/eid1009.040179
AMA Brooker S, Mohammed N, Adil K, et al. Leishmaniasis in Refugee and Local Pakistani Populations. Emerging Infectious Diseases. 2004;10(9):1681-1684. doi:10.3201/eid1009.040179.
APA Brooker, S., Mohammed, N., Adil, K., Agha, S., Reithinger, R., Rowland, M....Kolaczinski, J. (2004). Leishmaniasis in Refugee and Local Pakistani Populations. Emerging Infectious Diseases, 10(9), 1681-1684. https://dx.doi.org/10.3201/eid1009.040179.

Botulism Type E Outbreak Associated with Eating a Beached Whale, Alaska [PDF - 626 KB - 3 pages]
J. B. Mclaughlin et al.

We report an outbreak of botulism that occurred in July 2002 in a group of 12 Alaskan Yu’pik Eskimos who ate blubber and skin from a beached beluga whale. Botulism death rates among Alaska Natives have declined in the last 20 years, yet incidence has increased.

EID Mclaughlin JB, Sobel J, Lynn T, Funk E, Middaugh JP. Botulism Type E Outbreak Associated with Eating a Beached Whale, Alaska. Emerg Infect Dis. 2004;10(9):1685-1687. https://dx.doi.org/10.3201/eid1009.040131
AMA Mclaughlin JB, Sobel J, Lynn T, et al. Botulism Type E Outbreak Associated with Eating a Beached Whale, Alaska. Emerging Infectious Diseases. 2004;10(9):1685-1687. doi:10.3201/eid1009.040131.
APA Mclaughlin, J. B., Sobel, J., Lynn, T., Funk, E., & Middaugh, J. P. (2004). Botulism Type E Outbreak Associated with Eating a Beached Whale, Alaska. Emerging Infectious Diseases, 10(9), 1685-1687. https://dx.doi.org/10.3201/eid1009.040131.
Letters

Toronto Emergency Medical Services and SARS [PDF - 23 KB - 2 pages]
A. Silverman et al.
EID Silverman A, Simor A, Loutfy MR. Toronto Emergency Medical Services and SARS. Emerg Infect Dis. 2004;10(9):1688-1689. https://dx.doi.org/10.3201/eid1009.040170
AMA Silverman A, Simor A, Loutfy MR. Toronto Emergency Medical Services and SARS. Emerging Infectious Diseases. 2004;10(9):1688-1689. doi:10.3201/eid1009.040170.
APA Silverman, A., Simor, A., & Loutfy, M. R. (2004). Toronto Emergency Medical Services and SARS. Emerging Infectious Diseases, 10(9), 1688-1689. https://dx.doi.org/10.3201/eid1009.040170.

SARS during Pregnancy, United States [PDF - 22 KB - 2 pages]
L. A. Stockman et al.
EID Stockman LA, Lowther SA, Coy K, Saw J, Parashar UD. SARS during Pregnancy, United States. Emerg Infect Dis. 2004;10(9):1689-1690. https://dx.doi.org/10.3201/eid1009.040244
AMA Stockman LA, Lowther SA, Coy K, et al. SARS during Pregnancy, United States. Emerging Infectious Diseases. 2004;10(9):1689-1690. doi:10.3201/eid1009.040244.
APA Stockman, L. A., Lowther, S. A., Coy, K., Saw, J., & Parashar, U. D. (2004). SARS during Pregnancy, United States. Emerging Infectious Diseases, 10(9), 1689-1690. https://dx.doi.org/10.3201/eid1009.040244.

Eosinophilic Pleural Effusion in Gnathostomiasis [PDF - 25 KB - 2 pages]
P. Parola et al.
EID Parola P, Bordmann G, Brouqui P, Delmont J. Eosinophilic Pleural Effusion in Gnathostomiasis. Emerg Infect Dis. 2004;10(9):1690-1691. https://dx.doi.org/10.3201/eid1009.030671
AMA Parola P, Bordmann G, Brouqui P, et al. Eosinophilic Pleural Effusion in Gnathostomiasis. Emerging Infectious Diseases. 2004;10(9):1690-1691. doi:10.3201/eid1009.030671.
APA Parola, P., Bordmann, G., Brouqui, P., & Delmont, J. (2004). Eosinophilic Pleural Effusion in Gnathostomiasis. Emerging Infectious Diseases, 10(9), 1690-1691. https://dx.doi.org/10.3201/eid1009.030671.

Methicillin-resistant Staphylococcus aureus, Pakistan, 1996–2003 [PDF - 25 KB - 2 pages]
T. Butt et al.
EID Butt T, Ahmad RN, Usman M, Mahmood A. Methicillin-resistant Staphylococcus aureus, Pakistan, 1996–2003. Emerg Infect Dis. 2004;10(9):1691-1692. https://dx.doi.org/10.3201/eid1009.030844
AMA Butt T, Ahmad RN, Usman M, et al. Methicillin-resistant Staphylococcus aureus, Pakistan, 1996–2003. Emerging Infectious Diseases. 2004;10(9):1691-1692. doi:10.3201/eid1009.030844.
APA Butt, T., Ahmad, R. N., Usman, M., & Mahmood, A. (2004). Methicillin-resistant Staphylococcus aureus, Pakistan, 1996–2003. Emerging Infectious Diseases, 10(9), 1691-1692. https://dx.doi.org/10.3201/eid1009.030844.

Borrelia valaisiana in Cerebrospinal Fluid [PDF - 24 KB - 2 pages]
E. Diza et al.
EID Diza E, Papa A, Vezyri E, Tsounis S, Milonas I, Antoniadis A. Borrelia valaisiana in Cerebrospinal Fluid. Emerg Infect Dis. 2004;10(9):1692-1693. https://dx.doi.org/10.3201/eid1009.030439
AMA Diza E, Papa A, Vezyri E, et al. Borrelia valaisiana in Cerebrospinal Fluid. Emerging Infectious Diseases. 2004;10(9):1692-1693. doi:10.3201/eid1009.030439.
APA Diza, E., Papa, A., Vezyri, E., Tsounis, S., Milonas, I., & Antoniadis, A. (2004). Borrelia valaisiana in Cerebrospinal Fluid. Emerging Infectious Diseases, 10(9), 1692-1693. https://dx.doi.org/10.3201/eid1009.030439.

Baylisascaris procyonis in California [PDF - 26 KB - 2 pages]
L. Moore et al.
EID Moore L, Ash L, Sorvillo FJ, Berlin O. Baylisascaris procyonis in California. Emerg Infect Dis. 2004;10(9):1693-1694. https://dx.doi.org/10.3201/eid1009.040034
AMA Moore L, Ash L, Sorvillo FJ, et al. Baylisascaris procyonis in California. Emerging Infectious Diseases. 2004;10(9):1693-1694. doi:10.3201/eid1009.040034.
APA Moore, L., Ash, L., Sorvillo, F. J., & Berlin, O. (2004). Baylisascaris procyonis in California. Emerging Infectious Diseases, 10(9), 1693-1694. https://dx.doi.org/10.3201/eid1009.040034.

Streptococcus iniae Discitis in Singapore [PDF - 54 KB - 3 pages]
T. H. Koh et al.
EID Koh TH, Kurup A, Chen J. Streptococcus iniae Discitis in Singapore. Emerg Infect Dis. 2004;10(9):1694-1696. https://dx.doi.org/10.3201/eid1009.040029
AMA Koh TH, Kurup A, Chen J. Streptococcus iniae Discitis in Singapore. Emerging Infectious Diseases. 2004;10(9):1694-1696. doi:10.3201/eid1009.040029.
APA Koh, T. H., Kurup, A., & Chen, J. (2004). Streptococcus iniae Discitis in Singapore. Emerging Infectious Diseases, 10(9), 1694-1696. https://dx.doi.org/10.3201/eid1009.040029.

Rubella Epidemic Strain, Greece, 1999 [PDF - 25 KB - 2 pages]
A. Papa et al.
EID Papa A, Gioula G, Antoniadis A, Kyriazopoulou-Dalaina V. Rubella Epidemic Strain, Greece, 1999. Emerg Infect Dis. 2004;10(9):1696-1697. https://dx.doi.org/10.3201/eid1009.040117
AMA Papa A, Gioula G, Antoniadis A, et al. Rubella Epidemic Strain, Greece, 1999. Emerging Infectious Diseases. 2004;10(9):1696-1697. doi:10.3201/eid1009.040117.
APA Papa, A., Gioula, G., Antoniadis, A., & Kyriazopoulou-Dalaina, V. (2004). Rubella Epidemic Strain, Greece, 1999. Emerging Infectious Diseases, 10(9), 1696-1697. https://dx.doi.org/10.3201/eid1009.040117.

CTX-M β-Lactamase-producing Escherichia coli in Long-term Care Facilities, France [PDF - 26 KB - 2 pages]
N. Kassis-Chikhani et al.
EID Kassis-Chikhani N, Vimont S, Asselat K, Trivalle C, Minassian B, Sengelin C, et al. CTX-M β-Lactamase-producing Escherichia coli in Long-term Care Facilities, France. Emerg Infect Dis. 2004;10(9):1697-1698. https://dx.doi.org/10.3201/eid1009.030969
AMA Kassis-Chikhani N, Vimont S, Asselat K, et al. CTX-M β-Lactamase-producing Escherichia coli in Long-term Care Facilities, France. Emerging Infectious Diseases. 2004;10(9):1697-1698. doi:10.3201/eid1009.030969.
APA Kassis-Chikhani, N., Vimont, S., Asselat, K., Trivalle, C., Minassian, B., Sengelin, C....Arlet, G. (2004). CTX-M β-Lactamase-producing Escherichia coli in Long-term Care Facilities, France. Emerging Infectious Diseases, 10(9), 1697-1698. https://dx.doi.org/10.3201/eid1009.030969.

Do Antiborrelial Antibodies Suggest Lyme Disease in Cuba? [PDF - 30 KB - 3 pages]
I. Rodríguez et al.
EID Rodríguez I, Fernández C, Cinco M, Pedroso R, Fuentes O. Do Antiborrelial Antibodies Suggest Lyme Disease in Cuba?. Emerg Infect Dis. 2004;10(9):1698-1700. https://dx.doi.org/10.3201/eid1009.031048
AMA Rodríguez I, Fernández C, Cinco M, et al. Do Antiborrelial Antibodies Suggest Lyme Disease in Cuba?. Emerging Infectious Diseases. 2004;10(9):1698-1700. doi:10.3201/eid1009.031048.
APA Rodríguez, I., Fernández, C., Cinco, M., Pedroso, R., & Fuentes, O. (2004). Do Antiborrelial Antibodies Suggest Lyme Disease in Cuba?. Emerging Infectious Diseases, 10(9), 1698-1700. https://dx.doi.org/10.3201/eid1009.031048.

Human Herpesvirus 6 Encephalomyelitis [PDF - 49 KB - 3 pages]
J. L. Soto-Hernandez et al.
EID Soto-Hernandez JL, Denes E, Ranger-Rogez S. Human Herpesvirus 6 Encephalomyelitis. Emerg Infect Dis. 2004;10(9):1700-1702. https://dx.doi.org/10.3201/eid1009.040365
AMA Soto-Hernandez JL, Denes E, Ranger-Rogez S. Human Herpesvirus 6 Encephalomyelitis. Emerging Infectious Diseases. 2004;10(9):1700-1702. doi:10.3201/eid1009.040365.
APA Soto-Hernandez, J. L., Denes, E., & Ranger-Rogez, S. (2004). Human Herpesvirus 6 Encephalomyelitis. Emerging Infectious Diseases, 10(9), 1700-1702. https://dx.doi.org/10.3201/eid1009.040365.

Vancomycin Heteroresistance in Methicillin-resistant Staphylococcus aureus, Taiwan [PDF - 51 KB - 3 pages]
J. Wang et al.
EID Wang J, Tseng S, Hsueh P, Hiramatsu K. Vancomycin Heteroresistance in Methicillin-resistant Staphylococcus aureus, Taiwan. Emerg Infect Dis. 2004;10(9):1702-1704. https://dx.doi.org/10.3201/eid1009.040239
AMA Wang J, Tseng S, Hsueh P, et al. Vancomycin Heteroresistance in Methicillin-resistant Staphylococcus aureus, Taiwan. Emerging Infectious Diseases. 2004;10(9):1702-1704. doi:10.3201/eid1009.040239.
APA Wang, J., Tseng, S., Hsueh, P., & Hiramatsu, K. (2004). Vancomycin Heteroresistance in Methicillin-resistant Staphylococcus aureus, Taiwan. Emerging Infectious Diseases, 10(9), 1702-1704. https://dx.doi.org/10.3201/eid1009.040239.
Books and Media

A Clinician’s Dictionary of Pathogenic Microorganisms [PDF - 48 KB - 1 page]
D. Raoult
EID Raoult D. A Clinician’s Dictionary of Pathogenic Microorganisms. Emerg Infect Dis. 2004;10(9):1705. https://dx.doi.org/10.3201/eid1009.040540
AMA Raoult D. A Clinician’s Dictionary of Pathogenic Microorganisms. Emerging Infectious Diseases. 2004;10(9):1705. doi:10.3201/eid1009.040540.
APA Raoult, D. (2004). A Clinician’s Dictionary of Pathogenic Microorganisms. Emerging Infectious Diseases, 10(9), 1705. https://dx.doi.org/10.3201/eid1009.040540.

Cryptosporidium: From Molecules to Disease
T. J. Wade
EID Wade TJ. Cryptosporidium: From Molecules to Disease. Emerg Infect Dis. 2004;10(9):1705-1706. https://dx.doi.org/10.3201/eid1009.040566
AMA Wade TJ. Cryptosporidium: From Molecules to Disease. Emerging Infectious Diseases. 2004;10(9):1705-1706. doi:10.3201/eid1009.040566.
APA Wade, T. J. (2004). Cryptosporidium: From Molecules to Disease. Emerging Infectious Diseases, 10(9), 1705-1706. https://dx.doi.org/10.3201/eid1009.040566.
About the Cover

Measurable Indicators and Public Health [PDF - 116 KB - 2 pages]
P. Potter
EID Potter P. Measurable Indicators and Public Health. Emerg Infect Dis. 2004;10(9):1709-1710. https://dx.doi.org/10.3201/eid1009.ac1009
AMA Potter P. Measurable Indicators and Public Health. Emerging Infectious Diseases. 2004;10(9):1709-1710. doi:10.3201/eid1009.ac1009.
APA Potter, P. (2004). Measurable Indicators and Public Health. Emerging Infectious Diseases, 10(9), 1709-1710. https://dx.doi.org/10.3201/eid1009.ac1009.
Conference Summaries

Transnational Issues in Quarantine [PDF - 15 KB - 1 page]
C. DiGiovanni et al.
EID DiGiovanni C, Conley J, Hamon D, Pimsler M. Transnational Issues in Quarantine. Emerg Infect Dis. 2004;10(9):1707. https://dx.doi.org/10.3201/eid1009.040281
AMA DiGiovanni C, Conley J, Hamon D, et al. Transnational Issues in Quarantine. Emerging Infectious Diseases. 2004;10(9):1707. doi:10.3201/eid1009.040281.
APA DiGiovanni, C., Conley, J., Hamon, D., & Pimsler, M. (2004). Transnational Issues in Quarantine. Emerging Infectious Diseases, 10(9), 1707. https://dx.doi.org/10.3201/eid1009.040281.
Corrections

Correction, Vol. 10, No. 7 [PDF - 14 KB - 1 page]
EID Correction, Vol. 10, No. 7. Emerg Infect Dis. 2004;10(9):1708. https://dx.doi.org/10.3201/eid1009.c11009
AMA Correction, Vol. 10, No. 7. Emerging Infectious Diseases. 2004;10(9):1708. doi:10.3201/eid1009.c11009.
APA (2004). Correction, Vol. 10, No. 7. Emerging Infectious Diseases, 10(9), 1708. https://dx.doi.org/10.3201/eid1009.c11009.

Correction, Vol. 10, No. 8 [PDF - 14 KB - 1 page]
EID Correction, Vol. 10, No. 8. Emerg Infect Dis. 2004;10(9):1708. https://dx.doi.org/10.3201/eid1009.c21009
AMA Correction, Vol. 10, No. 8. Emerging Infectious Diseases. 2004;10(9):1708. doi:10.3201/eid1009.c21009.
APA (2004). Correction, Vol. 10, No. 8. Emerging Infectious Diseases, 10(9), 1708. https://dx.doi.org/10.3201/eid1009.c21009.
News and Notes

Ethics and Epidemics
R. Baker et al.
EID Baker R, Shelton W, Strosberg M. Ethics and Epidemics. Emerg Infect Dis. 2004;10(9):1707-1708. https://dx.doi.org/10.3201/eid1009.040407
AMA Baker R, Shelton W, Strosberg M. Ethics and Epidemics. Emerging Infectious Diseases. 2004;10(9):1707-1708. doi:10.3201/eid1009.040407.
APA Baker, R., Shelton, W., & Strosberg, M. (2004). Ethics and Epidemics. Emerging Infectious Diseases, 10(9), 1707-1708. https://dx.doi.org/10.3201/eid1009.040407.
Page created: March 03, 2014
Page updated: March 03, 2014
Page reviewed: March 03, 2014
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
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