Perspective
Economics of Preventing Hospital Infection
The economics of preventing hospital-acquired infections is most often described in general terms. The underlying concepts and mechanisms are rarely made explicit but should be understood for research and policy-making. We define the key economic concepts and specify an illustrative model that uses hypothetical data to identify how two related questions might be addressed: 1) how much should be invested for infection control, and 2) what are the most appropriate infection-control programs? We aim to make explicit the economics of preventing hospital-acquired infections.
EID | Graves N. Economics of Preventing Hospital Infection. Emerg Infect Dis. 2004;10(4):561-566. https://doi.org/10.3201/eid1004.020754 |
---|---|
AMA | Graves N. Economics of Preventing Hospital Infection. Emerging Infectious Diseases. 2004;10(4):561-566. doi:10.3201/eid1004.020754. |
APA | Graves, N. (2004). Economics of Preventing Hospital Infection. Emerging Infectious Diseases, 10(4), 561-566. https://doi.org/10.3201/eid1004.020754. |
Reanalyzing the 1900–1920 Sleeping Sickness Epidemic in Uganda
Sleeping sickness has long been a major public health problem in Uganda. From 1900 to 1920, more than 250,000 people died in an epidemic that affected the southern part of the country, particularly the Busoga region. The epidemic has traditionally been ascribed to T. b. gambiense, a parasite now confined to central and western Africa. The Busoga region still reports sleeping sickness, although it is caused by Trypanosoma brucei rhodesiense, commonly believed to have spread to Uganda from Zambia in the 1940s. Our analysis of clinical data recorded in the early 1900s shows that the clinical course of sleeping sickness cases during the 1900–1920 epidemic in Uganda was markedly different from T.b. gambiense cases, but similar to T.b. rhodesiense. These findings suggest that T.b. rhodesiense was present in Uganda and contributed to the epidemic. The historic context is reassessed in the light of these data.
EID | Fèvre E, Coleman P, Welburn S, Maudlin I. Reanalyzing the 1900–1920 Sleeping Sickness Epidemic in Uganda. Emerg Infect Dis. 2004;10(4):567-573. https://doi.org/10.3201/eid1004.020626 |
---|---|
AMA | Fèvre E, Coleman P, Welburn S, et al. Reanalyzing the 1900–1920 Sleeping Sickness Epidemic in Uganda. Emerging Infectious Diseases. 2004;10(4):567-573. doi:10.3201/eid1004.020626. |
APA | Fèvre, E., Coleman, P., Welburn, S., & Maudlin, I. (2004). Reanalyzing the 1900–1920 Sleeping Sickness Epidemic in Uganda. Emerging Infectious Diseases, 10(4), 567-573. https://doi.org/10.3201/eid1004.020626. |
Synopses
Pediatric Influenza Prevention and Control
Global evaluation of influenza vaccination in children indicates that current recommendations are not followed. Most children at high risk for influenza-related complications do not receive the vaccine, and increased efforts are needed to protect them. Furthermore, immunizing healthy infants 6–23 months of age and their close contacts should be strongly encouraged. Vaccinations are recommended for children with recurrent acute otitis media or recurrent respiratory tract infections and possibly for healthy daycare and school-age children because of the potential socioeconomic implications of influenza. Issues that need to be addressed include educating physicians and parents concerning influenza-related illness and complications, cost-effectiveness and safety of licensed vaccines, adequate vaccine supply, and availability of intranasal products.
EID | Principi N, Esposito S. Pediatric Influenza Prevention and Control. Emerg Infect Dis. 2004;10(4):574-580. https://doi.org/10.3201/eid1004.030398 |
---|---|
AMA | Principi N, Esposito S. Pediatric Influenza Prevention and Control. Emerging Infectious Diseases. 2004;10(4):574-580. doi:10.3201/eid1004.030398. |
APA | Principi, N., & Esposito, S. (2004). Pediatric Influenza Prevention and Control. Emerging Infectious Diseases, 10(4), 574-580. https://doi.org/10.3201/eid1004.030398. |
Research
Inhibition of SARS Coronavirus Infection In Vitro with Clinically Approved Antiviral Drugs
Severe acute respiratory syndrome (SARS) is an infectious disease caused by a newly identified human coronavirus (SARS-CoV). Currently, no effective drug exists to treat SARS-CoV infection. In this study, we investigated whether a panel of commercially available antiviral drugs exhibit in vitro anti–SARS-CoV activity. A drug-screening assay that scores for virus-induced cytopathic effects on cultured cells was used. Tested were 19 clinically approved compounds from several major antiviral pharmacologic classes: nucleoside analogs, interferons, protease inhibitors, reverse transcriptase inhibitors, and neuraminidase inhibitors. Complete inhibition of cytopathic effects of SARS-CoV in culture was observed for interferon subtypes, β-1b, α-n1, α-n3, and human leukocyte interferon α. These findings support clinical testing of approved interferons for the treatment of SARS.
EID | Tan EL, Ooi EE, Lin C, Tan HC, Ling AE, Lim B, et al. Inhibition of SARS Coronavirus Infection In Vitro with Clinically Approved Antiviral Drugs. Emerg Infect Dis. 2004;10(4):581-586. https://doi.org/10.3201/eid1004.030458 |
---|---|
AMA | Tan EL, Ooi EE, Lin C, et al. Inhibition of SARS Coronavirus Infection In Vitro with Clinically Approved Antiviral Drugs. Emerging Infectious Diseases. 2004;10(4):581-586. doi:10.3201/eid1004.030458. |
APA | Tan, E. L., Ooi, E. E., Lin, C., Tan, H. C., Ling, A. E., Lim, B....Stanton, L. W. (2004). Inhibition of SARS Coronavirus Infection In Vitro with Clinically Approved Antiviral Drugs. Emerging Infectious Diseases, 10(4), 581-586. https://doi.org/10.3201/eid1004.030458. |
SARS Transmission, Risk Factors, and Prevention in Hong Kong
We analyzed information obtained from 1,192 patients with probable severe acute respiratory syndrome (SARS) reported in Hong Kong. Among them, 26.6% were hospital workers, 16.1% were household members of SARS patients and had probable secondary infections, 14.3% were Amoy Garden residents, 4.9% were inpatients, and 20.1% were contacts of SARS patients who were not family members. The remaining 347 case-patients (29.1%) did not have “known” sources of infection. Excluding those <16 years of age, 330 patients with cases from “undefined” sources were used in a 1:2 matched case-control study. Multivariate analysis of this case-control study showed that having visited mainland China, hospitals, or the Amoy Gardens were risk factors (odds ratio [OR] 1.95 to 7.63). In addition, frequent mask use in public venues, frequent hand washing, and disinfecting the living quarters were significant protective factors (OR 0.36 to 0.58). In Hong Kong, therefore, community-acquired infection did not make up most transmissions, and public health measures have contributed substantially to the control of the SARS epidemic.
EID | Lau J, Tsui H, Lau M, Yang X. SARS Transmission, Risk Factors, and Prevention in Hong Kong. Emerg Infect Dis. 2004;10(4):587-592. https://doi.org/10.3201/eid1004.030628 |
---|---|
AMA | Lau J, Tsui H, Lau M, et al. SARS Transmission, Risk Factors, and Prevention in Hong Kong. Emerging Infectious Diseases. 2004;10(4):587-592. doi:10.3201/eid1004.030628. |
APA | Lau, J., Tsui, H., Lau, M., & Yang, X. (2004). SARS Transmission, Risk Factors, and Prevention in Hong Kong. Emerging Infectious Diseases, 10(4), 587-592. https://doi.org/10.3201/eid1004.030628. |
Myanmar Dengue Outbreak Associated with Displacement of Serotypes 2, 3, and 4 by Dengue 1
In 2001, Myanmar (Burma) had its largest outbreak of dengue—15,361 reported cases of dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), including 192 deaths. That year, 95% of dengue viruses isolated from patients were serotype 1 viruses belonging to two lineages that had diverged from an earlier, now extinct, lineage sometime before 1998. The ratio of DHF to DSS cases in 2001 was not significantly different from that in 2000, when 1,816 cases of DHF/DSS were reported and dengue 1 also was the most frequently isolated serotype. However, the 2001 ratio was significantly higher than that in 1998 (also an outbreak year) and in 1999, when all four serotypes were detected and serotypes 1, 2, and 3 were recovered in similar numbers. The large number of clinical cases in 2001 may have been due, in part, to a preponderance of infections with dengue 1 viruses.
EID | Thu HM, Lowry K, Myint TT, Shwe TN, Han AM, Khin KK, et al. Myanmar Dengue Outbreak Associated with Displacement of Serotypes 2, 3, and 4 by Dengue 1. Emerg Infect Dis. 2004;10(4):593-597. https://doi.org/10.3201/eid1004.030216 |
---|---|
AMA | Thu HM, Lowry K, Myint TT, et al. Myanmar Dengue Outbreak Associated with Displacement of Serotypes 2, 3, and 4 by Dengue 1. Emerging Infectious Diseases. 2004;10(4):593-597. doi:10.3201/eid1004.030216. |
APA | Thu, H. M., Lowry, K., Myint, T. T., Shwe, T. N., Han, A. M., Khin, K. K....Aaskov, J. G. (2004). Myanmar Dengue Outbreak Associated with Displacement of Serotypes 2, 3, and 4 by Dengue 1. Emerging Infectious Diseases, 10(4), 593-597. https://doi.org/10.3201/eid1004.030216. |
Predicting Geographic Variation in Cutaneous Leishmaniasis, Colombia
Approximately 6,000 cases of cutaneous leishmaniasis are reported annually in Colombia, a greater than twofold increase since the 1980s. Such reports certainly underestimate true incidence, and their geographic distribution is likely biased by local health service effectiveness. We investigated how well freely available environmental data explain the distribution of cases among 1,079 municipalities. For each municipality, a unique predictive logistic regression model was derived from the association among remaining municipalities between elevation, land cover (preclassified maps derived from satellite images), or both, and the odds of at least one case being reported. Land cover had greater predictive power than elevation; using both datasets improved accuracy. Fitting separate models to different ecologic zones, reflecting transmission cycle diversity, enhanced the accuracy of predictions. We derived measures that can be directly related to disease control decisions and show how results can vary, depending on the threshold selected for predicting a disease-positive municipality. The results identify areas where disease is most likely to be underreported.
EID | King RJ, Campbell-Lendrum DH, Davies CR. Predicting Geographic Variation in Cutaneous Leishmaniasis, Colombia. Emerg Infect Dis. 2004;10(4):598-607. https://doi.org/10.3201/eid1004.030241 |
---|---|
AMA | King RJ, Campbell-Lendrum DH, Davies CR. Predicting Geographic Variation in Cutaneous Leishmaniasis, Colombia. Emerging Infectious Diseases. 2004;10(4):598-607. doi:10.3201/eid1004.030241. |
APA | King, R. J., Campbell-Lendrum, D. H., & Davies, C. R. (2004). Predicting Geographic Variation in Cutaneous Leishmaniasis, Colombia. Emerging Infectious Diseases, 10(4), 598-607. https://doi.org/10.3201/eid1004.030241. |
Epidemiologic Determinants for Modeling Pneumonic Plague Outbreaks
Pneumonic plague poses a potentially increasing risk to humans in plague nonendemic regions either as a consequence of an aerosolized release or through importation of the disease. Pneumonic plague is person-to-person transmissible. We provide a quantitative assessment of transmissibility based on past outbreaks that shows that the average number of secondary cases per primary case (R0) was 1.3 (variance = 3.1), assuming a geometric probability distribution, prior to outbreak control measures. We also show that the latent and infectious periods can be approximated by using lognormal distributions with means (SD) of 4.3 (1.8) and 2.5 (1.2) days. Based on this parameter estimation, we construct a Markov-chain epidemic model to demonstrate the potential impact of delays in implementing outbreak control measures and increasing numbers of index cases on the incidence of cases in simulated outbreaks.
EID | Gani R, Leach S. Epidemiologic Determinants for Modeling Pneumonic Plague Outbreaks. Emerg Infect Dis. 2004;10(4):608-614. https://doi.org/10.3201/eid1004.030509 |
---|---|
AMA | Gani R, Leach S. Epidemiologic Determinants for Modeling Pneumonic Plague Outbreaks. Emerging Infectious Diseases. 2004;10(4):608-614. doi:10.3201/eid1004.030509. |
APA | Gani, R., & Leach, S. (2004). Epidemiologic Determinants for Modeling Pneumonic Plague Outbreaks. Emerging Infectious Diseases, 10(4), 608-614. https://doi.org/10.3201/eid1004.030509. |
Dengue Spatial and Temporal Patterns, French Guiana, 2001
To study a 2001 dengue fever outbreak in Iracoubo, French Guiana, we recorded the location of all patients’ homes and the date when symptoms were first observed. A geographic information system was used to integrate the patient-related information. The Knox test, a classic space-time analysis technique, was used to detect spatiotemporal clustering. Analysis of the relative-risk (RR) variations when space and time distances vary, highlighted the maximum space and time extent of a dengue transmission focus. The results show that heterogeneity in the RR variations in space and time corresponds to known entomologic and epidemiologic factors, such as the mosquito feeding cycle and host-seeking behavior. This finding demonstrates the relevance and potential of the use of GIS and spatial statistics for elaborating a dengue fever surveillance strategy.
EID | Tran A, Deparis X, Dussart P, Morvan J, Rabarison P, Remy F, et al. Dengue Spatial and Temporal Patterns, French Guiana, 2001. Emerg Infect Dis. 2004;10(4):615-621. https://doi.org/10.3201/eid1004.030186 |
---|---|
AMA | Tran A, Deparis X, Dussart P, et al. Dengue Spatial and Temporal Patterns, French Guiana, 2001. Emerging Infectious Diseases. 2004;10(4):615-621. doi:10.3201/eid1004.030186. |
APA | Tran, A., Deparis, X., Dussart, P., Morvan, J., Rabarison, P., Remy, F....Gardon, J. (2004). Dengue Spatial and Temporal Patterns, French Guiana, 2001. Emerging Infectious Diseases, 10(4), 615-621. https://doi.org/10.3201/eid1004.030186. |
Babesia divergens–like Infection, Washington State
Most reported U.S. zoonotic cases of babesiosis have occurred in the Northeast and been caused by Babesia microti. In Washington State, three cases of babesiosis have been reported previously, which were caused by WA1 (for “Washington 1”)-type parasites. We investigated a case of babesiosis in Washington in an 82–year-old man whose spleen had been removed and whose parasitemia level was 41.4%. The complete 18S ribosomal RNA gene of the parasite was amplified from specimens of his whole blood by polymerase chain reaction. Phylogenetic analysis showed the parasite is most closely related, but not identical, to B. divergens (similarity score, 99.5%), a bovine parasite in Europe. By indirect fluorescent-antibody testing, his serum reacted to B. divergens but not to B. microti or WA1 antigens. This case demonstrates that babesiosis can be caused by novel parasites detectable by manual examination of blood smears but not by serologic or molecular testing for B. microti or WA1-type parasites.
EID | Herwaldt BL, de Bruyn G, Pieniazek NJ, Homer M, Lofy KH, Slemenda SB, et al. Babesia divergens–like Infection, Washington State. Emerg Infect Dis. 2004;10(4):622-629. https://doi.org/10.3201/eid1004.030377 |
---|---|
AMA | Herwaldt BL, de Bruyn G, Pieniazek NJ, et al. Babesia divergens–like Infection, Washington State. Emerging Infectious Diseases. 2004;10(4):622-629. doi:10.3201/eid1004.030377. |
APA | Herwaldt, B. L., de Bruyn, G., Pieniazek, N. J., Homer, M., Lofy, K. H., Slemenda, S. B....Limaye, A. P. (2004). Babesia divergens–like Infection, Washington State. Emerging Infectious Diseases, 10(4), 622-629. https://doi.org/10.3201/eid1004.030377. |
Influenza A Virus PB1-F2 Gene in Recent Taiwanese Isolates
Influenza A virus contains eight RNA segments and encodes 10 viral proteins. However, an 11th protein, called PB1-F2, was found in A/Puerto Rico/8/34 (H1N1). This novel protein is translated from an alternative open reading frame (ORF) in the PB1 gene. We analyzed the PB1 gene of 42 recent influenza A isolates in Taiwan, including 24 H1N1 and 18 H3N2 strains. One H1N1 isolate and 17 H3N2 isolates contained the entire PB1-F2 ORF of 90 residues, three amino acids (aa) longer than the PB1-F2 of A/Puerto Rico/8/34 at the C terminal. The one remaining H3N2 isolate encoded a truncated PB1-F2 with 79 residues. The other 23 H1N1 isolates contained a truncated PB1-F2 of 57 aa. Phylogenetic analysis of both the HA and the PB1 genes showed that they shared similar clustering of these Taiwanese isolates, suggesting that no obvious reassortment occurred between the two genomic segments.
EID | Chen G, Yang C, Tsao K, Huang C, Lee L, Yang W, et al. Influenza A Virus PB1-F2 Gene in Recent Taiwanese Isolates. Emerg Infect Dis. 2004;10(4):630-636. https://doi.org/10.3201/eid1004.030412 |
---|---|
AMA | Chen G, Yang C, Tsao K, et al. Influenza A Virus PB1-F2 Gene in Recent Taiwanese Isolates. Emerging Infectious Diseases. 2004;10(4):630-636. doi:10.3201/eid1004.030412. |
APA | Chen, G., Yang, C., Tsao, K., Huang, C., Lee, L., Yang, W....Shih, S. (2004). Influenza A Virus PB1-F2 Gene in Recent Taiwanese Isolates. Emerging Infectious Diseases, 10(4), 630-636. https://doi.org/10.3201/eid1004.030412. |
Coccidioidomycosis among Workers at an Archeological Site, Northeastern Utah
In 2001, an outbreak of acute respiratory disease occurred among persons working at a Native American archeological site at Dinosaur National Monument in northeastern Utah. Epidemiologic and environmental investigations were undertaken to determine the cause of the outbreak. A clinical case was defined by the presence of at least two of the following symptoms: self-reported fever, shortness of breath, or cough. Ten workers met the clinical case definition; 9 had serologic confirmation of coccidioidomycosis, and 8 were hospitalized. All 10 were present during sifting of dirt through screens on June 19; symptoms began 9–12 days later (median 10). Coccidioidomycosis also developed in a worker at the site in September 2001. A serosurvey among 40 other Dinosaur National Monument workers did not find serologic evidence of recent infection. This outbreak documents a new endemic focus of coccidioidomycosis, extending northward its known geographic distribution in Utah by approximately 200 miles.
EID | Petersen LR, Marshall SL, Barton C, Hajjeh RA, Lindsley MD, Warnock DW, et al. Coccidioidomycosis among Workers at an Archeological Site, Northeastern Utah. Emerg Infect Dis. 2004;10(4):637-642. https://doi.org/10.3201/eid1004.030446 |
---|---|
AMA | Petersen LR, Marshall SL, Barton C, et al. Coccidioidomycosis among Workers at an Archeological Site, Northeastern Utah. Emerging Infectious Diseases. 2004;10(4):637-642. doi:10.3201/eid1004.030446. |
APA | Petersen, L. R., Marshall, S. L., Barton, C., Hajjeh, R. A., Lindsley, M. D., Warnock, D. W....Morgan, J. (2004). Coccidioidomycosis among Workers at an Archeological Site, Northeastern Utah. Emerging Infectious Diseases, 10(4), 637-642. https://doi.org/10.3201/eid1004.030446. |
Maternal Malaria and Perinatal HIV Transmission, Western Kenya
To determine whether maternal placental malaria is associated with an increased risk for perinatal mother-to-child HIV transmission (MTCT), we studied HIV-positive women in western Kenya. We enrolled 512 mother-infant pairs; 128 (25.0%) women had malaria, and 102 (19.9%) infants acquired HIV perinatally. Log10 HIV viral load and episiotomy or perineal tear were associated with increased perinatal HIV transmission, whereas low-density malaria (<10,000 parasites/μL) was associated with reduced risk (adjusted relative risk [ARR] 0.4). Among women dually infected with malaria and HIV, high-density malaria (>10,000 parasites/μL) was associated with increased risk for perinatal MTCT (ARR 2.0), compared to low-density malaria. The interaction between placental malaria and MTCT appears to be variable and complex: placental malaria that is controlled at low density may cause an increase in broad-based immune responses that protect against MTCT; uncontrolled, high-density malaria may simultaneously disrupt placental architecture and generate substantial antigen stimulus to HIV replication and increase risk for MTCT.
EID | Ayisi JG, van Eijk AM, Newman RD, ter Kuile FO, Shi Y, Yang C, et al. Maternal Malaria and Perinatal HIV Transmission, Western Kenya. Emerg Infect Dis. 2004;10(4):643-652. https://doi.org/10.3201/eid1004.030303 |
---|---|
AMA | Ayisi JG, van Eijk AM, Newman RD, et al. Maternal Malaria and Perinatal HIV Transmission, Western Kenya. Emerging Infectious Diseases. 2004;10(4):643-652. doi:10.3201/eid1004.030303. |
APA | Ayisi, J. G., van Eijk, A. M., Newman, R. D., ter Kuile, F. O., Shi, Y., Yang, C....Nahlen, B. L. (2004). Maternal Malaria and Perinatal HIV Transmission, Western Kenya. Emerging Infectious Diseases, 10(4), 643-652. https://doi.org/10.3201/eid1004.030303. |
Ixodid and Argasid Tick Species and West Nile Virus
Control of West Nile virus (WNV) can only be effective if the vectors and reservoirs of the virus are identified and controlled. Although mosquitoes are the primary vectors, WNV has repeatedly been isolated from ticks. Therefore tick-borne transmission studies were performed with an ixodid (Ixodes ricinus) and an argasid tick species (Ornithodoros moubata). Both species became infected after feeding upon viremic hosts, but I. ricinus ticks were unable to maintain the virus. In contrast, O. moubata ticks were infected for at least 132 days, and the infection was maintained through molting and a second bloodmeal. Infected O. moubata ticks transmitted the virus to rodent hosts, albeit at a low level. Moreover, the virus was nonsystemically transmitted between infected and uninfected O. moubata ticks co-fed upon uninfected hosts. Although ticks are unlikely to play a major role in WNV transmission, our findings suggest that some species have the potential to act as reservoirs for the virus.
EID | Lawrie CH, Uzcátegui NY, Gould EA, Nuttall PA. Ixodid and Argasid Tick Species and West Nile Virus. Emerg Infect Dis. 2004;10(4):653-657. https://doi.org/10.3201/eid1004.030517 |
---|---|
AMA | Lawrie CH, Uzcátegui NY, Gould EA, et al. Ixodid and Argasid Tick Species and West Nile Virus. Emerging Infectious Diseases. 2004;10(4):653-657. doi:10.3201/eid1004.030517. |
APA | Lawrie, C. H., Uzcátegui, N. Y., Gould, E. A., & Nuttall, P. A. (2004). Ixodid and Argasid Tick Species and West Nile Virus. Emerging Infectious Diseases, 10(4), 653-657. https://doi.org/10.3201/eid1004.030517. |
Antigenic and Genetic Variability of Human Metapneumoviruses
Human metapneumovirus (HMPV) is a member of the subfamily Pneumovirinae within the family Paramyxoviridae. Other members of this subfamily, respiratory syncytial virus and avian pneumovirus, can be divided into subgroups based on genetic or antigenic differences or both. For HMPV, the existence of different genetic lineages has been described on the basis of variation in a limited set of available sequences. We address the antigenic relationship between genetic lineages in virus neutralization assays. In addition, we analyzed the genetic diversity of HMPV by phylogenetic analysis of sequences obtained for part of the fusion protein (n = 84) and the complete attachment protein open reading frames (n = 35). On the basis of sequence diversity between attachment protein genes and the differences in virus neutralization titers, two HMPV serotypes were defined. Each serotype could be divided into two genetic lineages, but these did not reflect major antigenic differences.
EID | van den Hoogen BG, Herfst S, Sprong L, Cane PA, Forleo-Neto E, de Swart RL, et al. Antigenic and Genetic Variability of Human Metapneumoviruses. Emerg Infect Dis. 2004;10(4):658-666. https://doi.org/10.3201/eid1004.030393 |
---|---|
AMA | van den Hoogen BG, Herfst S, Sprong L, et al. Antigenic and Genetic Variability of Human Metapneumoviruses. Emerging Infectious Diseases. 2004;10(4):658-666. doi:10.3201/eid1004.030393. |
APA | van den Hoogen, B. G., Herfst, S., Sprong, L., Cane, P. A., Forleo-Neto, E., de Swart, R. L....Fouchier, R. (2004). Antigenic and Genetic Variability of Human Metapneumoviruses. Emerging Infectious Diseases, 10(4), 658-666. https://doi.org/10.3201/eid1004.030393. |
Pneumocystis jiroveci Dihydropteroate Synthase Genotypes in Immunocompetent Infants and Immunosuppressed Adults, Amiens, France
To date, investigations of Pneumocystis jiroveci circulation in the human reservoir through the dihydropteroate synthase (DHPS) locus analysis have only been conducted by examining P. jirovecii isolates from immunosuppressed patients with Pneumocystis pneumonia (PCP). Our study identifies P. jirovecii genotypes at this locus in 33 immunocompetent infants colonized with P. jirovecii contemporaneously with a bronchiolitis episode and in 13 adults with PCP; both groups of patients were monitored in Amiens, France. The results have pointed out identical features of P. jirovecii DHPS genotypes in the two groups, suggesting that in these two groups, transmission cycles of P. jirovecii infections are linked. If these two groups represent sentinel populations for P. jirovecii infections, our results suggest that all persons parasitized by P. jirovecii, whatever their risk factor for infection and the form of parasitism they have, act as interwoven circulation networks of P. jirovecii.
EID | Totet A, Latouche S, Lacube P, Pautard J, Jounieaux V, Raccurt C, et al. Pneumocystis jiroveci Dihydropteroate Synthase Genotypes in Immunocompetent Infants and Immunosuppressed Adults, Amiens, France. Emerg Infect Dis. 2004;10(4):667-673. https://doi.org/10.3201/eid1004.030451 |
---|---|
AMA | Totet A, Latouche S, Lacube P, et al. Pneumocystis jiroveci Dihydropteroate Synthase Genotypes in Immunocompetent Infants and Immunosuppressed Adults, Amiens, France. Emerging Infectious Diseases. 2004;10(4):667-673. doi:10.3201/eid1004.030451. |
APA | Totet, A., Latouche, S., Lacube, P., Pautard, J., Jounieaux, V., Raccurt, C....Nevez, G. (2004). Pneumocystis jiroveci Dihydropteroate Synthase Genotypes in Immunocompetent Infants and Immunosuppressed Adults, Amiens, France. Emerging Infectious Diseases, 10(4), 667-673. https://doi.org/10.3201/eid1004.030451. |
PorA Variable Regions of Neisseria meningitidis
Subtypes, defined by variation in the outer membrane protein PorA, are an integral part of the characterization scheme for Neisseria meningitidis. Identification of these variants remains important as the PorA protein is a major immunogenic component of several meningococcal vaccines under development, and characteristics of PorA are used to provide detailed epidemiologic information. Historically, serosubtypes have been defined by reactivity with a set of monoclonal antibodies. However, nucleotide sequence analyses of porA genes have established that the panel of serosubtyping monoclonal antibodies is not exhaustive and many porA variants cannot be detected. In addition, the nomenclature system used to define subtypes is inadequate. We examined all available nucleotide sequences of the porA VR1 and VR2 regions to identify and define subtype families. A revised nomenclature scheme, compatible with the previous serologic nomenclature scheme, was devised. A Web-accessible database describing this nomenclature and its relationship to previous schemes was established (available from: http://neisseria.org/nm/typing/pora).
EID | Russell JE, Jolley KA, Feavers IM, Maiden MC, Suker J. PorA Variable Regions of Neisseria meningitidis. Emerg Infect Dis. 2004;10(4):674-678. https://doi.org/10.3201/eid1004.030247 |
---|---|
AMA | Russell JE, Jolley KA, Feavers IM, et al. PorA Variable Regions of Neisseria meningitidis. Emerging Infectious Diseases. 2004;10(4):674-678. doi:10.3201/eid1004.030247. |
APA | Russell, J. E., Jolley, K. A., Feavers, I. M., Maiden, M. C., & Suker, J. (2004). PorA Variable Regions of Neisseria meningitidis. Emerging Infectious Diseases, 10(4), 674-678. https://doi.org/10.3201/eid1004.030247. |
Antimicrobial Resistance Gene Delivery in Animal Feeds
Avoparcin, a glycopeptide antimicrobial agent related to vancomycin, has been used extensively as a growth promoter in animal feeds for more than 2 decades, and evidence has shown that such use contributed to the development of vancomycin-resistant enterococci. A cluster that includes three genes, vanH, vanA, and vanX, is required for high-level resistance to glycopeptides. In the vancomycin producer Amycolatopsis orientalis C329.2, homologs of these genes are present, suggesting an origin for the cluster. We found substantial bacterial DNA contamination in animal-feed-grade avoparcin. Furthermore, nucleotide sequences related to the cluster vanHAX are present in this DNA, suggesting that the prolonged use of avoparcin in agriculture led to the uptake of glycopeptide resistance genes by animal commensal bacteria, which were subsequently transferred to humans.
EID | Lu K, Asano R, Davies J. Antimicrobial Resistance Gene Delivery in Animal Feeds. Emerg Infect Dis. 2004;10(4):679-683. https://doi.org/10.3201/eid1004.030506 |
---|---|
AMA | Lu K, Asano R, Davies J. Antimicrobial Resistance Gene Delivery in Animal Feeds. Emerging Infectious Diseases. 2004;10(4):679-683. doi:10.3201/eid1004.030506. |
APA | Lu, K., Asano, R., & Davies, J. (2004). Antimicrobial Resistance Gene Delivery in Animal Feeds. Emerging Infectious Diseases, 10(4), 679-683. https://doi.org/10.3201/eid1004.030506. |
Flea-borne Bartonella grahamii and Bartonella taylorii in Bank Voles
Bartonella species are increasingly associated with a range of human and animal diseases. Despite this, we have a poor understanding of the ecology and epidemiology of many species, especially those circulating in wild populations. Previous studies have demonstrated that a diverse range of Bartonella species are abundant in wild rodent populations; little is known regarding their modes of transmission, although both direct and indirect routes have been suggested. In this study, with bank voles (Clethrionomys glareolus) as the host species, we demonstrate that the rodent flea Ctenophthalmus nobilis is a competent vector of at least two Bartonella species, B. grahamii, which has previously been associated with human infection, and B. taylorii. In contrast, no evidence of either horizontal or vertical transmission was seen in bank voles inoculated with B. taylorii maintained in an arthropod-free environment; this finding suggests that fleas may be essential for transmitting some Bartonella species.
EID | Bown KJ, Bennett M, Begon M. Flea-borne Bartonella grahamii and Bartonella taylorii in Bank Voles. Emerg Infect Dis. 2004;10(4):684-687. https://doi.org/10.3201/eid1004.030455 |
---|---|
AMA | Bown KJ, Bennett M, Begon M. Flea-borne Bartonella grahamii and Bartonella taylorii in Bank Voles. Emerging Infectious Diseases. 2004;10(4):684-687. doi:10.3201/eid1004.030455. |
APA | Bown, K. J., Bennett, M., & Begon, M. (2004). Flea-borne Bartonella grahamii and Bartonella taylorii in Bank Voles. Emerging Infectious Diseases, 10(4), 684-687. https://doi.org/10.3201/eid1004.030455. |
Restaurant Inspection Scores and Foodborne Disease
Restaurants in the United States are regularly inspected by health departments, but few data exist regarding the effect of restaurant inspections on food safety. We examined statewide inspection records from January 1993 through April 2000. Data were available from 167,574 restaurant inspections. From 1993 to 2000, mean scores rose steadily from 80.2 to 83.8. Mean inspection scores of individual inspectors were 69–92. None of the 12 most commonly cited violations were critical food safety hazards. Establishments scoring <60 had a mean improvement of 16 points on subsequent inspections. Mean scores of restaurants experiencing foodborne disease outbreaks did not differ from restaurants with no reported outbreaks. A variety of factors influence the uniformity of restaurant inspections. The restaurant inspection system should be examined to identify ways to ensure food safety.
EID | Jones TF, Pavlin BI, LaFleur BJ, Ingram LA, Schaffner W. Restaurant Inspection Scores and Foodborne Disease. Emerg Infect Dis. 2004;10(4):688-692. https://doi.org/10.3201/eid1004.030343 |
---|---|
AMA | Jones TF, Pavlin BI, LaFleur BJ, et al. Restaurant Inspection Scores and Foodborne Disease. Emerging Infectious Diseases. 2004;10(4):688-692. doi:10.3201/eid1004.030343. |
APA | Jones, T. F., Pavlin, B. I., LaFleur, B. J., Ingram, L. A., & Schaffner, W. (2004). Restaurant Inspection Scores and Foodborne Disease. Emerging Infectious Diseases, 10(4), 688-692. https://doi.org/10.3201/eid1004.030343. |
Recombination Resulting in Virulence Shift in Avian Influenza Outbreak, Chile
Influenza A viruses occur worldwide in wild birds and are occasionally associated with outbreaks in commercial chickens and turkeys. However, avian influenza viruses have not been isolated from wild birds or poultry in South America. A recent outbreak in chickens of H7N3 low pathogenic avian influenza (LPAI) occurred in Chile. One month later, after a sudden increase in deaths, H7N3 highly pathogenic avian influenza (HPAI) virus was isolated. Sequence analysis of all eight genes of the LPAI virus and the HPAI viruses showed minor differences between the viruses except at the hemagglutinin (HA) cleavage site. The LPAI virus had a cleavage site similar to other low pathogenic H7 viruses, but the HPAI isolates had a 30 nucleotide insert. The insertion likely occurred by recombination between the HA and nucleoprotein genes of the LPAI virus, resulting in a virulence shift. Sequence comparison of all eight gene segments showed the Chilean viruses were also distinct from all other avian influenza viruses and represent a distinct South American clade.
EID | Suarez DL, Senne DA, Banks J, Brown IH, Essen SC, Lee C, et al. Recombination Resulting in Virulence Shift in Avian Influenza Outbreak, Chile. Emerg Infect Dis. 2004;10(4):693-699. https://doi.org/10.3201/eid1004.030396 |
---|---|
AMA | Suarez DL, Senne DA, Banks J, et al. Recombination Resulting in Virulence Shift in Avian Influenza Outbreak, Chile. Emerging Infectious Diseases. 2004;10(4):693-699. doi:10.3201/eid1004.030396. |
APA | Suarez, D. L., Senne, D. A., Banks, J., Brown, I. H., Essen, S. C., Lee, C....Alexander, D. J. (2004). Recombination Resulting in Virulence Shift in Avian Influenza Outbreak, Chile. Emerging Infectious Diseases, 10(4), 693-699. https://doi.org/10.3201/eid1004.030396. |
Human Metapneumovirus Infection among Children Hospitalized with Acute Respiratory Illness
Recent studies have associated human Metapneumovirus (HMPV) infection in children with respiratory disease of similar severity as respiratory syncytial virus (RSV) infection. We studied 668 banked swab specimens (one per admission) collected from a population-based, prospective study of acute respiratory illness among inpatient children from two U.S. cities. Specimens were tested for HMPV, RSV, influenza, and parainfluenza viruses by reverse transcription–polymerase chain reaction assays. Twenty-six (3.9%) were positive for HMPV; 125 (18.7%) for RSV; 45 (6.7%) for parainfluenza 1, 2, or 3; and 23 (3.4%) for influenza. HMPV-positive children were significantly older than RSV-positive children. HMPV-positive children required medical intensive care and received supplemental oxygen in similar frequencies to RSV-positive children. Among children hospitalized with respiratory illness, the incidence of HMPV infection was less than RSV, but clinical disease severity mirrored that of RSV infection. Further investigations to better characterize HMPV infection and its clinical effect are needed.
EID | Mullins JA, Erdman DD, Weinberg GA, Edwards KM, Hall CB, Walker FJ, et al. Human Metapneumovirus Infection among Children Hospitalized with Acute Respiratory Illness. Emerg Infect Dis. 2004;10(4):700-705. https://doi.org/10.3201/eid1004.030555 |
---|---|
AMA | Mullins JA, Erdman DD, Weinberg GA, et al. Human Metapneumovirus Infection among Children Hospitalized with Acute Respiratory Illness. Emerging Infectious Diseases. 2004;10(4):700-705. doi:10.3201/eid1004.030555. |
APA | Mullins, J. A., Erdman, D. D., Weinberg, G. A., Edwards, K. M., Hall, C. B., Walker, F. J....Anderson, L. J. (2004). Human Metapneumovirus Infection among Children Hospitalized with Acute Respiratory Illness. Emerging Infectious Diseases, 10(4), 700-705. https://doi.org/10.3201/eid1004.030555. |
Dispatches
West Nile Virus, Guadeloupe
To determine whether West Nile virus (WNV) had reached the archipelago of Guadeloupe, a serologic study in horses and birds was conducted in 2002. Immunoglobulin (Ig) G, IgM, enzyme-linked immunosorbent assay, and seroneutralization tests identified WNV infection in horses and chickens. Six months later, a high rate of seroconversion was observed in horses.
EID | Quirin R, Salas M, Zientara S, Zeller H, Labie J, Murri S, et al. West Nile Virus, Guadeloupe. Emerg Infect Dis. 2004;10(4):706-708. https://doi.org/10.3201/eid1004.030465 |
---|---|
AMA | Quirin R, Salas M, Zientara S, et al. West Nile Virus, Guadeloupe. Emerging Infectious Diseases. 2004;10(4):706-708. doi:10.3201/eid1004.030465. |
APA | Quirin, R., Salas, M., Zientara, S., Zeller, H., Labie, J., Murri, S....Martinez, D. (2004). West Nile Virus, Guadeloupe. Emerging Infectious Diseases, 10(4), 706-708. https://doi.org/10.3201/eid1004.030465. |
West Nile Virus and High Death Rate in American Crows
We document effects of West Nile virus (WNV) on American Crows. More than two thirds of our crows died of WNV infection, peaking when the proportion of infected mosquitoes at roosts was greatest. WNV antibody prevalence in crows was low. Local ecologic effects can be dramatic as WNV inhabits new areas.
EID | Yaremych SA, Warner RE, Mankin PC, Brawn JD, Raim A, Novak R. West Nile Virus and High Death Rate in American Crows. Emerg Infect Dis. 2004;10(4):709-711. https://doi.org/10.3201/eid1004.030499 |
---|---|
AMA | Yaremych SA, Warner RE, Mankin PC, et al. West Nile Virus and High Death Rate in American Crows. Emerging Infectious Diseases. 2004;10(4):709-711. doi:10.3201/eid1004.030499. |
APA | Yaremych, S. A., Warner, R. E., Mankin, P. C., Brawn, J. D., Raim, A., & Novak, R. (2004). West Nile Virus and High Death Rate in American Crows. Emerging Infectious Diseases, 10(4), 709-711. https://doi.org/10.3201/eid1004.030499. |
West Nile Virus Encephalitis in a Barbary Macaque (Macaca sylvanus)
An aged Barbary ape (Macaca sylvanus) at the Toronto Zoo became infected with naturally acquired West Nile virus (WNV) encephalitis that caused neurologic signs, which, associated with other medical problems, led to euthanasia. The diagnosis was based on immunohistochemical assay of brain lesions, reverse transcriptase–polymerase chain reaction, and virus isolation.
EID | Ølberg R, Barker IK, Crawshaw GJ, Bertelsen MF, Drebot MA, Andonova M. West Nile Virus Encephalitis in a Barbary Macaque (Macaca sylvanus). Emerg Infect Dis. 2004;10(4):712-714. https://doi.org/10.3201/eid1004.030675 |
---|---|
AMA | Ølberg R, Barker IK, Crawshaw GJ, et al. West Nile Virus Encephalitis in a Barbary Macaque (Macaca sylvanus). Emerging Infectious Diseases. 2004;10(4):712-714. doi:10.3201/eid1004.030675. |
APA | Ølberg, R., Barker, I. K., Crawshaw, G. J., Bertelsen, M. F., Drebot, M. A., & Andonova, M. (2004). West Nile Virus Encephalitis in a Barbary Macaque (Macaca sylvanus). Emerging Infectious Diseases, 10(4), 712-714. https://doi.org/10.3201/eid1004.030675. |
Human Case of Lobomycosis
We describe a 42-year-old woman with histologically confirmed lobomycosis, a cutaneous fungal infection rarely reported outside of Latin America. Our case represents the first published report of imported human lobomycosis in Canada and the fifth in an industrialized country.
EID | Elsayed S, Kuhn SM, Barber D, Church DL, Adams S, Kasper R. Human Case of Lobomycosis. Emerg Infect Dis. 2004;10(4):715-718. https://doi.org/10.3201/eid1004.030416 |
---|---|
AMA | Elsayed S, Kuhn SM, Barber D, et al. Human Case of Lobomycosis. Emerging Infectious Diseases. 2004;10(4):715-718. doi:10.3201/eid1004.030416. |
APA | Elsayed, S., Kuhn, S. M., Barber, D., Church, D. L., Adams, S., & Kasper, R. (2004). Human Case of Lobomycosis. Emerging Infectious Diseases, 10(4), 715-718. https://doi.org/10.3201/eid1004.030416. |
Dengue 3 Epidemic, Havana, 2001
In June 2001, dengue transmission was detected in Havana, Cuba; 12,889 cases were reported. Dengue 3, the etiologic agent of the epidemic, caused the dengue hemorrhagic fever only in adults, with 78 cases and 3 deaths. After intensive vector control efforts, no new cases have been detected.
EID | Peláez O, Guzmán MG, Kourí G, Pérez R, San Martín JL, Vázquez S, et al. Dengue 3 Epidemic, Havana, 2001. Emerg Infect Dis. 2004;10(4):719-722. https://doi.org/10.3201/eid1004.030271 |
---|---|
AMA | Peláez O, Guzmán MG, Kourí G, et al. Dengue 3 Epidemic, Havana, 2001. Emerging Infectious Diseases. 2004;10(4):719-722. doi:10.3201/eid1004.030271. |
APA | Peláez, O., Guzmán, M. G., Kourí, G., Pérez, R., San Martín, J. L., Vázquez, S....Prado, I. (2004). Dengue 3 Epidemic, Havana, 2001. Emerging Infectious Diseases, 10(4), 719-722. https://doi.org/10.3201/eid1004.030271. |
Phocine Distemper in German Seals, 2002
Approximately 21,700 seals died during a morbillivirus epidemic in northwestern Europe in 2002. Phocine distemper virus 1 was isolated from seals in German waters. The sequence of the P gene showed 97% identity with the Dutch virus isolated in 1988. There was 100% identity with the Dutch isolate from 2002 and a single nucleotide mismatch with the Danish isolate.
EID | Müller G, Wohlsein P, Beineke A, Haas L, Greiser-Wilke I, Siebert U, et al. Phocine Distemper in German Seals, 2002. Emerg Infect Dis. 2004;10(4):723-725. https://doi.org/10.3201/eid1004.030591 |
---|---|
AMA | Müller G, Wohlsein P, Beineke A, et al. Phocine Distemper in German Seals, 2002. Emerging Infectious Diseases. 2004;10(4):723-725. doi:10.3201/eid1004.030591. |
APA | Müller, G., Wohlsein, P., Beineke, A., Haas, L., Greiser-Wilke, I., Siebert, U....Baumgärtner, W. (2004). Phocine Distemper in German Seals, 2002. Emerging Infectious Diseases, 10(4), 723-725. https://doi.org/10.3201/eid1004.030591. |
Human Challenge Pilot Study with Cyclospora cayetanensis
We describe a pilot study that attempted to infect human volunteers with Cyclospora cayetanensis. Seven healthy volunteers ingested an inoculum of Cyclospora oocysts (approximately 200–49,000 oocysts). The volunteers did not experience symptoms of gastroenteritis, and no oocysts were detected in any stool samples during the 16 weeks volunteers were monitored.
EID | Alfano-Sobsey EM, Eberhard ML, Seed JR, Weber DJ, Won KY, Nace EK, et al. Human Challenge Pilot Study with Cyclospora cayetanensis. Emerg Infect Dis. 2004;10(4):726-728. https://doi.org/10.3201/eid1004.030356 |
---|---|
AMA | Alfano-Sobsey EM, Eberhard ML, Seed JR, et al. Human Challenge Pilot Study with Cyclospora cayetanensis. Emerging Infectious Diseases. 2004;10(4):726-728. doi:10.3201/eid1004.030356. |
APA | Alfano-Sobsey, E. M., Eberhard, M. L., Seed, J. R., Weber, D. J., Won, K. Y., Nace, E. K....Moe, C. L. (2004). Human Challenge Pilot Study with Cyclospora cayetanensis. Emerging Infectious Diseases, 10(4), 726-728. https://doi.org/10.3201/eid1004.030356. |
Successful Treatment of Human Herpesvirus 6 Encephalomyelitis in Immunocompetent Patient
We report the case of human herpesvirus 6 (HHV-6) encephalomyelitis in an immunocompetent patient, which was confirmed by viral amplification from cerebrospinal fluid. Cidofovir was used followed by ganciclovir because of an adverse effect to probenecid. The patient recovered. HHV-6 should be recognized as one of the causes of encephalomyelitis.
EID | Denes E, Magy L, Pradeau K, Alain S, Weinbreck P, Ranger-Rogez S. Successful Treatment of Human Herpesvirus 6 Encephalomyelitis in Immunocompetent Patient. Emerg Infect Dis. 2004;10(4):729-731. https://doi.org/10.3201/eid1004.030587 |
---|---|
AMA | Denes E, Magy L, Pradeau K, et al. Successful Treatment of Human Herpesvirus 6 Encephalomyelitis in Immunocompetent Patient. Emerging Infectious Diseases. 2004;10(4):729-731. doi:10.3201/eid1004.030587. |
APA | Denes, E., Magy, L., Pradeau, K., Alain, S., Weinbreck, P., & Ranger-Rogez, S. (2004). Successful Treatment of Human Herpesvirus 6 Encephalomyelitis in Immunocompetent Patient. Emerging Infectious Diseases, 10(4), 729-731. https://doi.org/10.3201/eid1004.030587. |
Ruling Out Bacillus anthracis
Optimization of methods for ruling out Bacillus anthracis leads to increased yields, faster turnaround times, and a lighter workload. We used 72 environmental non–B. anthracis bacilli to validate methods for ruling out B. anthracis. Most effective were horse blood agar, motility testing after a 2-h incubation in trypticase soy broth, and screening with a B. anthracis–selective agar.
EID | Papaparaskevas J, Houhoula DP, Papadimitriou M, Saroglou G, Legakis NJ, Zerva L. Ruling Out Bacillus anthracis. Emerg Infect Dis. 2004;10(4):732-735. https://doi.org/10.3201/eid1004.030544 |
---|---|
AMA | Papaparaskevas J, Houhoula DP, Papadimitriou M, et al. Ruling Out Bacillus anthracis. Emerging Infectious Diseases. 2004;10(4):732-735. doi:10.3201/eid1004.030544. |
APA | Papaparaskevas, J., Houhoula, D. P., Papadimitriou, M., Saroglou, G., Legakis, N. J., & Zerva, L. (2004). Ruling Out Bacillus anthracis. Emerging Infectious Diseases, 10(4), 732-735. https://doi.org/10.3201/eid1004.030544. |
High Incidence of Pulmonary Tuberculosis a Decade after Immigration, Netherlands
Incidence rates of pulmonary tuberculosis among immigrants from high incidence countries remain high for at least a decade after immigration into the Netherlands. Possible explanations are reactivation of old infections and infection transmitted after immigration. Control policies should be determined on the basis of the as-yet unknown main causes of the persistent high incidence.
EID | Vos AM, Meima A, Verver S, Looman CW, Bos V, Borgdorff MW, et al. High Incidence of Pulmonary Tuberculosis a Decade after Immigration, Netherlands. Emerg Infect Dis. 2004;10(4):736-739. https://doi.org/10.3201/eid1004.030530 |
---|---|
AMA | Vos AM, Meima A, Verver S, et al. High Incidence of Pulmonary Tuberculosis a Decade after Immigration, Netherlands. Emerging Infectious Diseases. 2004;10(4):736-739. doi:10.3201/eid1004.030530. |
APA | Vos, A. M., Meima, A., Verver, S., Looman, C. W., Bos, V., Borgdorff, M. W....Habbema, J. D. (2004). High Incidence of Pulmonary Tuberculosis a Decade after Immigration, Netherlands. Emerging Infectious Diseases, 10(4), 736-739. https://doi.org/10.3201/eid1004.030530. |
Murine Typhus with Renal Involvement in Canary Islands, Spain
Murine typhus and “murine-thypus-like” disease are reemerging infectious diseases. In Canary Islands (Spain), a rather distinct clinical pattern characterized by higher incidence of complications, especially renal damage (including acute failure and urinalysis abnormalities), is apparent and highly suggestive. It could be related to different strains of Rickettsia typhi or other cross-reactive species.
EID | Hernández-Cabrera M, Angel-Moreno A, Santana E, Bolaños M, Francès A, Martín-Sánchez A, et al. Murine Typhus with Renal Involvement in Canary Islands, Spain. Emerg Infect Dis. 2004;10(4):740-743. https://doi.org/10.3201/eid1004.030532 |
---|---|
AMA | Hernández-Cabrera M, Angel-Moreno A, Santana E, et al. Murine Typhus with Renal Involvement in Canary Islands, Spain. Emerging Infectious Diseases. 2004;10(4):740-743. doi:10.3201/eid1004.030532. |
APA | Hernández-Cabrera, M., Angel-Moreno, A., Santana, E., Bolaños, M., Francès, A., Martín-Sánchez, A....Pérez-Arellano, J. (2004). Murine Typhus with Renal Involvement in Canary Islands, Spain. Emerging Infectious Diseases, 10(4), 740-743. https://doi.org/10.3201/eid1004.030532. |
Anaplasma phagocytophilum, Babesia microti, and Borrelia burgdorferi in Ixodes scapularis, Southern Coastal Maine
Ixodes scapularis (deer ticks) from Maine were tested for multiple infections by polymerase chain reaction and immunofluorescence. In 1995, 29.5%, 9.5%, and 1.9% of deer ticks were infected with Borrelia burgdorferi, Anaplasma phagocytophilum, and Babesia microti, respectively. In 1996 and 1997, the number of A. phagocytophilum-infected ticks markedly declined. In 1995 through 1996, 4 (1.3%) of 301 were co-infected.
EID | Holman MS, Caporale DA, Goldberg J, Lacombe EH, Lubelczyk CB, Rand PW, et al. Anaplasma phagocytophilum, Babesia microti, and Borrelia burgdorferi in Ixodes scapularis, Southern Coastal Maine. Emerg Infect Dis. 2004;10(4):744-746. https://doi.org/10.3201/eid1004.030566 |
---|---|
AMA | Holman MS, Caporale DA, Goldberg J, et al. Anaplasma phagocytophilum, Babesia microti, and Borrelia burgdorferi in Ixodes scapularis, Southern Coastal Maine. Emerging Infectious Diseases. 2004;10(4):744-746. doi:10.3201/eid1004.030566. |
APA | Holman, M. S., Caporale, D. A., Goldberg, J., Lacombe, E. H., Lubelczyk, C. B., Rand, P. W....Smith, R. P. (2004). Anaplasma phagocytophilum, Babesia microti, and Borrelia burgdorferi in Ixodes scapularis, Southern Coastal Maine. Emerging Infectious Diseases, 10(4), 744-746. https://doi.org/10.3201/eid1004.030566. |
Dengue Fever Outbreak in a Recreation Club, Dhaka, Bangladesh
An outbreak of dengue fever occurred among employees of a recreation club in Bangladesh. Occupational transmission was characterized by a 12% attack rate, no dengue among family contacts, and Aedes vectors in club areas. Early recognition of the outbreak likely limited its impact.
EID | Wagatsuma Y, Breiman RF, Hossain A, Rahman M. Dengue Fever Outbreak in a Recreation Club, Dhaka, Bangladesh. Emerg Infect Dis. 2004;10(4):747-750. https://doi.org/10.3201/eid1004.030330 |
---|---|
AMA | Wagatsuma Y, Breiman RF, Hossain A, et al. Dengue Fever Outbreak in a Recreation Club, Dhaka, Bangladesh. Emerging Infectious Diseases. 2004;10(4):747-750. doi:10.3201/eid1004.030330. |
APA | Wagatsuma, Y., Breiman, R. F., Hossain, A., & Rahman, M. (2004). Dengue Fever Outbreak in a Recreation Club, Dhaka, Bangladesh. Emerging Infectious Diseases, 10(4), 747-750. https://doi.org/10.3201/eid1004.030330. |
Letters
Mycobacterium tuberculosis Complex Drug Resistance in Italy
EID | Migliori GB, Centis R, Fattorini L, Besozzi G, Saltini C, Scarparo C, et al. Mycobacterium tuberculosis Complex Drug Resistance in Italy. Emerg Infect Dis. 2004;10(4):752-753. https://doi.org/10.3201/eid1004.030667 |
---|---|
AMA | Migliori GB, Centis R, Fattorini L, et al. Mycobacterium tuberculosis Complex Drug Resistance in Italy. Emerging Infectious Diseases. 2004;10(4):752-753. doi:10.3201/eid1004.030667. |
APA | Migliori, G. B., Centis, R., Fattorini, L., Besozzi, G., Saltini, C., Scarparo, C....Piersimoni, C. (2004). Mycobacterium tuberculosis Complex Drug Resistance in Italy. Emerging Infectious Diseases, 10(4), 752-753. https://doi.org/10.3201/eid1004.030667. |
Mollaret-like Cells in Patients with West Nile Virus Infection
EID | Procop GW, Yen-Lieberman B, Prayson RA, Gordon SM. Mollaret-like Cells in Patients with West Nile Virus Infection. Emerg Infect Dis. 2004;10(4):753-754. https://doi.org/10.3201/eid1004.030783 |
---|---|
AMA | Procop GW, Yen-Lieberman B, Prayson RA, et al. Mollaret-like Cells in Patients with West Nile Virus Infection. Emerging Infectious Diseases. 2004;10(4):753-754. doi:10.3201/eid1004.030783. |
APA | Procop, G. W., Yen-Lieberman, B., Prayson, R. A., & Gordon, S. M. (2004). Mollaret-like Cells in Patients with West Nile Virus Infection. Emerging Infectious Diseases, 10(4), 753-754. https://doi.org/10.3201/eid1004.030783. |
Newly Isolated Vibrio cholerae Non-O1, Non-O139 Phages
EID | Sarkar BL, Ghosh AN, Sen A, Rodrigues DP. Newly Isolated Vibrio cholerae Non-O1, Non-O139 Phages. Emerg Infect Dis. 2004;10(4):754-756. https://doi.org/10.3201/eid1004.030413 |
---|---|
AMA | Sarkar BL, Ghosh AN, Sen A, et al. Newly Isolated Vibrio cholerae Non-O1, Non-O139 Phages. Emerging Infectious Diseases. 2004;10(4):754-756. doi:10.3201/eid1004.030413. |
APA | Sarkar, B. L., Ghosh, A. N., Sen, A., & Rodrigues, D. P. (2004). Newly Isolated Vibrio cholerae Non-O1, Non-O139 Phages. Emerging Infectious Diseases, 10(4), 754-756. https://doi.org/10.3201/eid1004.030413. |
Salmonella Agona Harboring Genomic Island 1-A
EID | Doublet B, Butaye P, Imberechts H, Collard J, Chaslus-Dancla E, Cloeckaert A. Salmonella Agona Harboring Genomic Island 1-A. Emerg Infect Dis. 2004;10(4):756-758. https://doi.org/10.3201/eid1004.030417 |
---|---|
AMA | Doublet B, Butaye P, Imberechts H, et al. Salmonella Agona Harboring Genomic Island 1-A. Emerging Infectious Diseases. 2004;10(4):756-758. doi:10.3201/eid1004.030417. |
APA | Doublet, B., Butaye, P., Imberechts, H., Collard, J., Chaslus-Dancla, E., & Cloeckaert, A. (2004). Salmonella Agona Harboring Genomic Island 1-A. Emerging Infectious Diseases, 10(4), 756-758. https://doi.org/10.3201/eid1004.030417. |
Another Dimension
Threat of the Spores
EID | Vora SK. Threat of the Spores. Emerg Infect Dis. 2004;10(4):751. https://doi.org/10.3201/eid1004.031030 |
---|---|
AMA | Vora SK. Threat of the Spores. Emerging Infectious Diseases. 2004;10(4):751. doi:10.3201/eid1004.031030. |
APA | Vora, S. K. (2004). Threat of the Spores. Emerging Infectious Diseases, 10(4), 751. https://doi.org/10.3201/eid1004.031030. |
Corrections
Correction, Vol. 10, No. 3
EID | Correction, Vol. 10, No. 3. Emerg Infect Dis. 2004;10(4):761. https://doi.org/10.3201/eid1004.c11004 |
---|---|
AMA | Correction, Vol. 10, No. 3. Emerging Infectious Diseases. 2004;10(4):761. doi:10.3201/eid1004.c11004. |
APA | (2004). Correction, Vol. 10, No. 3. Emerging Infectious Diseases, 10(4), 761. https://doi.org/10.3201/eid1004.c11004. |
About the Cover
Paul Gauguin (1848–1903). I Raro te Oviri (Under the Pandanus) (1891)
EID | Potter P. Paul Gauguin (1848–1903). I Raro te Oviri (Under the Pandanus) (1891). Emerg Infect Dis. 2004;10(4):766-767. https://doi.org/10.3201/eid1004.ac1004 |
---|---|
AMA | Potter P. Paul Gauguin (1848–1903). I Raro te Oviri (Under the Pandanus) (1891). Emerging Infectious Diseases. 2004;10(4):766-767. doi:10.3201/eid1004.ac1004. |
APA | Potter, P. (2004). Paul Gauguin (1848–1903). I Raro te Oviri (Under the Pandanus) (1891). Emerging Infectious Diseases, 10(4), 766-767. https://doi.org/10.3201/eid1004.ac1004. |
News and Notes
Consequences of Bacterial Resistance to Antimicrobial Agents
EID | Desenclos JC, Guillemot D. Consequences of Bacterial Resistance to Antimicrobial Agents. Emerg Infect Dis. 2004;10(4):759-760. https://doi.org/10.3201/eid1004.030754 |
---|---|
AMA | Desenclos JC, Guillemot D. Consequences of Bacterial Resistance to Antimicrobial Agents. Emerging Infectious Diseases. 2004;10(4):759-760. doi:10.3201/eid1004.030754. |
APA | Desenclos, J. C., & Guillemot, D. (2004). Consequences of Bacterial Resistance to Antimicrobial Agents. Emerging Infectious Diseases, 10(4), 759-760. https://doi.org/10.3201/eid1004.030754. |
Vets, Meds, and Zoonotic Threats
The fourth international conference on emerging zoonoses (September 18–21, Ames, Iowa, USA) brought together 180 scientists and healthcare specialists from 18 countries working to control diseases transmitted from animals to humans. The meeting took place under the auspices of the Center of Food Security and Public Health, USA, and the Institute for International Cooperation in Animal Biologics (a collaborating center of the World Animal Health Organisation [OIE]).
EID | Pitlik S. Vets, Meds, and Zoonotic Threats. Emerg Infect Dis. 2004;10(4):760-761. https://doi.org/10.3201/eid1004.030805 |
---|---|
AMA | Pitlik S. Vets, Meds, and Zoonotic Threats. Emerging Infectious Diseases. 2004;10(4):760-761. doi:10.3201/eid1004.030805. |
APA | Pitlik, S. (2004). Vets, Meds, and Zoonotic Threats. Emerging Infectious Diseases, 10(4), 760-761. https://doi.org/10.3201/eid1004.030805. |
In Memoriam Robert Ellis Shope 1929–2004
EID | Murphy FA, Calisher CH, Tesh RB, Walker DH. In Memoriam Robert Ellis Shope 1929–2004. Emerg Infect Dis. 2004;10(4):762-765. https://doi.org/10.3201/eid1004.im1004 |
---|---|
AMA | Murphy FA, Calisher CH, Tesh RB, et al. In Memoriam Robert Ellis Shope 1929–2004. Emerging Infectious Diseases. 2004;10(4):762-765. doi:10.3201/eid1004.im1004. |
APA | Murphy, F. A., Calisher, C. H., Tesh, R. B., & Walker, D. H. (2004). In Memoriam Robert Ellis Shope 1929–2004. Emerging Infectious Diseases, 10(4), 762-765. https://doi.org/10.3201/eid1004.im1004. |