Skip directly to search Skip directly to A to Z list Skip directly to page options Skip directly to site content

Volume 9, Number 8—August 2003

Volume 9, Number 8—August 2003   PDF Version [PDF - 6.69 MB - 141 pages]

Perspective

  • Porcine Reproductive and Respiratory Syndrome Virus: Origin Hypothesis PDF Version [PDF - 222 KB - 6 pages]
    P. G. Plagemann
        View Abstract

    Porcine reproductive and respiratory syndrome is a serious swine disease that appeared suddenly in the midwestern United States and central Europe approximately 14 years ago; the disease has now spread worldwide. In North America and Europe, the syndrome is caused by two genotypes of porcine reproductive and respiratory syndrome virus (PRRSV), an arterivirus whose genomes diverge by approximately 40%. My hypothesis, which explains the origin and evolution of the two distinct PRRSV genotypes, is that a mutant of a closely related arterivirus of mice (lactate dehydrogenase-elevating virus) infected wild boars in central Europe. These wild boars functioned as intermediate hosts and spread the virus to North Carolina in imported, infected European wild boars in 1912; the virus then evolved independently on the two continents in the prevalent wild hog populations for approximately 70 years until independently entering the domestic pig population.

        Cite This Article
    EID Plagemann PG. Porcine Reproductive and Respiratory Syndrome Virus: Origin Hypothesis. Emerg Infect Dis. 2003;9(8):903-908. https://dx.doi.org/10.3201/eid0908.030232
    AMA Plagemann PG. Porcine Reproductive and Respiratory Syndrome Virus: Origin Hypothesis. Emerging Infectious Diseases. 2003;9(8):903-908. doi:10.3201/eid0908.030232.
    APA Plagemann, P. G. (2003). Porcine Reproductive and Respiratory Syndrome Virus: Origin Hypothesis. Emerging Infectious Diseases, 9(8), 903-908. https://dx.doi.org/10.3201/eid0908.030232.
  • Detecting Bioterror Attacks by Screening Blood Donors: A Best-Case Analysis PDF Version [PDF - 344 KB - 6 pages]
    E. H. Kaplan et al.
        View Abstract

    To assess whether screening blood donors could provide early warning of a bioterror attack, we combined stochastic models of blood donation and the workings of blood tests with an epidemic model to derive the probability distribution of the time to detect an attack under assumptions favorable to blood donor screening. Comparing the attack detection delay to the incubation times of the most feared bioterror agents shows that even under such optimistic conditions, victims of a bioterror attack would likely exhibit symptoms before the attack was detected through blood donor screening. For example, an attack infecting 100 persons with a noncontagious agent such as Bacillus anthracis would only have a 26% chance of being detected within 25 days; yet, at an assumed additional charge of $10 per test, donor screening would cost $139 million per year. Furthermore, even if screening tests were 99.99% specific, 1,390 false-positive results would occur each year. Therefore, screening blood donors for bioterror agents should not be used to detect a bioterror attack.

        Cite This Article
    EID Kaplan EH, Patton CA, FitzGerald WP, Wein LM. Detecting Bioterror Attacks by Screening Blood Donors: A Best-Case Analysis. Emerg Infect Dis. 2003;9(8):909-914. https://dx.doi.org/10.3201/eid0908.030079
    AMA Kaplan EH, Patton CA, FitzGerald WP, et al. Detecting Bioterror Attacks by Screening Blood Donors: A Best-Case Analysis. Emerging Infectious Diseases. 2003;9(8):909-914. doi:10.3201/eid0908.030079.
    APA Kaplan, E. H., Patton, C. A., FitzGerald, W. P., & Wein, L. M. (2003). Detecting Bioterror Attacks by Screening Blood Donors: A Best-Case Analysis. Emerging Infectious Diseases, 9(8), 909-914. https://dx.doi.org/10.3201/eid0908.030079.

Research

  • Legionnaires’ Disease Outbreak in Murcia, Spain PDF Version [PDF - 279 KB - 7 pages]
    A. García-Fulgueiras et al.
        View Abstract

    An explosive outbreak of Legionnaires’ disease occurred in Murcia, Spain, in July 2001. More than 800 suspected cases were reported; 449 of these cases were confirmed, which made this the world’s largest outbreak of the disease reported to date. Dates of onset for confirmed cases ranged from June 26 to July 19 , with a case-fatality rate of 1%. The epidemic curve and geographic pattern from the 600 completed epidemiologic questionnaires indicated an outdoor point-source exposure in the northern part of the city. A case-control study matching 85 patients living outside the city of Murcia with two controls each was undertaken to identify the outbreak source; the epidemiologic investigation implicated the cooling towers at a city hospital. An environmental isolate from these towers with an identical molecular pattern as the clinical isolates was subsequently identified and supported that epidemiologic conclusion.

        Cite This Article
    EID García-Fulgueiras A, Navarro C, Fenoll D, García J, González-Diego P, Jiménez-Buñuales T, et al. Legionnaires’ Disease Outbreak in Murcia, Spain. Emerg Infect Dis. 2003;9(8):915-921. https://dx.doi.org/10.3201/eid0908.030337
    AMA García-Fulgueiras A, Navarro C, Fenoll D, et al. Legionnaires’ Disease Outbreak in Murcia, Spain. Emerging Infectious Diseases. 2003;9(8):915-921. doi:10.3201/eid0908.030337.
    APA García-Fulgueiras, A., Navarro, C., Fenoll, D., García, J., González-Diego, P., Jiménez-Buñuales, T....Pelaz, C. (2003). Legionnaires’ Disease Outbreak in Murcia, Spain. Emerging Infectious Diseases, 9(8), 915-921. https://dx.doi.org/10.3201/eid0908.030337.
  • Survival of Batrachochytrium dendrobatidis in Water: Quarantine and Disease Control Implications PDF Version [PDF - 249 KB - 4 pages]
    M. L. Johnson and R. Speare
        View Abstract

    Amphibian chytridiomycosis is an emerging infectious disease of amphibians thought to be moved between countries by trade in infected amphibians. The causative fungus, Batrachochytrium dendrobatidis, produces aquatic, motile zoospores; infections have been achieved in experiments by exposing amphibians to water containing zoospores. However, the ability of this fungus to survive in the environment in the absence of an amphibian host is unknown. We show that B. dendrobatidis will survive in tap water and in deionized water for 3 and 4 weeks, respectively. In lake water, infectivity was observed for 7 weeks after introduction. The knowledge that water can remain infective for up to 7 weeks is important for the formulation of disease control and quarantine strategies for the management of water that has been in contact with amphibians.

        Cite This Article
    EID Johnson ML, Speare R. Survival of Batrachochytrium dendrobatidis in Water: Quarantine and Disease Control Implications. Emerg Infect Dis. 2003;9(8):922-925. https://dx.doi.org/10.3201/eid0908.030145
    AMA Johnson ML, Speare R. Survival of Batrachochytrium dendrobatidis in Water: Quarantine and Disease Control Implications. Emerging Infectious Diseases. 2003;9(8):922-925. doi:10.3201/eid0908.030145.
    APA Johnson, M. L., & Speare, R. (2003). Survival of Batrachochytrium dendrobatidis in Water: Quarantine and Disease Control Implications. Emerging Infectious Diseases, 9(8), 922-925. https://dx.doi.org/10.3201/eid0908.030145.
  • Enzootic Transmission of Yellow Fever Virus in Peru PDF Version [PDF - 427 KB - 8 pages]
    J. E. Bryant et al.
        View Abstract

    The prevailing paradigm of yellow fever virus (YFV) ecology in South America is that of wandering epizootics. The virus is believed to move from place to place in epizootic waves involving monkeys and mosquitoes, rather than persistently circulating within particular locales. After a large outbreak of YFV illness in Peru in 1995, we used phylogenetic analyses of virus isolates to reexamine the hypothesis of virus movement. We sequenced a 670-nucleotide fragment of the prM/E gene region of from 25 Peruvian YFV samples collected from 1977 to 1999, and delineated six clades representing the states (Departments) of Puno, Pasco, Junin, Ayacucho, San Martin/Huanuco, and Cusco. The concurrent appearance of at least four variants during the 1995 epidemic and the genetic stability of separate virus lineages over time, indicate that Peruvian YFV is locally maintained and circulates continuously in discrete foci of enzootic transmission.

        Cite This Article
    EID Bryant JE, Wang H, Cabezas C, Ramirez G, Watts DM, Russell K, et al. Enzootic Transmission of Yellow Fever Virus in Peru. Emerg Infect Dis. 2003;9(8):926-933. https://dx.doi.org/10.3201/eid0908.030075
    AMA Bryant JE, Wang H, Cabezas C, et al. Enzootic Transmission of Yellow Fever Virus in Peru. Emerging Infectious Diseases. 2003;9(8):926-933. doi:10.3201/eid0908.030075.
    APA Bryant, J. E., Wang, H., Cabezas, C., Ramirez, G., Watts, D. M., Russell, K....Barrett, A. (2003). Enzootic Transmission of Yellow Fever Virus in Peru. Emerging Infectious Diseases, 9(8), 926-933. https://dx.doi.org/10.3201/eid0908.030075.
  • Molecular Analysis of Echovirus 13 Isolates and Aseptic Meningitis, Spain PDF Version [PDF - 366 KB - 8 pages]
    A. Avellón et al.
        View Abstract

    Echovirus 13 (EV13), considered rare, was reported worldwide in 2000, mostly related to aseptic meningitis outbreaks. In Spain, 135 EV13 isolates were identified. The genetic relationships between 64 representative strains from Spain and other reported isolates from the United States, Germany, Italy, Japan, and Sweden were described by analyzing the partial sequence of the major capsid protein (VP1) gene. The strains from Spain were clearly identified as EV13 (79.5% similarity with the EV13 reference strain) and were grouped phylogenetically into two different clusters (by origination on either the Iberian Peninsula or Canary Islands). Isolates from Germany from 2000 clustered with the Canary Islands group. The isolates from other countries obtained before 2000 were genetically distant. Changes in EV13 coding sequence involved several differences in the C-terminal extreme of the VP1 protein. Part of the neutralizing antigenic site III has been described in this genome region in poliovirus and swine vesicular disease virus.

        Cite This Article
    EID Avellón A, Casas I, Trallero G, Pérez C, Tenorio A, Palacios G, et al. Molecular Analysis of Echovirus 13 Isolates and Aseptic Meningitis, Spain. Emerg Infect Dis. 2003;9(8):934-941. https://dx.doi.org/10.3201/eid0908.030080
    AMA Avellón A, Casas I, Trallero G, et al. Molecular Analysis of Echovirus 13 Isolates and Aseptic Meningitis, Spain. Emerging Infectious Diseases. 2003;9(8):934-941. doi:10.3201/eid0908.030080.
    APA Avellón, A., Casas, I., Trallero, G., Pérez, C., Tenorio, A., & Palacios, G. (2003). Molecular Analysis of Echovirus 13 Isolates and Aseptic Meningitis, Spain. Emerging Infectious Diseases, 9(8), 934-941. https://dx.doi.org/10.3201/eid0908.030080.
  • Molecular Characterization of a Non–Babesia divergens Organism Causing Zoonotic Babesiosis in Europe PDF Version [PDF - 286 KB - 6 pages]
    B. L. Herwaldt et al.
        View Abstract

    In Europe, most reported human cases of babesiosis have been attributed, without strong molecular evidence, to infection with the bovine parasite Babesia divergens. We investigated the first known human cases of babesiosis in Italy and Austria, which occurred in two asplenic men. The complete 18S ribosomal RNA (18S rRNA) gene was amplified from specimens of their whole blood by polymerase chain reaction (PCR). With phylogenetic analysis, we compared the DNA sequences of the PCR products with those for other Babesia spp. The DNA sequences were identical for the organism from the two patients. In phylogenetic analysis, the organism clusters with B. odocoilei, a parasite of white-tailed deer; these two organisms form a sister group with B. divergens. This evidence indicates the patients were not infected with B. divergens but with an organism with previously unreported molecular characteristics for the 18S rRNA gene.

        Cite This Article
    EID Herwaldt BL, Cacciò S, Gherlinzoni F, Aspöck H, Slemenda SB, Piccaluga P, et al. Molecular Characterization of a Non–Babesia divergens Organism Causing Zoonotic Babesiosis in Europe. Emerg Infect Dis. 2003;9(8):943-948. https://dx.doi.org/10.3201/eid0908.020748
    AMA Herwaldt BL, Cacciò S, Gherlinzoni F, et al. Molecular Characterization of a Non–Babesia divergens Organism Causing Zoonotic Babesiosis in Europe. Emerging Infectious Diseases. 2003;9(8):943-948. doi:10.3201/eid0908.020748.
    APA Herwaldt, B. L., Cacciò, S., Gherlinzoni, F., Aspöck, H., Slemenda, S. B., Piccaluga, P....Pieniazek, N. J. (2003). Molecular Characterization of a Non–Babesia divergens Organism Causing Zoonotic Babesiosis in Europe. Emerging Infectious Diseases, 9(8), 943-948. https://dx.doi.org/10.3201/eid0908.020748.
  • Severe Tungiasis in Underprivileged Communities: Case Series from Brazil PDF Version [PDF - 306 KB - 7 pages]
    H. Feldmeier et al.
        View Abstract

    Tungiasis is caused by infestation with the sand flea (Tunga penetrans). This ectoparasitosis is endemic in economically depressed communities in South American and African countries. Tungiasis is usually considered an entomologic nuisance and does not receive much attention from healthcare professionals. During a study on tungiasis-related disease in an economically depressed area in Fortaleza, northeast Brazil, we identified 16 persons infested with an extremely high number of parasites. These patients had >50 lesions each and showed signs of intense acute and chronic inflammation. Superinfection of the lesions had led to pustule formation, suppuration, and ulceration. Debilitating sequelae, such as loss of nails and difficulty in walking, were constant. In economically depressed urban neighborhoods characterized by a high transmission potential, poor housing conditions, social neglect, and inadequate healthcare behavior, tungiasis may develop into severe disease.

        Cite This Article
    EID Feldmeier H, Eisele M, Sabóia-Moura RC, Heukelbach J. Severe Tungiasis in Underprivileged Communities: Case Series from Brazil. Emerg Infect Dis. 2003;9(8):949-955. https://dx.doi.org/10.3201/eid0908.030041
    AMA Feldmeier H, Eisele M, Sabóia-Moura RC, et al. Severe Tungiasis in Underprivileged Communities: Case Series from Brazil. Emerging Infectious Diseases. 2003;9(8):949-955. doi:10.3201/eid0908.030041.
    APA Feldmeier, H., Eisele, M., Sabóia-Moura, R. C., & Heukelbach, J. (2003). Severe Tungiasis in Underprivileged Communities: Case Series from Brazil. Emerging Infectious Diseases, 9(8), 949-955. https://dx.doi.org/10.3201/eid0908.030041.
  • Pseudomonas aeruginosa and the Oropharyngeal Ecosystem of Tube-Fed Patients PDF Version [PDF - 322 KB - 4 pages]
    A. Leibovitz et al.
        View Abstract

    We evaluated whether elderly patients fed with nasogastric tubes (NGT) are predisposed to Pseudomonas aeruginosa colonization in the oropharynx. Fifty-three patients on NGT feeding and 50 orally fed controls with similar clinical characteristics were studied. The tongue dorsum was swabbed and cultured. P. aeruginosa was isolated in 18 (34%) of the NGT-fed group but in no controls (p<0.001). Other gram-negative bacteria were cultured from 34 (64%) of NGT-fed patients as compared with 4 (8%) of controls (p<0.001). Antibiotic susceptibility of the oropharyngeal P. aeruginosa isolates was compared with that of isolates from sputum cultures obtained from our hospital’s bacteriologic laboratory. The oropharyngeal isolates showed a higher rate of resistance; differences were significant for amikacin (p<0.03). Scanning electron microscope studies showed a biofilm containing P. aeruginosa organisms. The pulsed-field gel electrophoresis profile of these organisms was similar to that of P. aeruginosa isolates from the oropharynx. NGT-fed patients may serve as vectors of resistant P. aeruginosa strains.

        Cite This Article
    EID Leibovitz A, Dan M, Zinger J, Carmeli Y, Habot B, Segal R, et al. Pseudomonas aeruginosa and the Oropharyngeal Ecosystem of Tube-Fed Patients. Emerg Infect Dis. 2003;9(8):956-959. https://dx.doi.org/10.3201/eid0908.030054
    AMA Leibovitz A, Dan M, Zinger J, et al. Pseudomonas aeruginosa and the Oropharyngeal Ecosystem of Tube-Fed Patients. Emerging Infectious Diseases. 2003;9(8):956-959. doi:10.3201/eid0908.030054.
    APA Leibovitz, A., Dan, M., Zinger, J., Carmeli, Y., Habot, B., & Segal, R. (2003). Pseudomonas aeruginosa and the Oropharyngeal Ecosystem of Tube-Fed Patients. Emerging Infectious Diseases, 9(8), 956-959. https://dx.doi.org/10.3201/eid0908.030054.
  • Nonmalarial Infant Deaths and DDT Use for Malaria Control PDF Version [PDF - 192 KB - 5 pages]
    A. Chen and W. J. Rogan
        View Abstract

    Although dichlorodiphenyl trichloroethane (DDT) is being banned worldwide, countries in sub-Saharan Africa have sought exemptions for malaria control. Few studies show illness in children from the use of DDT, and the possibility of risks to them from DDT use has been minimized. However, plausible if inconclusive studies associate DDT with more preterm births and shorter duration of lactation, which raise the possibility that DDT does indeed have such toxicity. Assuming that these associations are causal, we estimated the increase in infant deaths that might result from DDT spraying. The estimated increases are of the same order of magnitude as the decreases from effective malaria control. Unintended consequences of DDT use need to be part of the discussion of modern vector control policy.

        Cite This Article
    EID Chen A, Rogan WJ. Nonmalarial Infant Deaths and DDT Use for Malaria Control. Emerg Infect Dis. 2003;9(8):960-964. https://dx.doi.org/10.3201/eid0908.030082
    AMA Chen A, Rogan WJ. Nonmalarial Infant Deaths and DDT Use for Malaria Control. Emerging Infectious Diseases. 2003;9(8):960-964. doi:10.3201/eid0908.030082.
    APA Chen, A., & Rogan, W. J. (2003). Nonmalarial Infant Deaths and DDT Use for Malaria Control. Emerging Infectious Diseases, 9(8), 960-964. https://dx.doi.org/10.3201/eid0908.030082.
  • Multidrug-Resistant Tuberculosis in HIV-Negative Patients, Buenos Aires, Argentina PDF Version [PDF - 235 KB - 5 pages]
    D. Palmero et al.
        View Abstract

    Initial multidrug-resistant (MDR) tuberculosis (TB) in HIV-negative patients treated at a Buenos Aires referral hospital from 1991 to 2000 was examined by using molecular clustering of available isolates. Of 291 HIV-negative MDRTB patients, 79 were initially MDR. We observed an ascending trend of initial MDRTB during this decade (p=0.0033). The M strain, which was responsible for an institutional AIDS-associated outbreak that peaked in 1995 to 1997, caused 24 of the 49 initial MDRTB cases available for restriction fragment length polymorphism. Of those, 21 were diagnosed in 1997 or later. Hospital exposure increased the risk of acquiring M strain–associated MDRTB by approximately two and a half times. The emergence of initial MDRTB among HIV-negative patients after 1997 was apparently a sequel of the AIDS-related outbreak. Because the prevalence of M strain–associated disease in the study population did not level out by the end of the decade, further expansion of this disease is possible.

        Cite This Article
    EID Palmero D, Ritacco V, Ambroggi M, Natiello M, Barrera L, Capone L, et al. Multidrug-Resistant Tuberculosis in HIV-Negative Patients, Buenos Aires, Argentina. Emerg Infect Dis. 2003;9(8):965-969. https://dx.doi.org/10.3201/eid0908.020474
    AMA Palmero D, Ritacco V, Ambroggi M, et al. Multidrug-Resistant Tuberculosis in HIV-Negative Patients, Buenos Aires, Argentina. Emerging Infectious Diseases. 2003;9(8):965-969. doi:10.3201/eid0908.020474.
    APA Palmero, D., Ritacco, V., Ambroggi, M., Natiello, M., Barrera, L., Capone, L....Abbate, E. (2003). Multidrug-Resistant Tuberculosis in HIV-Negative Patients, Buenos Aires, Argentina. Emerging Infectious Diseases, 9(8), 965-969. https://dx.doi.org/10.3201/eid0908.020474.
  • Invasive Group A Streptococcal Disease: Risk Factors for Adults PDF Version [PDF - 279 KB - 8 pages]
    S. H. Factor et al.
        View Abstract

    We conducted a case-control study to identify risk factors for invasive group A streptococcal (GAS) infections, which can be fatal. Case-patients were identified when Streptoccus pyogenes was isolated from a normally sterile site and control subjects (two or more) were identified and matched to case-patients by using sequential-digit telephone dialing. All participants were noninstitutionalized surveillance area residents, >18 years of age. Conditional logistic regression identified the risk factors for invasive GAS infection: in adults 18 to 44 years of age, exposure to one or more children with sore throats (relative risk [RR]=4.93, p=0.02), HIV infection (RR =15.01, p=0.04), and history of injecting drug use (RR=14.71, p=0.003); in adults >45 years of age, number of persons in the home (RR=2.68, p=0.004), diabetes (RR= 2.27, p=0.03), cardiac disease (RR=3.24, p=0.006), cancer (RR= 3.54, p=0.006), and corticosteroid use (RR=5.18, p=0.03). Thus, host and environmental factors increased the risk for invasive GAS disease.

        Cite This Article
    EID Factor SH, Levine OS, Schwartz B, Harrison LH, Farley MM, McGeer A, et al. Invasive Group A Streptococcal Disease: Risk Factors for Adults. Emerg Infect Dis. 2003;9(8):970-977. https://dx.doi.org/10.3201/eid0908.020745
    AMA Factor SH, Levine OS, Schwartz B, et al. Invasive Group A Streptococcal Disease: Risk Factors for Adults. Emerging Infectious Diseases. 2003;9(8):970-977. doi:10.3201/eid0908.020745.
    APA Factor, S. H., Levine, O. S., Schwartz, B., Harrison, L. H., Farley, M. M., McGeer, A....Schuchat, A. (2003). Invasive Group A Streptococcal Disease: Risk Factors for Adults. Emerging Infectious Diseases, 9(8), 970-977. https://dx.doi.org/10.3201/eid0908.020745.
  • Community-Acquired Methicillin-Resistant Staphylococcus aureus Carrying Panton-Valentine Leukocidin Genes: Worldwide Emergence PDF Version [PDF - 353 KB - 7 pages]
    F. Vandenesch et al.
        View Abstract

    Infections caused by community-acquired (CA)-methicillin resistant Staphylococcus aureus (MRSA) have been reported worldwide. We assessed whether any common genetic markers existed among 117 CA-MRSA isolates from the United States, France, Switzerland, Australia, New Zealand, and Western Samoa by performing polymerase chain reaction for 24 virulence factors and the methicillin-resistance determinant. The genetic background of the strain was analyzed by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST). The CA-MRSA strains shared a type IV SCCmec cassette and the Panton-Valentine leukocidin locus, whereas the distribution of the other toxin genes was quite specific to the strains from each continent. PFGE and MLST analysis indicated distinct genetic backgrounds associated with each geographic origin, although predominantly restricted to the agr3 background. Within each continent, the genetic background of CA-MRSA strains did not correspond to that of the hospital-acquired MRSA.

        Cite This Article
    EID Vandenesch F, Naimi T, Enright MC, Lina G, Nimmo GR, Heffernan H, et al. Community-Acquired Methicillin-Resistant Staphylococcus aureus Carrying Panton-Valentine Leukocidin Genes: Worldwide Emergence. Emerg Infect Dis. 2003;9(8):978-984. https://dx.doi.org/10.3201/eid0908.030089
    AMA Vandenesch F, Naimi T, Enright MC, et al. Community-Acquired Methicillin-Resistant Staphylococcus aureus Carrying Panton-Valentine Leukocidin Genes: Worldwide Emergence. Emerging Infectious Diseases. 2003;9(8):978-984. doi:10.3201/eid0908.030089.
    APA Vandenesch, F., Naimi, T., Enright, M. C., Lina, G., Nimmo, G. R., Heffernan, H....Etienne, J. (2003). Community-Acquired Methicillin-Resistant Staphylococcus aureus Carrying Panton-Valentine Leukocidin Genes: Worldwide Emergence. Emerging Infectious Diseases, 9(8), 978-984. https://dx.doi.org/10.3201/eid0908.030089.
  • Candidemia in Finland, 1995–1999 PDF Version [PDF - 343 KB - 6 pages]
    E. Poikonen et al.
        View Abstract

    We analyzed laboratory-based surveillance candidemia data from the National Infectious Disease Register in Finland and reviewed cases of candidemia from one tertiary-care hospital from 1995 to 1999. A total of 479 candidemia cases were reported to the Register. The annual incidence rose from 1.7 per 100,000 population in 1995 to 2.2 in 1999. Species other than Candida albicans accounted for 30% of cases without change in the proportion. A total of 79 cases of candidemia were identified at the hospital; the rate varied from 0.03 to 0.05 per 1,000 patient-days by year. Predisposing factors included indwelling catheters (81%), gastrointestinal surgery (27%), hematologic malignancy (25%), other types of surgery (21%), and solid malignancies (20%). Crude 7-day and 30-day case-fatality ratios were 15% and 35%, respectively. The rate of candidemia increased in Finland but is still substantially lower than in the United States. No shift to non–C. albicans species could be detected.

        Cite This Article
    EID Poikonen E, Lyytikäinen O, Anttila V, Ruutu P. Candidemia in Finland, 1995–1999. Emerg Infect Dis. 2003;9(8):985-990. https://dx.doi.org/10.3201/eid0908.030069
    AMA Poikonen E, Lyytikäinen O, Anttila V, et al. Candidemia in Finland, 1995–1999. Emerging Infectious Diseases. 2003;9(8):985-990. doi:10.3201/eid0908.030069.
    APA Poikonen, E., Lyytikäinen, O., Anttila, V., & Ruutu, P. (2003). Candidemia in Finland, 1995–1999. Emerging Infectious Diseases, 9(8), 985-990. https://dx.doi.org/10.3201/eid0908.030069.

Dispatches

  • Severe Acute Respiratory Syndrome: Temporal Stability and Geographic Variation in Death Rates and Doubling Times PDF Version [PDF - 259 KB - 4 pages]
    A. P. Galvani et al.
        View Abstract

    We analyzed temporal stability and geographic trends in cumulative case-fatality rates and average doubling times of severe acute respiratory syndrome (SARS). In part, we account for correlations between case-fatality rates and doubling times through differences in control measures. Factors that may alter future estimates of case-fatality rates, reasons for heterogeneity in doubling times among countries, and implications for the control of SARS are discussed.

        Cite This Article
    EID Galvani AP, Lei X, Jewell NP. Severe Acute Respiratory Syndrome: Temporal Stability and Geographic Variation in Death Rates and Doubling Times. Emerg Infect Dis. 2003;9(8):991-994. https://dx.doi.org/10.3201/eid0908.030334
    AMA Galvani AP, Lei X, Jewell NP. Severe Acute Respiratory Syndrome: Temporal Stability and Geographic Variation in Death Rates and Doubling Times. Emerging Infectious Diseases. 2003;9(8):991-994. doi:10.3201/eid0908.030334.
    APA Galvani, A. P., Lei, X., & Jewell, N. P. (2003). Severe Acute Respiratory Syndrome: Temporal Stability and Geographic Variation in Death Rates and Doubling Times. Emerging Infectious Diseases, 9(8), 991-994. https://dx.doi.org/10.3201/eid0908.030334.
  • Emerging Pathogen in Wild Amphibians and Frogs (Rana catesbeiana) Farmed for International Trade PDF Version [PDF - 242 KB - 4 pages]
    R. Mazzoni et al.
        View Abstract

    Chytridiomycosis is an emerging disease responsible for global decline and extinction of amphibians. We report the causative agent, Batrachochytrium dendrobatidis, in North American bullfrogs (Rana catesbeiana) farmed for the international restaurant trade. Our findings suggest that international trade may play a key role in the global dissemination of this and other emerging infectious diseases in wildlife.

        Cite This Article
    EID Mazzoni R, Cunningham AA, Daszak P, Apolo A, Perdomo E, Speranza G, et al. Emerging Pathogen in Wild Amphibians and Frogs (Rana catesbeiana) Farmed for International Trade. Emerg Infect Dis. 2003;9(8):995-998. https://dx.doi.org/10.3201/eid0908.030030
    AMA Mazzoni R, Cunningham AA, Daszak P, et al. Emerging Pathogen in Wild Amphibians and Frogs (Rana catesbeiana) Farmed for International Trade. Emerging Infectious Diseases. 2003;9(8):995-998. doi:10.3201/eid0908.030030.
    APA Mazzoni, R., Cunningham, A. A., Daszak, P., Apolo, A., Perdomo, E., & Speranza, G. (2003). Emerging Pathogen in Wild Amphibians and Frogs (Rana catesbeiana) Farmed for International Trade. Emerging Infectious Diseases, 9(8), 995-998. https://dx.doi.org/10.3201/eid0908.030030.
  • NmcA Carbapenem-hydrolyzing Enzyme in Enterobacter cloacae in North America PDF Version [PDF - 298 KB - 4 pages]
    S. Pottumarthy et al.
        View Abstract

    An imipenem-resistant Enterobacter cloacae isolate was recovered from the blood of a patient with a hematologic malignancy. Analytical isoelectric focusing, inhibitor studies, hydrolysis, induction assays, and molecular sequencing methods confirmed the presence of a NmcA carbapenem-hydrolyzing enzyme. This first report of NmcA detected in North America warrants further investigation into its distribution and clinical impact.

        Cite This Article
    EID Pottumarthy S, Moland ES, Juretschko S, Swanzy SR, Thomson KS, Fritsche TR, et al. NmcA Carbapenem-hydrolyzing Enzyme in Enterobacter cloacae in North America. Emerg Infect Dis. 2003;9(8):999-1002. https://dx.doi.org/10.3201/eid0908.030096
    AMA Pottumarthy S, Moland ES, Juretschko S, et al. NmcA Carbapenem-hydrolyzing Enzyme in Enterobacter cloacae in North America. Emerging Infectious Diseases. 2003;9(8):999-1002. doi:10.3201/eid0908.030096.
    APA Pottumarthy, S., Moland, E. S., Juretschko, S., Swanzy, S. R., Thomson, K. S., & Fritsche, T. R. (2003). NmcA Carbapenem-hydrolyzing Enzyme in Enterobacter cloacae in North America. Emerging Infectious Diseases, 9(8), 999-1002. https://dx.doi.org/10.3201/eid0908.030096.
  • Fluid Intake and Decreased Risk for Hospitalization for Dengue Fever, Nicaragua PDF Version [PDF - 338 KB - 4 pages]
    E. Harris et al.
        View Abstract

    In a hospital and health center-based study in Nicaragua, fluid intake during the 24 hours before being seen by a clinician was statistically associated with decreased risk for hospitalization of dengue fever patients. Similar results were obtained for children <15 years of age and older adolescents and adults in independent analyses.

        Cite This Article
    EID Harris E, Pérez L, Phares CR, Pérez Md, Idiaquez W, Rocha J, et al. Fluid Intake and Decreased Risk for Hospitalization for Dengue Fever, Nicaragua. Emerg Infect Dis. 2003;9(8):1003-1006. https://dx.doi.org/10.3201/eid0908.020456
    AMA Harris E, Pérez L, Phares CR, et al. Fluid Intake and Decreased Risk for Hospitalization for Dengue Fever, Nicaragua. Emerging Infectious Diseases. 2003;9(8):1003-1006. doi:10.3201/eid0908.020456.
    APA Harris, E., Pérez, L., Phares, C. R., Pérez, M. d., Idiaquez, W., Rocha, J....Balmaseda, A. (2003). Fluid Intake and Decreased Risk for Hospitalization for Dengue Fever, Nicaragua. Emerging Infectious Diseases, 9(8), 1003-1006. https://dx.doi.org/10.3201/eid0908.020456.
  • From Pig to Pacifier: Chitterling-Associated Yersiniosis Outbreak among Black Infants PDF Version [PDF - 175 KB - 3 pages]
    T. F. Jones et al.
        View Abstract

    In this case-control study of Yersinia enterocolitica infections among black infants, chitterling preparation was significantly associated with illness (p<0.001). Of 13 samples of chitterlings tested, 2 were positive for Yersinia intermedia and 5 for Salmonella. Decontamination of chitterlings before sale with methods such as irradiation should be strongly considered.

        Cite This Article
    EID Jones TF, Buckingham SC, Bopp CA, Ribot E, Schaffner W. From Pig to Pacifier: Chitterling-Associated Yersiniosis Outbreak among Black Infants. Emerg Infect Dis. 2003;9(8):1007-1009. https://dx.doi.org/10.3201/eid0908.030103
    AMA Jones TF, Buckingham SC, Bopp CA, et al. From Pig to Pacifier: Chitterling-Associated Yersiniosis Outbreak among Black Infants. Emerging Infectious Diseases. 2003;9(8):1007-1009. doi:10.3201/eid0908.030103.
    APA Jones, T. F., Buckingham, S. C., Bopp, C. A., Ribot, E., & Schaffner, W. (2003). From Pig to Pacifier: Chitterling-Associated Yersiniosis Outbreak among Black Infants. Emerging Infectious Diseases, 9(8), 1007-1009. https://dx.doi.org/10.3201/eid0908.030103.
  • Acute Hemorrhagic Conjunctivitis caused by Coxsackievirus A24 Variant, South Korea, 2002 PDF Version [PDF - 185 KB - 3 pages]
    G. Kayali et al.
        View Abstract

    In summer 2002, a nationwide outbreak of acute hemorrhagic conjunctivitis occurred in South Korea. The etiologic agent was confirmed as coxsackievirus A24 variant (CA24v) by virus isolation and sequencing of a part of the VP1 gene. Phylogentic analysis, based on the protease 3C sequences, showed that the Korean isolates were clustered into a lineage distinct from the CA24v isolates reported in previous outbreaks in Asia.

        Cite This Article
    EID Kayali G, Park S, Choi Y, Kim H, Lee K, Park W, et al. Acute Hemorrhagic Conjunctivitis caused by Coxsackievirus A24 Variant, South Korea, 2002. Emerg Infect Dis. 2003;9(8):1010-1012. https://dx.doi.org/10.3201/eid0908.030190
    AMA Kayali G, Park S, Choi Y, et al. Acute Hemorrhagic Conjunctivitis caused by Coxsackievirus A24 Variant, South Korea, 2002. Emerging Infectious Diseases. 2003;9(8):1010-1012. doi:10.3201/eid0908.030190.
    APA Kayali, G., Park, S., Choi, Y., Kim, H., Lee, K., Park, W....Choe, K. (2003). Acute Hemorrhagic Conjunctivitis caused by Coxsackievirus A24 Variant, South Korea, 2002. Emerging Infectious Diseases, 9(8), 1010-1012. https://dx.doi.org/10.3201/eid0908.030190.
  • Nonhemolytic, Nonmotile Gram-Positive Rods Indicative of Bacillus anthracis PDF Version [PDF - 178 KB - 3 pages]
    E. G. Dib et al.
        View Abstract

    We report a 40-year-old female patient who was admitted to the hospital because of a left ovarian mass torsion. A nonhemolytic, nonmotile Bacillus, suspicious of Bacillus anthracis, was isolated from a blood culture. We discuss the evaluation that led to the final identification of the bacterium as B. megaterium.

        Cite This Article
    EID Dib EG, Dib SA, Korkmaz DA, Mobarakai NK, Glaser JB. Nonhemolytic, Nonmotile Gram-Positive Rods Indicative of Bacillus anthracis. Emerg Infect Dis. 2003;9(8):1013-1015. https://dx.doi.org/10.3201/eid0908.030205
    AMA Dib EG, Dib SA, Korkmaz DA, et al. Nonhemolytic, Nonmotile Gram-Positive Rods Indicative of Bacillus anthracis. Emerging Infectious Diseases. 2003;9(8):1013-1015. doi:10.3201/eid0908.030205.
    APA Dib, E. G., Dib, S. A., Korkmaz, D. A., Mobarakai, N. K., & Glaser, J. B. (2003). Nonhemolytic, Nonmotile Gram-Positive Rods Indicative of Bacillus anthracis. Emerging Infectious Diseases, 9(8), 1013-1015. https://dx.doi.org/10.3201/eid0908.030205.

Another Dimension

  • Eating Dirt PDF Version [PDF - 147 KB - 6 pages]
    G. N. Callahan
        View Abstract

    Please
This earth is blessed
Do not play in it
Sign on the wall of El Santuario de Chimayo, New Mexico

        Cite This Article
    EID Callahan GN. Eating Dirt. Emerg Infect Dis. 2003;9(8):1016-1021. https://dx.doi.org/10.3201/eid0908.030033
    AMA Callahan GN. Eating Dirt. Emerging Infectious Diseases. 2003;9(8):1016-1021. doi:10.3201/eid0908.030033.
    APA Callahan, G. N. (2003). Eating Dirt. Emerging Infectious Diseases, 9(8), 1016-1021. https://dx.doi.org/10.3201/eid0908.030033.

Letters

  • Carbapenem-Resistant Pseudomonas aeruginosa–Carrying VIM-2 Metallo-β-Lactamase Determinants, Croatia PDF Version [PDF - 160 KB - 2 pages]
    S. Sardelic et al.
            Cite This Article
    EID Sardelic S, Pallecchi L, Punda-Polic V, Rossolini G. Carbapenem-Resistant Pseudomonas aeruginosa–Carrying VIM-2 Metallo-β-Lactamase Determinants, Croatia. Emerg Infect Dis. 2003;9(8):1022-1023. https://dx.doi.org/10.3201/eid0908.020373
    AMA Sardelic S, Pallecchi L, Punda-Polic V, et al. Carbapenem-Resistant Pseudomonas aeruginosa–Carrying VIM-2 Metallo-β-Lactamase Determinants, Croatia. Emerging Infectious Diseases. 2003;9(8):1022-1023. doi:10.3201/eid0908.020373.
    APA Sardelic, S., Pallecchi, L., Punda-Polic, V., & Rossolini, G. (2003). Carbapenem-Resistant Pseudomonas aeruginosa–Carrying VIM-2 Metallo-β-Lactamase Determinants, Croatia. Emerging Infectious Diseases, 9(8), 1022-1023. https://dx.doi.org/10.3201/eid0908.020373.
  • Rickettsia felis in the United Kingdom PDF Version [PDF - 161 KB - 2 pages]
    M. J. Kenny et al.
            Cite This Article
    EID Kenny MJ, Birtles RJ, Day MJ, Shaw SE. Rickettsia felis in the United Kingdom. Emerg Infect Dis. 2003;9(8):1023-1024. https://dx.doi.org/10.3201/eid0908.030314
    AMA Kenny MJ, Birtles RJ, Day MJ, et al. Rickettsia felis in the United Kingdom. Emerging Infectious Diseases. 2003;9(8):1023-1024. doi:10.3201/eid0908.030314.
    APA Kenny, M. J., Birtles, R. J., Day, M. J., & Shaw, S. E. (2003). Rickettsia felis in the United Kingdom. Emerging Infectious Diseases, 9(8), 1023-1024. https://dx.doi.org/10.3201/eid0908.030314.
  • Community Transmission of Extended-Spectrum β-Lactamase PDF Version [PDF - 160 KB - 2 pages]
    B. Mirelis et al.
            Cite This Article
    EID Mirelis B, Navarro F, Miró E, Mesa RJ, Coll P, Prats G, et al. Community Transmission of Extended-Spectrum β-Lactamase. Emerg Infect Dis. 2003;9(8):1024-1025. https://dx.doi.org/10.3201/eid0908.030094
    AMA Mirelis B, Navarro F, Miró E, et al. Community Transmission of Extended-Spectrum β-Lactamase. Emerging Infectious Diseases. 2003;9(8):1024-1025. doi:10.3201/eid0908.030094.
    APA Mirelis, B., Navarro, F., Miró, E., Mesa, R. J., Coll, P., & Prats, G. (2003). Community Transmission of Extended-Spectrum β-Lactamase. Emerging Infectious Diseases, 9(8), 1024-1025. https://dx.doi.org/10.3201/eid0908.030094.
  • Polymyxin-Resistant Acinetobacter spp. Isolates: What is Next? PDF Version [PDF - 165 KB - 3 pages]
    A. O. Reis et al.
            Cite This Article
    EID Reis AO, Luz DA, Tognim MC, Sader HS, Gales AC. Polymyxin-Resistant Acinetobacter spp. Isolates: What is Next?. Emerg Infect Dis. 2003;9(8):1025-1027. https://dx.doi.org/10.3201/eid0908.030052
    AMA Reis AO, Luz DA, Tognim MC, et al. Polymyxin-Resistant Acinetobacter spp. Isolates: What is Next?. Emerging Infectious Diseases. 2003;9(8):1025-1027. doi:10.3201/eid0908.030052.
    APA Reis, A. O., Luz, D. A., Tognim, M. C., Sader, H. S., & Gales, A. C. (2003). Polymyxin-Resistant Acinetobacter spp. Isolates: What is Next?. Emerging Infectious Diseases, 9(8), 1025-1027. https://dx.doi.org/10.3201/eid0908.030052.
  • Multidrug-Resistant Shiga Toxin–Producing Escherichia coli O118:H16 in Latin America PDF Version [PDF - 158 KB - 2 pages]
    A. F. Pestana de Castro et al.
            Cite This Article
    EID Pestana de Castro AF, Guerra B, Leomil L, Aidar-Ugrinovitch L, Beutin L. Multidrug-Resistant Shiga Toxin–Producing Escherichia coli O118:H16 in Latin America. Emerg Infect Dis. 2003;9(8):1027-1028. https://dx.doi.org/10.3201/eid0908.030062
    AMA Pestana de Castro AF, Guerra B, Leomil L, et al. Multidrug-Resistant Shiga Toxin–Producing Escherichia coli O118:H16 in Latin America. Emerging Infectious Diseases. 2003;9(8):1027-1028. doi:10.3201/eid0908.030062.
    APA Pestana de Castro, A. F., Guerra, B., Leomil, L., Aidar-Ugrinovitch, L., & Beutin, L. (2003). Multidrug-Resistant Shiga Toxin–Producing Escherichia coli O118:H16 in Latin America. Emerging Infectious Diseases, 9(8), 1027-1028. https://dx.doi.org/10.3201/eid0908.030062.

About the Cover

  • Jan Steen (c. 1625–1679). Beware of Luxury (c. 1665). PDF Version [PDF - 129 KB - 1 page]
    P. Potter
            Cite This Article
    EID Potter P. Jan Steen (c. 1625–1679). Beware of Luxury (c. 1665).. Emerg Infect Dis. 2003;9(8):1035. https://dx.doi.org/10.3201/eid0908.AC0908
    AMA Potter P. Jan Steen (c. 1625–1679). Beware of Luxury (c. 1665).. Emerging Infectious Diseases. 2003;9(8):1035. doi:10.3201/eid0908.AC0908.
    APA Potter, P. (2003). Jan Steen (c. 1625–1679). Beware of Luxury (c. 1665).. Emerging Infectious Diseases, 9(8), 1035. https://dx.doi.org/10.3201/eid0908.AC0908.

Corrections

  • Correction, Vol. 9, No. 6 PDF Version [PDF - 120 KB - 1 page]
            Cite This Article
    EID Correction, Vol. 9, No. 6. Emerg Infect Dis. 2003;9(8):1028. https://dx.doi.org/10.3201/eid0908.C10908
    AMA Correction, Vol. 9, No. 6. Emerging Infectious Diseases. 2003;9(8):1028. doi:10.3201/eid0908.C10908.
    APA (2003). Correction, Vol. 9, No. 6. Emerging Infectious Diseases, 9(8), 1028. https://dx.doi.org/10.3201/eid0908.C10908.

News and Notes

  • Emergence and Control of Zoonotic Viral Encephalitis PDF Version [PDF - 138 KB - 2 pages]
    C. H. Calisher et al.
            Cite This Article
    EID Calisher CH, Dodet B, Griffin D. Emergence and Control of Zoonotic Viral Encephalitis. Emerg Infect Dis. 2003;9(8):1029-1030. https://dx.doi.org/10.3201/eid0908.030319
    AMA Calisher CH, Dodet B, Griffin D. Emergence and Control of Zoonotic Viral Encephalitis. Emerging Infectious Diseases. 2003;9(8):1029-1030. doi:10.3201/eid0908.030319.
    APA Calisher, C. H., Dodet, B., & Griffin, D. (2003). Emergence and Control of Zoonotic Viral Encephalitis. Emerging Infectious Diseases, 9(8), 1029-1030. https://dx.doi.org/10.3201/eid0908.030319.
  • New and Reemerging Infectious Diseases PDF Version [PDF - 158 KB - 4 pages]
    R. Docampo
            Cite This Article
    EID Docampo R. New and Reemerging Infectious Diseases. Emerg Infect Dis. 2003;9(8):1030-1033. https://dx.doi.org/10.3201/eid0908.030324
    AMA Docampo R. New and Reemerging Infectious Diseases. Emerging Infectious Diseases. 2003;9(8):1030-1033. doi:10.3201/eid0908.030324.
    APA Docampo, R. (2003). New and Reemerging Infectious Diseases. Emerging Infectious Diseases, 9(8), 1030-1033. https://dx.doi.org/10.3201/eid0908.030324.
TOP