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Issue Cover for Volume 10, Number 1—January 2004

Volume 10, Number 1—January 2004

[PDF - 4.90 MB - 171 pages]

Perspective

Salmonella Enteritidis Infections, United States, 1985–1999 [PDF - 236 KB - 7 pages]
M. E. Patrick et al.

Salmonella enterica serotype Enteritidis emerged as an important illness during the 1980s. Investigations showed that consumption of undercooked eggs was the major risk factor for disease, and a variety of prevention and control efforts were initiated during the 1990s. We describe sporadic infections and outbreaks of S. Enteritidis in the United States from 1985 through 1999 and discuss prevention and control efforts. After reaching a high of 3.9 per 100,000 population in 1995, S. Enteritidis infections declined to 1.98 per 100,000 in 1999. While the total number of outbreaks decreased by half, those in the western states tripled. Outbreaks of S. Enteritidis phage type 4 infections accounted for 49% of outbreaks in 1999. Outbreak-associated deaths in health facilities decreased from 14 in 1987 to 0 in 1999. Overall, rates of sporadic S. Enteritidis infection, outbreaks, and deaths have declined dramatically. For further reductions, control measures should continue to be applied along the entire farm-to-table continuum.

EID Patrick ME, Adcock PM, Gomez TM, Altekruse SF, Holland BH, Tauxe RV, et al. Salmonella Enteritidis Infections, United States, 1985–1999. Emerg Infect Dis. 2004;10(1):1-7. https://dx.doi.org/10.3201/eid1001.020572
AMA Patrick ME, Adcock PM, Gomez TM, et al. Salmonella Enteritidis Infections, United States, 1985–1999. Emerging Infectious Diseases. 2004;10(1):1-7. doi:10.3201/eid1001.020572.
APA Patrick, M. E., Adcock, P. M., Gomez, T. M., Altekruse, S. F., Holland, B. H., Tauxe, R. V....Swerdlow, D. L. (2004). Salmonella Enteritidis Infections, United States, 1985–1999. Emerging Infectious Diseases, 10(1), 1-7. https://dx.doi.org/10.3201/eid1001.020572.

Emerging Issues in Virus Taxonomy [PDF - 138 KB - 6 pages]
M. H. van Regenmortel and B. W. Mahy

Viruses occupy a unique position in biology. Although they possess some of the properties of living systems such as having a genome, they are actually nonliving infectious entities and should not be considered microorganisms. A clear distinction should be drawn between the terms virus, virion, and virus species. Species is the most fundamental taxonomic category used in all biological classification. In 1991, the International Committee on Taxonomy of Viruses (ICTV) decided that the category of virus species should be used in virus classification together with the categories of genus and family. More than 50 ICTV study groups were given the task of demarcating the 1,550 viral species that were recognized in the 7th ICTV report, which was published in 2000. We briefly describe the changes in virus classification that were introduced in that report. We also discuss recent proposals to introduce a nonlatinized binomial nomenclature for virus species.

EID van Regenmortel MH, Mahy BW. Emerging Issues in Virus Taxonomy. Emerg Infect Dis. 2004;10(1):8-13. https://dx.doi.org/10.3201/eid1001.030279
AMA van Regenmortel MH, Mahy BW. Emerging Issues in Virus Taxonomy. Emerging Infectious Diseases. 2004;10(1):8-13. doi:10.3201/eid1001.030279.
APA van Regenmortel, M. H., & Mahy, B. W. (2004). Emerging Issues in Virus Taxonomy. Emerging Infectious Diseases, 10(1), 8-13. https://dx.doi.org/10.3201/eid1001.030279.
Synopses

Fungal Biofilms and Drug Resistance [PDF - 170 KB - 6 pages]
M. A. Jabra-Rizk et al.

Candida species, including the novel opportunistic pathogen Candida dubliniensis, are now emerging as major agents of nosocomial infections. Many such manifestations of infections associated with the formation of Candida biofilms include those occurring on devices such as indwelling intravascular catheters. Fungal biofilm-associated infections are frequently refractory to conventional therapy because of resistance to antimicrobial agents. This resistance could be in part due to the surface-induced upregulation of drug efflux pumps. Biofilm-associated Candida show uniform resistance to a wide spectrum of the currently available conventional antifungal agents, which implies that antimicrobial drugs that specifically target biofilm-associated infections are needed. The novel classes of antifungal agents, the lipid formulation of amphotericins, and the echinocandins have demonstrated unique antifungal activity against the resistant Candida biofilms, providing a breakthrough in the treatment of life-threatening invasive systemic mycoses. The use of drugs effective in combating biofilm-associated infections could lead to major developments in the treatment of fungal implant infections.

EID Jabra-Rizk MA, Falkler WA, Meiller TF. Fungal Biofilms and Drug Resistance. Emerg Infect Dis. 2004;10(1):14-19. https://dx.doi.org/10.3201/eid1001.030119
AMA Jabra-Rizk MA, Falkler WA, Meiller TF. Fungal Biofilms and Drug Resistance. Emerging Infectious Diseases. 2004;10(1):14-19. doi:10.3201/eid1001.030119.
APA Jabra-Rizk, M. A., Falkler, W. A., & Meiller, T. F. (2004). Fungal Biofilms and Drug Resistance. Emerging Infectious Diseases, 10(1), 14-19. https://dx.doi.org/10.3201/eid1001.030119.
Research

Severe Acute Respiratory Syndrome–associated Coronavirus in Lung Tissue [PDF - 230 KB - 5 pages]
T. Mazzulli et al.

Efforts to contain severe acute respiratory syndrome (SARS) have been limited by the lack of a standardized, sensitive, and specific test for SARS-associated coronavirus (CoV). We used a standardized reverse transcription-polymerase chain reaction assay to detect SARS-CoV in lung samples obtained from well-characterized patients who died of SARS and from those who died of other reasons. SARS-CoV was detected in all 22 postmortem lung tissues (to 109 viral copies/g) from 11 patients with probable SARS but was not detected in any of the 23 lung control samples (sample analysis was blinded). The sensitivity and specificity (95% confidence interval) were 100% (84.6% to 100%) and 100% (85.1% to 100%), respectively. Viral loads were significantly associated with a shorter course of illness but not with the use of ribavirin or steroids. CoV was consistently identified in the lungs of all patients who died of SARS but not in control patients, supporting a primary role for CoV in deaths.

EID Mazzulli T, Farcas GA, Poutanen SM, Willey BM, Low DE, Butany J, et al. Severe Acute Respiratory Syndrome–associated Coronavirus in Lung Tissue. Emerg Infect Dis. 2004;10(1):20-24. https://dx.doi.org/10.3201/eid1001.030404
AMA Mazzulli T, Farcas GA, Poutanen SM, et al. Severe Acute Respiratory Syndrome–associated Coronavirus in Lung Tissue. Emerging Infectious Diseases. 2004;10(1):20-24. doi:10.3201/eid1001.030404.
APA Mazzulli, T., Farcas, G. A., Poutanen, S. M., Willey, B. M., Low, D. E., Butany, J....Kain, K. C. (2004). Severe Acute Respiratory Syndrome–associated Coronavirus in Lung Tissue. Emerging Infectious Diseases, 10(1), 20-24. https://dx.doi.org/10.3201/eid1001.030404.

Severe Acute Respiratory Syndrome, Beijing, 2003 [PDF - 103 KB - 7 pages]
W. Liang et al.

The largest outbreak of severe acute respiratory syndrome (SARS) struck Beijing in spring 2003. Multiple importations of SARS to Beijing initiated transmission in several healthcare facilities. Beijing’s outbreak began March 5; by late April, daily hospital admissions for SARS exceeded 100 for several days; 2,521 cases of probable SARS occurred. Attack rates were highest in those 20–39 years of age; 1% of cases occurred in children <10 years. The case-fatality rate was highest among patients >65 years (27.7% vs. 4.8% for those 20–64 years, p < 0.001). Healthcare workers accounted for 16% of probable cases. The proportion of case-patients without known contact to a SARS patient increased significantly in May. Implementation of early detection, isolation, contact tracing, quarantine, triage of case-patients to designated SARS hospitals, and community mobilization ended the outbreak.

EID Liang W, Zhu Z, Guo J, Liu Z, He X, Zhou W, et al. Severe Acute Respiratory Syndrome, Beijing, 2003. Emerg Infect Dis. 2004;10(1):25-31. https://dx.doi.org/10.3201/eid1001.030553
AMA Liang W, Zhu Z, Guo J, et al. Severe Acute Respiratory Syndrome, Beijing, 2003. Emerging Infectious Diseases. 2004;10(1):25-31. doi:10.3201/eid1001.030553.
APA Liang, W., Zhu, Z., Guo, J., Liu, Z., He, X., Zhou, W....Schuchat, A. (2004). Severe Acute Respiratory Syndrome, Beijing, 2003. Emerging Infectious Diseases, 10(1), 25-31. https://dx.doi.org/10.3201/eid1001.030553.

Influenza Epidemics in the United States, France, and Australia, 1972–1997 [PDF - 450 KB - 8 pages]
C. Viboud et al.

Influenza epidemics occur once a year during the winter in temperate areas. Little is known about the similarities between epidemics at different locations. We have analyzed pneumonia and influenza deaths from 1972 to 1997 in the United States, France, and Australia to examine the correlation over space and time between the three countries. We found a high correlation in both areas between France and the United States (correlation in impact, Spearman’s ρ = 0.76, p < 0.001, and test for synchrony in timing of epidemics, p < 0.001). We did not find a similar correlation between the United States and Australia or between France and Australia, when considering a systematic half-year lead or delay of influenza epidemics in Australia as compared with those in the United States or France. These results support a high correlation at the hemisphere level and suggest that the global interhemispheric circulation of epidemics follows an irregular pathway with recurrent changes in the leading hemisphere.

EID Viboud C, Boëlle P, Pakdaman K, Carrat F, Valleron A, Flahault A. Influenza Epidemics in the United States, France, and Australia, 1972–1997. Emerg Infect Dis. 2004;10(1):32-39. https://dx.doi.org/10.3201/eid1001.020705
AMA Viboud C, Boëlle P, Pakdaman K, et al. Influenza Epidemics in the United States, France, and Australia, 1972–1997. Emerging Infectious Diseases. 2004;10(1):32-39. doi:10.3201/eid1001.020705.
APA Viboud, C., Boëlle, P., Pakdaman, K., Carrat, F., Valleron, A., & Flahault, A. (2004). Influenza Epidemics in the United States, France, and Australia, 1972–1997. Emerging Infectious Diseases, 10(1), 32-39. https://dx.doi.org/10.3201/eid1001.020705.

Ecologic and Geographic Distribution of Filovirus Disease [PDF - 373 KB - 8 pages]
A. T. Peterson et al.

We used ecologic niche modeling of outbreaks and sporadic cases of filovirus-associated hemorrhagic fever (HF) to provide a large-scale perspective on the geographic and ecologic distributions of Ebola and Marburg viruses. We predicted that filovirus would occur across the Afrotropics: Ebola HF in the humid rain forests of central and western Africa, and Marburg HF in the drier and more open areas of central and eastern Africa. Most of the predicted geographic extent of Ebola HF has been observed; Marburg HF has the potential to occur farther south and east. Ecologic conditions appropriate for Ebola HF are also present in Southeast Asia and the Philippines, where Ebola Reston is hypothesized to be distributed. This first large-scale ecologic analysis provides a framework for a more informed search for taxa that could constitute the natural reservoir for this virus family.

EID Peterson AT, Bauer JT, Mills JN. Ecologic and Geographic Distribution of Filovirus Disease. Emerg Infect Dis. 2004;10(1):40-47. https://dx.doi.org/10.3201/eid1001.030125
AMA Peterson AT, Bauer JT, Mills JN. Ecologic and Geographic Distribution of Filovirus Disease. Emerging Infectious Diseases. 2004;10(1):40-47. doi:10.3201/eid1001.030125.
APA Peterson, A. T., Bauer, J. T., & Mills, J. N. (2004). Ecologic and Geographic Distribution of Filovirus Disease. Emerging Infectious Diseases, 10(1), 40-47. https://dx.doi.org/10.3201/eid1001.030125.

Fatal Infectious Disease Surveillance in a Medical Examiner Database [PDF - 163 KB - 7 pages]
M. I. Wolfe et al.

Increasing infectious disease deaths, the emergence of new infections, and bioterrorism have made surveillance for infectious diseases a public health concern. Medical examiners and coroners certify approximately 20% of all deaths that occur within the United States and can be a key source of information regarding infectious disease deaths. We hypothesized that a computer-assisted search tool (algorithm) could detect infectious disease deaths from a medical examiner database, thereby reducing the time and resources required to perform such surveillance manually. We developed two algorithms, applied them to a medical examiner database, and verified the cases identified against the opinion of a panel of experts. The algorithms detected deaths with infectious components with sensitivities from 67% to 94%, and predictive value positives ranging from 8% to 49%. Algorithms can be useful for surveillance in medical examiner offices that have limited resources or for conducting surveillance across medical examiner jurisdictions.

EID Wolfe MI, Nolte KB, Yoon SS. Fatal Infectious Disease Surveillance in a Medical Examiner Database. Emerg Infect Dis. 2004;10(1):48-53. https://dx.doi.org/10.3201/eid1001.020764
AMA Wolfe MI, Nolte KB, Yoon SS. Fatal Infectious Disease Surveillance in a Medical Examiner Database. Emerging Infectious Diseases. 2004;10(1):48-53. doi:10.3201/eid1001.020764.
APA Wolfe, M. I., Nolte, K. B., & Yoon, S. S. (2004). Fatal Infectious Disease Surveillance in a Medical Examiner Database. Emerging Infectious Diseases, 10(1), 48-53. https://dx.doi.org/10.3201/eid1001.020764.

Hospital-reported Pneumococcal Susceptibility to Penicillin [PDF - 84 KB - 6 pages]
J. P. Metlay et al.

Geographic variation in drug susceptibility among isolates of Streptococcus pneumoniae has influenced national treatment guidelines for community-acquired pneumonia. Whether individual hospital susceptibility data provide reliable and valid information for providers is unclear. We examined the geographic and temporal variability in hospital-reported rates of pneumococcal susceptibility. We surveyed all 52 hospitals that provided acute adult care in the five counties surrounding Philadelphia and collected data on levels of penicillin susceptibility among all pneumococcal blood isolates from 1998 to 2000. In 1998, pneumococcal nonsusceptibility to penicillin varied from 0% to 67% of all blood isolates across the 33 hospitals with >10 isolates in that year. Hospital location did not correlate with the level of reported pneumococcal susceptibility (p = 0.8). In addition, correlations were not significant in reported pneumococcal susceptibility to penicillin within individual hospitals during the 3 years.

EID Metlay JP, Branas CC, Fishman NO. Hospital-reported Pneumococcal Susceptibility to Penicillin. Emerg Infect Dis. 2004;10(1):54-59. https://dx.doi.org/10.3201/eid1001.030140
AMA Metlay JP, Branas CC, Fishman NO. Hospital-reported Pneumococcal Susceptibility to Penicillin. Emerging Infectious Diseases. 2004;10(1):54-59. doi:10.3201/eid1001.030140.
APA Metlay, J. P., Branas, C. C., & Fishman, N. O. (2004). Hospital-reported Pneumococcal Susceptibility to Penicillin. Emerging Infectious Diseases, 10(1), 54-59. https://dx.doi.org/10.3201/eid1001.030140.

Ciprofloxacin-resistant Salmonella enterica Typhimurium and Choleraesuis from Pigs to Humans, Taiwan [PDF - 260 KB - 9 pages]
P. Hsueh et al.

We evaluated the disk susceptibility data of 671 nontyphoid Salmonella isolates collected from different parts of Taiwan from March 2001 to August 2001 and 1,261 nontyphoid Salmonella isolates from the National Taiwan University Hospital from 1996 to 2001. Overall, ciprofloxacn resistance was found in 2.7% (18/671) of all nontyphoid Salmonella isolates, in 1.4% (5/347) of Salmonella enterica serotype Typhimurium and in 7.5% (8/107) in S. enterica serotype Choleraesuis nationwide. MICs of six newer fluoroquinolones were determined for the following isolates: 37 isolates of ciprofloxacin-resistant (human) S. enterica Typhimurium (N = 26) and Choleraesuis (N = 11), 10 isolates of ciprofloxacin-susceptible (MIC <1 μg/mL) (human) isolates of these two serotypes, and 15 swine isolates from S. enterica Choleraesuis (N = 13) and Typhmurium (N = 2) with reduced susceptibility to ciprofloxacin (MIC >0.12 μg/mL). Sequence analysis of the gryA, gyrB, parC, parE, and acrR genes, ciprofloxacin accumulation; and genotypes generated by pulsed-field gel electrophoresis with three restriction enzymes (SpeI, XbaI, and BlnI) were performed. All 26 S. enterica Typhimurium isolates from humans and pigs belonged to genotype I. For S. enterica Choleraesuis isolates, 91% (10/11) of human isolates and 54% (7/13) of swine isolates belonged to genotype B. These two genotypes isolates from humans all exhibited a high-level of resistance to ciprofloxacin (MIC 16–64 μg/mL). They had two-base substitutions in the gyrA gene at codons 83 (Ser83Phe) and 87 (Asp87Gly or Asp87Asn) and in the parC gene at codon 80 (Ser80Arg, Ser80Ile, or Ser84Lys). Our investigation documented that not only did these two S. enterica isolates have a high prevalence of ciprofloxacin resistance nationwide but also that some closely related ciprofloxacin-resistant strains are disseminated from pigs to humans.

EID Hsueh P, Teng L, Tseng S, Chang C, Wan J, Yan J, et al. Ciprofloxacin-resistant Salmonella enterica Typhimurium and Choleraesuis from Pigs to Humans, Taiwan. Emerg Infect Dis. 2004;10(1):60-68. https://dx.doi.org/10.3201/eid1001.030171
AMA Hsueh P, Teng L, Tseng S, et al. Ciprofloxacin-resistant Salmonella enterica Typhimurium and Choleraesuis from Pigs to Humans, Taiwan. Emerging Infectious Diseases. 2004;10(1):60-68. doi:10.3201/eid1001.030171.
APA Hsueh, P., Teng, L., Tseng, S., Chang, C., Wan, J., Yan, J....Luh, K. (2004). Ciprofloxacin-resistant Salmonella enterica Typhimurium and Choleraesuis from Pigs to Humans, Taiwan. Emerging Infectious Diseases, 10(1), 60-68. https://dx.doi.org/10.3201/eid1001.030171.

Escherichia coli Producing CTX-M-2 β-Lactamase in Cattle, Japan [PDF - 104 KB - 7 pages]
Y. Shiraki et al.

From November 2000 to June 2001, Escherichia coli strains producing CTX-M-2 β-lactamase were isolated from 6 (1.5%) of 396 cattle fecal samples and 2 (0.7%) of 270 surface swabs of cattle carcasses in Japan. The blaCTX-M-2 gene responsible for CTX-M-2 production was encoded on transferable plasmids, and the gene was transferred to E. coli CSH2 with a very high frequency (2 x 10-4 to 6 x 10-1 per donor cells) by conjugation. Random amplified polymorphic DNA analysis of nine isolates showed at least five different patterns. These findings suggest that CTX-M-2 producers might have originated from cattle through the use of cephalosporins such as ceftiofur and that cattle could be a reservoir of CTX-M-2–producing E. coli. Continuous and strategic surveillance of antimicrobial-resistant bacteria in livestock is essential to suppress further dissemination of these bacteria into society at large.

EID Shiraki Y, Shibata N, Doi Y, Arakawa Y. Escherichia coli Producing CTX-M-2 β-Lactamase in Cattle, Japan. Emerg Infect Dis. 2004;10(1):69-75. https://dx.doi.org/10.3201/eid1001.030219
AMA Shiraki Y, Shibata N, Doi Y, et al. Escherichia coli Producing CTX-M-2 β-Lactamase in Cattle, Japan. Emerging Infectious Diseases. 2004;10(1):69-75. doi:10.3201/eid1001.030219.
APA Shiraki, Y., Shibata, N., Doi, Y., & Arakawa, Y. (2004). Escherichia coli Producing CTX-M-2 β-Lactamase in Cattle, Japan. Emerging Infectious Diseases, 10(1), 69-75. https://dx.doi.org/10.3201/eid1001.030219.

Nosocomial Bloodstream Infection and Clinical Sepsis [PDF - 128 KB - 6 pages]
S. Hugonnet et al.

Primary bloodstream infection (BSI) is a leading, preventable infectious complication in critically ill patients and has a negative impact on patients’ outcome. Surveillance definitions for primary BSI distinguish those that are microbiologically documented from those that are not. The latter is known as clinical sepsis, but information on its epidemiologic importance is limited. We analyzed prospective on-site surveillance data of nosocomial infections in a medical intensive care unit. Of the 113 episodes of primary BSI, 33 (29%) were microbiologically documented. The overall BSI infection rate was 19.8 episodes per 1,000 central-line days (confidence interval [CI] 95%, 16.1 to 23.6); the rate fell to 5.8 (CI 3.8 to 7.8) when only microbiologically documented episodes were considered. Exposure to vascular devices was similar in patients with clinical sepsis and patients with microbiologically documented BSI. We conclude that laboratory-based surveillance alone will underestimate the incidence of primary BSI and thus jeopardize benchmarking.

EID Hugonnet S, Sax H, Eggimann P, Chevrolet J, Pittet D. Nosocomial Bloodstream Infection and Clinical Sepsis. Emerg Infect Dis. 2004;10(1):76-81. https://dx.doi.org/10.3201/eid1001.030407
AMA Hugonnet S, Sax H, Eggimann P, et al. Nosocomial Bloodstream Infection and Clinical Sepsis. Emerging Infectious Diseases. 2004;10(1):76-81. doi:10.3201/eid1001.030407.
APA Hugonnet, S., Sax, H., Eggimann, P., Chevrolet, J., & Pittet, D. (2004). Nosocomial Bloodstream Infection and Clinical Sepsis. Emerging Infectious Diseases, 10(1), 76-81. https://dx.doi.org/10.3201/eid1001.030407.

Experimental Infection of Cats and Dogs with West Nile Virus [PDF - 181 KB - 7 pages]
L. E. Austgen et al.

Domestic dogs and cats were infected by mosquito bite and evaluated as hosts for West Nile virus (WNV). Viremia of low magnitude and short duration developed in four dogs but they did not display signs of disease. Four cats became viremic, with peak titers ranging from 103.0 to 104.0 PFU/mL. Three of the cats showed mild, non-neurologic signs of disease. WNV was not isolated from saliva of either dogs or cats during the period of viremia. An additional group of four cats were exposed to WNV orally, through ingestion of infected mice. Two cats consumed an infected mouse on three consecutive days, and two cats ate a single infected mouse. Viremia developed in all of these cats with a magnitude and duration similar to that seen in cats infected by mosquito bite, but none of the four showed clinical signs. These results suggest that dogs and cats are readily infected by WNV. The high efficiency of oral transmission observed with cats suggests that infected prey animals may serve as an important source of infection to carnivores. Neither species is likely to function as an epidemiologically important amplifying host, although the peak viremia observed in cats may be high enough to infect mosquitoes at low efficiency.

EID Austgen LE, Bowen RA, Bunning ML, Davis BS, Mitchell CJ, Chang GJ. Experimental Infection of Cats and Dogs with West Nile Virus. Emerg Infect Dis. 2004;10(1):82-88. https://dx.doi.org/10.3201/eid1001.020616
AMA Austgen LE, Bowen RA, Bunning ML, et al. Experimental Infection of Cats and Dogs with West Nile Virus. Emerging Infectious Diseases. 2004;10(1):82-88. doi:10.3201/eid1001.020616.
APA Austgen, L. E., Bowen, R. A., Bunning, M. L., Davis, B. S., Mitchell, C. J., & Chang, G. J. (2004). Experimental Infection of Cats and Dogs with West Nile Virus. Emerging Infectious Diseases, 10(1), 82-88. https://dx.doi.org/10.3201/eid1001.020616.

Fluoroquinolones Protective against Cephalosporin Resistance in Gram-negative Nosocomial Pathogens [PDF - 318 KB - 6 pages]
M. J. Schwaber et al.

In a matched case-control study, we studied the effect of prior receipt of fluoroquinolones on isolation of three third-generation cephalosporin-resistant gram-negative nosocomial pathogens. Two hundred eighty-two cases with a third-generation cephalosporin-resistant pathogen (203 with Enterobacter spp., 50 with Pseudomonas aeruginosa, and 29 with Klebsiella pneumoniae) were matched on length of stay to controls in a 1:2 ratio. Case-patients and controls were similar in age (mean 62 years) and sex (54% male). Variables predicting third-generation cephalosporin resistance were surgery (p = 0.005); intensive care unit stay (p < 0.001); and receipt of a β-lactam/β-lactamase inhibitor (p < 0.001), a ureidopenicillin (p = 0.002), or a third-generation cephalosporin (p < 0.001). Receipt of a fluoroquinolone was protective against isolation of a third-generation cephalosporin-resistant pathogen (p = 0.005). Interventional studies are required to determine whether replacing third-generation cephalosporins with fluoroquinolones will be effective in reducing cephalosporin resistance and the effect of such interventions on fluoroquinolone resistance.

EID Schwaber MJ, Cosgrove SE, Gold HS, Kaye KS, Carmeli Y. Fluoroquinolones Protective against Cephalosporin Resistance in Gram-negative Nosocomial Pathogens. Emerg Infect Dis. 2004;10(1):94-99. https://dx.doi.org/10.3201/eid1001.020663
AMA Schwaber MJ, Cosgrove SE, Gold HS, et al. Fluoroquinolones Protective against Cephalosporin Resistance in Gram-negative Nosocomial Pathogens. Emerging Infectious Diseases. 2004;10(1):94-99. doi:10.3201/eid1001.020663.
APA Schwaber, M. J., Cosgrove, S. E., Gold, H. S., Kaye, K. S., & Carmeli, Y. (2004). Fluoroquinolones Protective against Cephalosporin Resistance in Gram-negative Nosocomial Pathogens. Emerging Infectious Diseases, 10(1), 94-99. https://dx.doi.org/10.3201/eid1001.020663.

Evaluating Detection and Diagnostic Decision Support Systems for Bioterrorism Response [PDF - 147 KB - 9 pages]
D. M. Bravata et al.

We evaluated the usefulness of detection systems and diagnostic decision support systems for bioterrorism response. We performed a systematic review by searching relevant databases (e.g., MEDLINE) and Web sites for reports of detection systems and diagnostic decision support systems that could be used during bioterrorism responses. We reviewed over 24,000 citations and identified 55 detection systems and 23 diagnostic decision support systems. Only 35 systems have been evaluated: 4 reported both sensitivity and specificity, 13 were compared to a reference standard, and 31 were evaluated for their timeliness. Most evaluations of detection systems and some evaluations of diagnostic systems for bioterrorism responses are critically deficient. Because false-positive and false-negative rates are unknown for most systems, decision making on the basis of these systems is seriously compromised. We describe a framework for the design of future evaluations of such systems.

EID Bravata DM, Sundaram V, McDonald KM, Smith WM, Szeto H, Schleinitz MD, et al. Evaluating Detection and Diagnostic Decision Support Systems for Bioterrorism Response. Emerg Infect Dis. 2004;10(1):100-108. https://dx.doi.org/10.3201/eid1001.030243
AMA Bravata DM, Sundaram V, McDonald KM, et al. Evaluating Detection and Diagnostic Decision Support Systems for Bioterrorism Response. Emerging Infectious Diseases. 2004;10(1):100-108. doi:10.3201/eid1001.030243.
APA Bravata, D. M., Sundaram, V., McDonald, K. M., Smith, W. M., Szeto, H., Schleinitz, M. D....Owens, D. K. (2004). Evaluating Detection and Diagnostic Decision Support Systems for Bioterrorism Response. Emerging Infectious Diseases, 10(1), 100-108. https://dx.doi.org/10.3201/eid1001.030243.

Respiratory and Urinary Tract Infections, Arthritis, and Asthma Associated with HTLV-I and HTLV-II Infection [PDF - 135 KB - 8 pages]
E. L. Murphy et al.

Human T-lymphotropic virus types I and II (HTLV-I and -II) cause myelopathy; HTLV-I, but not HTLV-II, causes adult T-cell leukemia. Whether HTLV-II is associated with other diseases is unknown. Using survival analysis, we studied medical history data from a prospective cohort of HTLV-I– and HTLV-II–infected and –uninfected blood donors, all HIV seronegative. A total of 152 HTLV-I, 387 HTLV-II, and 799 uninfected donors were enrolled and followed for a median of 4.4, 4.3, and 4.4 years, respectively. HTLV-II participants had significantly increased incidences of acute bronchitis (incidence ratio [IR] = 1.68), bladder or kidney infection (IR = 1.55), arthritis (IR = 2.66), and asthma (IR = 3.28), and a borderline increase in pneumonia (IR = 1.82, 95% confidence interval [CI] 0.98 to 3.38). HTLV-I participants had significantly increased incidences of bladder or kidney infection (IR = 1.82), and arthritis (IR = 2.84). We conclude that HTLV-II infection may inhibit immunologic responses to respiratory infections and that both HTLV-I and -II may induce inflammatory or autoimmune reactions.

EID Murphy EL, Wang B, Sacher RA, Fridey J, Smith JW, Nass CC, et al. Respiratory and Urinary Tract Infections, Arthritis, and Asthma Associated with HTLV-I and HTLV-II Infection. Emerg Infect Dis. 2004;10(1):109-116. https://dx.doi.org/10.3201/eid1001.020714
AMA Murphy EL, Wang B, Sacher RA, et al. Respiratory and Urinary Tract Infections, Arthritis, and Asthma Associated with HTLV-I and HTLV-II Infection. Emerging Infectious Diseases. 2004;10(1):109-116. doi:10.3201/eid1001.020714.
APA Murphy, E. L., Wang, B., Sacher, R. A., Fridey, J., Smith, J. W., Nass, C. C....Schreiber, G. B. (2004). Respiratory and Urinary Tract Infections, Arthritis, and Asthma Associated with HTLV-I and HTLV-II Infection. Emerging Infectious Diseases, 10(1), 109-116. https://dx.doi.org/10.3201/eid1001.020714.
Historical Review

Bacillus anthracis Bioterrorism Incident, Kameido, Tokyo, 1993 [PDF - 249 KB - 4 pages]
H. Takahashi et al.

In July 1993, a liquid suspension of Bacillus anthracis was aerosolized from the roof of an eight-story building in Kameido, Tokyo, Japan, by the religious group Aum Shinrikyo. During 1999 to 2001, microbiologic tests were conducted on a liquid environmental sample originally collected during the 1993 incident. Nonencapsulated isolates of B. anthracis were cultured from the liquid. Multiple-locus, variable-number tandem repeat analysis found all isolates to be identical to a strain used in Japan to vaccinate animals against anthrax, which was consistent with the Aum Shinrikyo members’ testimony about the strain source. In 1999, a retrospective case-detection survey was conducted to identify potential human anthrax cases associated with the incident, but none were found. The use of an attenuated B. anthracis strain, low spore concentrations, ineffective dispersal, a clogged spray device, and inactivation of the spores by sunlight are all likely contributing factors to the lack of human cases.

EID Takahashi H, Keim P, Kaufmann AF, Keys C, Smith KL, Taniguchi K, et al. Bacillus anthracis Bioterrorism Incident, Kameido, Tokyo, 1993. Emerg Infect Dis. 2004;10(1):117-120. https://dx.doi.org/10.3201/eid1001.030238
AMA Takahashi H, Keim P, Kaufmann AF, et al. Bacillus anthracis Bioterrorism Incident, Kameido, Tokyo, 1993. Emerging Infectious Diseases. 2004;10(1):117-120. doi:10.3201/eid1001.030238.
APA Takahashi, H., Keim, P., Kaufmann, A. F., Keys, C., Smith, K. L., Taniguchi, K....Kurata, T. (2004). Bacillus anthracis Bioterrorism Incident, Kameido, Tokyo, 1993. Emerging Infectious Diseases, 10(1), 117-120. https://dx.doi.org/10.3201/eid1001.030238.
Dispatches

Panton-Valentine Leukocidin and Staphyloccoccal Skin Infections in Schoolchildren [PDF - 239 KB - 4 pages]
K. Boubaker et al.

The Panton-Valentine leukocidin is associated with staphylococcal skin and pulmonary infections. We describe a school outbreak of skin infections and the public health response to it. Nasal carriage of a Panton-Valentine leukocidin–positive Staphylococcus aureus clone was detected only in previously ill classmates and their family members.

EID Boubaker K, Diebold P, Blanc DS, Vandenesch F, Praz G, Dupuis G, et al. Panton-Valentine Leukocidin and Staphyloccoccal Skin Infections in Schoolchildren. Emerg Infect Dis. 2004;10(1):121-124. https://dx.doi.org/10.3201/eid1001.030144
AMA Boubaker K, Diebold P, Blanc DS, et al. Panton-Valentine Leukocidin and Staphyloccoccal Skin Infections in Schoolchildren. Emerging Infectious Diseases. 2004;10(1):121-124. doi:10.3201/eid1001.030144.
APA Boubaker, K., Diebold, P., Blanc, D. S., Vandenesch, F., Praz, G., Dupuis, G....Troillet, N. (2004). Panton-Valentine Leukocidin and Staphyloccoccal Skin Infections in Schoolchildren. Emerging Infectious Diseases, 10(1), 121-124. https://dx.doi.org/10.3201/eid1001.030144.

Rickettsia mongolotimonae Infection in South Africa [PDF - 45 KB - 2 pages]
A. Pretorius and R. J. Birtles

We report the first laboratory-confirmed case of Rickettsia mongolotimonae infection in Africa. The patient sought treatment for an eschar on his toe; lymphangitis, severe headaches, and fever subsequently developed. After a regimen of doxycycline, symptoms rapidly resolved. R. mongolotimonae infection was diagnosed retrospectively by serologic tests and molecular-based detection of the organism in biopsy specimens of eschar material.

EID Pretorius A, Birtles RJ. Rickettsia mongolotimonae Infection in South Africa. Emerg Infect Dis. 2004;10(1):125-126. https://dx.doi.org/10.3201/eid1001.020662
AMA Pretorius A, Birtles RJ. Rickettsia mongolotimonae Infection in South Africa. Emerging Infectious Diseases. 2004;10(1):125-126. doi:10.3201/eid1001.020662.
APA Pretorius, A., & Birtles, R. J. (2004). Rickettsia mongolotimonae Infection in South Africa. Emerging Infectious Diseases, 10(1), 125-126. https://dx.doi.org/10.3201/eid1001.020662.

Domestically Acquired Campylobacter Infections in Finland [PDF - 203 KB - 4 pages]
A. Vierikko et al.

Campylobacter jejuni isolates (n = 533) from domestic cases diagnosed in Finland during a 3-month peak period were studied. The highest rate was observed among those 70–74 years of age. Domestic C. jejuni isolates were especially frequent in the eastern districts. Six serotypes covered 61% of all C. jejuni isolates.

EID Vierikko A, Hänninen M, Siitonen A, Ruutu P, Rautelin H. Domestically Acquired Campylobacter Infections in Finland. Emerg Infect Dis. 2004;10(1):127-130. https://dx.doi.org/10.3201/eid1001.020636
AMA Vierikko A, Hänninen M, Siitonen A, et al. Domestically Acquired Campylobacter Infections in Finland. Emerging Infectious Diseases. 2004;10(1):127-130. doi:10.3201/eid1001.020636.
APA Vierikko, A., Hänninen, M., Siitonen, A., Ruutu, P., & Rautelin, H. (2004). Domestically Acquired Campylobacter Infections in Finland. Emerging Infectious Diseases, 10(1), 127-130. https://dx.doi.org/10.3201/eid1001.020636.

Salmonella Serovars from Humans and Other Sources in Thailand, 1993–2002 [PDF - 230 KB - 6 pages]
A. Bangtrakulnonth et al.

We serotyped 44,087 Salmonella isolates from humans and 26,148 from other sources from 1993 through 2002. The most common serovar causing human salmonellosis in Thailand was Salmonella enterica Weltevreden. Serovars causing human infections in Thailand differ from those in other countries and seem to be related to Salmonella serovars in different food products and reservoirs.

EID Bangtrakulnonth A, Pornreongwong S, Pulsrikarn C, Sawanpanyalert P, Hendriksen RS, Wong DM, et al. Salmonella Serovars from Humans and Other Sources in Thailand, 1993–2002. Emerg Infect Dis. 2004;10(1):131-136. https://dx.doi.org/10.3201/eid1001.020781
AMA Bangtrakulnonth A, Pornreongwong S, Pulsrikarn C, et al. Salmonella Serovars from Humans and Other Sources in Thailand, 1993–2002. Emerging Infectious Diseases. 2004;10(1):131-136. doi:10.3201/eid1001.020781.
APA Bangtrakulnonth, A., Pornreongwong, S., Pulsrikarn, C., Sawanpanyalert, P., Hendriksen, R. S., Wong, D. M....Aarestrup, F. M. (2004). Salmonella Serovars from Humans and Other Sources in Thailand, 1993–2002. Emerging Infectious Diseases, 10(1), 131-136. https://dx.doi.org/10.3201/eid1001.020781.

Myiasis During Adventure Sports Race [PDF - 77 KB - 3 pages]
M. Seppänen et al.

Travelers who have visited tropical areas may exhibit aggressive forms of obligatory myiases, in which the larvae (maggots) invasively feed on living tissue. The risk of a traveler’s acquiring a screwworm infestation has been considered negligible, but with the increasing popularity of adventure sports and wildlife travel, this risk may need to be reassessed.

EID Seppänen M, Virolainen-Julkunen A, Kakko I, Vilkamaa P, Meri S. Myiasis During Adventure Sports Race. Emerg Infect Dis. 2004;10(1):137-139. https://dx.doi.org/10.3201/eid1001.020825
AMA Seppänen M, Virolainen-Julkunen A, Kakko I, et al. Myiasis During Adventure Sports Race. Emerging Infectious Diseases. 2004;10(1):137-139. doi:10.3201/eid1001.020825.
APA Seppänen, M., Virolainen-Julkunen, A., Kakko, I., Vilkamaa, P., & Meri, S. (2004). Myiasis During Adventure Sports Race. Emerging Infectious Diseases, 10(1), 137-139. https://dx.doi.org/10.3201/eid1001.020825.

Estimating the Public Health Impact of Rabies [PDF - 160 KB - 3 pages]
P. G. Coleman et al.

Rabies is a fatal, preventable zoonosis, but it is not effectively controlled throughout much of the developing world. The impetus for control is hampered by a lack of awareness of its true impact. We estimate a disability-adjusted life year (DALY) score for rabies to quantify the disease impact relative to other diseases to set priorities for public health interventions.

EID Coleman PG, Fèvre EM, Cleaveland S. Estimating the Public Health Impact of Rabies. Emerg Infect Dis. 2004;10(1):140-142. https://dx.doi.org/10.3201/eid1001.020744
AMA Coleman PG, Fèvre EM, Cleaveland S. Estimating the Public Health Impact of Rabies. Emerging Infectious Diseases. 2004;10(1):140-142. doi:10.3201/eid1001.020744.
APA Coleman, P. G., Fèvre, E. M., & Cleaveland, S. (2004). Estimating the Public Health Impact of Rabies. Emerging Infectious Diseases, 10(1), 140-142. https://dx.doi.org/10.3201/eid1001.020744.

Antifungal Susceptibilities of Cryptococcus neoformans [PDF - 37 KB - 3 pages]
L. K. Archibald et al.

Susceptibility profiles of medically important fungi in less-developed countries remain uncharacterized. We measured the MICs of amphotericin B, 5-flucytosine, fluconazole, itraconazole, and ketoconazole for Cryptococcus neoformans clinical isolates from Thailand, Malawi, and the United States and found no evidence of resistance or MIC profile differences among the countries.

EID Archibald LK, Tuohy MJ, Wilson DA, Nwanyanwu O, Kazembe PN, Tansuphasawadikul S, et al. Antifungal Susceptibilities of Cryptococcus neoformans. Emerg Infect Dis. 2004;10(1):143-145. https://dx.doi.org/10.3201/eid1001.020779
AMA Archibald LK, Tuohy MJ, Wilson DA, et al. Antifungal Susceptibilities of Cryptococcus neoformans. Emerging Infectious Diseases. 2004;10(1):143-145. doi:10.3201/eid1001.020779.
APA Archibald, L. K., Tuohy, M. J., Wilson, D. A., Nwanyanwu, O., Kazembe, P. N., Tansuphasawadikul, S....Procop, G. W. (2004). Antifungal Susceptibilities of Cryptococcus neoformans. Emerging Infectious Diseases, 10(1), 143-145. https://dx.doi.org/10.3201/eid1001.020779.

Human Infection with M- Strain of Brucella canis [PDF - 65 KB - 3 pages]
J. C. Wallach et al.

The less mucoid strain of Brucella canis or M- strain is used for the serologic diagnosis of canine brucellosis. While this strain is avirulent in dogs, we report the case of clinical brucellosis that developed in a laboratory worker a few days after handling live M- cells for antigen production.

EID Wallach JC, Giambartolomei GH, Baldi PC, Fossati CA. Human Infection with M- Strain of Brucella canis. Emerg Infect Dis. 2004;10(1):146-148. https://dx.doi.org/10.3201/eid1001.020622
AMA Wallach JC, Giambartolomei GH, Baldi PC, et al. Human Infection with M- Strain of Brucella canis. Emerging Infectious Diseases. 2004;10(1):146-148. doi:10.3201/eid1001.020622.
APA Wallach, J. C., Giambartolomei, G. H., Baldi, P. C., & Fossati, C. A. (2004). Human Infection with M- Strain of Brucella canis. Emerging Infectious Diseases, 10(1), 146-148. https://dx.doi.org/10.3201/eid1001.020622.

Adenovirus Type 7 Genomic-Type Variant, New York City, 1999 [PDF - 233 KB - 4 pages]
J. A. Calder et al.

An outbreak of respiratory illness occurred in a long-term care facility in New York City. Investigation of the outbreak identified confirmed or suspected adenoviral infection in 84% of the residents from October 19 to December 18, 1999. Further identification by type-specific neutralization and restriction analysis identified a new genomic variant of adenovirus type 7.

EID Calder JA, Erdman DD, Ackelsberg J, Cato SW, Deutsch V, Lechich AJ, et al. Adenovirus Type 7 Genomic-Type Variant, New York City, 1999. Emerg Infect Dis. 2004;10(1):149-152. https://dx.doi.org/10.3201/eid1001.020605
AMA Calder JA, Erdman DD, Ackelsberg J, et al. Adenovirus Type 7 Genomic-Type Variant, New York City, 1999. Emerging Infectious Diseases. 2004;10(1):149-152. doi:10.3201/eid1001.020605.
APA Calder, J. A., Erdman, D. D., Ackelsberg, J., Cato, S. W., Deutsch, V., Lechich, A. J....Schofield, B. S. (2004). Adenovirus Type 7 Genomic-Type Variant, New York City, 1999. Emerging Infectious Diseases, 10(1), 149-152. https://dx.doi.org/10.3201/eid1001.020605.
Commentaries

Virus Taxonomy: One Step Forward, Two Steps Back [PDF - 48 KB - 2 pages]
M. L. Eberhard
EID Eberhard ML. Virus Taxonomy: One Step Forward, Two Steps Back. Emerg Infect Dis. 2004;10(1):153-154. https://dx.doi.org/10.3201/eid1001.030945
AMA Eberhard ML. Virus Taxonomy: One Step Forward, Two Steps Back. Emerging Infectious Diseases. 2004;10(1):153-154. doi:10.3201/eid1001.030945.
APA Eberhard, M. L. (2004). Virus Taxonomy: One Step Forward, Two Steps Back. Emerging Infectious Diseases, 10(1), 153-154. https://dx.doi.org/10.3201/eid1001.030945.
Letters

Haemophilus influenzae Type b Meningitis in Children, Eritrea [PDF - 30 KB - 2 pages]
D. G. Naik and M. Seyoum
EID Naik DG, Seyoum M. Haemophilus influenzae Type b Meningitis in Children, Eritrea. Emerg Infect Dis. 2004;10(1):155-156. https://dx.doi.org/10.3201/eid1001.030132
AMA Naik DG, Seyoum M. Haemophilus influenzae Type b Meningitis in Children, Eritrea. Emerging Infectious Diseases. 2004;10(1):155-156. doi:10.3201/eid1001.030132.
APA Naik, D. G., & Seyoum, M. (2004). Haemophilus influenzae Type b Meningitis in Children, Eritrea. Emerging Infectious Diseases, 10(1), 155-156. https://dx.doi.org/10.3201/eid1001.030132.

Quinolone Safety and Efficacy More Important than Potency [PDF - 25 KB - 2 pages]
R. Frothingham
EID Frothingham R. Quinolone Safety and Efficacy More Important than Potency. Emerg Infect Dis. 2004;10(1):156-157. https://dx.doi.org/10.3201/eid1001.030307
AMA Frothingham R. Quinolone Safety and Efficacy More Important than Potency. Emerging Infectious Diseases. 2004;10(1):156-157. doi:10.3201/eid1001.030307.
APA Frothingham, R. (2004). Quinolone Safety and Efficacy More Important than Potency. Emerging Infectious Diseases, 10(1), 156-157. https://dx.doi.org/10.3201/eid1001.030307.

Vancomycin-resistant Enterococcus faecalis in Serbia [PDF - 26 KB - 2 pages]
B. Stošović et al.
EID Stošović B, Stepanović S, Donabedian S, Tošić T, Jovanović M. Vancomycin-resistant Enterococcus faecalis in Serbia. Emerg Infect Dis. 2004;10(1):157-158. https://dx.doi.org/10.3201/eid1001.020790
AMA Stošović B, Stepanović S, Donabedian S, et al. Vancomycin-resistant Enterococcus faecalis in Serbia. Emerging Infectious Diseases. 2004;10(1):157-158. doi:10.3201/eid1001.020790.
APA Stošović, B., Stepanović, S., Donabedian, S., Tošić, T., & Jovanović, M. (2004). Vancomycin-resistant Enterococcus faecalis in Serbia. Emerging Infectious Diseases, 10(1), 157-158. https://dx.doi.org/10.3201/eid1001.020790.

Q Fever in Como, Northern Italy [PDF - 25 KB - 2 pages]
D. Santoro et al.
EID Santoro D, Giura R, Colombo MC, Antonelli P, Gramegna M, Gandola O, et al. Q Fever in Como, Northern Italy. Emerg Infect Dis. 2004;10(1):159-160. https://dx.doi.org/10.3201/eid1001.030467
AMA Santoro D, Giura R, Colombo MC, et al. Q Fever in Como, Northern Italy. Emerging Infectious Diseases. 2004;10(1):159-160. doi:10.3201/eid1001.030467.
APA Santoro, D., Giura, R., Colombo, M. C., Antonelli, P., Gramegna, M., Gandola, O....Gridavilla, G. (2004). Q Fever in Como, Northern Italy. Emerging Infectious Diseases, 10(1), 159-160. https://dx.doi.org/10.3201/eid1001.030467.
About the Cover

Johannes [Jan] Vermeer (1632–1675). The Astronomer (1668) [PDF - 158 KB - 2 pages]
P. Potter
EID Potter P. Johannes [Jan] Vermeer (1632–1675). The Astronomer (1668). Emerg Infect Dis. 2004;10(1):162-163. https://dx.doi.org/10.3201/eid1001.ac1001
AMA Potter P. Johannes [Jan] Vermeer (1632–1675). The Astronomer (1668). Emerging Infectious Diseases. 2004;10(1):162-163. doi:10.3201/eid1001.ac1001.
APA Potter, P. (2004). Johannes [Jan] Vermeer (1632–1675). The Astronomer (1668). Emerging Infectious Diseases, 10(1), 162-163. https://dx.doi.org/10.3201/eid1001.ac1001.
Corrections

Correction Vol. 9, No. 6 [PDF - 14 KB - 1 page]
EID Correction Vol. 9, No. 6. Emerg Infect Dis. 2004;10(1):160. https://dx.doi.org/10.3201/eid1001.c11001
AMA Correction Vol. 9, No. 6. Emerging Infectious Diseases. 2004;10(1):160. doi:10.3201/eid1001.c11001.
APA (2004). Correction Vol. 9, No. 6. Emerging Infectious Diseases, 10(1), 160. https://dx.doi.org/10.3201/eid1001.c11001.

Correction Vol. 9, No. 11 [PDF - 14 KB - 1 page]
EID Correction Vol. 9, No. 11. Emerg Infect Dis. 2004;10(1):160. https://dx.doi.org/10.3201/eid1001.c21001
AMA Correction Vol. 9, No. 11. Emerging Infectious Diseases. 2004;10(1):160. doi:10.3201/eid1001.c21001.
APA (2004). Correction Vol. 9, No. 11. Emerging Infectious Diseases, 10(1), 160. https://dx.doi.org/10.3201/eid1001.c21001.
Page created: July 10, 2012
Page updated: July 10, 2012
Page reviewed: July 10, 2012
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
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