Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Issue Cover for Volume 4, Number 2—June 1998

Volume 4, Number 2—June 1998

[PDF - 10.70 MB - 195 pages]

Perspective

Emerging Infectious Diseases—Southeast Asia [PDF - 31 KB - 3 pages]
S. K. Lam
EID Lam SK. Emerging Infectious Diseases—Southeast Asia. Emerg Infect Dis. 1998;4(2):145-147. https://doi.org/10.3201/eid0402.980201
AMA Lam SK. Emerging Infectious Diseases—Southeast Asia. Emerging Infectious Diseases. 1998;4(2):145-147. doi:10.3201/eid0402.980201.
APA Lam, S. K. (1998). Emerging Infectious Diseases—Southeast Asia. Emerging Infectious Diseases, 4(2), 145-147. https://doi.org/10.3201/eid0402.980201.

Wild Primate Populations in Emerging Infectious Disease Research: The Missing Link? [PDF - 411 KB - 10 pages]
N. D. Wolfe et al.

Wild primate populations, an unexplored source of information regarding emerging infectious disease, may hold valuable clues to the origins and evolution of some important pathogens. Primates can act as reservoirs for human pathogens. As members of biologically diverse habitats, they serve as sentinels for surveillance of emerging pathogens and provide models for basic research on natural transmission dynamics. Since emerging infectious diseases also pose serious threats to endangered and threatened primate species, studies of these diseases in primate populations can benefit conservation efforts and may provide the missing link between laboratory studies and the well-recognized needs of early disease detection, identification, and surveillance.

EID Wolfe ND, Escalante AA, Karesh WB, Kilbourn A, Spielman A, Lal AA. Wild Primate Populations in Emerging Infectious Disease Research: The Missing Link?. Emerg Infect Dis. 1998;4(2):149-158. https://doi.org/10.3201/eid0402.980202
AMA Wolfe ND, Escalante AA, Karesh WB, et al. Wild Primate Populations in Emerging Infectious Disease Research: The Missing Link?. Emerging Infectious Diseases. 1998;4(2):149-158. doi:10.3201/eid0402.980202.
APA Wolfe, N. D., Escalante, A. A., Karesh, W. B., Kilbourn, A., Spielman, A., & Lal, A. A. (1998). Wild Primate Populations in Emerging Infectious Disease Research: The Missing Link?. Emerging Infectious Diseases, 4(2), 149-158. https://doi.org/10.3201/eid0402.980202.

Accommodating Error Analysis in Comparison and Clustering of Molecular Fingerprints [PDF - 108 KB - 10 pages]
H. Salamon et al.

Molecular epidemiologic studies of infectious diseases rely on pathogen genotype comparisons, which usually yield patterns comprising sets of DNA fragments (DNA fingerprints). We use a highly developed genotyping system, IS6110-based restriction fragment length polymorphism analysis of Mycobacterium tuberculosis, to develop a computational method that automates comparison of large numbers of fingerprints. Because error in fragment length measurements is proportional to fragment length and is positively correlated for fragments within a lane, an align-and-count method that compensates for relative scaling of lanes reliably counts matching fragments between lanes. Results of a two-step method we developed to cluster identical fingerprints agree closely with 5 years of computer-assisted visual matching among 1,335 M. tuberculosis fingerprints. Fully documented and validated methods of automated comparison and clustering will greatly expand the scope of molecular epidemiology.

EID Salamon H, Segal MR, Ponce de Leon A, Small PM. Accommodating Error Analysis in Comparison and Clustering of Molecular Fingerprints. Emerg Infect Dis. 1998;4(2):159-168. https://doi.org/10.3201/eid0402.980203
AMA Salamon H, Segal MR, Ponce de Leon A, et al. Accommodating Error Analysis in Comparison and Clustering of Molecular Fingerprints. Emerging Infectious Diseases. 1998;4(2):159-168. doi:10.3201/eid0402.980203.
APA Salamon, H., Segal, M. R., Ponce de Leon, A., & Small, P. M. (1998). Accommodating Error Analysis in Comparison and Clustering of Molecular Fingerprints. Emerging Infectious Diseases, 4(2), 159-168. https://doi.org/10.3201/eid0402.980203.

Legal Issues Associated with Antimicrobial Drug Resistance [PDF - 41 KB - 9 pages]
D. P. Fidler

An effective public health strategy against the development of antimicrobial drug resistance needs to be informed by legal as well as scientific analysis. This article describes some legal issues arising from current efforts against antimicrobial resistance and underscores the interdependence between law and public health in these efforts.

EID Fidler DP. Legal Issues Associated with Antimicrobial Drug Resistance. Emerg Infect Dis. 1998;4(2):169-177. https://doi.org/10.3201/eid0402.980204
AMA Fidler DP. Legal Issues Associated with Antimicrobial Drug Resistance. Emerging Infectious Diseases. 1998;4(2):169-177. doi:10.3201/eid0402.980204.
APA Fidler, D. P. (1998). Legal Issues Associated with Antimicrobial Drug Resistance. Emerging Infectious Diseases, 4(2), 169-177. https://doi.org/10.3201/eid0402.980204.

Rickettsial Pathogens and Their Arthropod Vectors [PDF - 97 KB - 8 pages]
A. F. Azad and C. B. Beard

Rickettsial diseases, important causes of illness and death worldwide, exist primarily in endemic and enzootic foci that occasionally give rise to sporadic or seasonal outbreaks. Rickettsial pathogens are highly specialized for obligate intracellular survival in both the vertebrate host and the invertebrate vector. While studies often focus primarily on the vertebrate host, the arthropod vector is often more important in the natural maintenance of the pathogen. Consequently, coevolution of rickettsiae with arthropods is responsible for many features of the host-pathogen relationship that are unique among arthropod-borne diseases, including efficient pathogen replication, long-term maintenance of infection, and transstadial and transovarial transmission. This article examines the common features of the host-pathogen relationship and of the arthropod vectors of the typhus and spotted fever group rickettsiae.

EID Azad AF, Beard CB. Rickettsial Pathogens and Their Arthropod Vectors. Emerg Infect Dis. 1998;4(2):179-186. https://doi.org/10.3201/eid0402.980205
AMA Azad AF, Beard CB. Rickettsial Pathogens and Their Arthropod Vectors. Emerging Infectious Diseases. 1998;4(2):179-186. doi:10.3201/eid0402.980205.
APA Azad, A. F., & Beard, C. B. (1998). Rickettsial Pathogens and Their Arthropod Vectors. Emerging Infectious Diseases, 4(2), 179-186. https://doi.org/10.3201/eid0402.980205.

Could Myocarditis, Insulin-Dependent Diabetes Mellitus, and Guillain-Barré Syndrome Be Caused by One or More Infectious Agents Carried by Rodents? [PDF - 602 KB - 7 pages]
B. Niklasson et al.

The numbers of small rodents in northern Sweden fluctuate heavily, peaking every 3 or 4 years. We found that the incidence of Guillain-Barré syndrome and insulin-dependent diabetes mellitus, as well as the number of deaths caused by myocarditis, followed the fluctuations in numbers of bank voles, although with different time lags. An environmental factor, such as an infectious agent, has been suggested for all three diseases. We hypothesize that Guillain-Barré syndrome, myocarditis, and insulin-dependent diabetes mellitus in humans in Sweden are caused by one or more infectious agents carried by small rodents. Also, a group of novel picornaviruses recently isolated from these small rodents is being investigated as the possible etiologic agent(s).

EID Niklasson B, Hörnfeldt B, Lundman B. Could Myocarditis, Insulin-Dependent Diabetes Mellitus, and Guillain-Barré Syndrome Be Caused by One or More Infectious Agents Carried by Rodents?. Emerg Infect Dis. 1998;4(2):187-193. https://doi.org/10.3201/eid0402.980206
AMA Niklasson B, Hörnfeldt B, Lundman B. Could Myocarditis, Insulin-Dependent Diabetes Mellitus, and Guillain-Barré Syndrome Be Caused by One or More Infectious Agents Carried by Rodents?. Emerging Infectious Diseases. 1998;4(2):187-193. doi:10.3201/eid0402.980206.
APA Niklasson, B., Hörnfeldt, B., & Lundman, B. (1998). Could Myocarditis, Insulin-Dependent Diabetes Mellitus, and Guillain-Barré Syndrome Be Caused by One or More Infectious Agents Carried by Rodents?. Emerging Infectious Diseases, 4(2), 187-193. https://doi.org/10.3201/eid0402.980206.

Multidrug-Resistant Mycobacterium tuberculosis: Molecular Perspectives [PDF - 514 KB - 15 pages]
A. Rattan et al.

Multidrug-resistant strains of Mycobacterium tuberculosis seriously threaten tuberculosis (TB) control and prevention efforts. Molecular studies of the mechanism of action of antitubercular drugs have elucidated the genetic basis of drug resistance in M. tuberculosis. Drug resistance in M. tuberculosis is attributed primarily to the accumulation of mutations in the drug target genes; these mutations lead either to an altered target (e.g., RNA polymerase and catalase-peroxidase in rifampicin and isoniazid resistance, respectively) or to a change in titration of the drug (e.g., InhA in isoniazid resistance). Development of specific mechanism–based inhibitors and techniques to rapidly detect multidrug resistance will require further studies addressing the drug and drug-target interaction.

EID Rattan A, Kalia A, Ahmad N. Multidrug-Resistant Mycobacterium tuberculosis: Molecular Perspectives. Emerg Infect Dis. 1998;4(2):195-209. https://doi.org/10.3201/eid0402.980207
AMA Rattan A, Kalia A, Ahmad N. Multidrug-Resistant Mycobacterium tuberculosis: Molecular Perspectives. Emerging Infectious Diseases. 1998;4(2):195-209. doi:10.3201/eid0402.980207.
APA Rattan, A., Kalia, A., & Ahmad, N. (1998). Multidrug-Resistant Mycobacterium tuberculosis: Molecular Perspectives. Emerging Infectious Diseases, 4(2), 195-209. https://doi.org/10.3201/eid0402.980207.
Synopses

Hospitalizations for Unexplained Illnesses among U.S. Veterans of the Persian Gulf War [PDF - 57 KB - 9 pages]
J. D. Knoke and G. C. Gray

Persian Gulf War veterans have reported a variety of symptoms, many of which have not led to conventional diagnoses. We ascertained all active-duty U.S. military personnel deployed to the Persian Gulf War (552,111) and all Gulf War era military personnel not deployed (1,479,751) and compared their postwar hospitalization records (until 1 April 1996) for one or more of 77 diagnoses under the International Classification of Diseases (ICD-9) system. The diagnoses were assembled by the Emerging Infections Program, Centers for Disease Control and Prevention, and are here termed "unexplained illnesses." Deployed veterans were found to have a slightly higher risk of hospitalization for unexplained illness than the nondeployed. Most of the excess hospitalizations for the deployed were due to the diagnosis "illness of unknown cause" (ICD-9 code 799.9), and most occurred in participants of the Comprehensive Clinical Evaluation Program who were admitted for evaluation only. When the effect of participation in this program was removed, the deployed had a slightly lower risk than the nondeployed. These findings suggest that active-duty Gulf War veterans did not have excess unexplained illnesses resulting in hospitalization in the 4.67-year period following deployment.

EID Knoke JD, Gray GC. Hospitalizations for Unexplained Illnesses among U.S. Veterans of the Persian Gulf War. Emerg Infect Dis. 1998;4(2):211-219. https://doi.org/10.3201/eid0402.980208
AMA Knoke JD, Gray GC. Hospitalizations for Unexplained Illnesses among U.S. Veterans of the Persian Gulf War. Emerging Infectious Diseases. 1998;4(2):211-219. doi:10.3201/eid0402.980208.
APA Knoke, J. D., & Gray, G. C. (1998). Hospitalizations for Unexplained Illnesses among U.S. Veterans of the Persian Gulf War. Emerging Infectious Diseases, 4(2), 211-219. https://doi.org/10.3201/eid0402.980208.

Agricultural Use of Burkholderia (Pseudomonas) cepacia: A Threat to Human Health? [PDF - 331 KB - 7 pages]
A. H. Holmes et al.

In the past 2 decades, Burkholderia cepacia has emerged as a human pathogen causing numerous outbreaks, particularly among cystic fibrosis (CF) patients. One highly transmissible strain has spread across North America and Britain, and another between hospitalized CF and non-CF patients. Meanwhile, the organism has been developed as a biopesticide for protecting crops against fungal diseases and has potential as a bioremediation agent for breaking down recalcitrant herbicides and pesticides. However, B. cepacia is inherently resistant to multiple antibiotics; selection of strains "safe" for environmental application is not at present possible phenotypically or genotypically; molecular epidemiology and phylogenetic studies demonstrate that highly transmissible strains emerge randomly; and the organism has a capacity for rapid mutation and adaptation (facilitated by numerous insertion sequences), and a large, complex genome divided into separate chromosomes. Therefore, the widespread agricultural use of B. cepacia should be approached with caution.

EID Holmes AH, Govan J, Goldstein R. Agricultural Use of Burkholderia (Pseudomonas) cepacia: A Threat to Human Health?. Emerg Infect Dis. 1998;4(2):221-227. https://doi.org/10.3201/eid0402.980209
AMA Holmes AH, Govan J, Goldstein R. Agricultural Use of Burkholderia (Pseudomonas) cepacia: A Threat to Human Health?. Emerging Infectious Diseases. 1998;4(2):221-227. doi:10.3201/eid0402.980209.
APA Holmes, A. H., Govan, J., & Goldstein, R. (1998). Agricultural Use of Burkholderia (Pseudomonas) cepacia: A Threat to Human Health?. Emerging Infectious Diseases, 4(2), 221-227. https://doi.org/10.3201/eid0402.980209.

Haemophilus influenzae Invasive Disease in the United States, 1994–1995: Near Disappearance of a Vaccine-Preventable Childhood Disease [PDF - 136 KB - 9 pages]
K. M. Bisgard et al.

We analyzed national Haemophilus influenzae (Hi) surveillance data from 1994 and 1995 to describe the epidemiology of Hi invasive disease among persons of all ages. Serotype data were available for 376 (56%) of 669 reported Hi cases among children aged 4 years or younger; 184 (49%) were H. influenzae type b (Hib). Among children aged 4 or younger, incidence (per 100,000) of all Hi invasive disease was 1.8 in 1994 and 1.6 (p < 0.05) in 1995. Children aged 5 months or younger had the highest average annual incidence rate of Hib invasive disease (2.2 per 100,000); children aged 6 to 11 months had the next highest rate (1.2 per 100,000) (p < 0.05). Of 181 children with Hib invasive disease whose age in months was known, 85 (47%) were too young (aged 5 months or younger) to have completed a primary series with an Hib-containing vaccine. Of the 83 children with known vaccination status who were eligible to receive a primary series (aged 6 months or older), 52 (63%) were undervaccinated, and the remaining 31 (37%) had completed a primary series in which vaccine failed. Among persons aged 5 years or older with Hi invasive disease, the lowest average annual incidence was among those 20 to 39 years of age (0.15 per 100,000), and the highest was among those aged 80 years or older (2.26 per 100,000). Among persons aged 5 years or older, serotype data were available for 1,372 (71%) of the 1,940 Hi invasive disease cases; 159 (28%) of the 568 Hi cases with known serotype were due to Hib.

EID Bisgard KM, Kao AS, Leake J, Strebel PM, Perkins BA, Wharton M. Haemophilus influenzae Invasive Disease in the United States, 1994–1995: Near Disappearance of a Vaccine-Preventable Childhood Disease. Emerg Infect Dis. 1998;4(2):229-237. https://doi.org/10.3201/eid0402.980210
AMA Bisgard KM, Kao AS, Leake J, et al. Haemophilus influenzae Invasive Disease in the United States, 1994–1995: Near Disappearance of a Vaccine-Preventable Childhood Disease. Emerging Infectious Diseases. 1998;4(2):229-237. doi:10.3201/eid0402.980210.
APA Bisgard, K. M., Kao, A. S., Leake, J., Strebel, P. M., Perkins, B. A., & Wharton, M. (1998). Haemophilus influenzae Invasive Disease in the United States, 1994–1995: Near Disappearance of a Vaccine-Preventable Childhood Disease. Emerging Infectious Diseases, 4(2), 229-237. https://doi.org/10.3201/eid0402.980210.

Multiple-Drug Resistant Enterococci: The Nature of the Problem and an Agenda for the Future [PDF - 196 KB - 11 pages]
M. M. Huycke et al.

Enterococci, leading causes of nosocomial bacteremia, surgical wound infection, and urinary tract infection, are becoming resistant to many and sometimes all standard therapies. New rapid surveillance methods are highlighting the importance of examining enterococcal isolates at the species level. Most enterococcal infections are caused by Enterococcus faecalis, which are more likely to express traits related to overt virulence but—for the moment—also more likely to retain sensitivity to at least one effective antibiotic. The remaining infections are mostly caused by E. faecium, a species virtually devoid of known overt pathogenic traits but more likely to be resistant to even antibiotics of last resort. Effective control of multiple-drug resistant enterococci will require 1) better understanding of the interaction between enterococci, the hospital environment, and humans, 2) prudent antibiotic use, 3) better contact isolation in hospitals and other patient care environments, and 4) improved surveillance. Equally important is renewed vigor in the search for additional drugs, accompanied by the evolution of new therapeutic paradigms less vulnerable to the cycle of drug introduction and drug resistance.

EID Huycke MM, Sahm DF, Gilmore MS. Multiple-Drug Resistant Enterococci: The Nature of the Problem and an Agenda for the Future. Emerg Infect Dis. 1998;4(2):239-249. https://doi.org/10.3201/eid0402.980211
AMA Huycke MM, Sahm DF, Gilmore MS. Multiple-Drug Resistant Enterococci: The Nature of the Problem and an Agenda for the Future. Emerging Infectious Diseases. 1998;4(2):239-249. doi:10.3201/eid0402.980211.
APA Huycke, M. M., Sahm, D. F., & Gilmore, M. S. (1998). Multiple-Drug Resistant Enterococci: The Nature of the Problem and an Agenda for the Future. Emerging Infectious Diseases, 4(2), 239-249. https://doi.org/10.3201/eid0402.980211.

Enteroaggregative Escherichia coli [PDF - 234 KB - 11 pages]
J. P. Nataro et al.

Enteroaggregative Escherichia coli (EAEC), an increasingly recognized cause of diarrhea in children in developing countries, has been particularly associated with persistent diarrhea (more than 14 days), a major cause of illness and death. Recent outbreaks implicate EAEC as a cause of foodborne illness in industrialized countries. The pathogenesis of EAEC infection is not well understood, but a model can be proposed in which EAEC adhere to the intestinal mucosa and elaborate enterotoxins and cytotoxins, which result in secretory diarrhea and mucosal damage. EAEC's ability to stimulate the release of inflammatory mediators may also play a role in intestinal illness.

EID Nataro JP, Steiner T, Guerrant RL. Enteroaggregative Escherichia coli. Emerg Infect Dis. 1998;4(2):251-261. https://doi.org/10.3201/eid0402.980212
AMA Nataro JP, Steiner T, Guerrant RL. Enteroaggregative Escherichia coli. Emerging Infectious Diseases. 1998;4(2):251-261. doi:10.3201/eid0402.980212.
APA Nataro, J. P., Steiner, T., & Guerrant, R. L. (1998). Enteroaggregative Escherichia coli. Emerging Infectious Diseases, 4(2), 251-261. https://doi.org/10.3201/eid0402.980212.

Campylobacter jejuni Strains from Patients with Guillain-Barré Syndrome [PDF - 35 KB - 6 pages]
B. M. Allos et al.

Guillain-Barré syndrome (GBS), an acute demyelinating peripheral neuropathy, may be triggered by an acute infectious illness; infection with Campylobacter jejuni is the most frequently reported antecedent event. In Japan, O:19 is the most common serotype among GBS-associated C. jejuni strains. To determine whether serotype O:19 occurs among GBS-associated strains in the United States and Europe, we serotyped seven such strains and found that two (29%) of seven GBS-associated strains from patients in the United States and Germany were serotype O:19. To determine whether GBS-associated strains may be resistant to killing by normal human serum (NHS), we studied the serum susceptibility of 17 GBS- and 27 enteritis-associated strains (including many O:19 and non-O:19 strains) using C. jejuni antibody positive (pool 1) or negative (pool 2) human serum. Using pool 1 serum we found that one (6%) of 18 serotype O:19 strains compared with 11 (42%) of 26 non-O:19 strains were killed; results using pool 2 serum were nearly identical. Finally, 8 O:19 and 8 non-O:19 strains were not significantly different in their ability to bind complement component C3. Serotype O:19 C. jejuni strains were overrepresented among GBS-associated strains in the United States and Germany and were significantly more serum-resistant than non-O:19 strains. The mechanism of this resistance appears unrelated to C3 binding.

EID Allos BM, Lippy FT, Carlsen A, Washburn RG, Blaser MJ. Campylobacter jejuni Strains from Patients with Guillain-Barré Syndrome. Emerg Infect Dis. 1998;4(2):263-268. https://doi.org/10.3201/eid0402.980213
AMA Allos BM, Lippy FT, Carlsen A, et al. Campylobacter jejuni Strains from Patients with Guillain-Barré Syndrome. Emerging Infectious Diseases. 1998;4(2):263-268. doi:10.3201/eid0402.980213.
APA Allos, B. M., Lippy, F. T., Carlsen, A., Washburn, R. G., & Blaser, M. J. (1998). Campylobacter jejuni Strains from Patients with Guillain-Barré Syndrome. Emerging Infectious Diseases, 4(2), 263-268. https://doi.org/10.3201/eid0402.980213.
Dispatches

An Apparently New Virus (Family Paramyxoviridae) Infectious for Pigs, Humans, and Fruit Bats [PDF - 100 KB - 3 pages]
A. W. Philbey et al.

We isolated an apparently new virus in the family Paramyxoviridae from stillborn piglets with deformities at a piggery in New South Wales, Australia. In 1997, the pregnancy rate and litter size at the piggery decreased markedly, while the proportion of mummified fetuses increased. We found serologic evidence of infection in pigs at the affected piggery and two associated piggeries, in humans exposed to infected pigs, and in fruit bats. Menangle virus is proposed as a common name for this agent, should further studies confirm that it is a newly recognized virus.

EID Philbey AW, Kirkland PD, Ross AD, Davis RJ, Gleeson AB, Love RJ, et al. An Apparently New Virus (Family Paramyxoviridae) Infectious for Pigs, Humans, and Fruit Bats. Emerg Infect Dis. 1998;4(2):269-271. https://doi.org/10.3201/eid0402.980214
AMA Philbey AW, Kirkland PD, Ross AD, et al. An Apparently New Virus (Family Paramyxoviridae) Infectious for Pigs, Humans, and Fruit Bats. Emerging Infectious Diseases. 1998;4(2):269-271. doi:10.3201/eid0402.980214.
APA Philbey, A. W., Kirkland, P. D., Ross, A. D., Davis, R. J., Gleeson, A. B., Love, R. J....Hyatt, A. D. (1998). An Apparently New Virus (Family Paramyxoviridae) Infectious for Pigs, Humans, and Fruit Bats. Emerging Infectious Diseases, 4(2), 269-271. https://doi.org/10.3201/eid0402.980214.

Probable Human Infection with a Newly Described Virus in the Family Paramyxoviridae [PDF - 18 KB - 3 pages]
K. Chant et al.

After an apparently new virus in the family Paramyxoviridae was isolated from pigs in August 1997, an investigation was carried out to assess its risk for humans. More than 250 persons with potential exposure to infected pigs were tested serologically. Two piggery workers with intense occupational exposure had high convalescent-phase antibody titers to this new virus. In early June 1997, both workers had an influenzalike illness with rash; serologic testing showed no alternative cause. Strong evidence indicates that the two men became ill from this new virus, but the mode of transmission from pigs to humans remains unknown.

EID Chant K, Chan R, Smith M, Dwyer DE, Kirkland PD. Probable Human Infection with a Newly Described Virus in the Family Paramyxoviridae. Emerg Infect Dis. 1998;4(2):273-275. https://doi.org/10.3201/eid0402.980215
AMA Chant K, Chan R, Smith M, et al. Probable Human Infection with a Newly Described Virus in the Family Paramyxoviridae. Emerging Infectious Diseases. 1998;4(2):273-275. doi:10.3201/eid0402.980215.
APA Chant, K., Chan, R., Smith, M., Dwyer, D. E., & Kirkland, P. D. (1998). Probable Human Infection with a Newly Described Virus in the Family Paramyxoviridae. Emerging Infectious Diseases, 4(2), 273-275. https://doi.org/10.3201/eid0402.980215.

Emergence of the M Phenotype of Erythromycin-Resistant Pneumococci in South Africa [PDF - 29 KB - 5 pages]
C. A. Widdowson and K. P. Klugman

Erythromycin-resistant pneumococci have been isolated in South Africa since 1978; however, from 1987 to 1996, resistance to macrolides was only detected in 270 (2.7%) of 9,868 blood or cerebrospinal fluid (CSF) pneumococcal isolates, most of which were obtained from the public sector. In South Africa, macrolide use in the public sector is estimated at 56% of that in the private sector. Most erythromycin-resistant strains (89%) exhibited resistance to erythromycin and clindamycin (macrolide-lincosamide-streptogramin B phenotype). In the United States, most erythromycin-resistant pneumococci exhibit the newly described M phenotype (resistance to erythromycin alone), associated with the mefE gene. The M phenotype in South Africa increased significantly in the last 10 years, from 1 of 5,115 to 28 of 4,735 of blood and CSF isolates received from 1987 to 1991 compared with 1992 to 1996 (p = 5x10-7). These data suggest that, although macrolide resistance in pneumococci remains low in the public sector, the mefE gene is rapidly emerging in South Africa.

EID Widdowson CA, Klugman KP. Emergence of the M Phenotype of Erythromycin-Resistant Pneumococci in South Africa. Emerg Infect Dis. 1998;4(2):277-281. https://doi.org/10.3201/eid0402.980216
AMA Widdowson CA, Klugman KP. Emergence of the M Phenotype of Erythromycin-Resistant Pneumococci in South Africa. Emerging Infectious Diseases. 1998;4(2):277-281. doi:10.3201/eid0402.980216.
APA Widdowson, C. A., & Klugman, K. P. (1998). Emergence of the M Phenotype of Erythromycin-Resistant Pneumococci in South Africa. Emerging Infectious Diseases, 4(2), 277-281. https://doi.org/10.3201/eid0402.980216.

Mycobacterium tuberculosis infection as a Zoonotic Disease: Transmission between Humans and Elephants [PDF - 29 KB - 5 pages]
K. Michalak et al.

Between 1994 and 1996, three elephants from an exotic animal farm in Illinois died of pulmonary disease due to Mycobacterium tuberculosis. In October 1996, a fourth living elephant was culture-positive for M. tuberculosis. Twenty-two handlers at the farm were screened for tuberculosis (TB); eleven had positive reactions to intradermal injection with purified protein derivative. One had smear-negative, culture-positive active TB. DNA fingerprint comparison by IS6110 and TBN12 typing showed that the isolates from the four elephants and the handler with active TB were the same strain. This investigation indicates transmission of M. tuberculosis between humans and elephants.

EID Michalak K, Austin C, Diesel S, Bacon JM, Zimmerman P, Maslow JN. Mycobacterium tuberculosis infection as a Zoonotic Disease: Transmission between Humans and Elephants. Emerg Infect Dis. 1998;4(2):283-287. https://doi.org/10.3201/eid0402.980217
AMA Michalak K, Austin C, Diesel S, et al. Mycobacterium tuberculosis infection as a Zoonotic Disease: Transmission between Humans and Elephants. Emerging Infectious Diseases. 1998;4(2):283-287. doi:10.3201/eid0402.980217.
APA Michalak, K., Austin, C., Diesel, S., Bacon, J. M., Zimmerman, P., & Maslow, J. N. (1998). Mycobacterium tuberculosis infection as a Zoonotic Disease: Transmission between Humans and Elephants. Emerging Infectious Diseases, 4(2), 283-287. https://doi.org/10.3201/eid0402.980217.

New Vectors of Rift Valley Fever in West Africa [PDF - 71 KB - 5 pages]
D. Fontenille et al.

After an outbreak of Rift Valley fever in Southern Mauritania in 1987, entomologic studies were conducted in a bordering region in Sénégal from 1991 to 1996 to identify the sylvatic vectors of Rift Valley fever virus. The virus was isolated from the floodwater mosquitoes Aedes vexans and Ae. ochraceus. In 1974 and 1983, the virus had been isolated from Ae. dalzieli. Although these vectors differ from the main vectors in East and South Africa, they use the same type of breeding sites and also feed on cattle and sheep. Although enzootic vectors have now been identified in West Africa, the factors causing outbreaks remain unclear.

EID Fontenille D, Traore-Lamizana M, Diallo M, Thonnon J, Digoutte J, Zeller H. New Vectors of Rift Valley Fever in West Africa. Emerg Infect Dis. 1998;4(2):289-293. https://doi.org/10.3201/eid0402.980218
AMA Fontenille D, Traore-Lamizana M, Diallo M, et al. New Vectors of Rift Valley Fever in West Africa. Emerging Infectious Diseases. 1998;4(2):289-293. doi:10.3201/eid0402.980218.
APA Fontenille, D., Traore-Lamizana, M., Diallo, M., Thonnon, J., Digoutte, J., & Zeller, H. (1998). New Vectors of Rift Valley Fever in West Africa. Emerging Infectious Diseases, 4(2), 289-293. https://doi.org/10.3201/eid0402.980218.

Reemergence of Plasmodium vivax Malaria in the Republic of Korea [PDF - 19 KB - 3 pages]
B. H. Feighner et al.

Plasmodium vivax malaria reemerged in the Republic of Korea in 1993. The number of cases has tripled each year since, with more than 1,600 cases reported in 1997. All 27 cases in U.S. troops resolved uneventfully with chloroquine/primaquine therapy. Disease is localized along the western Demilitarized Zone and presents minimal risk to tourists.

EID Feighner BH, Pak SI, Novakoski WL, Kelsey LL, Strickman D. Reemergence of Plasmodium vivax Malaria in the Republic of Korea. Emerg Infect Dis. 1998;4(2):295-297. https://doi.org/10.3201/eid0402.980219
AMA Feighner BH, Pak SI, Novakoski WL, et al. Reemergence of Plasmodium vivax Malaria in the Republic of Korea. Emerging Infectious Diseases. 1998;4(2):295-297. doi:10.3201/eid0402.980219.
APA Feighner, B. H., Pak, S. I., Novakoski, W. L., Kelsey, L. L., & Strickman, D. (1998). Reemergence of Plasmodium vivax Malaria in the Republic of Korea. Emerging Infectious Diseases, 4(2), 295-297. https://doi.org/10.3201/eid0402.980219.

Molecular and Epidemiologic Analysis of Dengue Virus Isolates from Somalia [PDF - 48 KB - 5 pages]
N. Kanesa-thasan et al.

Nucleotide sequence analysis was performed on 14 dengue virus isolates (13 dengue-2 viruses and 1 dengue-3 virus) recovered from febrile soldiers in Somalia in 1993. The dengue-2 viruses were most closely related to dengue-2 virus recovered in Somalia in 1984. However, differences in nucleotide sequence (0.35% to 1.35%) were evident among the 1993 isolates. These differences were closely associated with the geographic location of the infection as well as with different times of infection at the same location. Genetic difference between strains was not associated with differences in clinical features. Molecular analysis of dengue viruses is a useful adjunct to epidemiologic investigation of their distribution over distance and time.

EID Kanesa-thasan N, Chang GJ, Smoak BL, Magill A, Burrous MJ, Hoke CH. Molecular and Epidemiologic Analysis of Dengue Virus Isolates from Somalia. Emerg Infect Dis. 1998;4(2):299-303. https://doi.org/10.3201/eid0402.980220
AMA Kanesa-thasan N, Chang GJ, Smoak BL, et al. Molecular and Epidemiologic Analysis of Dengue Virus Isolates from Somalia. Emerging Infectious Diseases. 1998;4(2):299-303. doi:10.3201/eid0402.980220.
APA Kanesa-thasan, N., Chang, G. J., Smoak, B. L., Magill, A., Burrous, M. J., & Hoke, C. H. (1998). Molecular and Epidemiologic Analysis of Dengue Virus Isolates from Somalia. Emerging Infectious Diseases, 4(2), 299-303. https://doi.org/10.3201/eid0402.980220.

Molecular Characterization of a Novel Rickettsia Species from Ixodes scapularis in Texas [PDF - 48 KB - 5 pages]
A. N. Billings et al.

A novel Rickettsia species of undetermined pathogenicity was detected in Ixodes scapularis. DNA sequencing showed the highest nucleotide sequence similarities with R. australis for the 17 kDa gene, R. helvetica for gltA, and R. montana for rompA. The new organism, provisionally designated as genotype Cooleyi, is highly divergent in three conserved genes from recognized Rickettsia species.

EID Billings AN, Teltow GJ, Vasilakis N, Walker DH. Molecular Characterization of a Novel Rickettsia Species from Ixodes scapularis in Texas. Emerg Infect Dis. 1998;4(2):305-309. https://doi.org/10.3201/eid0402.980221
AMA Billings AN, Teltow GJ, Vasilakis N, et al. Molecular Characterization of a Novel Rickettsia Species from Ixodes scapularis in Texas. Emerging Infectious Diseases. 1998;4(2):305-309. doi:10.3201/eid0402.980221.
APA Billings, A. N., Teltow, G. J., Vasilakis, N., & Walker, D. H. (1998). Molecular Characterization of a Novel Rickettsia Species from Ixodes scapularis in Texas. Emerging Infectious Diseases, 4(2), 305-309. https://doi.org/10.3201/eid0402.980221.

Dual Infection with Ehrlichia chaffeensis and a Spotted Fever Group Rickettsia: A Case Report [PDF - 85 KB - 6 pages]
D. J. Sexton et al.

Well-documented cases of simultaneous human infection with more than one tick-borne pathogen are rare. To our knowledge only two dual infections have been reported: simultaneous human infection with the agent of human granulocytic ehrlichiosis and Borrelia burgdorferi and simultaneous human infection with B. burgdorferi and Babesia microti (1-2). Rocky Mountain spotted fever has long been known to be endemic in North Carolina; cases of human ehrlichial infection were recognized there soon after Ehrlichia chaffeensis was recognized as an important cause of tick-borne disease in the southeastern United States. Because both Rocky Mountain spotted fever and ehrlichiosis are prevalent in North Carolina, occasional cases of simultaneous human infection by rickettsial and ehrlichial agents would not be surprising; however, no such cases seem to have been reported.

EID Sexton DJ, Corey GR, Carpenter C, Kong LQ, Gandhi T, Breitschwerdt EB, et al. Dual Infection with Ehrlichia chaffeensis and a Spotted Fever Group Rickettsia: A Case Report. Emerg Infect Dis. 1998;4(2):311-316. https://doi.org/10.3201/eid0402.980222
AMA Sexton DJ, Corey GR, Carpenter C, et al. Dual Infection with Ehrlichia chaffeensis and a Spotted Fever Group Rickettsia: A Case Report. Emerging Infectious Diseases. 1998;4(2):311-316. doi:10.3201/eid0402.980222.
APA Sexton, D. J., Corey, G. R., Carpenter, C., Kong, L. Q., Gandhi, T., Breitschwerdt, E. B....Dumler, S. J. (1998). Dual Infection with Ehrlichia chaffeensis and a Spotted Fever Group Rickettsia: A Case Report. Emerging Infectious Diseases, 4(2), 311-316. https://doi.org/10.3201/eid0402.980222.

Molecular Fingerprinting of Multidrug-Resistant Salmonella enterica Serotype Typhi [PDF - 116 KB - 4 pages]
M. D. Hampton et al.

For epidemiologic investigations, the primary subdivision of Salmonella Typhi is vi-phage typing; 106 Vi-phage types are defined. For multidrug-resistant strains the most common types have been M1 (Pakistan) and E1 (India, Pakistan, Bangladesh, and the Arabian Gulf); a strain untypable with the Vi phages has been responsible for a major epidemic in Tajikistan. Most often, isolates from the Indian subcontinent have been resistant to ampicillin, chloramphenicol, streptomycin, sulfonamides, tetracyclines, and trimethoprim; but in the 1997 Tajikistan outbreak, the epidemic strain was also resistant to ciprofloxacin. For multidrug-resistant strains, subdivision within phage type can be achieved by plasmid profile typing and pulsed-field gel electrophoresis.

EID Hampton MD, Ward LR, Rowe B, Threlfall EJ. Molecular Fingerprinting of Multidrug-Resistant Salmonella enterica Serotype Typhi. Emerg Infect Dis. 1998;4(2):317-320. https://doi.org/10.3201/eid0402.980223
AMA Hampton MD, Ward LR, Rowe B, et al. Molecular Fingerprinting of Multidrug-Resistant Salmonella enterica Serotype Typhi. Emerging Infectious Diseases. 1998;4(2):317-320. doi:10.3201/eid0402.980223.
APA Hampton, M. D., Ward, L. R., Rowe, B., & Threlfall, E. J. (1998). Molecular Fingerprinting of Multidrug-Resistant Salmonella enterica Serotype Typhi. Emerging Infectious Diseases, 4(2), 317-320. https://doi.org/10.3201/eid0402.980223.

Clostridium septicum Infection and Hemolytic Uremic Syndrome [PDF - 23 KB - 4 pages]
M. Barnham and N. Weightman

Five cases of Clostridium septicum infection secondary to Escherichia coli O157induced hemolytic uremic syndrome have been reported. We report on three cases (one of which is included in the above five) of dual Cl. septicum and E. coli infection; all three patients were exposed to farm animals. A common zoonotic source for Cl. septicum and E. coli O157 infections should be considered. Patients with hemolytic uremic syndrome should be treated aggressively and monitored closely for Cl. septicum superinfection.

EID Barnham M, Weightman N. Clostridium septicum Infection and Hemolytic Uremic Syndrome. Emerg Infect Dis. 1998;4(2):321-324. https://doi.org/10.3201/eid0402.980224
AMA Barnham M, Weightman N. Clostridium septicum Infection and Hemolytic Uremic Syndrome. Emerging Infectious Diseases. 1998;4(2):321-324. doi:10.3201/eid0402.980224.
APA Barnham, M., & Weightman, N. (1998). Clostridium septicum Infection and Hemolytic Uremic Syndrome. Emerging Infectious Diseases, 4(2), 321-324. https://doi.org/10.3201/eid0402.980224.

Persistent Infection of Pets within a Household with Three Bartonella Species [PDF - 132 KB - 4 pages]
D. L. Kordick and E. B. Breitschwerdt

We monitored by blood culture and immunofluorescence assay (IFA) bartonella infection in one dog and eight cats in a household to determine the prevalence and persistence of the infection as well as its transmissibility to humans. Ectoparasite control was rigorously exercised. During a 3-year period, Bartonella clarridgeiae was recovered from one cat on two occasions, and B. henselae was isolated from another cat on four occasions. During a 16-month period, B. vinsonii subsp. berkhoffii was isolated from the dog on 8 of 10 culture attempts. Despite extensive household contact, the pet owner was seronegative to all three species by IFA for Bartonella-specific immunoglobulin G.

EID Kordick DL, Breitschwerdt EB. Persistent Infection of Pets within a Household with Three Bartonella Species. Emerg Infect Dis. 1998;4(2):325-328. https://doi.org/10.3201/eid0402.980225
AMA Kordick DL, Breitschwerdt EB. Persistent Infection of Pets within a Household with Three Bartonella Species. Emerging Infectious Diseases. 1998;4(2):325-328. doi:10.3201/eid0402.980225.
APA Kordick, D. L., & Breitschwerdt, E. B. (1998). Persistent Infection of Pets within a Household with Three Bartonella Species. Emerging Infectious Diseases, 4(2), 325-328. https://doi.org/10.3201/eid0402.980225.

Using Nurse Hot Line Calls for Disease Surveillance [PDF - 36 KB - 4 pages]
J. S. Rodman et al.

Nurse hot line calls are a potential source of public health surveillance data and may help identify epidemics of emerging infectious diseases. In this study, nurse hot line data from Milwaukee, Wisconsin, showed more than a 17-fold increase in calls for diarrhea during the 1993 Milwaukee cryptosporidiosis outbreak. Moreover, consistent patterns of seasonal variation in diarrhea- and vomiting-related calls were detected from the Baltimore, Maryland, and Albuquerque, New Mexico, hot lines. Analysis of nurse hot line calls may provide an inexpensive and timely method for improving disease surveillance.

EID Rodman JS, Frost F, Jakubowski W. Using Nurse Hot Line Calls for Disease Surveillance. Emerg Infect Dis. 1998;4(2):329-332. https://doi.org/10.3201/eid0402.980226
AMA Rodman JS, Frost F, Jakubowski W. Using Nurse Hot Line Calls for Disease Surveillance. Emerging Infectious Diseases. 1998;4(2):329-332. doi:10.3201/eid0402.980226.
APA Rodman, J. S., Frost, F., & Jakubowski, W. (1998). Using Nurse Hot Line Calls for Disease Surveillance. Emerging Infectious Diseases, 4(2), 329-332. https://doi.org/10.3201/eid0402.980226.
Commentaries

Vector-borne Disease Surveillance and Natural Disasters [PDF - 15 KB - 2 pages]
R. S. Nasci and C. G. Moore
EID Nasci RS, Moore CG. Vector-borne Disease Surveillance and Natural Disasters. Emerg Infect Dis. 1998;4(2):333-334. https://doi.org/10.3201/eid0402.980227
AMA Nasci RS, Moore CG. Vector-borne Disease Surveillance and Natural Disasters. Emerging Infectious Diseases. 1998;4(2):333-334. doi:10.3201/eid0402.980227.
APA Nasci, R. S., & Moore, C. G. (1998). Vector-borne Disease Surveillance and Natural Disasters. Emerging Infectious Diseases, 4(2), 333-334. https://doi.org/10.3201/eid0402.980227.
Letters

Similarity of Chemokines Charge and the V3 Domain of HIV-1 env Protein [PDF - 122 KB - 2 pages]
B. Berkhout and A. T. Das
EID Berkhout B, Das AT. Similarity of Chemokines Charge and the V3 Domain of HIV-1 env Protein. Emerg Infect Dis. 1998;4(2):335-336. https://doi.org/10.3201/eid0402.980228
AMA Berkhout B, Das AT. Similarity of Chemokines Charge and the V3 Domain of HIV-1 env Protein. Emerging Infectious Diseases. 1998;4(2):335-336. doi:10.3201/eid0402.980228.
APA Berkhout, B., & Das, A. T. (1998). Similarity of Chemokines Charge and the V3 Domain of HIV-1 env Protein. Emerging Infectious Diseases, 4(2), 335-336. https://doi.org/10.3201/eid0402.980228.

Detection of Glycoprotein of Burkholderia pseudomallei [PDF - 18 KB - 2 pages]
N. P. Khrapova et al.
EID Khrapova NP, Tikhonov NG, Prokhvatilova YV. Detection of Glycoprotein of Burkholderia pseudomallei. Emerg Infect Dis. 1998;4(2):336-337. https://doi.org/10.3201/eid0402.980229
AMA Khrapova NP, Tikhonov NG, Prokhvatilova YV. Detection of Glycoprotein of Burkholderia pseudomallei. Emerging Infectious Diseases. 1998;4(2):336-337. doi:10.3201/eid0402.980229.
APA Khrapova, N. P., Tikhonov, N. G., & Prokhvatilova, Y. V. (1998). Detection of Glycoprotein of Burkholderia pseudomallei. Emerging Infectious Diseases, 4(2), 336-337. https://doi.org/10.3201/eid0402.980229.

Forging New Perspectives on Disease Surveillance [PDF - 18 KB - 2 pages]
H. Feldbaum
EID Feldbaum H. Forging New Perspectives on Disease Surveillance. Emerg Infect Dis. 1998;4(2):337-338. https://doi.org/10.3201/eid0402.980230
AMA Feldbaum H. Forging New Perspectives on Disease Surveillance. Emerging Infectious Diseases. 1998;4(2):337-338. doi:10.3201/eid0402.980230.
APA Feldbaum, H. (1998). Forging New Perspectives on Disease Surveillance. Emerging Infectious Diseases, 4(2), 337-338. https://doi.org/10.3201/eid0402.980230.

Provide a Context for Disease Emergence [PDF - 19 KB - 3 pages]
T. D. St. George
EID St. George TD. Provide a Context for Disease Emergence. Emerg Infect Dis. 1998;4(2):338-340. https://doi.org/10.3201/eid0402.980231
AMA St. George TD. Provide a Context for Disease Emergence. Emerging Infectious Diseases. 1998;4(2):338-340. doi:10.3201/eid0402.980231.
APA St. George, T. D. (1998). Provide a Context for Disease Emergence. Emerging Infectious Diseases, 4(2), 338-340. https://doi.org/10.3201/eid0402.980231.

Resistance to Dryness of Escherichia coli O157:H7 Strains from Outbreak in Sakai City, Japan, 1996 [PDF - 19 KB - 2 pages]
Y. Iijima et al.
EID Iijima Y, Matsumoto M, Higuchi K, Furuta T, Honda T. Resistance to Dryness of Escherichia coli O157:H7 Strains from Outbreak in Sakai City, Japan, 1996. Emerg Infect Dis. 1998;4(2):340-341. https://doi.org/10.3201/eid0402.980232
AMA Iijima Y, Matsumoto M, Higuchi K, et al. Resistance to Dryness of Escherichia coli O157:H7 Strains from Outbreak in Sakai City, Japan, 1996. Emerging Infectious Diseases. 1998;4(2):340-341. doi:10.3201/eid0402.980232.
APA Iijima, Y., Matsumoto, M., Higuchi, K., Furuta, T., & Honda, T. (1998). Resistance to Dryness of Escherichia coli O157:H7 Strains from Outbreak in Sakai City, Japan, 1996. Emerging Infectious Diseases, 4(2), 340-341. https://doi.org/10.3201/eid0402.980232.

Irradiation Pasteurization of Solid Foods [PDF - 14 KB - 1 page]
S. Moses and R. C. Brunham
EID Moses S, Brunham RC. Irradiation Pasteurization of Solid Foods. Emerg Infect Dis. 1998;4(2):341. https://doi.org/10.3201/eid0402.980233
AMA Moses S, Brunham RC. Irradiation Pasteurization of Solid Foods. Emerging Infectious Diseases. 1998;4(2):341. doi:10.3201/eid0402.980233.
APA Moses, S., & Brunham, R. C. (1998). Irradiation Pasteurization of Solid Foods. Emerging Infectious Diseases, 4(2), 341. https://doi.org/10.3201/eid0402.980233.

Emerging Infectious Diseases in Brazil [PDF - 19 KB - 2 pages]
L. Jacintho da Silva
EID Jacintho da Silva L. Emerging Infectious Diseases in Brazil. Emerg Infect Dis. 1998;4(2):341-342. https://doi.org/10.3201/eid0402.980234
AMA Jacintho da Silva L. Emerging Infectious Diseases in Brazil. Emerging Infectious Diseases. 1998;4(2):341-342. doi:10.3201/eid0402.980234.
APA Jacintho da Silva, L. (1998). Emerging Infectious Diseases in Brazil. Emerging Infectious Diseases, 4(2), 341-342. https://doi.org/10.3201/eid0402.980234.

Reply to L.J. da Silva [PDF - 12 KB - 1 page]
H. Momen
EID Momen H. Reply to L.J. da Silva. Emerg Infect Dis. 1998;4(2):343. https://doi.org/10.3201/eid0402.980235
AMA Momen H. Reply to L.J. da Silva. Emerging Infectious Diseases. 1998;4(2):343. doi:10.3201/eid0402.980235.
APA Momen, H. (1998). Reply to L.J. da Silva. Emerging Infectious Diseases, 4(2), 343. https://doi.org/10.3201/eid0402.980235.

A Brief Update on Rabbit Hemorrhagic Disease Virus [PDF - 16 KB - 2 pages]
L. Capucci and A. Lavazza
EID Capucci L, Lavazza A. A Brief Update on Rabbit Hemorrhagic Disease Virus. Emerg Infect Dis. 1998;4(2):343-344. https://doi.org/10.3201/eid0402.980236
AMA Capucci L, Lavazza A. A Brief Update on Rabbit Hemorrhagic Disease Virus. Emerging Infectious Diseases. 1998;4(2):343-344. doi:10.3201/eid0402.980236.
APA Capucci, L., & Lavazza, A. (1998). A Brief Update on Rabbit Hemorrhagic Disease Virus. Emerging Infectious Diseases, 4(2), 343-344. https://doi.org/10.3201/eid0402.980236.

Rabbit Hemorrhagic Disease [PDF - 18 KB - 2 pages]
C. Mead
EID Mead C. Rabbit Hemorrhagic Disease. Emerg Infect Dis. 1998;4(2):344-345. https://doi.org/10.3201/eid0402.980237
AMA Mead C. Rabbit Hemorrhagic Disease. Emerging Infectious Diseases. 1998;4(2):344-345. doi:10.3201/eid0402.980237.
APA Mead, C. (1998). Rabbit Hemorrhagic Disease. Emerging Infectious Diseases, 4(2), 344-345. https://doi.org/10.3201/eid0402.980237.

Reply to Drs. Capucci, Lavazza, and Mead [PDF - 16 KB - 2 pages]
A. W. Smith et al.
EID Smith AW, Cherry NJ, Matson DO. Reply to Drs. Capucci, Lavazza, and Mead. Emerg Infect Dis. 1998;4(2):345-346. https://doi.org/10.3201/eid0402.980238
AMA Smith AW, Cherry NJ, Matson DO. Reply to Drs. Capucci, Lavazza, and Mead. Emerging Infectious Diseases. 1998;4(2):345-346. doi:10.3201/eid0402.980238.
APA Smith, A. W., Cherry, N. J., & Matson, D. O. (1998). Reply to Drs. Capucci, Lavazza, and Mead. Emerging Infectious Diseases, 4(2), 345-346. https://doi.org/10.3201/eid0402.980238.
About the Cover

Freedom of Childhood
Conference Summaries

Conference on Global Disease Elimination and Eradication as Public Health Strategies, February 26, 1998 [PDF - 19 KB - 3 pages]
D. Conlon
EID Conlon D. Conference on Global Disease Elimination and Eradication as Public Health Strategies, February 26, 1998. Emerg Infect Dis. 1998;4(2):349-351. https://doi.org/10.3201/eid0402.980240
AMA Conlon D. Conference on Global Disease Elimination and Eradication as Public Health Strategies, February 26, 1998. Emerging Infectious Diseases. 1998;4(2):349-351. doi:10.3201/eid0402.980240.
APA Conlon, D. (1998). Conference on Global Disease Elimination and Eradication as Public Health Strategies, February 26, 1998. Emerging Infectious Diseases, 4(2), 349-351. https://doi.org/10.3201/eid0402.980240.
Corrections

Correction: Vol. 4, No. 1 [PDF - 11 KB - 1 page]
EID Correction: Vol. 4, No. 1. Emerg Infect Dis. 1998;4(2):351. https://doi.org/10.3201/eid0402.c10402
AMA Correction: Vol. 4, No. 1. Emerging Infectious Diseases. 1998;4(2):351. doi:10.3201/eid0402.c10402.
APA (1998). Correction: Vol. 4, No. 1. Emerging Infectious Diseases, 4(2), 351. https://doi.org/10.3201/eid0402.c10402.
News and Notes

The National Food Safety Initiative [PDF - 19 KB - 3 pages]
S. Binder et al.
EID Binder S, Khabbaz R, Swaminathan B, Tauxe R, Potter M. The National Food Safety Initiative. Emerg Infect Dis. 1998;4(2):347-349. https://doi.org/10.3201/eid0402.980239
AMA Binder S, Khabbaz R, Swaminathan B, et al. The National Food Safety Initiative. Emerging Infectious Diseases. 1998;4(2):347-349. doi:10.3201/eid0402.980239.
APA Binder, S., Khabbaz, R., Swaminathan, B., Tauxe, R., & Potter, M. (1998). The National Food Safety Initiative. Emerging Infectious Diseases, 4(2), 347-349. https://doi.org/10.3201/eid0402.980239.
Page created: June 07, 2012
Page updated: June 07, 2012
Page reviewed: June 07, 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.
edit_01 ScholarOne Submission Portal
Issue Select
GO
GO

Spotlight Topics

 

Get Email Updates

To receive email updates about this page, enter your email address:

file_external