Emerging Infectious Diseases

Published by Centers for Disease Control and Prevention (CDC)


In response.
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November 2014


66 Reads

Van-Mai Cao-Lormeau

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June 2013


116 Reads


In response.

November 2013


53 Reads






Table 2 . Specimens chosen for more detailed virus genetic analysis, Saudi Arabia and Yemen 
Genetic Analysis of Viruses Associated with Emergence of Rift Valley Fever in Saudi Arabia and Yemen, 2000-01

January 2003


76 Reads

The first confirmed Rift Valley fever outbreak outside Africa was reported in September 2000, in the Arabian Peninsula. As of February 2001, a total of 884 hospitalized patients were identified in Saudi Arabia, with 124 deaths. In Yemen, 1,087 cases were estimated to have occurred, with 121 deaths. Laboratory diagnosis of Rift Valley fever virus (RVFV) infections included virus genetic detection and characterization of clinical specimens by reverse transcription-polymerase chain reaction, in addition to serologic tests and virus isolation. Genetic analysis of selected regions of virus S, M, and L RNA genome segments indicated little genetic variation among the viruses associated with disease. The Saudi Arabia and Yemen viruses were almost identical to those associated with earlier RVF epidemics in East Africa. Analysis of S, M, and L RNA genome segment sequence differences showed similar phylogenetic relationships among these viruses, indicating that genetic reassortment did not play an important role in the emergence of this virus in the Arabian Peninsula. These results are consistent with the recent introduction of RVFV into the Arabian Peninsula from East Africa.

Influenza AH1N2 Viruses, United Kingdom, 2001–02 Influenza Season

March 2003


235 Reads

During the winter of 2001-02, influenza AH1N2 viruses were detected for the first time in humans in the U.K. The H1N2 viruses co-circulated with H3N2 viruses and a very small number of H1N1 viruses and were isolated in the community and hospitalized patients, predominantly from children <15 years of age. Characterization of H1N2 viruses indicated that they were antigenically and genetically homogeneous, deriving the hemagglutinin (HA) gene from recently circulating A/New Caledonia/20/99-like H1N1 viruses, whereas the other seven genes originated from recently circulating H3N2 viruses. Retrospective reverse transcription-polymerase chain reaction analysis of influenza A H1 viruses isolated in the U.K. during the previous winter identified a single H1N2 virus, isolated in March 2001, indicating that H1N2 viruses did not widely circulate in the U.K. before September 2001. The reassortment event is estimated to have occurred between 1999 and early 2001, and the emergence of H1N2 viruses in humans reinforces the need for frequent surveillance of circulating viruses.

Clostridium difficile Ribotype 027, Toxinotype III, the Netherlands

June 2006


78 Reads

Outbreaks due to Clostridium difficile polymerase chain reaction (PCR) ribotype 027, toxinotype III, were detected in 7 hospitals in the Netherlands from April 2005 to February 2006. One hospital experienced at the same time a second outbreak due to a toxin A-negative C. difficile PCR ribotype 017 toxinotype VIII strain. The outbreaks are difficult to control.

Figure. Results of PCR ribotyping of Clostridium diffi cile 027 strains from Chile. M indicates the 100-bp DNA ladder; lane 2, R20291; lane 2, PUC47; lane 3, PUC51. A) PCR ribotyping of C. diffi cile isolates. PCR results show that that the band pattern of the ribosomal intergenic regions of strains PUC47 and PUC51 are similar to those of the reference (epidemic) strain R20291. B) Cluster analysis of strains PUC47, PUC51, and the epidemic strain 027 R20291 shows >99% similarity and that they belong to the same epidemic clade. Scale bar indicates percent identity.  
Epidemic Clostridium difficile Ribotype 027 in Chile

August 2012


99 Reads

TO THE EDITOR: The increased severity of Clostridium difficile infection is primarily attributed to the appearance of an epidemic strain characterized as PCR ribotype 027 (1). The only report that identified epidemic C. difficile ribotype 027 in an American country outside of North America comes from Costa Rica, raising the possibility that strains 027 might also be present in other countries of Latin America (2). Several studies between 2001 and 2009 have been conducted in South American countries to detect the incidence of C. difficile infection in hospitalized patients, but they did not identify which C. difficile strains were causing these infections (3).

Severe Community-acquired Pneumonia Due to Staphylococcus aureus, 2003–04 Influenza Season

July 2006


87 Reads

During the 2003-04 influenza season, 17 cases of Staphylococcus aureus community-acquired pneumonia (CAP) were reported from 9 states; 15 (88%) were associated with methicillin-resistant S. aureus (MRSA). The median age of patients was 21 years; 5 (29%) had underlying diseases, and 4 (24%) had risk factors for MRSA. Twelve (71%) had laboratory evidence of influenza virus infection. All but 1 patient, who died on arrival, were hospitalized. Death occurred in 5 (4 with MRSA). S. aureus isolates were available from 13 (76%) patients (11 MRSA). Toxin genes were detected in all isolates; 11 (85%) had only genes for Panton-Valentine leukocidin. All isolates had community-associated pulsed-field gel electrophoresis patterns; all MRSA isolates had the staphylococcal cassette chromosome mec type IVa. In communities with a high prevalence of MRSA, empiric therapy of severe CAP during periods of high influenza activity should include consideration for MRSA.

Influenza Vaccine Effectiveness among US Military Basic Trainees, 2005–06 Season

May 2007


66 Reads

Virtually all US military basic trainees receive seasonal influenza vaccine. Surveillance data collected from December 2005 through March 2006 were evaluated to estimate effectiveness of the influenza vaccine at 6 US military basic training centers. Vaccine effectiveness against laboratory-confirmed influenza was 92% (95% confidence interval 85%-96%).

Rapid determination of HLA B*07 ligands from the West Nile virus NY99 genome

August 2001


39 Reads

Defined T cell epitopes for West Nile (WN) virus may be useful for developing subunit vaccines against WN virus infection and diagnostic reagents to detect WN virus-specific immune response. We applied a bioinformatics (EpiMatrix) approach to search the WN virus NY99 genome for HLA B*07 restricted cytotoxic T cell (CTL) epitopes. Ninety-five of 3,433 WN virus peptides scored above a predetermined cutoff, suggesting that these would be likely to bind to HLA B*07 and would also be likely candidate CTL epitopes. Compared with other methods for genome mapping, derivation of these ligands was rapid and inexpensive. Major histocompatibility complex ligands identified by this method may be used to screen T cells from WN virus-exposed persons for cell-mediated response to WN virus or to develop diagnostic reagents for immunopathogenesis studies and epidemiologic surveillance.

Figure 1. Phylogenetic reconstruction of the H1 genes of infl uenza viruses A (H1N1) in Norway, 2007-08 season. The analysis was performed on an alignment spanning positions 84-1054 of viral RNA segment 4. Pairwise distances were calculated by using the Kimura 2-parameter model with a transition:transversion ratio of 2.0; the phylogenetic tree was constructed by the neighbor-joining method, as implemented in the programs DNADIST and NEIGHBOR in the PHYLIP package (14,15). Published sequences were obtained from the Infl uenza Sequence Database, Los Alamos National Laboratory (16). Boldface indicates viruses from the 2007-08 infl uenza season in Norway; red indicates oseltamivir-resistant viruses; blue, susceptible viruses. New sequences presented in this analysis have been deposited in GenBank (accession nos. CY036664-CY036694).
Table 2 . Reported associations for patients infected with oseltamivir-resistant or oseltamivir-susceptible influenza virus A (H1N1), 2007-08 influenza season, Norway*
Figure 4. Proportion of oseltamivir-resistant in fl uenza viruses A (H1N1) in the 2007–08 in fl uenza season in Norway, by county of sampling. The total number of samples analyzed for each county is given inside each county. 
Oseltamivir-Resistant Influenza Viruses A (H1N1), Norway, 2007–08

March 2009


97 Reads

In Norway in January 2008, unprecedented levels of oseltamivir resistance were found in 12 of 16 influenza viruses A (H1N1) tested. To investigate the epidemiologic and clinical characteristics of these viruses, we used sequence analysis to test all available subtype H1N1 viruses from the 2007-08 season for resistance. Questionnaires from physicians provided information on predisposing diseases, oseltamivir use, symptoms, and complications. Clinical data were obtained for 265 patients. In total, 183 (67.3%) of 272 viruses were oseltamivir resistant. Resistance was not associated with prior use of antiviral drugs. Symptoms and hospitalization rates did not differ for patients infected with a resistant or a susceptible virus. Oseltamivir-resistant influenza viruses A (H1N1) did not show diminished capability to spread in the absence of selective pressure. The ability of these viruses to sustain their fitness and spread among persons should be considered when shaping future strategies for treating and preventing seasonal and pandemic influenza.

Figure 2. Total number of in fl uenza virus detections, by type and subtype and by week, Europe, winter 2007–08. 
Figure 3. Total in fl uenza A viruses subtyped as H1N1 and number of oseltamivir-resistant or oseltamivir-sensitive viruses among the subset of in fl uenza viruses A (H1N1) for which oseltamivir susceptibility was determined, by week, Europe, winter 2007–08. 
Figure 5. Weighted average prevalence of oseltamvir-resistant infl uenza viruses A (H1N1), Europe, winter 2007-08. The light gray region indicates the 95% confi dence interval.
Figure 6. Phylogenetic comparisons of the hemagglutinin (A) and neuraminidase (B) genes of infl uenza viruses A (H1N1). Sequences of oseltamivir-resistant viruses, possessing the H275Y (H274Y in N2 numbering) mutation are in boldface; vaccine strains are in italics. Common amino acid changes that distinguish clades 1 and 2 and subgroups of clade 2 are shown. Scale bars indicate 0.01 nucleotide substitutions per site.
Oseltamivir-Resistant Influenza Virus A (H1N1), Europe, 2007-08 Season

May 2009


201 Reads

In Europe, the 2007-08 winter season was dominated by influenza virus A (H1N1) circulation through week 7, followed by influenza B virus from week 8 onward. Oseltamivir-resistant influenza viruses A (H1N1) (ORVs) with H275Y mutation in the neuraminidase emerged independently of drug use. By country, the proportion of ORVs ranged from 0% to 68%, with the highest proportion in Norway. The average weighted prevalence of ORVs across Europe increased gradually over time, from near 0 in week 40 of 2007 to 56% in week 19 of 2008 (mean 20%). Neuraminidase genes of ORVs possessing the H275Y substitution formed a homogeneous subgroup closely related to, but distinguishable from, those of oseltamivir-sensitive influenza viruses A (H1N1). Minor variants of ORVs emerged independently, indicating multiclonal ORVs. Overall, the clinical effect of ORVs in Europe, measured by influenza-like illness or acute respiratory infection, was unremarkable and consistent with normal seasonal activity.

No Association between 2008-09 Influenza Vaccine and Influenza A(H1N1)pdm09 Virus Infection, Manitoba, Canada, 2009

May 2012


57 Reads

We conducted a population-based study in Manitoba, Canada, to investigate whether use of inactivated trivalent influenza vaccine (TIV) during the 2008-09 influenza season was associated with subsequent infection with influenza A(H1N1)pdm09 virus during the first wave of the 2009 pandemic. Data were obtained from a provincewide population-based immunization registry and laboratory-based influenza surveillance system. The test-negative case-control study included 831 case-patients with confirmed influenza A(H1N1)pdm09 virus infection and 2,479 controls, participants with test results negative for influenza A and B viruses. For the association of TIV receipt with influenza A(H1N1)pdm09 virus infection, the fully adjusted odds ratio was 1.0 (95% CI 0.7-1.4). Among case-patients, receipt of 2008-09 TIV was associated with a statistically nonsignificant 49% reduction in risk for hospitalization. In agreement with study findings outside Canada, our study in Manitoba indicates that the 2008-09 TIV neither increased nor decreased the risk for infection with influenza A(H1N1)pdm09 virus.

Levin, B. R. The evolution and maintenance of virulence in microparasites. Emerg. Infect. Dis. 2, 93-102
In recent years, population and evolutionary biologists have questioned the traditional view that parasite-mediated morbidity and mortality¿virulence¿is a primitive character and an artifact of recent associations between parasites and their hosts. A number of hypotheses have been proposed that favor virulence and suggest that it will be maintained by natural selection. According to some of these hypotheses, the pathogenicity of HIV, Vibrio cholerae, Mycobacterium tuberculosis,theShigella,as well as Plasmodium falciparum,and many other microparasites, are not only maintained by natural selection, but their virulence increases or decreases as an evolutionary response to changes in environmental conditions or the density and/or behavior of the human population. Other hypotheses propose that the virulence of microparasites is not directly favored by natural selection; rather, microparasite-mediated morbidity and mortality are either coincidental to parasite-expressed characters (virulence determinants that evolved for other functions) or the product of short-sighted evolution in infected hosts. These hypotheses for the evolution and maintenance of microparasite virulence are critically reviewed, and suggestions are made for testing them experimentally.

Figure 1. Antimicrobial susceptibility of Salmonella enterica serotype Typhimurium definitive phage type (DT) 12 and DT 120 isolates, England and Wales, 1991–2000. A, S. Typhimurium DT 12; B, S. Typhimurium DT 120. Clear bar, sensitive; diagonal screened bar, resistance to ampicillin , chloramphenicol, streptomycin, sulfonamides, and tetracyclines (ACSSuT; includes resistant-type ACSSuT and ACSSuT plus additional resistances to Tm, Cp L, or both); black bar, other resistance patterns.  
Figure 2. Dendrogram showing the relationships of pulsed-field gel electrophoresis profiles by the nearest neighbor technique. *Includes resistant (R)-type ACSSuT and ACSSuT plus additional resistances to Tm, Cp L, or both. A = ampicillin, C = chloramphenicol, Fu = furazolidone, K = kanamycin, Ne = neomycin, S = streptomycin, Su = sulfonamides, T = tetracyclines, Tm = trimethoprim, Cp L = ciprofloxacin.  
Multiply Resistant (MR) Salmonella enterica serotype Typhimurium DT 12 and DT 120: A case of MR DT 104 in disguise?

May 2002


82 Reads

Multiresistant Salmonella enterica serotype Typhimurium definitive phage type (DT) 12 and DT 120 are more closely related to DT 104 than to non-multiresistant strains of their respective phage types. Multiresistant DT 12 and DT 120 appear to have arisen due to changes in phage susceptibility of DT 104 rather than horizontal transfer of resistance genes.

Enterovirus 104 Infection in Adult, Japan, 2011

May 2012


54 Reads

TO THE EDITOR: Human enterovirus (HEV) C (family Picornaviridae, genus Enterovirus) consists of 3 types of poliovirus (1, 2, and 3), 9 types of coxsackievirus A (CV-A1, 11, 13, 17, 19, 20, 21, 22, and 24), and 9 types of enterovirus (EV) (95, 96, 99, 102, 104, 105, 109, 113, and 116) (www.picornaviridae.com/enterovirus/hev-c/hev-c.htm). EV-104 was first identified in 2009 in Switzerland in 8 children who had pneumonia or acute otitis media (1). To our knowledge, there has been only 1 other report of EV-104, detected in Italy in 3 adults and 2 children who had upper respiratory tract infection (RTI) (2). We report the detection of a novel EV-104 strain in an adult with upper RTI in Japan.

Table 2 . Percentage composition of isoleucine and valine at position 221 in the neuraminidase of virus isolates and clinical specimens with reduced susceptibility to oseltamivir and peramivir, North Carolina, USA, 201011 influenza season*
Figure. Phylogenetic analysis of A) hemagglutinin and B) neuraminidase genes of Victoria lineage type B infl uenza viruses (n = 89). Red indicates the 2010-2011 Northern Hemisphere vaccine strain; blue indicates the cluster of infl uenza B viruses identifi ed in North Carolina carrying the I221V substitution in the neuraminidase; green indicates viruses collected from North Carolina with wild-type sequence at position 221 in the neuraminidase; black indicates representatives of globally circulating infl uenza B viruses. Month of collection is shown after virus strain designation. Evolutionary distances were computed by using the Tamura-Nei method (www. megasoftware.net/WebHelp/part_iv___evolutionary_ analysis/computing_evolutionary_distances/distance_ models/nucleotide_substitution_models/hc_tamura_ nei_distance.htm). Scale bars indicate number of base substitutions per site.  
Influenza B Viruses with Mutation in the Neuraminidase Active Site, North Carolina, USA, 2010–11

November 2011


63 Reads

Oseltamivir is 1 of 2 antiviral medications available for the treatment of influenza B virus infections. We describe and characterize a cluster of influenza B viruses circulating in North Carolina with a mutation in the neuraminidase active site that may reduce susceptibility to oseltamivir and the investigational drug peramivir but not to zanamivir.

Neisseria meningitidis ST-11 Clonal Complex, Chile 2012

February 2015


127 Reads

Serogroup W Neisseria meningitidis was the main cause of invasive meningococcal disease in Chile during 2012. The case-fatality rate for this disease was higher than in previous years. Genotyping of meningococci isolated from case-patients identified the hypervirulent lineage W:P1.5,2:ST-11, which contained allele 22 of the fHbp gene.

Figure. Geographic distribution of oseltamivir-resistant pandemic (H1N1) 2009 viruses in the United States, October 1, 2010-July 31, 2011. Numerators are number of oseltamivir-resistant viruses identifi ed by state public health laboratories; denominators are number of pandemic (H1N1) 2009-positive specimens submitted by each state for susceptibility testing. Gray shading indicates states that had >1 infection with oseltamivir-resistant virus. 
Oseltamivir-Resistant Pandemic (H1N1) 2009 Virus Infections, United States, 2010–11

February 2012


57 Reads

During October 2010-July 2011, 1.0% of pandemic (H1N1) 2009 viruses in the United States were oseltamivir resistant, compared with 0.5% during the 2009-10 influenza season. Of resistant viruses from 2010-11 and 2009-10, 26% and 89%, respectively, were from persons exposed to oseltamivir before specimen collection. Findings suggest limited community transmission of oseltamivir-resistant virus.

Severe Pneumonia Caused by Legionella pneumophila Serogroup 11, Italy

November 2012


56 Reads

TO THE EDITOR: Legionella pneumophila serogroups (SGs) 1-16 cause pneumonia in humans. Although SG 1 is the serogroup most commonly associated with disease (1), we report a case of community-acquired legionellosis caused by SG 11.

Clarke B, Hiltz M, Musgrave H, Forward KR.. Cephamycin resistance in clinical isolates and labotatory-derived strains of Escherichia coli, Nova Scotia, Canada. Emerging Infect Dis 9: 1254-1259

November 2003


34 Reads

AmpC β-lactamase, altered porins, or both are usually responsible for cefoxitin resistance in Escherichia coli. We examined the relative importance of each. We studied 18 strains of clinical isolates with reduced cefoxitin susceptibility and 10 initially-susceptible strains passaged through cefoxitin-gradient plates. Of 18 wild-resistant strains, 9 had identical promoter mutations (including creation of a consensus 17-bp spacer) and related pulsed-field gel electrophoresis patterns; the other 9 strains were unrelated. Nine strains had attenuator mutations; two strains did not express OmpC or OmpF. After serial passage, 8 of 10 strains developed cefoxitin resistance, none developed promoter or attenuator mutations, 6 lost both the OmpC and OmpF porin proteins, and 1 showed decreased production of both. One strain had neither porin alteration or increased AmpC production. Porin mutants may occur more commonly and be less fit and less inclined to spread or cause disease than strains with increased β-lactamase expression.

Genetic Variants of Echovirus 13, Northern India, 2010

February 2013


52 Reads

Nonpolio acute flaccid paralysis is increasing in India. To determine viral causes, we conducted cell culture and molecular analysis identification of nonpolio human enteroviruses associated with acute flaccid paralysis during March-August 2010 in northern India. The predominant nonpolio enterovirus found was echovirus 13, a serotype rarely isolated in India.

Statewide School-located Influenza Vaccination Program for Children 5–13 Years of Age, Hawaii, USA

February 2010


96 Reads

New guidance recommends annual influenza vaccination for all children 5-18 years of age in the United States. During 2007-2008, Hawaii offered inactivated and live attenuated influenza vaccine at school-located clinics for grades kindergarten through 8. Most (90%) public and private schools participated, and 622 clinics were conducted at 340 schools. Of 132,775 children 5-13 years of age, 60,760 (46%) were vaccinated. The proportion vaccinated peaked at 54% for those 6 years of age and declined for older cohorts. More than 90% of schoolchildren transited the clinic in <10 minutes. A total of 16,920 staff-hours were expended; estimated cost per dose administered was $27 and included vaccine purchase and administration, health staffing resources, printing costs, data management, and promotion. This program demonstrates the feasibility of conducting mass school-located influenza vaccination programs in public and private schools statewide, as might be indicated to respond to pandemic influenza.

Biological Warfare at the 1346 Siege of Caffa

October 2002


6,373 Reads

On the basis of a 14th-century account by the Genoese Gabriele de' Mussi, the Black Death is widely believed to have reached Europe from the Crimea as the result of a biological warfare attack. This is not only of great historical interest but also relevant to current efforts to evaluate the threat of military or terrorist use of biological weapons. Based on published translations of the de' Mussi manuscript, other 14th-century accounts of the Black Death, and secondary scholarly literature, I conclude that the claim that biological warfare was used at Caffa is plausible and provides the best explanation of the entry of plague into the city. This theory is consistent with the technology of the times and with contemporary notions of disease causation; however, the entry of plague into Europe from the Crimea likely occurred independent of this event.

Figure 1. Meningococcal disease in Kingdom of Saudi Arabia, by month, 1995–2000. Cases of meningococcal disease with dates converted from Islamic calendar months. The period of the Hajj pilgrimage for each year is underscored.  
Serogroup W-135 Meningococcal Disease during the Hajj, 2000

July 2003


105 Reads

An outbreak of serogroup W-135 meningococcal disease occurred during the 2000 Hajj in Saudi Arabia. Disease was reported worldwide in Hajj pilgrims and their close contacts; however, most cases were identified in Saudi Arabia. Trends in Saudi meningococcal disease were evaluated and the epidemiology of Saudi cases from this outbreak described. Saudi national meningococcal disease incidence data for 1990 to 2000 were reviewed; cases from January 24 to June 5, 2000, were retrospectively reviewed. The 2000 Hajj outbreak consisted of distinct serogroup A and serogroup W-135 outbreaks. Of 253 identified cases in Saudi Arabia, 161 (64%) had serogroup identification; serogroups W-135 and A caused 93 (37%) and 60 (24%) cases with attack rates of 9 and 6 cases per 100,000 population, respectively. The 2000 Hajj outbreak was the first large serogroup W-135 meningococcal disease outbreak identified worldwide. Enhanced surveillance for serogroup W-135, especially in Africa, is essential to control this emerging epidemic disease.

Absence of Neisseria meningitidis W-135 Electrophoretic Type 37 during the Hajj, 2002

July 2003


40 Reads

We document the absence of carriage of Neisseria meningitidis W-135 of the sequence type 11 in returning pilgrims after the Hajj 2002. This finding contrasts with the 15% carriage rate we previously reported in pilgrims returning from the Hajj 2001. The epidemiology of carriage may be changing or may have been controlled by vaccination and a policy of administering antibiotics to pilgrims from countries with a high incidence of meningococcal disease.

Novel G10P[14] Rotavirus Strain, Northern Territory, Australia

August 2013


65 Reads

We identified a genotype G10P[14] rotavirus strain in 5 children and 1 adult with acute gastroenteritis from the Northern Territory, Australia. Full genome sequence analysis identified an artiodactyl-like (bovine, ovine, and camelid) G10-P[14]-I2-R2-C2-M2-A11-N2-T6-E2-H3 genome constellation. This finding suggests artiodactyl-to-human transmission and strengthens the need to continue rotavirus strain surveillance.

Adenovirus Serotype 14 Infection, New Brunswick, Canada, 2011

January 2013


73 Reads

We describe 3 culture-proven cases of adenovirus serotype 14 infection in New Brunswick, Canada, during the summer of 2011. Strains isolated from severely ill patients were closely related to strains of a genomic variant, adenovirus 14p1, circulating in the United States and Ireland. Physicians in Canada should be aware of this emerging adenovirus.

Figure 1. Circular map of plasmid pCT. Open reading frames are color coded as follows: brown, pseudogenes; orange, hypothetic proteins; light pink, insertion sequences; light blue, tra locus; green, pil locus; dark pink, antimicrobial drug resistance gene; yellow, putative sigma factor; red, replication-associated genes. Arrows show the direction of transcription. pCT, IncK plasmid. 
Figure 2. Artemis Comparison Tool (Sanger, Cambridge, UK) comparisons of IncK plasmid (pCT) with other plasmids. Complete DNA sequence plasmid comparisons. Bands of color indicate homology between sequences. Red lines show sequence in the same con fi rmation; blue lines indicate sequence inversion. The pCT sequence is represented as the top line of each comparison compared with pO26_vir (GenBank accession no. FJ38659) (A); R387 (B); R64 (accession no. AP005147) (C); and pEK204 (accession no. EU935740) (D) on each bottom line. 
Figure 3. Phylogenetic analysis of nikB in IncI complex plasmids from Escherichia coli . DNA sequences of nikB PCR amplicons and sequences obtained from public resources were aligned and analyzed by using MEGA 4.0 ( 29 ). A neighbor-joining tree was constructed by using complete deletion modeling and computed by using the maximum composite likelihood method ( 30 ). The phylogenetic tree was linearized assuming equal evolutionary rates in all lineages. Circles, nikB sequences from plasmids isolated from veterinary isolates from the United Kingdom; triangles, nikB sequences of plasmids from Escherichia coli isolated from humans; squares, nikB sequences of plasmids obtained from GenBank or the Sanger Institute; shaded shapes, plasmids identi fi ed as pCT-like by using PCR in this study; asterisks, plasmids encoding bla CTX-M-14 . pCT, 
Complete Sequence and Molecular Epidemiology of IncK Epidemic Plasmid Encoding blaCTX-M-14

April 2011


664 Reads

Antimicrobial drug resistance is a global challenge for the 21st century with the emergence of resistant bacterial strains worldwide. Transferable resistance to β-lactam antimicrobial drugs, mediated by production of extended-spectrum β-lactamases (ESBLs), is of particular concern. In 2004, an ESBL-carrying IncK plasmid (pCT) was isolated from cattle in the United Kingdom. The sequence was a 93,629-bp plasmid encoding a single antimicrobial drug resistance gene, blaCTX-M-14. From this information, PCRs identifying novel features of pCT were designed and applied to isolates from several countries, showing that the plasmid has disseminated worldwide in bacteria from humans and animals. Complete DNA sequences can be used as a platform to develop rapid epidemiologic tools to identify and trace the spread of plasmids in clinically relevant pathogens, thus facilitating a better understanding of their distribution and ability to transfer between bacteria of humans and animals.

Figure 2. Evolutionary relationships among influenza A (H1N1)pdm09 virus neuraminidase genes, United States, 2013–14. Phylogenetic tree was generated by using MEGA software v5.2 (http://www.megasoftware. net/) and the neighbor-joining method. Evolutionary distances were computed by using the maximum composite likelihood model. Analysis included 100 representative A(H1N1)pdm09 neuraminidase gene sequences. Scale bar indicates nucleotide substitutions per site. Solid circles indicate oseltamivirresistant H275Y markers. A/ California/07/2009 (current Northern Hemisphere vaccine strain) virus was used as a reference for ancestry (root) and numbering. F, Centers for Disease Control and Prevention reference antigen; Oct, October 2013; Nov, November 2013; Dec, December 2013; Jan, January 2014; Feb, February 2014; GLY, glycosylation.  
Oseltamivir-Resistant Influenza A(H1N1)pdm09 Viruses, United States, 2013–14

January 2015


201 Reads

We report characteristics of oseltamivir-resistant influenza A(H1N1)pdm09 viruses and patients infected with these viruses in the United States. During 2013–14, fifty-nine (1.2%) of 4,968 analyzed US influenza A(H1N1)pdm09 viruses had the H275Y oseltamivir resistance–conferring neuraminidase substitution. Our results emphasize the need for local surveillance for neuraminidase inhibitor susceptibility among circulating influenza viruses. © 2015, Centers for Disease Control and Prevention (CDC). All rights reserved.

Figure 1. Maximum-likelihood trees of the full-length fi ber (A), E1A (B), and hexon (C) open reading frames of adenovirus B2 subgenera. Phylogenetic analysis was performed by using reference sequences from GenBank for the adenovirus B2 subgenera, including prototype reference strains. The query sequences from this study are identical and are represented in boldface. The tree was built in PAUP* (23) on the basis of the HKY85 model of evolution and for the fi ber tree also with a β distribution and used midpoint rooting. Bootstrap resampling (n = 1,000) was performed by using the neighbor-joining algorithm. Scale bars indicate nucleotide substitutions per site.  
Figure 2. Comparative restriction enzyme analysis of viral DNA extracted from the prototype human adenovirus (HAdV) 14 de Wit strain and the fi rst detected HAdV-14 case isolated in Dublin, Ireland, November 2009. All odd-numbered lanes (e.g., 1, 3) contain the de Wit strain and all even-numbered lanes (e.g., 2, 4) contain the Dublin 2009 strain, with restriction enzyme digests as follows: lanes 1 and 2 with BamHI; lanes 3 and 4 with BclI; lanes 5 and 6 with BglII; lanes 7 and 8 with BstEII; lanes 9 and 10 with DraI; lanes 11 and 12 with HindIII; lanes 13 and 14 with PstI; lanes 15 and 16 with SmaI; lanes 17 and 18 with XbaI. Outer lanes are molecular markers (1 Kb +100 bp; BioRad, Hercules, CA, USA).  
Deaths Associated with Human Adenovirus-14p1 Infections, Europe, 2009–2010

August 2011


204 Reads

Human adenovirus (HAdV) serotype 14 is rarely identified. However, an emerging variant, termed HAdV-14p1, recently has been described in the United States in association with outbreaks of acute respiratory disease with high rates of illness and death. We retrospectively analyzed specimens confirmed positive for HAdV by immunofluorescence, virus culture, or real-time PCR during July 1, 2009-July 31, 2010, and describe 9 cases of HAdV-14p1 infection with characteristic mutations in the fiber and E1A genes that are phylogenetically indistinguishable from the viruses previously detected in the United States. Three patients died; 2 were immunocompromised, and 1 was an immunocompetent adult. We propose that surveillance should be increased for HAdV-14p1 and recommend that this virus be considered in the differential diagnosis of sudden-onset acute respiratory disease, particularly fatal infections, for which an etiology is not clear.

15th International Workshop on Campylobacter, Helicobacter and Related Organisms

July 2010


115 Reads

The purpose of this communication is to update the veterinary public health community as to what poultry-related interventions were presented at the recent biennial International Workshop on Campylobacter, Helicobacter and Related Organisms (CHRO), which was held in Niigata, Japan, September 2-5, 2009. More than 30 years have passed since the publication of Martin Skirrow's seminal paper in the British Medical Journal in which he described Campylobacter enteritis as a new disease (1). This publication precipitated a global interest in thermophilic campylobacters. Three decades later, these organisms still pose a grave threat to public health. Furthermore, 10 years have passed since Parkhill et al. published the genome sequence of Campylobacter jejuni NCTC11168 (2).

Figure. Pulsed-fi eld gel electrophoresis after SmaI digestion of Streptococcus suis serotype 16 strain SS07 and a representative set of S. suis serotype 2 strains isolated from patients with meningitis in southern Vietnam. A dendrogram was generated by Dice analysis (optimization 0.5%, band tolerance 1%) and cluster analysis with unweighted pair group method with arithmetic average, using Bionumerics software (Applied Maths, Sint- Martens-Latem, Belgium). Numbers in dendrogram indicate percentage of similarity. Arrow numbers indicate molecular size (kb).  
Human Case of Streptococcus suis Serotype 16 Infection

February 2008


1,567 Reads

Streptococcus suis infection is an emerging zoonosis in Southeast Asia. We report a fatal case of S. suis serotype 16 infection in a Vietnamese man in 2001.

First Epidemic of Echovirus 16 Meningitis in Cuba

October 2001


61 Reads

From April to September 2000, an epidemic of aseptic meningitis spread throughout Cuba, with 16,943 reported cases. Virologic studies identified echovirus 16 as the cause of this epidemic. This is the first reported isolate of echovirus 16 from patients with viral meningitis in Cuba.

Fatal Coxsackievirus A-16 Pneumonitis in Adult

August 2007


91 Reads

Coxsackievirus A-16 (CVA-16) is the agent of hand, foot, and mouth disease in children. We report a case of fatal pneumonitis in an adult due to a CVA-16 strain with a low (78.6%) rate of sequence homology with the reference strain. A modified, more virulent, strain of CVA-16 could be emerging.

Figure 1. Native American tribes of southeastern Massachusetts in ≈1620. 
Figure 2. Plymouth, Massachusetts, harbor showing extensive Native American settlement (a sketch by Samuel de Champlain from his voyage of 1606). 
Figure 3. Leptospiral life cycle. 
New Hypothesis for Cause of Epidemic among Native Americans, New England, 1616–1619

February 2010


5,214 Reads

In the years before English settlers established the Plymouth colony (1616-1619), most Native Americans living on the southeastern coast of present-day Massachusetts died from a mysterious disease. Classic explanations have included yellow fever, smallpox, and plague. Chickenpox and trichinosis are among more recent proposals. We suggest an additional candidate: leptospirosis complicated by Weil syndrome. Rodent reservoirs from European ships infected indigenous reservoirs and contaminated land and fresh water. Local ecology and high-risk quotidian practices of the native population favored exposure and were not shared by Europeans. Reduction of the population may have been incremental, episodic, and continuous; local customs continuously exposed this population to hyperendemic leptospiral infection over months or years, and only a fraction survived. Previous proposals do not adequately account for signature signs (epistaxis, jaundice) and do not consider customs that may have been instrumental to the near annihilation of Native Americans, which facilitated successful colonization of the Massachusetts Bay area.

Figure 1. A) Time series of summer Palmer Drought Severity Index (PDSI) averaged for 78 grid points in central Mexico, 1665–1918. Data were obtained from Cook et al. ( 12,13 ) and Therrell et al. ( 14 ). B) Time series of June–July PDSI reconstructed from the Cuahtemoc la Fragua tree-ring chronology in east-central Mexico by using an average of 22 grid locations from the monthly PDSI dataset of R.R. Heim, Jr. (National Climatic Data Center, Ashville, NC, USA). Circles indicate typhus epidemics. Red lines indicate high-frequency yearly variability of moisture reconstruction. Black lines indicate smoothed lower-frequency representation of this variability. Horizontal lines indicate average PDSI for period. 
Figure 2. A) Superposed epoch analysis ( 20 ) of summer Palmer Drought Severity Index (PDSI) for central Mexico averaged for the 22 periods that had typhus epidemics (1655, 1710–1712, 1714, 1742, 1761–1762, 1785–1787, 1799–1802, 1805–1806, 1811–1812, 1821–1823, 1825–1828, 1835–1838, 1847–1848, 1861–1864, 1865–1868, 1870–1873, 1875–1877, 1884–1886, 1894–1895, 1902–1903, 1909–1911, and 1915–1918). Horizontal line indicates PDSI = 0. JJ, June–July; JJA, June–July–August. B) Superimposed epoch analysis of June–July PDSI for east- central Mexico also averaged for the 22 periods that had typhus epidemics. Superimposed epoch analyses were performed by using the Dendrochronology Program Library ( 21,22 ). Horizontal line indicates mean PDSI. 
Figure 3. Tree-ring-reconstructed summer Palmer Drought Severity Index (PDSI) during A) 22 and B) 15 typhus epidemics in Mexico, 1665-1918. Drought conditions are indicated by negative values on the PDSI scale. Reconstructed summer PDSI values during the 15 typhus epidemic years with the most negative PDSI values for central Mexico are mapped in panel B. JJA, June-July-August.
Drought and Epidemic Typhus, Central Mexico, 1655–1918
Epidemic typhus is an infectious disease caused by the bacterium Rickettsia prowazekii and transmitted by body lice (Pediculus humanus corporis). This disease occurs where conditions are crowded and unsanitary. This disease accompanied war, famine, and poverty for centuries. Historical and proxy climate data indicate that drought was a major factor in the development of typhus epidemics in Mexico during 1655-1918. Evidence was found for 22 large typhus epidemics in central Mexico, and tree-ring chronologies were used to reconstruct moisture levels over central Mexico for the past 500 years. Below-average tree growth, reconstructed drought, and low crop yields occurred during 19 of these 22 typhus epidemics. Historical documents describe how drought created large numbers of environmental refugees that fled the famine-stricken countryside for food relief in towns. These refugees often ended up in improvised shelters in which crowding encouraged conditions necessary for spread of typhus.

Figure 1. Geographic distribution of hospitals where 16S rRNA methylase gene-positive strains were isolated. Of 16 hospitals, 4 were located in the Kanto area (Gunma and Tokyo), 6 in the Chubu area (Aichi, Gifu, and Shizuoka), 1 in the Koushin-etsu area (Nagano), 4 in the Kinki area (Osaka, Nara, and Hyogo), and 1 in the Kyushu area (Miyazaki). This distribution suggests a sparse but diffuse spread of 16S rRNA methylase-producing, gram-negative pathogenic microbes in Japan. Bacterial species and type of 16S rRNA methylase identified in each hospital are shown in Table 2.
Figure 2. A) Pulsed-field gel electrophoresis (PFGE) fingerprinting patterns of SpeI-digested total DNA preparations from Pseudomonas aeruginosa. M, Lambda ladder PFGE molecular mass marker (Bio-Rad, Hercules, CA, USA). Strains 103 and 109 show similar patterns, which suggests probable nosocomial transmission of rmtA-positive strains in hospital C. Strains 113, 127, and 158 also demonstrate similar patterns, which implies possible nosocomial transmission in hospital D. However, 2 different PFGE patterns are observed in hospitals C, D, and F, which suggests transfer of plasmids carrying 16S rRNA-methylase genes among P. aeruginosa strains with different genetic backgrounds. B) SmaIdigested total DNA preparations from Acinetobacter baumannii isolated from hospital S. Three strains demonstrate the same PFGE pattern, which suggests probable nosocomial transmission of armA-positive A. baumannii in hospital S. M, lambda ladder lowrange PFGE molecular mass marker (New England Biolabs, Ipswich, MA, USA).
16S rRNA Methylase–producing, Gram-Negative Pathogens, Japan

May 2007


145 Reads

To investigate the exact isolation frequency of 16S rRNA methylase-producing, gram-negative pathogenic bacteria, we tested 87,626 clinical isolates from 169 hospitals. Twenty-six strains from 16 hospitals harbored 16S rRNA methylase genes, which suggests sparse but diffuse spread of pan-aminoglycoside-resistant microbes in Japan.

Table 1 continued. Descriptions and GenBank accession numbers of 107 Bacillus species strains analyzed in this study 
Table 3 . 16S rRNA gene types identified among 125 Bacillus spp. strains analyzed in this study (n=107) and available at GenBank (n=18) 
Sequencing of 16S rRNA Gene: A Rapid Tool for Identification of Bacillus anthracis

November 2002


840 Reads

In a bioterrorism event, a tool is needed to rapidly differentiate Bacillus anthracis from other closely related spore-forming Bacillus species. During the recent outbreak of bioterrorism-associated anthrax, we sequenced the 16S rRNA generom these species to evaluate the potential of 16S rRNA gene sequencing as a diagnostic tool. We found eight distinct 16S types among all 107 16S rRNA gene seqs fuences that differed from each other at 1 to 8 positions (0.06% to 0.5%). All 86 B. anthracis had an identical 16S gene sequence, designated type 6; 16S type 10 was seen in all B. thuringiensis strains; six other 16S types were found among the 10 B. cereus strains. This report describes the first demonstration of an exclusive association of a distinct 16S sequence with B. anthracis. Consequently, we were able to rapidly identify suspected isolates and to detect the B. anthracis 16S rRNA gene directly from culture-negative clinical specimens from seven patients with laboratory-confirmed anthrax.

Figure 1.-The 16th-century population collapse in Mexico, based on estimates of Cook and Simpson (1). The 1545 and 1576 cocoliztli epidemics appear to have been hemorrhagic fevers caused by an indigenous viral agent and aggravated by unusual climatic conditions. The Mexican population did not recover to pre-Hispanic levels until the 20th century.  
Figure 2.-Winter-spring precipitation reconstructed from tree ring data, Durango, Mexico (normalized and smoothed to highlight decennial variability). The tree-ring estimates explain 56% of the variance in precipitation for Durango and are consistent with independent precipitation data. This reconstruction is well correlated with the all-Mexico rainfall index (r = 0.76; p < 0.001) and with precipitation over north central Mexico, where the cocoliztli epidemics appear to have been most severe. Note the unprecedented 16th-century magadrought during both cocoliztli epidemics.  
Figure 3.-The winter-spring precipitation totals estimated for each year in Durango, 1540-1548 (top), 1571-1579 (middle), compared with the Palmer drought index, southwestern USA 1988-1995 (bottom). A tenfold increase in deer mice was witnessed in the southwestern USA during the 1993 outbreak, a year of abundant precipitation following a prolonged drought. The similar dry-wet pattern reconstructed for the 1545 epidemic of cocoliztli may have impacted the population dynamics of the suspected rodent host to aggravate the epidemic.  
Megadrought and Megadeath in 16th Century Mexico

May 2002


2,031 Reads

The native population collapse in 16th century Mexico was a demographic catastrophe with one of the highest death rates in history. Recently developed tree-ring evidence has allowed the levels of precipitation to be reconstructed for north central Mexico, adding to the growing body of epidemiologic evidence and indicating that the 1545 and 1576 epidemics of cocoliztli (Nahuatl for "pest") were indigenous hemorrhagic fevers transmitted by rodent hosts and aggravated by extreme drought conditions.