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1.  Gene Sequencing for Routine Verification of Pyrazinamide Resistance in Mycobacterium tuberculosis: a Role for pncA but Not rpsA 
Journal of Clinical Microbiology  2012;50(11):3726-3728.
Pyrazinamide (PZA) is an important component of first-line therapy for the treatment of tuberculosis. Here, we evaluate targeted gene sequencing as a supplement to phenotypic PZA susceptibility testing of Mycobacterium tuberculosis. Routine sequencing of pncA, but not rpsA, is effective for verification of PZA susceptibility results.
PMCID: PMC3486241  PMID: 22895038
2.  Opinions Differ by Expertise in Mycobacterium avium Complex Disease 
Rationale: Pulmonary Mycobacterium avium complex treatment guidelines rely largely on expert opinion. The extent to which nonexperts agree with recommendations of experts in this clinical area is unknown.
Objectives: We sought to compare practices and perceptions of prognosis between experts and nonexperts.
Methods: We surveyed respirologists (Ontario, Canada, “nonexperts”) and experts from nontuberculous mycobacterial disease centers of excellence (Canada and United States).
Measurements and Main Results: Forty-six Ontario respirologists (29% of 160) and 19 experts (73% of 26) participated. There was agreement between nonexperts and experts regarding disease duration before diagnosis (2 yr), likelihood of spontaneous remission (7–15%), typical duration of treatment (18 mo), first choice of therapy (guideline regimens), a subgroup of patients for whom less-intensive regimens are favored (10% after recurrence), likelihood of recurrence (30%), and median survival (10 yr in most patients). Noted differences were that nonexperts estimated fewer patients with a positive culture had disease (30% vs. 50%, P = 0.02), used intensive guidelines therapy less often in new cases (50% vs. 79%, P = 0.02), and perceived a slightly lower success rate with guidelines therapy (65% vs. 75%, P = 0.047). Response ranges were wider for nonexperts, significantly so for selection of intensive guidelines therapy in new (P = 0.01) and recurrent (P = 0.04) cases.
Conclusion: Experts and nonexperts agreed on many issues. However, nonexperts perceived lower rates of disease among patients with isolates, tended to use less aggressive treatment approaches, and perceived lower success rates. Significant variability was observed in responses—often wider among nonexperts. Although these results are likely biased by referral, they may identify important areas for targeted education.
PMCID: PMC3972981  PMID: 24083335
Mycobacterium avium-intracellulare infection; Mycobacterium infections, nontuberculous; nontuberculous mycobacteria; practice guidelines
4.  Marked Microevolution of a Unique Mycobacterium tuberculosis Strain in 17 Years of Ongoing Transmission in a High Risk Population 
PLoS ONE  2014;9(11):e112928.
The transmission and persistence of Mycobacterium tuberculosis within high risk populations is a threat to tuberculosis (TB) control. In the current study, we used whole genome sequencing (WGS) to decipher the transmission dynamics and microevolution of M. tuberculosis ON-A, an endemic strain responsible for an ongoing outbreak of TB in an urban homeless/under-housed population. Sixty-one M. tuberculosis isolates representing 57 TB cases from 1997 to 2013 were subjected to WGS. Sequencing data was integrated with available epidemiological information and analyzed to determine how the M. tuberculosis ON-A strain has evolved during almost two decades of active transmission. WGS offers higher discriminatory power than traditional genotyping techniques, dividing the M. tuberculosis ON-A strain into 6 sub-clusters, each defined by unique single nucleotide polymorphism profiles. One sub-cluster, designated ON-ANM (Natural Mutant; 26 isolates from 24 cases) was also defined by a large, 15 kb genomic deletion. WGS analysis reveals the existence of multiple transmission chains within the same population/setting. Our results help validate the utility of WGS as a powerful tool for identifying genomic changes and adaptation of M. tuberculosis.
PMCID: PMC4236100  PMID: 25405861
5.  Complete Sequence of pOZ176, a 500-Kilobase IncP-2 Plasmid Encoding IMP-9-Mediated Carbapenem Resistance, from Outbreak Isolate Pseudomonas aeruginosa 96 
Pseudomonas aeruginosa 96 (PA96) was isolated during a multicenter surveillance study in Guangzhou, China, in 2000. Whole-genome sequencing of this outbreak strain facilitated analysis of its IncP-2 carbapenem-resistant plasmid, pOZ176. The plasmid had a length of 500,839 bp and an average percent G+C content of 57%. Of the 618 predicted open reading frames, 65% encode hypothetical proteins. The pOZ176 backbone is not closely related to any plasmids thus far sequenced, but some similarity to pQBR103 of Pseudomonas fluorescens SBW25 was observed. Two multiresistant class 1 integrons and several insertion sequences were identified. The blaIMP-9-carrying integron contained aacA4→blaIMP-9→aacA4, flanked upstream by Tn21 tnpMRA and downstream by a complete tni operon of Tn402 and a mer module, named Tn6016. The second integron carried aacA4→catB8a→blaOXA-10 and was flanked by Tn1403-like tnpRA and a sul1-type 3′ conserved sequence (3′-CS), named Tn6217. Other features include three resistance genes similar to those of Tn5, a tellurite resistance operon, and two pil operons. The replication and maintenance systems exhibit similarity to a genomic island of Ralstonia solanacearum GM1000. Codon usage analysis suggests the recent acquisition of blaIMP-9. The origins of the integrons on pOZ176 indicated separate horizontal gene transfer events driven by antibiotic selection. The novel mosaic structure of pOZ176 suggests that it is derived from environmental bacteria.
PMCID: PMC3719692  PMID: 23716048
6.  Emergence of non-serotype b encapsulated Haemophilus influenzae as a cause of pediatric meningitis in northwestern Ontario 
Before the introduction of the conjugate vaccine, Haemophilus influenzae serotype b (Hib) was the leading cause of bacterial meningitis in children. Although successful in reducing Hib cases, the vaccine confers no protection against other serotypes of H influenzae, such as a (Hia), or f (Hif). The emergence of invasive disease caused by non-Hib in northwestern Ontario (38 cases between 2002 and 2008) with predominance of Hia was previously reported by the authors. At that time, no cases of pediatric meningitis caused by H influenzae were recorded in the region. Continued surveillance identified 12 new cases of invasive non-Hib between January 2009 and July 2011. Among these cases, three young children developed meningitis with severe complications caused by Hia or Hif. The present article describes these cases along with the characteristics of recent H influenzae isolates from the region, (ie, their genetic background and antibiotic sensitivity). The findings point to the clonal nature of circulating Hia strains as well as to an increase in frequency and severity of pediatric invasive H influenzae infections in northwestern Ontario.
PMCID: PMC3630022  PMID: 24421786
Case series; Haemophilus influenzae; Meningitis; Serotype a; Serotype f
7.  Antimicrobial resistance and antimicrobial use associated with laboratory-confirmed cases of Campylobacter infection in two health units in Ontario 
A population-based study was conducted over a two-year period in the Perth District (PD) and Wellington-Dufferin-Guelph (WDG) health units in Ontario to document antimicrobial resistance and antimicrobial use associated with clinical cases of laboratory-confirmed campylobacteriosis.
Etest (bioMérieux SA, France) was used to determine the minimum inhibitory concentration of amoxicillin/clavulanic acid, ampicillin, chloramphenicol, ciprofloxacin (CIP), clindamycin, erythromycin (ERY), gentamicin, nalidixic acid and tetracycline. Data regarding antimicrobial use were collected from 250 cases.
Of the 250 cases, 165 (65.7%) reported staying home or being hospitalized due to campylobacteriosis. Fifty-four per cent of cases (135 of 249) reported taking antimicrobials to treat campylobacteriosis. In 115 cases (51.1%), fecal culture results were not used for treatment decisions because they were not available before the initiation of antimicrobial treatment and/or they were not available before the cessation of symptoms. Of the 250 cases, 124 (49.6%) had available Campylobacter isolates, of which 66 (53.2%) were resistant to at least one of the antimicrobials tested. No resistance to ampicillin, chloramphenicol or gentamicin was found in these isolates. Six isolates (4.8%) were resistant to CIP. Two isolates (1.6%) were resistant to ERY; however, no isolates were resistant to both CIP and ERY.
Prudent use practices should be promoted among physicians to reduce the use of antimicrobials for the treatment of gastroenteritis in general and campylobacteriosis in particular, as well as to minimize the future development of resistance to these antimicrobials in Campylobacter species.
PMCID: PMC3630032  PMID: 24421795
Antimicrobial resistance; Antimicrobial use; Campylobacter; Canada; Ontario
8.  Pulmonary Nontuberculous Mycobacterial Disease, Ontario, Canada, 1998–2010 
Emerging Infectious Diseases  2013;19(11):1889-1891.
We measured the prevalence and temporal trends of pulmonary nontuberculous mycobacterial disease among residents of Ontario, Canada, during 1998–2010. Five-year prevalence increased from 29.3 cases/100,000 persons in 1998–2002 to 41.3/100,000 in 2006–2010 (p<0.0001). Improved laboratory methods did not explain this increase, suggesting a surge in disease prevalence.
PMCID: PMC3837646  PMID: 24210012
atypical mycobacteria; atypical Mycobacterium; epidemiology; Mycobacterium avium-intracellulare; Mycobacterium avium-intracellulare complex; mycobacterium intracellulare; nontuberculous Mycobacterium; Canada; Ontario; tuberculosis and other mycobacteria; bacteria
9.  Antimicrobial Susceptibilities of Clinical Isolates of HACEK Organisms 
The “HACEK” organisms are a group of fastidious Gram-negative bacteria that cause a variety of infections, including infective endocarditis. Antimicrobial susceptibility testing is not universally available, and therapy for these infections is often empirical. We report the antimicrobial susceptibilities of 70 clinical HACEK isolates to 18 antimicrobials. All isolates were susceptible to ceftriaxone and levofloxacin, indicating that these agents remain appropriate empirical choices for the treatment of infections with this group of organisms.
PMCID: PMC3623346  PMID: 23403420
10.  Homologous Recombination Drives Both Sequence Diversity and Gene Content Variation in Neisseria meningitidis 
Genome Biology and Evolution  2013;5(9):1611-1627.
The study of genetic and phenotypic variation is fundamental for understanding the dynamics of bacterial genome evolution and untangling the evolution and epidemiology of bacterial pathogens. Neisseria meningitidis (Nm) is among the most intriguing bacterial pathogens in genomic studies due to its dynamic population structure and complex forms of pathogenicity. Extensive genomic variation within identical clonal complexes (CCs) in Nm has been recently reported and suggested to be the result of homologous recombination, but the extent to which recombination contributes to genomic variation within identical CCs has remained unclear. In this study, we sequenced two Nm strains of identical serogroup (C) and multi-locus sequence type (ST60), and conducted a systematic analysis with an additional 34 Nm genomes. Our results revealed that all gene content variation between the two ST60 genomes was introduced by homologous recombination at the conserved flanking genes, and 94.25% or more of sequence divergence was caused by homologous recombination. Recombination was found in genes associated with virulence factors, antigenic outer membrane proteins, and vaccine targets, suggesting an important role of homologous recombination in rapidly altering the pathogenicity and antigenicity of Nm. Recombination was also evident in genes of the restriction and modification systems, which may undermine barriers to DNA exchange. In conclusion, homologous recombination can drive both gene content variation and sequence divergence in Nm. These findings shed new light on the understanding of the rapid pathoadaptive evolution of Nm and other recombinogenic bacterial pathogens.
PMCID: PMC3787668  PMID: 23902748
horizontal gene transfer; homologous recombination; clonal complex; MLST; nonvertical gene; restriction modification systems
11.  Comparative Genomic Analyses of Streptococcus pseudopneumoniae Provide Insight into Virulence and Commensalism Dynamics 
PLoS ONE  2013;8(6):e65670.
Streptococcus pseudopneumoniae (SPPN) is a recently described species of the viridans group streptococci (VGS). Although the pathogenic potential of S. pseudopneumoniae remains uncertain, it is most commonly isolated from patients with underlying medical conditions, such as chronic obstructive pulmonary disease. S. pseudopneumoniae can be distinguished from the closely related species, S. pneumoniae and S. mitis, by phenotypic characteristics, including optochin resistance in the presence of 5% CO2, bile insolubility, and the lack of the pneumococcal capsule. Previously, we reported the draft genome sequence of S. pseudopneumoniae IS7493, a clinical isolate obtained from an immunocompromised patient with documented pneumonia. Here, we use comparative genomics approaches to identify similarities and key differences between S. pseudopneumoniae IS7493, S. pneumoniae and S. mitis. The genome structure of S. pseudopneumoniae IS7493 is most closely related to that of S. pneumoniae R6, but several recombination events are evident. Analysis of gene content reveals numerous unique features that distinguish S. pseudopneumoniae from other streptococci. The presence of loci for competence, iron transport, pneumolysin production and antimicrobial resistance reinforce the phylogenetic position of S. pseudopneumoniae as an intermediate species between S. pneumoniae and S. mitis. Additionally, the presence of several virulence factors and antibiotic resistance mechanisms suggest the potential of this commensal species to become pathogenic or to contribute to increasing antibiotic resistance levels seen among the VGS.
PMCID: PMC3686770  PMID: 23840352
12.  Invasive Potential of Nonencapsulated Disease Isolates of Neisseria meningitidis 
Infection and Immunity  2012;80(7):2346-2353.
The capsule of Neisseria meningitidis is the major virulence factor that enables this bacterium to overcome host immunity elicited by complement and phagocytes, rendering it capable of surviving in blood. As such, nonencapsulated N. meningitidis isolates are generally considered nonpathogenic. Here, we consider the inherent virulence of two nonencapsulated N. meningitidis isolates obtained from our national surveillance of infected blood cultures in Canada. Capsule deficiency of both strains was confirmed by serology and PCR for the ctrA to ctrD genes and siaA to siaC genes, as well as siaD genes specific to serogroups B, C, Y, and W135. In both strains, the capsule synthesis genes were replaced by the capsule null locus, cnl-2. In accordance with a lack of capsule, both strains were fully susceptible to killing by both human and baby rabbit complement. However, in the presence of cytidine-5′ monophospho-N-acetylneuraminic acid (CMP-NANA), allowing for lipooligosaccharide (LOS) sialylation, a significant increase of resistance to complement killing was observed. Mass spectrometry of purified LOS did not reveal any uncommon modifications that would explain their invasive phenotype. Finally, in a mouse intraperitoneal challenge model, these nonencapsulated isolates displayed enhanced virulence relative to an isogenic mutant of serogroup B strain MC58 lacking capsule (MC58ΔsiaD). Virulence of all nonencapsulated isolates tested was below that of encapsulated serogroup B strains MC58 and B16B6. However, whereas no mortality was observed with MC58ΔsiaD, 5/10 mice succumbed to infection with strain 2275 and 2/11 mice succumbed to strain 2274. Our results suggest the acquisition of a new virulence phenotype by these nonencapsulated strains.
PMCID: PMC3416473  PMID: 22508859
14.  The Impact of Infection on Population Health: Results of the Ontario Burden of Infectious Diseases Study 
PLoS ONE  2012;7(9):e44103.
Evidence-based priority setting is increasingly important for rationally distributing scarce health resources and for guiding future health research. We sought to quantify the contribution of a wide range of infectious diseases to the overall infectious disease burden in a high-income setting.
Methodology/Principal Findings
We used health-adjusted life years (HALYs), a composite measure comprising premature mortality and reduced functioning due to disease, to estimate the burden of 51 infectious diseases and associated syndromes in Ontario using 2005–2007 data. Deaths were estimated from vital statistics data and disease incidence was estimated from reportable disease, healthcare utilization, and cancer registry data, supplemented by local modeling studies and national and international epidemiologic studies. The 51 infectious agents and associated syndromes accounted for 729 lost HALYs, 44.2 deaths, and 58,987 incident cases per 100,000 population annually. The most burdensome infectious agents were: hepatitis C virus, Streptococcus pneumoniae, Escherichia coli, human papillomavirus, hepatitis B virus, human immunodeficiency virus, Staphylococcus aureus, influenza virus, Clostridium difficile, and rhinovirus. The top five, ten, and 20 pathogens accounted for 46%, 67%, and 75% of the total infectious disease burden, respectively. Marked sex-specific differences in disease burden were observed for some pathogens. The main limitations of this study were the exclusion of certain infectious diseases due to data availability issues, not considering the impact of co-infections and co-morbidity, and the inability to assess the burden of milder infections that do not result in healthcare utilization.
Infectious diseases continue to cause a substantial health burden in high-income settings such as Ontario. Most of this burden is attributable to a relatively small number of infectious agents, for which many effective interventions have been previously identified. Therefore, these findings should be used to guide public health policy, planning, and research.
PMCID: PMC3433488  PMID: 22962601
15.  Epidemiology of serogroup B invasive meningococcal disease in Ontario, Canada, 2000 to 2010 
BMC Infectious Diseases  2012;12:202.
Invasive meningococcal disease (IMD) caused by serogroup B is the last major serogroup in Canada to become vaccine-preventable. The anticipated availability of vaccines targeting this serogroup prompted an assessment of the epidemiology of serogroup B disease in Ontario, Canada.
We retrieved information on confirmed IMD cases reported to Ontario’s reportable disease database between January 1, 2000 and December 31, 2010 and probabilistically-linked these cases to Public Health Ontario Laboratory records. Rates were calculated with denominator data obtained from Statistics Canada. We calculated a crude number needed to vaccinate using the inverse of the infant (<1 year) age-specific incidence multiplied by expected vaccine efficacies between 70% and 80%, and assuming only direct protection (no herd effects).
A total of 259 serogroup B IMD cases were identified in Ontario over the 11-year period. Serogroup B was the most common cause of IMD. Incidence ranged from 0.11 to 0.27/100,000/year, and fluctuated over time. Cases ranged in age from 13 days to 101 years; 21.4% occurred in infants, of which 72.7% were <6 months. Infants had the highest incidence (3.70/100,000). Case-fatality ratio was 10.7% overall. If we assume that all infant cases would be preventable by vaccination, we would need to vaccinate between 33,784 and 38,610 infants to prevent one case of disease.
Although rare, the proportion of IMD caused by serogroup B has increased and currently causes most IMD in Ontario, with infants having the highest risk of disease. Although serogroup B meningococcal vaccines are highly anticipated, our findings suggest that decisions regarding publicly funding serogroup B meningococcal vaccines will be difficult and may not be based on disease burden alone.
PMCID: PMC3472197  PMID: 22928839
Invasive meningococcal disease; Neisseria meningitidis; Serogroup B; Epidemiology; Surveillance; Ontario; Canada
16.  Phylogenetic Incongruence in E. coli O104: Understanding the Evolutionary Relationships of Emerging Pathogens in the Face of Homologous Recombination 
PLoS ONE  2012;7(4):e33971.
Escherichia coli O104:H4 was identified as an emerging pathogen during the spring and summer of 2011 and was responsible for a widespread outbreak that resulted in the deaths of 50 people and sickened over 4075. Traditional phenotypic and genotypic assays, such as serotyping, pulsed field gel electrophoresis (PFGE), and multilocus sequence typing (MLST), permit identification and classification of bacterial pathogens, but cannot accurately resolve relationships among genotypically similar but pathotypically different isolates. To understand the evolutionary origins of E. coli O104:H4, we sequenced two strains isolated in Ontario, Canada. One was epidemiologically linked to the 2011 outbreak, and the second, unrelated isolate, was obtained in 2010. MLST analysis indicated that both isolates are of the same sequence type (ST678), but whole-genome sequencing revealed differences in chromosomal and plasmid content. Through comprehensive phylogenetic analysis of five O104:H4 ST678 genomes, we identified 167 genes in three gene clusters that have undergone homologous recombination with distantly related E. coli strains. These recombination events have resulted in unexpectedly high sequence diversity within the same sequence type. Failure to recognize or adjust for homologous recombination can result in phylogenetic incongruence. Understanding the extent of homologous recombination among different strains of the same sequence type may explain the pathotypic differences between the ON2010 and ON2011 strains and help shed new light on the emergence of this new pathogen.
PMCID: PMC3320906  PMID: 22493677
17.  Escherichia coli O104:H4 Infections and International Travel 
Emerging Infectious Diseases  2012;18(3):473-476.
We analyzed travel-associated clinical isolates of Escherichia coli O104:H4, including 1 from the 2011 German outbreak and 1 from a patient who returned from the Philippines in 2010, by genome sequencing and optical mapping. Despite extensive genomic similarity between these strains, key differences included the distribution of toxin and antimicrobial drug–resistance determinants.
PMCID: PMC3309582  PMID: 22377016
Escherichia coli; Shiga toxin; genomics; bacteria; international travel; foodborne infections; travel-related infections; E. coli
18.  Extensive Genomic Variation within Clonal Complexes of Neisseria meningitidis 
Genome Biology and Evolution  2011;3:1406-1418.
Meningococcal disease is a widely distributed complex disease affecting all age categories. It can cause severe meningitis and septicemia, especially in unvaccinated infants and young children. The causative agent, Neisseria meningitidis (Nm), can be phenotypically and genetically differentiated into serogroups and sequence types (STs) and has a highly dynamic population structure. To obtain a deeper understanding of the epidemiology of Nm, we sequenced seven Nm genomes. Large-scale genomic analysis was conducted with these 7 Nm genomes, 27 additional Nm genomes from GenBank, and 4 other Neisseria genomes. We observed extensive homologous recombination in all gene functional categories among different Nm genomes. Homologous recombination is so frequent that it has resulted in numerous chimeric open reading frames, including genes in the capsule biosynthesis cluster and loci targeted by commercial vaccines. Our results reveal that, despite widespread use, evolutionary relationships inferred from the standard seven-gene multilocus sequence typing (MLST) method could not predict virulence gene content or strain phenotype. In fact, up to 28% of the virulence-associated genes could differ between strains of identical STs. Consistent with previous studies, we found that allelic recombination is also associated with alterations in antibiotic susceptibility. Overall, these findings emphasize the extensive genomic plasticity of Nm and the limitations of standard molecular methods to quantify this genotypic and phenotypic diversity.
PMCID: PMC3242501  PMID: 22084315
homologous recombination; horizontal gene transfer; genome evolution; multilocus sequence typing; virulence gene
19.  Evaluation of CLSI Agar Dilution Method and Trek Sensititre Broth Microdilution Panel for Determining Antimicrobial Susceptibility of Streptococcus pneumoniae▿ 
Journal of Clinical Microbiology  2011;49(2):704-706.
Both the CLSI agar dilution method and Trek Sensititre broth microdilution panel for Streptococcus pneumoniae antimicrobial susceptibility testing were evaluated against the reference CLSI broth microdilution method using the most recently published CLSI breakpoints. While agar dilution was not an optimal method, the commercial panel appeared to be an acceptable method, with minor errors encountered for ceftriaxone, penicillin, and meropenem.
PMCID: PMC3043519  PMID: 21123533
20.  Respiratory Infection in Institutions during Early Stages of Pandemic (H1N1) 2009, Canada 
Emerging Infectious Diseases  2009;15(12):2001-2003.
Outbreaks of respiratory infection in institutions in Ontario, Canada were studied from April 20 to June 12, 2009, during the early stages of the emergence of influenza A pandemic (H1N1) 2009. Despite widespread presence of influenza in the general population, only 2 of 83 outbreaks evaluated by molecular methods were associated with pandemic (H1N1) 2009.
PMCID: PMC3044548  PMID: 19961686
Influenza; H1N1; disease outbreaks; nursing homes; respiratory tract infections; long-term care facilities; viruses; Canada; expedited; dispatch
21.  Risk of ruling out severe acute respiratory syndrome by ruling in another diagnosis: Variable incidence of atypical bacteria coinfection based on diagnostic assays 
Severe acute respiratory syndrome (SARS) caused the first epidemic of the 21st century and continues to threaten the global community.
To assess the incidence of coinfection in patients confirmed to have SARS-associated coronavirus (SARS-CoV) infection, and thus, to determine the risk of ruling out SARS by ruling in another diagnosis.
The present report is a retrospective study evaluating the incidence and impact of laboratory-confirmed SARS-CoV and other pulmonary pathogens in 117 patients. These patients were evaluated in a Toronto, Ontario, community hospital identified as the epicentre for the second SARS outbreak.
Coinfection with other pulmonary pathogens occured in patients with SARS. Seventy-three per cent of the patient population evaluated had laboratory-confirmed SARS-CoV infection. Serology showing acute or recent Chlamydophila pneumoniae or Mycoplasma pneumoniae infection revealed an incidence of 30% and 9%, respectively, in those with SARS. These rates are similar to previously published studies on coinfection in pneumonia. All nucleic acid diagnostic assays were negative for C pneumoniae and M pneumoniae in respiratory samples from patients with SARS having serological evidence for these atypical pathogens.
Diagnostic assays for well-recognized pulmonary pathogens have limitations, and ruling out SARS-CoV by ruling in another pulmonary pathogen carries significant risk. Despite positive serology for atypical pathogens, in a setting where clinical suspicion for SARS is high, specific tests for SARS should be performed to confirm or exclude a diagnosis.
PMCID: PMC2539008  PMID: 16470249
Coinfection; Coronavirus; Epidemic; Pneumonia; SARS

Results 1-21 (21)