EDITORIAL
10.1111/1469-0691.12654
Editorial: Emerging clones of bacterial epidemics in the genomic area D. Raoult Unite de Recherche en Maladies Infectieuses et Tropicales Emergentes, Faculte de Medecine, CNRS-IRD UMR 6236, Universite de la Mediterranee, Marseille, France E-mail: [email protected] Article published online: 30 April 2014
We are in the middle of a paradigm shift in bacterial infectious diseases. Thus, bacteria in their pathogenic role have, for now, been defined at the species level. There has been, moreover, confusion in the taxonomy. Indeed, doctors want to name bacteria, agents or epidemic diseases with a specific species name, whereas taxonomists focus on other elements, including genetic, metabolic and morphological factors. For example, the agent of typhoid fever, Salmonella typhi, finally lost its species name, whereas it corresponds to a pathovar, which doctors need to name. Thus, the former Salmonella typhi, which should be called, according to genetic definitions, Salmonella enterica serotype typhi, is now written Salmonella Typhi, as a compromise between medical doctors and taxonomists [1]. The situation is the same for many bacterial agents of disease that are, in fact, microbial clones. The continuous emergence of new virulent microbial clones among populations of pathogenic, or non-pathogenic, bacteria is a major element that genomics now allows the study of. Several studies are presented in this issue; the work of Wren [2] on Clostridium difficile shows that a particularly dangerous clone, O27, appeared a few years ago and has been spreading across the planet, with greater infectiousness and mortality than others. Thus, the detection of O27 has become essential, to enable adequate measures to be taken. Another clear example is the Beijing genotype of Mycobacterium tuberculosis, recent work on which has been published in the journal [3]; it appeared 30 years ago as the epidemic clone of M. tuberculosis capable of carrying multiple resistance determinants, and now represents 10% of M. tuberculosis isolates worldwide. Most other clones have an endemic dissemination and represent very contagious microorganisms; there is a tuberculosis pandemic linked to Beijing whose distribution and severity are very different from those of other older clones of M. tuberculosis. The situation is the same for plague: it has been shown through palaeomicrobiology studies of the Justinian plague, then the plague of the Middle Ages [4], that the three major
pandemics corresponded to particularly virulent Yersinia pestis clones that diffused at high speed through different continents. For the work on Neisseria meningitidis reported by Read [5], a genomic surprise was that the clone currently circulating in the UK could be either serotype A or serotype C, which challenges our classification of N. meningitidis and may change vaccine strategies. Indeed, if the vaccine strategies of encirclement are based on the identification of the serotype, it will not be possible to control the epidemics. Moreover, regarding cholera genomics, studies have shown that, in the midst of a very large population of Vibrio cholerae existing in the environment, only a few clones have the potential to spread and generate epidemics and pandemics. For example, the observed epidemic in Haiti was caused by a virulent and pathogenic clone already detected in Nepal and carried by Nepalese United Nations’soldiers; this triggered an extremely deadly epidemic, and it is the same clone, and not multiple clones, in the environment of Haiti [6]. Finally, multiple clones will continue to appear in our environment. This was the case, for example, with Escherichia coli in a German outbreak of severe gastroenteritis, which was also clarified, thanks to the identification of a specific genomic clone [7]. This is also the case for E. coli clones responsible for urinary tract infections and resistant exclusively to co-trimoxazole [7]. Finally, other clones will appear that are capable of generating epidemics, such the clone detected in Sweden of Chlamydia trachomatis [8], which escaped detection with molecular diagnostic techniques by presenting a mutation of the gene that is most commonly used for PCR! In total, our understanding of epidemics of bacterial origin is being substantially increased by genomics, which shows us that most epidemics are caused by individual clones that merit a specific identification and require us to redefine particular isolation and preventive measures because of their epidemic and pathological specificity.
ª2014 The Author Clinical Microbiology and Infection ª2014 European Society of Clinical Microbiology and Infectious Diseases
372
Clinical Microbiology and Infection, Volume 20 Number 5, May 2014
Transparency Declaration The author declares no conflict of interest.
References 1. Ruby T, McLaughlin L, Gopinath S, Monack D. Salmonella’s long-term relationship with its host. FEMS Microbiol Rev 2012; 36: 600–615. 2. Valiente E, Cairns MD, Wren BW. The Clostridium difficile PCR ribotype 027 lineage: a pathogen on the move. Clin Microbiol Infect 2014; 20: 396–404.
CMI
3. Borgdorff MW, van Soolingen D. The re-emergence of tuberculosis: what have we learnt from molecular epidemiology? Clin Microbiol Infect 2013; 19: 889–901. 4. Raoult–D, Mouffok N, Bitam I, Piarroux R, Drancourt M. Plague: history and contemporary analysis. J Infect 2013; 66: 18–26. 5. Read R. Neisseria meningitidis; clones, carriage and disease. Clin Microbiol Infect 2014; 20: 391–395. 6. Moore S, Thomson N, Mutreja A, Piarroux R. Widespread epidemic cholera due to a restricted subset of Vibrio cholerae clones. Clin Microbiol Infect 2014; 20: 373–379. 7. Riley LW. Pandemic lineages of extraintestinal pathogenic Escherichia coli. Clin Microbiol Infect 2014; 20: 380–390. 8. Jurstrand M, Fredlund H, Unemo M. The new variant of Chlamydia trachomatis was present as early as 2003 in Orebro County, Sweden, but remained undetected until 2006. Sex Transm Infect 2013; 89: 607–608.
ª2014 The Author Clinical Microbiology and Infection ª2014 European Society of Clinical Microbiology and Infectious Diseases, CMI, 20, 371–372
10.1111/1469-0691.12654
Editorial: Emerging clones of bacterial epidemics in the genomic area D. Raoult Unite de Recherche en Maladies Infectieuses et Tropicales Emergentes, Faculte de Medecine, CNRS-IRD UMR 6236, Universite de la Mediterranee, Marseille, France E-mail: [email protected] Article published online: 30 April 2014
We are in the middle of a paradigm shift in bacterial infectious diseases. Thus, bacteria in their pathogenic role have, for now, been defined at the species level. There has been, moreover, confusion in the taxonomy. Indeed, doctors want to name bacteria, agents or epidemic diseases with a specific species name, whereas taxonomists focus on other elements, including genetic, metabolic and morphological factors. For example, the agent of typhoid fever, Salmonella typhi, finally lost its species name, whereas it corresponds to a pathovar, which doctors need to name. Thus, the former Salmonella typhi, which should be called, according to genetic definitions, Salmonella enterica serotype typhi, is now written Salmonella Typhi, as a compromise between medical doctors and taxonomists [1]. The situation is the same for many bacterial agents of disease that are, in fact, microbial clones. The continuous emergence of new virulent microbial clones among populations of pathogenic, or non-pathogenic, bacteria is a major element that genomics now allows the study of. Several studies are presented in this issue; the work of Wren [2] on Clostridium difficile shows that a particularly dangerous clone, O27, appeared a few years ago and has been spreading across the planet, with greater infectiousness and mortality than others. Thus, the detection of O27 has become essential, to enable adequate measures to be taken. Another clear example is the Beijing genotype of Mycobacterium tuberculosis, recent work on which has been published in the journal [3]; it appeared 30 years ago as the epidemic clone of M. tuberculosis capable of carrying multiple resistance determinants, and now represents 10% of M. tuberculosis isolates worldwide. Most other clones have an endemic dissemination and represent very contagious microorganisms; there is a tuberculosis pandemic linked to Beijing whose distribution and severity are very different from those of other older clones of M. tuberculosis. The situation is the same for plague: it has been shown through palaeomicrobiology studies of the Justinian plague, then the plague of the Middle Ages [4], that the three major
pandemics corresponded to particularly virulent Yersinia pestis clones that diffused at high speed through different continents. For the work on Neisseria meningitidis reported by Read [5], a genomic surprise was that the clone currently circulating in the UK could be either serotype A or serotype C, which challenges our classification of N. meningitidis and may change vaccine strategies. Indeed, if the vaccine strategies of encirclement are based on the identification of the serotype, it will not be possible to control the epidemics. Moreover, regarding cholera genomics, studies have shown that, in the midst of a very large population of Vibrio cholerae existing in the environment, only a few clones have the potential to spread and generate epidemics and pandemics. For example, the observed epidemic in Haiti was caused by a virulent and pathogenic clone already detected in Nepal and carried by Nepalese United Nations’soldiers; this triggered an extremely deadly epidemic, and it is the same clone, and not multiple clones, in the environment of Haiti [6]. Finally, multiple clones will continue to appear in our environment. This was the case, for example, with Escherichia coli in a German outbreak of severe gastroenteritis, which was also clarified, thanks to the identification of a specific genomic clone [7]. This is also the case for E. coli clones responsible for urinary tract infections and resistant exclusively to co-trimoxazole [7]. Finally, other clones will appear that are capable of generating epidemics, such the clone detected in Sweden of Chlamydia trachomatis [8], which escaped detection with molecular diagnostic techniques by presenting a mutation of the gene that is most commonly used for PCR! In total, our understanding of epidemics of bacterial origin is being substantially increased by genomics, which shows us that most epidemics are caused by individual clones that merit a specific identification and require us to redefine particular isolation and preventive measures because of their epidemic and pathological specificity.
ª2014 The Author Clinical Microbiology and Infection ª2014 European Society of Clinical Microbiology and Infectious Diseases
372
Clinical Microbiology and Infection, Volume 20 Number 5, May 2014
Transparency Declaration The author declares no conflict of interest.
References 1. Ruby T, McLaughlin L, Gopinath S, Monack D. Salmonella’s long-term relationship with its host. FEMS Microbiol Rev 2012; 36: 600–615. 2. Valiente E, Cairns MD, Wren BW. The Clostridium difficile PCR ribotype 027 lineage: a pathogen on the move. Clin Microbiol Infect 2014; 20: 396–404.
CMI
3. Borgdorff MW, van Soolingen D. The re-emergence of tuberculosis: what have we learnt from molecular epidemiology? Clin Microbiol Infect 2013; 19: 889–901. 4. Raoult–D, Mouffok N, Bitam I, Piarroux R, Drancourt M. Plague: history and contemporary analysis. J Infect 2013; 66: 18–26. 5. Read R. Neisseria meningitidis; clones, carriage and disease. Clin Microbiol Infect 2014; 20: 391–395. 6. Moore S, Thomson N, Mutreja A, Piarroux R. Widespread epidemic cholera due to a restricted subset of Vibrio cholerae clones. Clin Microbiol Infect 2014; 20: 373–379. 7. Riley LW. Pandemic lineages of extraintestinal pathogenic Escherichia coli. Clin Microbiol Infect 2014; 20: 380–390. 8. Jurstrand M, Fredlund H, Unemo M. The new variant of Chlamydia trachomatis was present as early as 2003 in Orebro County, Sweden, but remained undetected until 2006. Sex Transm Infect 2013; 89: 607–608.
ª2014 The Author Clinical Microbiology and Infection ª2014 European Society of Clinical Microbiology and Infectious Diseases, CMI, 20, 371–372
