Genetic attribution of bacterial genotypes has become a major tool in the investigation of the epidemiology of campylobacteriosis and has implicated retail chicken meat as the major source of human infection in several countries. To investigate the robustness of this approach to the provenance of the reference data sets used, a collection of 742 Campylobacter jejuni and 261 Campylobacter coli isolates obtained from United Kingdomsourced chicken meat was established and typed by multilocus sequence typing. Comparative analyses of the data with those from other isolates sourced from a variety of host animals and countries were undertaken by genetic attribution, genealogical, and population genetic approaches. The genotypes from the United Kingdom data set were highly diverse, yet structured into sequence types, clonal complexes, and genealogical groups very similar to those seen in chicken isolates from the Netherlands, the United States, and Senegal, but more distinct from isolates obtained from ruminant, swine, and wild bird sources. Assignment analyses consistently grouped isolates from different host animal sources regardless of geographical source; these associations were more robust than geographic associations across isolates from three continents. We conclude that, notwithstanding the high diversity of these pathogens, there is a strong signal of association of multilocus genotypes with particular hosts, which is greater than the geographic signal. These findings are consistent with local and international transmission of host-associated lineages among food animal species and provide a foundation for further improvements in genetic attribution.Members of the genus Campylobacter, specifically Campylobacter jejuni and Campylobacter coli, are major causes of human morbidity worldwide and are the most common bacterial cause of gastroenteritis in industrialized countries (4). These bacteria are commonly found as apparently harmless members of the gut microbiota of many farmed and wild mammals and birds. This, together with the sporadic nature of most human disease, has contributed to the remaining uncertainty regarding the relative importance of different potential sources of human infection (34), inhibiting the implementation of effective public health interventions, which may have major economic consequences on intensive food production. Human infection with C. jejuni and C. coli has been epidemiologically linked to contact with pets and farm animals and to consumption of red meat, water, milk, and poultry (17,20,34).The advent of multilocus sequence typing (MLST) for both C. jejuni and C. coli and its application to large and diverse isolate collections have enhanced understanding of the ecology (38) and epidemiology (10) of these important pathogens. It has been shown that there is substantial genetic differentiation between farmed ruminants and chickens (29) and even greater differentiation between farmed chickens and wild birds at the same farm site (5). Furthermore, MLST supports the application of popul...

The distributions of the mec regulator genes mecI and mecR1, which were identified on the chromosome of mecA-carrying Staphylococcus aureus N315, in methicillin-resistant staphylococci isolated in Japan and various countries were studied. Screening by dot blot hybridization by using polymerase chain reaction (PCR)-amplified probes revealed that at least the 5'-end region of the mecR1 gene was present in all strains tested, whereas about 40% of the strains were negative for the mecI gene. The data suggested that these regulator genes were the original components of the additional mec region DNA of methicillin-resistant S. aureus as well as methicillin-resistant, coagulase-negative staphylococci of seven staphylococcal species (S. epidermidis, S. haemolyticus, S. hominis, S. sciuri, S. capitis, S. caprae, and S. warneri). The mecI gene, which presumably codes for the repressor protein of the mecA gene, was found to harbor a point mutation in all six mecI-positive methicillin-resistant S. aureus strains, and their basal level of mecA gene transcription was elevated compared with that of strain N315, which harbors a presumably intact counterpart of the mecI gene. The data suggested that the mecI gene encodes for a strong repressor function on mecA gene transcription and is deleted or mutated in clinical methicillin-resistant S. aureus strains with high levels of resistance to methicillin.

ObjectivesTo review Campylobacter cases in England and Wales over 2 decades and examine the main factors/mechanisms driving the changing epidemiology.DesignA descriptive study of Campylobacter patients between 1989 and 2011. Cases over 3 years were linked anonymously to postcode, population density, deprivation indices and census data. Cases over 5 years were anonymously linked to local weather exposure estimates.SettingPatients were from general practice, hospital and environmental health investigations through primary diagnostic laboratories across England and Wales.ParticipantsThere were 1 109 406 cases.Outcome measuresDescription of changes in Campylobacter epidemiology over 23 years and how the main drivers may influence these.ResultsThere was an increase in Campylobacter cases over the past 23 years, with the largest increase in people over 50 years. Changes in the underlying population have contributed to this, including the impacts of population increases after World War I, World War II and the ‘baby boom’ of the 1960s. A recent increase in risk or ascertainment within this population has caused an increase in cases in all age groups from 2004 to 2011. The seasonal increase in cases between weeks 18 (Early May) and 22 (Early June) was consistent across ages, years and regions and was most marked in children and in more rural regions. Campylobacter prevalence by week in each region correlated with temperature 2 weeks before. There were higher prevalences in areas with a low population density, low deprivation and lower percentage of people of ethnic origin. Data from sero–phage and multilocus sequence typing show a few common types and many uncommon types.ConclusionsThe drivers/mechanisms influencing seasonality, age distribution, population density, socioeconomic and long-term differences are diverse and their relative contributions remain to be established. Surveillance and typing provide insights into Campylobacter epidemiology and sources of infection, providing a sound basis for targeted interventions.

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A typing procedure for Staphylococcus aureus was developed based on improved PCR amplification of the coagulase gene and restriction fragment length polymorphism (RFLP) analysis of the product. All coagulasepositive staphylococci produced a single PCR amplification product of either 875, 660, 603, or 547 bp. Those strains of epidemic methicillin-resistant S. aureus 16 (EMRSA-16) studied all gave a product of 547 bp. PCR products were digested with AluI and CfoI, and the fragments were separated by gel electrophoresis. Ten distinct RFLP patterns were found among 85 isolates of methicillin-resistant S. aureus (MRSA) and 10 propagating strains (PS) of methicillin-sensitive S. aureus (MSSA) examined. RFLP patterns 1, 2, and 3 were specific to strains of EMRSA-3, -15, and -16, respectively. By contrast, RFLP patterns 4 and 5 were seen with a heterogeneous collection of strains, together with drug-resistant forms of S. aureus isolated in Europe and four propagating strains used for the international phage set. RFLP pattern 6 was given by the Airedale isolate and PS 95. RFLP pattern 7 encompassed EMRSA-2 (isolate 331), PS 94, and PS 96. An isolate from Germany gave RFLP pattern 8. Eight strains of MSSA gave patterns similar to those of methicillin-resistant strains (RFLP patterns 3, 4, 5, 6, and 7), but two, PS 42E and PS 71, gave unique RFLP patterns 9 and 10, respectively. The coagulase gene PCR products for 24 isolates of MRSA and two isolates of MSSA were sequenced for both strands. The sequences were aligned, and evolutionary lineages were inferred based on pairwise distances between isolates.