Indications of in vivo transfer of an epidemic R plasmid from Salmonella enteritidis to Escherichia coli of the normal human gut flora

Balis, Evagelos; Vatopoulos, Alkiviadis; Kanelopoulou, M; Mainas, Efstratios; Hatzoudis, George; Kontogianni, V; Malamou-Lada, H.; Kitsou-Kiriakopoulou, S; Kalapothaki, V.

doi:10.1128/jcm.34.4.977-979.1996

Cited by 45 publications

(17 citation statements)

References 24 publications

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“…The most numerous coliform bacillus in human isolates, E. coli, would be a good candidate for this. We have already shown that E. coli of the normal human faecal flora can harbor the same 34-MDa R plasmid as S. enteritidis simultaneously isolated from the same sample [26]. This is consistent with the hypothesis of in vivo transfer of resistance genes among Salmonella spp.…”

Section: Discussionsupporting

confidence: 88%

Molecular analysis of ampicillin-resistant sporadic Salmonella typhi and Salmonella paratyphi B clinical isolates

Tassios¹,

Vatopoulos

Mainas

et al. 1997

Clinical Microbiology and Infection

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OBJECTIVE: To study the mechanisms of antibiotic resistance in Salmonella typhi and Salmonella paratyphi B clinical isolates, and the clonality of resistant strains. METHODS: Antibiotic susceptibility was tested by disk-agar diffusion. Conjugation experiments and plasmid analysis by agarose gel electrophoresis after EcoRI digestion were followed by hybridization to a digoxigenin-labeled TEM-type beta-lactamase probe. DNA fingerprints were obtained by pulsed-field gel electrophoresis of Xbal-digested chromosomal DNA. RESULTS: Three S. typhi isolates (7% of the isolates studied), of which one was ampicillin resistant and the other two multiresistant (ampicillin, chloramphenicol, tetracycline, sulfamethoxazole/trimethoprim and streptomycin), and two ampicillin-resistant S. paratyphi B isolates (25% of the isolates studied) were further evaluated. A 34-MDa conjugative plasmid, previously isolated from Salmonella enteritidis, conferred ampicillin resistance. A 100-MDa conjugative plasmid encoded resistance to chloramphenicol, tetracycline and sulfamethoxazole/trimethoprim, as well as ampicillin. Chromosomal fingerprinting revealed two distinct resistant strains for each serovar which were different from a matched set of sensitive S. typhi strains. CONCLUSIONS: Two conjugative, TEM-type beta-lactamase-encoding plasmids conferred ampicillin resistance to S. typhi and S. paratyphi B. The 34-MDa plasmid was identical to that previously characterized from S. enteritidis, while the 100-MDa plasmid also encoded resistance to chloramphenicol, tetracycline and sulfamethoxazole/trimethoprim. Resistant isolates did not belong to a single clone but rather represented distinct strains.

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Section: Discussionsupporting

confidence: 88%

Molecular analysis of ampicillin-resistant sporadic Salmonella typhi and Salmonella paratyphi B clinical isolates

Tassios¹,

Vatopoulos

Mainas

et al. 1997

Clinical Microbiology and Infection

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“…Some studies have investigated the transfer of antibiotic resistance genes (9,(36)(37)(38)(39) both across species and within them, but little has been reported on the transfer of key virulence factors, such as toxins. The possibility that plasmid transfer can occur inside animals has been considered since the 1960s and has been shown in a variety of models, mostly under antibiotic selective pressure (8,10,40,41). This study demonstrated that both the virulence and antibiotic resistance-encoding plasmids of necrotic enteritis-associated C. perfringens are conjugative within the chicken gastrointestinal tract, without selection.…”

Section: Ber-ne33 Ber-ne33/pnetb Pbd1 Pbd1/pnetb Ehe-ne18 Wer-ne36 Bementioning

confidence: 73%

Conjugation-Mediated Horizontal Gene Transfer of Clostridium perfringens Plasmids in the Chicken Gastrointestinal Tract Results in the Formation of New Virulent Strains

Lacey

Keyburn

Ford

et al. 2017

Appl Environ Microbiol

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is a gastrointestinal pathogen capable of causing disease in a variety of hosts. Necrotic enteritis in chickens is caused by strains that produce the pore-forming toxin NetB, the major virulence factor for this disease. Like many other toxins and antibiotic resistance genes, NetB is encoded on a conjugative plasmid. Conjugative transfer of the -containing plasmid pJIR3535 has been demonstrated with a null mutant. This study has investigated the effect of plasmid transfer on disease pathogenesis, with two genetically distinct transconjugants constructed under conditions, within the intestinal tract of chickens. This study also demonstrates that plasmid transfer can occur naturally in the host gut environment, without the need for antibiotic selective pressure to be applied. The demonstration of plasmid transfer within the chicken host may have implications for disease progression and pathogenesis of -mediated disease. Such horizontal gene transfer events are likely to be common in the clostridia and may be a key factor in strain evolution, both within animals and in the wider environment. is a major gastrointestinal pathogen of poultry. strains that express the NetB pore-forming toxin, which is encoded on a conjugative plasmid, cause necrotic enteritis. This study demonstrated that the conjugative transfer of the containing plasmid to two different non-pathogenic strains converted them into disease causing strains with similar disease-causing capability as the donor strain. Plasmid transfer of and antibiotic resistance was also demonstrated to occur within the gastrointestinal tract of chickens, with approximately 14% of isolates recovered comprising of three distinct, derived, transconjugant types. The demonstration of plasmid transfer indicates the potential importance of strain plasticity and the contribution of plasmids to strain virulence.

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“…However, there is a high degree of rapid plasmid-mediated transfer of CTX resistance between fecal E. coli and Salmonella, as well as other Enterobacteriaceae, and thus, commensal E. coli can be used as a reasonable surrogate to measure the development of resistance in bacterial enteric pathogens. [37][38][39] We have shown that daily CTX did not result in increased P. falciparum antifolate resistance; rather, daily CTX was associated with a reduced incidence of malaria and antifolateresistant genotypes compared with HIV-infected individuals not taking daily CTX. In contrast, daily CTX increased carriage of non-susceptible pneumococci and CTX-resistant E. coli and may accelerate the development of CTX resistance among respiratory and diarrheal pathogens, especially in areas with lower baseline CTX resistance.…”

Section: Discussionmentioning

confidence: 99%

Does Cotrimoxazole Prophylaxis for the Prevention of HIV-Associated Opportunistic Infections Select for Resistant Pathogens in Kenyan Adults?

Hamel¹,

Greene²,

Chiller³

et al. 2008

The American Journal of Tropical Medicine and Hygiene

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We assessed the effect of daily cotrimoxazole, essential for HIV care, on development of antifolate-resistant Plasmodium falciparum, naso-pharyngeal Streptococcus pneumoniae (pneumococcus), and commensal Escherichia coli. HIV-positive subjects with CD4 cell count < 350 cells/muL (lower-CD4; N = 692) received cotrimoxazole; HIV-positive with CD4 cell count > or = 350 cells/muL (higher-CD4; N = 336) and HIV-negative subjects (N = 132) received multivitamins. Specimens were collected at baseline, 2 weeks, monthly, and at sick visits during 6 months of follow-up to compare changes in resistance, with higher-CD4 as referent. P. falciparum parasitemia incidence density was 16 and 156/100 person-years in lower-CD4 and higher-CD4, respectively (adjusted rate ratio [ARR] = 0.11; 95% confidence interval [CI] = 0.06-0.15; P < 0.001) and 97/100 person-years in HIV-negative subjects (ARR = 0.62; 95% CI = 0.44-0.86; P = 005). Incidence density of triple and quintuple dihydrofolate-reductase/dihydropteroate-synthetase mutations was 90% reduced in lower-CD4 compared with referent. Overall, cotrimoxazole non-susceptibility was high among isolated pneumococcus (92%) and E. coli (76%) and increased significantly in lower-CD4 subjects by Week 2 (P < 0.005). Daily cotrimoxazole prevented malaria and reduced incidence of antifolate-resistant P. falciparum but contributed to increased pneumococcus and commensal Escherichia coli resistance.

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Indications of in vivo transfer of an epidemic R plasmid from Salmonella enteritidis to Escherichia coli of the normal human gut flora

Cited by 45 publications

References 24 publications

Molecular analysis of ampicillin-resistant sporadic Salmonella typhi and Salmonella paratyphi B clinical isolates

Molecular analysis of ampicillin-resistant sporadic Salmonella typhi and Salmonella paratyphi B clinical isolates

Conjugation-Mediated Horizontal Gene Transfer of Clostridium perfringens Plasmids in the Chicken Gastrointestinal Tract Results in the Formation of New Virulent Strains

Does Cotrimoxazole Prophylaxis for the Prevention of HIV-Associated Opportunistic Infections Select for Resistant Pathogens in Kenyan Adults?

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