Chloramphenicol resistance in clinical isolates of Yersinia enterocolitica serotype 0:3 biotype 4

1988 ◽  
Vol 21 (4) ◽  
pp. 506-508 ◽  
Author(s):  
EMILIO PÉREZ TRALLERO ◽  
GUSTAVO CILLA EGUILUZ ◽  
MERCEDES URBIETA EGANA
Pathology ◽  
1993 ◽  
Vol 25 (4) ◽  
pp. 385-387 ◽  
Author(s):  
Jeannette N. Pham ◽  
Sydney M. Bell

1991 ◽  
Vol 28 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Jeannette N. Pham ◽  
Sydney M. Bell ◽  
Josette Y. M. Lanzarone

2003 ◽  
Vol 131 (3) ◽  
pp. 1181-1186 ◽  
Author(s):  
I. G. WILSON

Campylobacter isolates from raw retail chickens (n=434) sampled between 1998 and 2000 were tested for resistance to 12 antibiotics. Among 208 campylobacters tested, more than 90% of isolates were susceptible to 4 out of 9 antibiotics (nalidixic acid, erythromycin, chloramphenicol and gentamicin). Most campylobacters were resistant to 3 antibiotics and multiple resistance was found in 4%. Ciprofloxacin resistance was 11%. Campylobacter contamination (28%) in imported chickens (n=150) was almost half that found in local whole chickens (50%), but the resistance of imported isolates (n=42) was similar to that of local campylobacters. Resistance in isolates from imported chicken breasts was generally more common, but to only 4 antibiotics. Resistance patterns of chicken isolates were compared to human clinical isolates (n=494), and a greater similarity was found between the clinical and local isolates than with imported campylobacters. Lower chloramphenicol resistance was found in clinical Campylobacter isolates than in those from chicken sources.


2002 ◽  
Vol 46 (9) ◽  
pp. 2977-2981 ◽  
Author(s):  
Beatriz Guerra ◽  
Sara Soto ◽  
Reiner Helmuth ◽  
M. Carmen Mendoza

ABSTRACT An unusual self-transferable virulence-resistance plasmid (pUO-StVR2) was found in nine multidrug-resistant (ACSSuT phenotype) Salmonella enterica serotype Typhimurium clinical isolates that were assigned to four different phage types and a single and distinctive XbaI pulsed-field gel electrophoresis profile. pUO-StVR2 is an IncFII plasmid of about 140 kb in length carrying the spvA, spvB, and spvC (Salmonella plasmid virulence) and rck (resistance to complement killing) genes. It also carries the oxa1/aadA1a (ampicillin resistance and streptomycin-spectinomycin resistance) gene cassette configuration located within a class 1 integron with qacEΔ1/sul1 (ammonium antiseptics resistance and sulfadiazine resistance); the transposon genes merA, tnpA, and tnpR (mercury resistance, transposase, and resolvase of Tn21, respectively); and the catA1 (chloramphenicol resistance) and tet(B) (tetracycline resistance) genes. The insertion of resistance genes into a Salmonella virulence plasmid constitutes a new and interesting example of plasmid evolution and presents a serious public health problem.


2004 ◽  
Vol 53 (11) ◽  
pp. 1065-1068 ◽  
Author(s):  
Itender Singh ◽  
Jugsharan S Virdi

Two hundred and fifty nine isolates of Yersinia enterocolitica and related species were examined for the production of heat-stable enterotoxin (Yersinia stable toxin; YST) as well as for the prevalence of enterotoxin genes, viz. ystA, ystB and ystC. Under the conventional conditions used for the production of Y. enterocolitica enterotoxin, i.e. in tryptic soy broth (TSB) supplemented with yeast extract at 28 °C for 48 h, 77.7 % of clinical isolates and 62.3 % of swine isolates showed enterotoxigenicity in infant mice. All isolates that produced enterotoxin at 28 °C also showed enterotoxic activity at 37 °C after 48 h incubation under an alkaline pH of 7.5, the pH present in the ileum. All Yersinia intermedia and Yersinia frederiksenii isolates were negative for enterotoxin production. All clinical isolates and 96.3 % of Y. enterocolitica isolates from swine hybridized with a probe for ystB, which indicated that the ystB gene was most prevalent in Y. enterocolitica biotype 1A strains. None of the Y. enterocolitica isolates showed hybridization with oligonucleotide probes for ystA or ystC. The study indicated that YST-b was the major contributor to diarrhoea produced by biotype 1A strains of Y. enterocolitica.


1998 ◽  
Vol 66 (3) ◽  
pp. 1113-1120 ◽  
Author(s):  
Travis Grant ◽  
Vicki Bennett-Wood ◽  
Roy M. Robins-Browne

ABSTRACT Yersinia enterocolitica is an important enteric pathogen which has well-defined virulence determinants that allow the bacteria to become established in their hosts and overcome host defenses. A number of strains obtained from patients with diarrhea, however, lack these genes. Accordingly, the mechanisms by which they cause disease are uncertain. Most of these isolates belong to biotype 1A. Strains of this biotype are also frequently isolated from a variety of nonclinical sources, such as food, soil, water, and healthy animals, and there is evidence that some of these strains are avirulent. In this study we investigated 111 strains of Y. enterocoliticabiotype 1A, 79 from symptomatic humans and 32 from nonclinical sources, for virulence-associated characteristics. DNA hybridization studies showed that none of the strains carried sequences homologous with pYV, the ∼70-kb Yersinia virulence plasmid. Some strains hybridized with DNA probes for one of the following chromosomal virulence-associated genes: ail (7.2%), myfA(11.7%), ystA (0.9%), and ystB (85%). In addition, 33 strains (29.7%) produced an enterotoxin that was reactive in infant mice. However, the frequencies of these virulence-associated properties in clinical and nonclinical isolates were similar. Clinical isolates invaded HEp-2 cells and Chinese hamster ovary cells to a significantly greater extent than nonclinical strains (P ≤ 0.002). In addition, clinical strains colonized the intestinal tracts of perorally inoculated mice for significantly longer periods than nonclinical isolates (P ≤ 0.01). Light and electron microscopic examination of tissue culture cells incubated with invasive yersiniae revealed that the bacteria invaded selected cells in large numbers but spared others, suggesting that biotype-1A strains of Y. enterocolitica may invade cells by a novel mechanism. These results indicate that some clinical isolates of Y. enterocolitica which lack classical virulence markers may be able to cause disease via virulence mechanisms which differ from those previously characterized in enteropathogenic Yersiniaspecies.


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