Biotype and antibiotic sensitivity of 100 clinical isolates of Yersinia enterocolitica

1991 ◽  
Vol 28 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Jeannette N. Pham ◽  
Sydney M. Bell ◽  
Josette Y. M. Lanzarone
Pathology ◽  
1993 ◽  
Vol 25 (4) ◽  
pp. 385-387 ◽  
Author(s):  
Jeannette N. Pham ◽  
Sydney M. Bell

2021 ◽  
Vol 8 ◽  
Author(s):  
Nurul Asyiqin Haulisah ◽  
Latiffah Hassan ◽  
Siti Khairani Bejo ◽  
Saleh Mohammed Jajere ◽  
Nur Indah Ahmad

Overuse of antimicrobials in livestock health and production beyond therapeutic needs has been highlighted in recent years as one of the major risk factors for the acceleration of antimicrobial resistance (AMR) of bacteria in both humans and animals. While there is an abundance of reports on AMR in clinical isolates from humans, information regarding the patterns of resistance in clinical isolates from animals is scarce. Hence, a situational analysis of AMR based on clinical isolates from a veterinary diagnostic laboratory was performed to examine the extent and patterns of resistance demonstrated by isolates from diseased food animals. Between 2015 and 2017, 241 cases of diseased livestock were received. Clinical specimens from ruminants (cattle, goats and sheep), and non-ruminants (pigs and chicken) were received for culture and sensitivity testing. A total of 701 isolates were recovered from these specimens. From ruminants, Escherichia coli (n = 77, 19.3%) predominated, followed by Staphylococcus aureus (n = 73, 18.3%). Antibiotic sensitivity testing (AST) revealed that E. coli resistance was highest for penicillin, streptomycin, and neomycin (77–93%). In addition, S. aureus was highly resistant to neomycin, followed by streptomycin and ampicillin (68–82%). More than 67% of E. coli isolates were multi-drug resistant (MDR) and only 2.6% were susceptible to all the tested antibiotics. Similarly, 65.6% of S. aureus isolates were MDR and only 5.5% were susceptible to all tested antibiotics. From non-ruminants, a total of 301 isolates were recovered. Escherichia coli (n = 108, 35.9%) and Staphylococcus spp. (n = 27, 9%) were the most frequent isolates obtained. For E. coli, the highest resistance was against amoxicillin, erythromycin, tetracycline, and neomycin (95–100%). Staphylococcus spp. had a high level of resistance to streptomycin, trimethoprim/sulfamethoxazole, tetracycline and gentamicin (80–100%). The MDR levels of E. coli and Staphylococcus spp. isolates from non-ruminants were 72.2 and 74.1%, respectively. Significantly higher resistance level were observed among isolates from non-ruminants compared to ruminants for tetracycline, amoxicillin, enrofloxacin, and trimethoprim/sulfamethoxazole.


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

2005 ◽  
Vol 49 (7) ◽  
pp. 2834-2839 ◽  
Author(s):  
Yumi Osaki ◽  
Yumiko Sanbongi ◽  
Midori Ishikawa ◽  
Hiroshi Kataoka ◽  
Takahisa Suzuki ◽  
...  

ABSTRACT To clarify the relationship between mutations commonly found for penicillin-binding protein 3 (PBP 3) of β-lactamase-nonproducing ampicillin-resistant (BLNAR) Haemophilus influenzae isolates and β-lactam resistance, single and multiple amino acid mutations at positions 377, 385, 389, 517, and 526 were introduced into PBP 3 of a β-lactam-susceptible Rd strain by site-directed mutagenesis. Twelve isogenic recombinant strains were challenged with nine β-lactam antibiotics. Replacement of the asparagine at position 526 with lysine (N526K) increased the resistance to imipenem eightfold and increased the resistance to various cephalosporins two- to eightfold. Substitution of threonine for serine at position 385 (S385T) and/or substitution of phenylalanine for leucine at position 389 (L389F), in addition to the N526K mutation, led to two- to fourfold additional increases in cephalosporin resistance. An isoleucine-to-methionine substitution at position 377 did not change the antibiotic sensitivity of any of the recombinant strains also carrying other PBP 3 mutations tested. Thirty-six clinical isolates carrying a PBP 3 gene (ftsI) with the S385T, L389F, R517H, and/or N526K mutation were chosen from among 279 clinical isolates collected in Japan, and the isolates were grouped into six classes on the basis of the patterns of the four mutations in PBP 3. Rd recombinants were made with each of the ftsI genes. The levels of resistance to β-lactams varied between recombinants of different classes but were comparable for those of the same class. The levels of resistance to cephalosporins of these recombinants were similar to those of the parent clinical isolates, while those to ampicillin and carbapenems were lower. These results indicate that resistance to β-lactams, at least to cephalosporins, depends in large part on the PBP 3 mutations R517H, N526K, S385T, and L389F.


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