Plasmid Profile Analysis and Antibiotic Resistance Patterns of Shigella Isolates from Kwale County, Kenya

John Njeru

doi:10.14737/journal.jimb/2015/3.3.66.74

Abstract

Shigellosis caused by multidrug-resistant (MDR) Shigella strains is an important cause of morbidity and mortality in developing countries. Shigella strains usually harbour heterogeneous population of plasmids which can confer resistance to different antibiotics. A hospital based survey was conducted to determine the pattern of antimi- crobial resistance and plasmid profiles in Shigella species from diarrheal patients in Kwale county. Twenty nine (8.1%) Shigella spp were obtained from 360 stool samples collected and each strain screened for antimicrobial resistance to common antimicrobial agents and presence of plasmids. High antibiotic resistance was found to Sulfamethoxazole-tri- methoprim (79%), Ampicillin (75.9%) and Streptomycin (75.9%). All isolates were sensitive to ciprofloxacin, ceph- alosporins and Aztreonam antibiotics. Ninety seven percent of the isolates screened contained one or more plasmids ranging from 1-6. Majority were small plasmids. Species specific plasmids of 3.2kb, 9.0kb, and 3.8kb were found in Shigella flexneri, Shigella dysenteriae and Shigella sonnei respectively, while 34.5% and 79.3% MDR strains harbored large (>100kb) and middle range self-transmissible plasmids (10-100kb). In all species, no association was found be- tween specific plasmid profile and antibiotic resistance patterns. Significant association was found between carriage of 80kb plasmid in S. dysenteriae (P<0.001), combined 48kb and 80kb plasmids in S. flexneri (P=0.002) and S. sonnei (P=0.041) and MDR phenotype. The middle range plasmids specified resistance to Sulfamethoxazole-trimethoprim, Ampicillin, Streptomycin and Tetracycline. This study reports the usefulness of plasmid profiling in detection and discrimination of Shigella strains in Kenya. The study also shows that middle range self-transferable R-plasmids are widespread among the circulating MDR Shigella strains indicating the important role of these genetic elements in the development and dissemination of multidrug resistance.

Highlights

Shigellosis is one of the most prevalent diarrheal diseases in the developing countries and a major cause of morbidity and mortality (Brooks et al, 2006; WHO, 1999; Jousilahti et al, 1997)
Fifteen multi drug resistance patterns were identified with sulfamethoxazole-trimethoprim, streptomycin, ampicillin and tetracycline (8 strains) and sulfamethoxazole-trimethoprim, streptomycin, ampicillin, tetracycline, chloramphenicol and gentamycin (3 strains) being the most predominant patterns Table 1
Transfer of ampicillin and streptomycin resistance was significantly associated with a single plasmid of 80kb while transfer of combined resistance to ampicillin, sulfamethoxazole-trimethoprim, streptomycin and tetracycline was associated with joint transfer of 48kb and the 80kb plasmids. These results suggest that the genes conferring resistance to ampicillin and streptomycin are located on the 80kb plasmid while those conferring resistance to sulfamethoxazole-trimethoprim and tetracycline are located on 48kb plasmid

Summary

Introduction

Shigellosis is one of the most prevalent diarrheal diseases in the developing countries and a major cause of morbidity and mortality (Brooks et al, 2006; WHO, 1999; Jousilahti et al, 1997). Shigellosis caused by antibiotic resistant Shigella is more frequent in African countries, reflecting the effect of widespread unregulated antimicrobial use. This has drastically reduced the antimiJuly 2015 | Volume 3 | Issue 3 | Page 66 crobial therapeutic options and increased cost of treatment (Tesfaye et al, 2014; Mandomando et al, 2009; Gururaja et al, 2008; Huruy et al, 2008; Bogaerts et al, 1997). Previous studies in Kenya have reported multi drug resistance in Shigella strains to the commonly used antibiotics such as ampicillin, tetracycline, chloramphenicol, sulphamethoxazole/ trimethoprim, nalidixic acid and gentamicin (Sang et al, 2012; Kariuki et al, 2006; Kariuki et al, 1996).

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Conclusion