**6.3 Antibiotic resistance in EIEC**

EIEC-related infection is self-limiting that could be managed with rehydration to replenish the loss electrolyte. Zinc supplementation and nutritional therapy with iron-rich green plantain have also been shown to reduce the severity and the duration of diarrheal illness. However, in rare cases of severe symptoms antimicrobial treatment therapy has been reported to be effective [3, 10]. Since *Shigella* and EIEC present similar symptoms and are often misdiagnosed, similar antimicrobials include azithromycin (macrolide), ceftriaxone, (cephalosporin), and ciprofloxacin (fluoroquinolone) are recommended [3, 159].

Like other *E. coli* pathotypes and *Shigella*, there is an emergence of multidrugresistant EIEC strains. In a study of EIEC isolates from adults with enteric infection in Cameroon, high resistance to ampicillin and sulfamethoxazole-trimethoprim was noted in 57.14% and 71.43%, respectively. Resistance determinants to ampicillin (*bla*TEM and *bla*Oxa) were found in 28.57% of the isolates. Additionally, *cat1* and *cat2* genes were noted in chloramphenicol resistant strains while *tetA*, *tetB* encoding resistance to tetracycline, *dfr12, dfr7, dfr1a* to sulphamethoxazole-trimethoprim, and *sul1* gene to sulfonamide were present in more than 85% of the EIEC isolates [169]. In a large-scale study of *Shigella* and EIEC isolates from eight countries in four continents between 1971 and 1999, 48% of EIEC isolates were resistant to tetracycline [170]. In another study, an EIEC O164 strain isolated from a traveler with diarrhea in Japan was found to be resistant to streptomycin, spectinomycin, co-trimoxazole, and ampicillin, with reduced susceptibility to ciprofloxacin [171]. In this strain, resistance determinant for trimethoprim (*dfrXII*), streptomycin and spectinomycin (*aadA2*), and an ORF of unknown function was carried on a class 1 integron located on a transferable plasmid. While ampicillin resistance gene *bla*TEM was detected, the reduced susceptibility to ciprofloxacin was reported to be due to a single mutation P158-to-S in *parC*.
