Antibiotic alternative against clostridial infections

Clostridium difficle infection has become a great cause of concern in the present world, and its antibiotic resistance is increasing day by day owing to the misuse and rapid use of antibiotics. Previous studies have shown that there is a strong association of CDAD or Clostridium difficle associated diarrhea with the use of wide spectrum antibiotics such as Clindamycin, cephalosporin penicillin and fluoroquinolone[1]. Antibiotic resistance supports this bacterium to grow, while the other beneficial gut microorganisms are killed in the presence of these antibiotics[2]. This change in the growth of the bacterium causes the emergence of hyper virulent strains of C. difficle. The most prominent type is polymerase chain reaction ribotype (RT027) which is responsible for severe infection[3].

According to the report from the Centers for Disease Control and Prevention (CDC), approximately 453,000 people get admitted into hospital and 29,000 succumb to death annually due to clostridial infection in the USA[4]. The prevalence of this clostridial infection caused by ribotype 027 has been started since the first decade of the present century. CDAD (Clostridium difficle associated Diarrhea) is currently the most frequently occurring nosocomial infection in many hospitals worldwide, imposing a substantial economic burden on the health care systems[5][6]. C. difficle is a Gram-positive, anaerobic spore forming bacillus of the genera clostridium found throughout the environment — in soil, water, air, human and animal feces, and food products, such as processed meats. It is the prime mover of nosocomial or hospital-acquired infection. It can be grown on laboratory media from the stools of adults, newborns and infants[6]. Disease transmission is occurred due to spore formation of this bacterium and this transmission is occurred by fecal oral root[7]. One of the causes of the increase in the incidence of CDI is that it can germinate on adverse conditions such as on exposure to heat, radiation, chemicals, and antibiotics[8]. After germination, the spores secretes enterotoxin (toxin A), and cytotoxin (toxin B) which is responsible for severe inflammation and epithelial damage resulting in few medical conditions such as secretory diarrhoea and pseudomembranous colitis[9].

Mainly vancomycin and metronidazole are preferred choices of antibiotics for treating C. difficile infection. However, C. difficile is acquiring a remarkable resistance and also a low susceptibility to both vancomycin and metronidazole[10][11]. Many other antibiotics currently used applied for the treatment of bacterial infections are losing effectiveness against C. difficle infection (CDI). These antibiotics includes clindamycin, aminoglycosides, erythromycin, lincomycin, penicillins, tetracyclines, cephalosporins, and fluoroquinolones[12].

Due to the aforementioned problems, one needs to look beyond the conventional antibiotic therapy for treating C. difficile infection (CDI), one novel approach could be by exploiting the bacteriocins as alternative therapeutics to antIbiotics in combating such infection. Bacteriocin is a small peptidic toxin, mainly produced by prokaryotes and is used to inhibit or kill the bacteria within the members of the same producer species or members of different bacterial genera[13]. It can be produced from both gram positive bacteria and gram negative bacteria [14]. Although there are many other bacteriocins observed, lacticin 3147, nisin and thuricin CD have remarkable effectiveness[15]. Lacticin 3147 can reduce the amount of C. difficile and don’t affect the non-spore forming bacteria. But there is a disadvantage of lacticin 3147. It can destroy wide spectrum gram-positive bacteria of the gut such as enterococci, lactobacilli, and Bifidobacterium[16]. Nisin can kill C. difficle along with varous gram positive bacteria. But it is not more effective than vancomycin[17]. On the other hand, thuricin CD is more effective than vancomycin against C. difficile. It is very effective in reducing C. difficile in a faecal environment containing high microbial load. ’ without perturbing or affecting the gut microbiota[18].

References:
[1] DOI:[10.1093/jac/dkw385].
[2] DOI:10.1177/2049936115622891
[3] PMCID:PMC4645450
[4] DOI:10.1056/NEJMoa1408913
[5] DOI:10.1128/CMR.00016-13
[6] https://doi.org/10.1038/emi.2013.62
[7] PMID: 24354025 [8] doi:  [10.1128/JB.01765-07] [9] DOI:10.1038/nrmicro2164
[10] Decreased Effectiveness of Metronidazole for the Treatment of Clostridium difficile Infection?
[11] doi:  [10.1128/AAC.00220-12]
[12] doi:  [10.1128/JCM.02250-16]. [13] DOI: 10.20959/wjpr201611-7261}
[14] DOI 10.1007/978-1-4419-7692-5_4
[15] doi:  [10.3389/fmicb.2015.01020]
[16] DOI:10.1099/jmm.0.47085-0
[17] DOI:10.1099/jmm.0.000202
[18]DOI:10.1099/mic.0.068767-0

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