Morphological, Physio-biochemical Properties and Antibiogram of the Clostridium chauvoei.

Abstract

Clostridium chauvoei is one of the deadly micro-organism that causes disease in cattle and sheep. We tested Clostridium chauvoei on different culture media, physio-biochemical agents and antibiotics. The best grwoth of organism was observed on blood and nutrient agar at pH 7.2-7.5, and temperature in between 37-40ºC. No effect of centrifugation was observed. Fourteen different antibiotics were tested against the Clostridium chauvoei. Highly effective antibiotics were chloramphenicol, tetracycline, baquiloprim/sulphadimidine, erythromycin, gentamicin, compound sulphonamides.

Multidrug Resistance in Clostridia

“…The less susceptible antibiotics included 55.2% for neomycin, 43.7% for kanamycin, and 62.5% for ampicillin. The species showed resistance against bacitracin, metronidazole, and lincomycin (Rais et al 2016). Another study reported sensitivity against penicillin, oxytetracycline and chlortetracycline.…”

A review of cardiac blackleg in cattle, and report of 2 cases without skeletal muscle involvement in Argentina

“…19 C. chauvoei is highly susceptible to several antimicrobials, including cephalothin, clindamycin, enrofloxacin, erythromycin, penicillin, chloramphenicol, tetracycline, sulfadimidine, and gentamicin. 46…”

“…The best growing conditions for C. chauvoei are on blood agar, pH 7.2–7.5, in strict anaerobic conditions at 37–40°C. 46 C. chauvoei colonies on blood agar are circular, raised, usually 2–4 mm in diameter, bright and semitransparent, although after 24 h of incubation they became completely opaque. Frequently, the colonies are surrounded by a variable zone of hemolysis on sheep blood agar.…”

“…19 C. chauvoei is highly susceptible to several antimicrobials, including cephalothin, clindamycin, enrofloxacin, erythromycin, penicillin, chloramphenicol, tetracycline, sulfadimidine, and gentamicin. 46 C. chauvoei produces 2 β-pore-forming toxins (β-PFTs) named C. chauvoei toxin A (CctA) and chauveolysin. The general mechanism of action of β-PFTs consists of formation of pores in the lipid cell membrane that results in the alteration of membrane permeability and subsequently cell death by necrosis or apoptosis depending on toxin concentration.…”