Clostridium difficilebacteria can exist everywhere from soil, air, water, animals and people. Thediscovery of the bacterium was in 1935, but only in 1978 was declared as”disease causing”. The name of the bacteria “difficile” comes from the factthat the bacteria was at the beginning very hard to distinguish and culture.Early examinations found that the bacteria was situated in the gastrointestinaltract of infants; consequently, researchers inferred that the species was atypical, commensal life form, the same as E. coli.
So, in the late 1970s,additionally investigations demonstrated that C. diff was in reality thecentral reason for pseudomembranous colitis.The primary contactwith another host is happening through an epithelial surface. This might be theskin or the interior mucosal surfaces of the respiratory, gastro-intestinal,and urogenital tracts. In the wake of reaching, the infectious agent has tofigure it out how to cling to the epithelial surface, and afterward colonizingit, or entering inside to duplicate.
Immediately after the person is infected,the bacteria gets installed in the GI tract and then efface past by, bowelmotion.The bacteria is agram-positive, anaerobic, spore forming rod-shaped micro-organism measuring 0.5-1.0×3.0-16.0µm.
It is saccharolytic and producesthree exotoxins: toxin A (TcdA) and B (TcdB) induce glycosylation of G-proteins(Rho, Rac, Cdc42) and finally affects actin polymerization leading to loss oftissue integrity. The 2 toxins, especially toxin B is associated with illnessin humans. The third toxin is a dual toxin that has ADP-ribosylating movement.The medical interrelationship are uncertain right now but can be associatedwith increased virulence.
Toxin A and B production is happening topmost in stationaryphase and during nutrient limitation. Carbohydrate limitation results in aswitch to amino acid fermentation, which in turn results in a shortage of aminoacids and toxin production. The expression of the toxin genesTcdA and TcdB iscontrolled by positive TcdD and negative TcdC regulations which respond tochanges in the environment. Toxin A is a 308 kDa protein and toxin B is a 270kDa protein. Each protein has an enzymatic active domain E glucosyltransferase,a domain responsible for binding B which consists of multiple oligopeptiderepeat units, and a domain T that is involved in translocation of the toxinacross the host cell membranes. The cultivation ofC.difficile depends strictly on anaerobic conditions and pre-diminished media.
On the particular cycloserine-cefoxitin-fructose agar, the colonies of thebacteria will appear yellow and flat, with a ground-glass appearance and anencompassing yellow corona. Sporulation is imperative for clostridium difficileto cause illness and the ability to resist on every surface and also resistantto numerous antibiotics and disinfectants, resulting in easing the process oftransmitting the bacteria. Clostridium difficileis associated with around 20 percent cases of antibiotic associated diarrhea.From 2001 and 2016 the rates of the infection have increased significantly,also a male is unlikely to get the infection compared to a women.
There are some majorrisk factors that are the main cause of clostridium difficile, such as:· Antibiotics: the bacteria is commonly correlated withantibiotics such as clindamycin, cephalosporin and fluoroquinolones.Plethora of research points out that the use of antibiotics forillnesses that don’t require antibiotic treatment is contributing to increasebacterial infection.· Medical environment: most of the individuals are getting theinfection in nursing homes, hospitals or another medical clinics, but theinfections outside this medical environments are growing rapidly. People canget the infection if they are touching infected objects or areas with feces andthen touch their mouth or mucous membranes.
Medical staff can spread thebacteria to patients, 13% of patients with at least 2 weeks stay in thehospital are likely to get the infection and more 4 weeks stay in the hospitalthe percentage is 50% of people getting the infection.· Acid suppression medication: The treatment tosuppress gastric acid increases the risk of developing clostridium difficile.H2blockers increase the risk 1.5-fold, proton pump inhibitors by 1.7 with once-daily use and2.4 with more than once-daily use.