bacteria can exist everywhere from soil, air, water, animals and people. The
discovery of the bacterium was in 1935, but only in 1978 was declared as
“disease causing”. The name of the bacteria “difficile” comes from the fact
that the bacteria was at the beginning very hard to distinguish and culture.
Early examinations found that the bacteria was situated in the gastrointestinal
tract of infants; consequently, researchers inferred that the species was a
typical, commensal life form, the same as E. coli. So, in the late 1970s,
additionally investigations demonstrated that C. diff was in reality the
central reason for pseudomembranous colitis.
The primary contact
with another host is happening through an epithelial surface. This might be the
skin or the interior mucosal surfaces of the respiratory, gastro-intestinal,
and urogenital tracts. In the wake of reaching, the infectious agent has to
figure it out how to cling to the epithelial surface, and afterward colonizing
it, or entering inside to duplicate. Immediately after the person is infected,
the bacteria gets installed in the GI tract and then efface past by, bowel
The bacteria is a
gram-positive, anaerobic, spore forming rod-shaped micro-organism measuring 0.5-1.0×3.0-16.0
It is saccharolytic and produces
three exotoxins: toxin A (TcdA) and B (TcdB) induce glycosylation of G-proteins
(Rho, Rac, Cdc42) and finally affects actin polymerization leading to loss of
tissue integrity. The 2 toxins, especially toxin B is associated with illness
in humans. The third toxin is a dual toxin that has ADP-ribosylating movement.
The medical interrelationship are uncertain right now but can be associated
with increased virulence. Toxin A and B production is happening topmost in stationary
phase and during nutrient limitation. Carbohydrate limitation results in a
switch to amino acid fermentation, which in turn results in a shortage of amino
acids and toxin production. The expression of the toxin genesTcdA and TcdB is
controlled by positive TcdD and negative TcdC regulations which respond to
changes in the environment. Toxin A is a 308 kDa protein and toxin B is a 270
kDa protein. Each protein has an enzymatic active domain E glucosyltransferase,
a domain responsible for binding B which consists of multiple oligopeptide
repeat units, and a domain T that is involved in translocation of the toxin
across the host cell membranes.
The cultivation of
C.difficile depends strictly on anaerobic conditions and pre-diminished media.
On the particular cycloserine-cefoxitin-fructose agar, the colonies of the
bacteria will appear yellow and flat, with a ground-glass appearance and an
encompassing yellow corona. Sporulation is imperative for clostridium difficile
to cause illness and the ability to resist on every surface and also resistant
to numerous antibiotics and disinfectants, resulting in easing the process of
transmitting the bacteria.
is 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 major
risk factors that are the main cause of clostridium difficile, such as:
Antibiotics: the bacteria is commonly correlated with
antibiotics such as clindamycin, cephalosporin and fluoroquinolones.
Plethora of research points out that the use of antibiotics for
illnesses that don’t require antibiotic treatment is contributing to increase
Medical environment: most of the individuals are getting the
infection in nursing homes, hospitals or another medical clinics, but the
infections outside this medical environments are growing rapidly. People can
get the infection if they are touching infected objects or areas with feces and
then touch their mouth or mucous membranes. Medical staff can spread the
bacteria to patients, 13% of patients with at least 2 weeks stay in the
hospital are likely to get the infection and more 4 weeks stay in the hospital
the percentage is 50% of people getting the infection.
Acid suppression medication: The treatment to
suppress gastric acid increases the risk of developing clostridium difficile.H2
blockers increase the risk 1.5-fold, proton pump inhibitors by 1.7 with once-daily use and
2.4 with more than once-daily use.