PATHOGENESISI OF CAMPYLOBACER
Introduction
Campylobacter is the most common cause of food-borne disease in many industrial
countries. These are curve- spiral, motile and non-spore-forming negative rods.
Campylobacter infection in human is directly related to more knowledge of biological area
of pathogen. The virulence mechanism of campylobacter jejuni is not fully known despite
the genetic information of different C.jejuni. Campylobacter range from mild to severe
diarrhoea diseases, and the incubation period also ranges from two to seven days and this is
a self-limiting illness (Dasti, et al. 2009).
Disease pathogenesis; The development in deciphering molecular mechanism of virulence
of campylobacter jejuni give an indication of a unique pathogen, the execution of N-linked
glycosylation of more than 30 proteins related to colonization, invasion and adherence.
Contamination of water, consumption of undercooked poultry and unpasteurized dairy
products is a known source of human infection. The mechanisms of the infection in the
tissue injury in the guts, the site of the tissue injury includes the small intestine and the
ileum as well as the colon. These resulted in the destruction of the epithelia cells.
Campylobacter colonised the intestines and gain access into the mucus layer covering of the
intestinal cells. Motility of campylobacter conferred by the polar flagella with combination
of their screw- cork forms allows them efficiently penetrates this mucus barrier ((Dasti, et al.
2009, Vliet &Ketley, 2001).
The diagram shows the life cycle of pathogenesis of Campylobacter
Steadiness of the food-borne bacterial pathogens; Unlike other food-borne bacterial
pathogens, campylobacter jejuni can only grow in an environment that due to its complex
nutrition requirements. Campylobacter uses intermediates of the tricarboxylic acid (TCA)
cycle as a source of energy and does not metabolize carbohydrates because it lacks the
glycolytic enzyme phosphofructokinase. Campylobacter jejuni mostly depends on
scavenging amino acid and keto acids from its intestinal microbial floral. (Ripabelli, et al
2008).
Bacterial factor: The invasions of the campylobacter are use as a measure of bacterial
virulence, reflecting the involvement of multiple bacterial structures and mechanism.
Bacterial factors bring in the host cells attack disease pathogenesis are capsular
polysaccharide, flagella apparatus, cytolethal distending toxin and post translation
glycosylation (Vliet &Ketley, 2001)
Capsule: The campylobacter bacteria with its common feature of capsular polysaccharide
play a vital role in bacteria survival and persistence in the environment, which contributes to
its pathogenesis. This capsular polysaccharide (CPSs) display different structural variation
misleading to the host antigens and the resistance phagocytises and the complementmediated killing. CPSs allow the bacterial to invade host immunity through several
mechanisms (Ripabelli, G. et al 2008)
Bacterial toxin effects: The effect of bacteria toxins, campylobacter jejuni present with
passing watery diarrhoea that developed to bloody diarrhoea, indicates the important roles
bacteria toxin exhibit in the disease. Cytolethal distending toxin (CDT) is the lone confirmed
campylobacter toxin recognized, with its cellular effect, which produces a number of
campylobacter species including campylobacter jejuni. This toxin induces the cell distension
in the different mammalian cell line, which characterized by elongation, swelling, and
eventually cell death. The tendency of the host to acquire the necessary nutrients iron,
contributes to the bacterial pathogenesis. When the concentration of iron in the body
system is low, tissues cannot support bacterial growth and iron limitation constitutes a nonspecific host defence. In not shell, campylobacter can use the advantage of low number of
iron compound. Campylobacter does not manufacture siderophores but can uses
siderophores ferrichrome and enterochelin produces from other organism. And as a
microaerophilic bacterial metabolised during normal metabolism and in transmission when
in contact with host defence (Zilbauer, et al. 2008)
Flagellin: Flagella structure in campylobacter contains a single unsheathed flagellum. Which
could be at one pole or both, this provides the organism with a high amount of motility. This
are used to overcome peristalsis and an entrance into the mucous layer of the epithelium
and secretes flagella and non-flagella proteins for the adhesion and invasion thereby
contributing to the bacterial virulence (Vliet &Ketley, 2001)
Diagram of Pathogencity-associated factor of campylobacter
REFFERENCE
Ripabelli, et al. (2008). Prevalence of virulence-associated genes and cytolethal distending
toxin production in Campylobacter spp. Isolated in Italy. Comparative Immunology,
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Dasti, J. I., et al. (2009). Campylobacter jejuni: A brief overview on pathogenicity-associated
factor and disease-mediating mechanisms, international journal of medical microbiology.
Elsevier, 300, pp.205-211.
Vliet, A. H. M. Van, and Ketley, J. M. (2001). Pathogenesis of enteric Campylobacter
infection. Journal of Applied Microbiology, 90, pp. 45s-56s.
Zilbauer, M., et al. (2008). Campylobacter jejuni-mediated disease pathogenesis: an update.
Transaction of the royal society of tropical medicine and Hygiene. Elsevier, 102, pp.123-129.