Cmpylobacter jejuni
Campylobacter, is a Zoonotic disease classified in the family of Campylobacteraceae, which are
curved, helical-shaped, non-sporulated, Gram-ve, motile, microaerophilic and thermophilic
microorganism. They exist in a large group of warm-blooded animals, specifically, birds which forms
their normal intestinal flora. Campylobacters have a single unipolar or bipolar flagellum to propel
them in a darting movement in a liquid medium. (colles et al, 2009).
According to Altekruse (1997) McFaydean and Stockman are the first person to identify
campylobacters in the tissue of an aborted sheep fetus. In 1957 isolated similar curved, helical
shaped bacteria from the stool of a children who has a bloody diarrhea. In 1972, microbiologists in
Belgium pioneered to isolate campylobacters from patients with bloody diarrhea. Currently C. jejuni
the causes of major food-borne gastroenteritis in the U.S.A and other developed countries.
Morphology
Van Putten et al (2009) stated the biochemical secretion involved in the pathogenesis and virulence
factors in C. Jejuni are adhesions, cytotoxins and endotoxins including a group of proteins
characterised as Campylobacter invasion antigens (Cia) to enable invade and colonize the jejunum.
Such as: Motility, Flagella, Adherence, Capsule CadF, JlpA, PEB1, LOS, MOMP, Toxin, CDT
Invasion: CiaB and
CiaC,
Secretion system: Type
IV secretion system
LOS(lipooligosaccharide)
Linton et al (2000) stated that LOS diversity is a very important factor which enables C. Jejuni to
colonize a variety of hosts, for adhesion, Phase variation and structural mimicry. The ability of the
organism to show variations at higher rate by creating molecular similarity by LOS proves its action
in avoiding host defence. The likeness of LOS molecular structures with gangliosides produces
cross reacting antibodies creates basis for association of C. jejuni with Guillain-Barre syndrome. It
is an acute form of neurological disease known to cause ascending paralysis of the peripheral nerves
that leads to the impairment of the respiratory muscle leading to death.
Picture: Curr. Top. Microbiol. Immunol, 337,197-229.)
Structure
Vlieti and Ketley (2001) states that Campylobacters are a group of spiral, curved Gram -ve bacilli
with polar flagella at either side of the bacteria. They are highly motile, urease negative, oxidase and
catalase positive and microaerophilic. Requires about 15% oxygen and 5% carbon dioxide
concentration for optimal growth.
Genetic Structure
The genetic sequence of C. jejuni was completed in 2000 in the Sanger Centre, their finding suggest
the genome of C. jejuni has 1.6 million bases, comprising of 1,654 coding genes. According to their
discovery C. jejuni is found to be the most gene-dense bacterium of all the sequenced
microorganisms, at least 94.3% of the genome contains protein coding gene.
Classification and Antigenic Types
According to Moran and Penner (1999) Campylobacter species contains several serogroups, based on
their lipopolysaccharide (O) and protein (H) antigens. However a small number of serogroups
account for majority of the human isolates in a specific geographic location. C jejuni contains several
surface-exposed antigens, such as porin and flagellin.
Life cycle
Their ability to survive host’s gut is very poor, and cannot replicate easily. The organism grows best
at 37 to 42 OC in microaerophilic environment and is labile to freezing, drying, acidic situations and
salinity (Altekruse et al, 1997).
Discussion;
According to Karlyshev (2005) surface glycans of microbial agents composed of glycolipid and
glycoprotein plays a major role in the interaction of cell-cell and host immune response. The survival
and pathogenecity of c. Jejuni is based upon the interaction of the campylobacter glycone with the
lipooligosacchride (LOS) Capsular O- and N-linked glycosylation, these proteins plays a major role
in the life cycle, infectivity and cross contamination of the bacteria to humans.
References:
Altekruse, F., Stern, J., Fields, P., David L. And Swerdlow, D. (1999) ‘Campylobacter jejuni—An
Emerging Foodborne Pathogen.’ Emerging Infectious diseases, 5 (1), 7-8.
F M Colles, FM., McCarthy, N D., Howe, J C., Devereux, C L., Gosler, A G and M C J Maiden (2009)
‘Dynamics of Campylobacter colonization of a natural host, Sturnus vulgaris (European Starling).’ Environ
Microbiol. January, 11(1), 258–267.
Karlyshev, AV., Ketley, JM. And Wren BW.(2005) ‘The Campylobacter jejuni glycome.’ FEMS
Microbiol Rev, 29 (2), 377-90.
Linton, D,. Karlyshev, A., Hitchen, P., Morris, H., Dell, A., Gregson, N. and Wren, B. (2000) ‘
Multiple N-acetyl neuraminic acid synthetase (neuB) genes in Campylobacter jejuni: identification
and characterization of the gene involved in sialylation of lipo-oligosaccharide.’ Mol. Microbiol,
35(5), 1120-1134.
Moran, A.P. and Penner, J. L. (1999) ‘Serotyping of Campylobacter jejuni based on heat stable
antigens: relevance, molecular basis and implications in pathogenesis.’ Journal of Applied
Microbiology, 86 (3), 361–377.
http://www.sanger.ac.uk/resour...cteria/campylobacter-coli.html
Van Putten JP, et al.(2009) ‘ Molecular mechanisms of Campylobacter infection.’ Curr. Top.
Microbiol. Immunol, 337, 197-229.