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Campylobacter: Health Effects and Toxicity

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DOI: 10.1016/B978-0-12-384947-2.00106-9

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Zautner A.E., and Masanta W.O. (2016) Campylobacter: Health Effects and Toxicity. In: Caballero, B., Finglas,
P., and Toldrá, F. (eds.) The Encyclopedia of Food and Health vol. 1, pp. 596-601. Oxford: Academic Press.

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 Author's personal copy

Campylobacter: Health Effects and Toxicity

AE Zautner and WO Masanta, Universitätsmedizin Göttingen, Göttingen, Germany
ã 2016 Elsevier Ltd. All rights reserved.

Introduction gastroenteritis. Interestingly, epidemiologic studies have con-

The name Campylobacter was coined from two Greek words:
kampὓlοB (kampylos) meaning curved and bakt!rΐa (bakteria)
meaning rod. The genus Campylobacter was initiated in 1963 by
Sebald and Véron upon observing a Vibrio-like bacterial strain
that had been isolated from abortion cases in ewes and cattle
could not ferment sugar and had a different G þ C content to
that of Vibrio cholerae. Chronologically, McFadyean and Stock-
man who had concluded that a Vibrio-like bacterium was
responsible for abortions in Devon longwoolled ewes in the
United Kingdom reported the first case in 1906. This was
closely followed by a similar report in 1918 by Smith and
Taylor who had observed that a Vibrio-like bacterium was
responsible for abortions in cattle in the United States of
America. Due to the similarity between these two bacteria,
Smith and Taylor had classified them into the genus Vibrio
and collectively named Vibrio fetus. This bacterium was
renamed as Campylobacter fetus, and to avoid such errors in
taxonomy and nomenclature of Vibrio-like bacteria that were
being isolated, Sebald and Véron initiated and defined the
genus Campylobacter as comprising Gram-negative, slender,
and curved bacteria, which are (a) motile by means of polar
flagella (Figure 1), (b) microaerophilic with a strictly respira-
tory metabolism, and (c) not producing acid in carbohydrate-
containing media and which have a DNA G þ C content of
29–36%. This contrasted the genus Vibrio, which had been
previously defined as comprising bacteria that ferment glucose
and have a DNA G þ C content between 40% and 53%. As a
result of improved taxonomy methods, particularly genotypic
methods, the genus Campylobacter presently has 25 species and
9 subspecies (see Table 1).
Unlike in sheep and cattle, the isolation of Campylobacter
spp. from human feces before 1968 was not possible because
an isolation technique had not been developed. All the Vibrio-
like bacteria that had been isolated in humans before originated
from blood samples. The first undisputable Campylobacter
human infection was reported in 1947 by Vinzent and co-
workers who identified V. fetus (presently C. fetus) to have
caused abortion in two women who had been admitted to the
hospital for four weeks due to fever. In 1957, Elizabeth King
isolated two Vibrio-like bacteria from the blood of patients with
diarrhea but failed to isolate any bacteria from the feces of the
patients. In spite of failure to isolate bacteria from the feces of
the patients, King concluded that Campylobacter caused the
enteric infections. Dekeyser and Butzler confirmed King’s con-
clusion in 1968. They isolated V. jejuni (presently C. jejuni) from
feces and blood of a 20-year-old female who was admitted in
July 1968 in St. Peter University Hospital in Brussels with severe
diarrhea and fever using a filtration technique. Since then, better
techniques for isolating and identifying Campylobacter from feces
have been developed. These techniques have revealed that
C. jejuni and C. coli are one major cause of human
stantly shown that C. jejuni is the leading cause of bacterial
gastroenteritis worldwide and C. coli is responsible for a signif-
icant lower percentage of cases. Therefore, in this chapter we
discuss (i) general characteristics of C. jejuni, (ii) epidemiology
of C. jejuni infections, (iii) C. jejuni enteritis and associated
postinfectious manifestations, (iv) pathogenesis of C. jejuni,
and (v) treatment of campylobacteriosis.
Characteristics of C. jejuni
C. jejuni are Gram-negative, nonspore-forming, microaerophilic
(5% oxygen), spiral-shaped rods measuring 1.5–3.5 mm in length
and 0.2–0.4 mm in width. They possess a single circular chromo-
some of 1.64–1.7 million base pairs (30.6% G þ C), which is
predicted to encode about 1650 proteins including 52 ribosomal
proteins. The bacterial cells have a unique corkscrew motility
propelled by flagella located at the poles of the bacterial cell.
The growth temperature ranges from 30 to 45 " C with an opti-
mum of 42 " C. C. jejuni does not multiply at temperatures below
30 " C but remains viable for many months at these temperatures.
Some studies have shown that C. jejuni cells remain viable at 4 " C
for up to 7 months. They grow in a pH range of 5.0–9.0 with an
optimum of 6.5–7.5. C. jejuni is sensitive to desiccation and heat
(it can be easily destroyed above 48 " C) and is unable to grow in
NaCl # 2%. In contrast to many other bacteria, amino and car-
bon acids are the major carbon sources because they do not
utilize glucose or other hexose sugars as carbon source. But
particular strains are able to metabolize L-fucose. C. jejuni survives
and thrives in a wide range of hosts.
Epidemiology
C. jejuni is the most prevalent cause of human gastroenteritis in
both developing and developed countries. In developing
countries, it mainly affects children below 5 years, while in
developed countries it mainly infects adults. In addition, in
developing countries, incidences of campylobacteriosis are not
season-specific but in developed countries most cases are
reported during summer.
In spite of these differences, C. jejuni are commensal organ-
isms in the intestines of wild birds and farm and domestic
animals including goats, sheep, cattle, swine, poultry, dogs,
and cats. Also, they are found in untreated water and water
bodies such as lakes, dams, and rivers. Consequently, contact
with farm and domesticated animals, raw milk, milk products,
untreated water, undercooked poultry, contaminated meat
products, barbecue meat, minced meat, both processed and
unprocessed sea foods, international travel, and restaurant
eating are major risk factors. Epidemiological and

596 Encyclopedia of Food and Health http://dx.doi.org/10.1016/B978-0-12-384947-2.00106-9

The Encyclopedia of Food and Health, (2016), vol. 1, pp. 596-601
 Author's personal copy
Campylobacter: Health Effects and Toxicity 597

microbiological studies have shown that poultry remains to be

Figure 1 Electron micrograph of C. jejuni strain B2. The bacterial cell
has at both poles a flagellum, which ensures its cellular motility. Thanks
to Michael Hoppert, Department of General Microbiology, University of
Göttingen for the picture.
the major source of human infection.
According to the European Food Safety Authority (EFSA),
214 000 cases of infection were reported in the year 2012 in the
European Union. It is assumed that the actual number of cases
of human campylobacteriosis is at approximately nine million
per year in the EU. The costs incurred by campylobacteriosis
for the public health systems and due to loss of productivity in
the EU are estimated by the EFSA to approximately EUR 2.4
billion per year. The disease burden of Campylobacter enteritis
and its postinfectious sequelae is approximately 0.35 million
disability-adjusted life years (DALYs) per year. Contaminated
broiler meat is assumed to account for 20–30% of the cases,
while 50–80% may be attributed to the chicken reservoir as a
whole (laying hens in addition to broilers).
The Foodborne Diseases Active Surveillance Network, a
collaboration among the Centers for Disease Control and Pre-
vention (CDC) and 10 US state health departments, estimates
the incidence per 100 000 population in 2012 to 14.30. Among
these Campylobacter isolates with species information, 90%
were C. jejuni, 8% were C. coli, and the remaining 2% belonged
to other Campylobacter species.

Table 1 The bacterial species included in the genus Campylobacter (in alphabetical order)

Species/subspecies/biovar Host/habitat References

C. avium Chicken, turkey Rossi et al. (2009)

C. canadensis Whooping crane Inglis et al. (2007)
C. coli Swine, poultry, sheep, dogs Skirrow (1977)
C. concisus Humans Love et al. (1984)
C. curvus Swine, humans Vandamme et al. (1991)
C. cuniculorum Rabbits Zanoni et al. (2009)
C. fetus ssp. fetus Sheep, goats, cattle van der Graaf-van Bloois et al. (2014)
C. fetus ssp. venerealis bv. intermedius Cattle
C. fetus ssp. venerealis Cattle
C. gracilis Dogs, humans Han et al. (1991)
C. helveticus Cats, dogs, humans Stanley et al. (1992)
C. hominis Humans Lawson et al. (1998)
C. hyointestinalis ssp. hyointestinalis Swine Gebhart et al. (1983)
C. hyointestinalis ssp. lawsonii Swine On et al. (1995)
C. insulaenigrae Seals, sea lions, elephant seals, Foster et al. (2004)
C. jejuni ssp. doylei Humans Steele and Owen (1988)
C. jejuni ssp. jejuni Cattle, chicken, sheep, swine, turkey, humans, Skirrow (1977)
wild birds, etc.
C. lanienae Swine, cattle Logan et al. (2000)
C. lari ssp. concheus Shellfish Debruyne et al. (2009)
C. lari ssp. lari Shellfish
C. laridis Humans Benjamin et al. (1983)
C. mucosalis Swine Lawson et al. (1975)
C. peloridis Shellfish Debruyne et al. (2009)
C. rectus Humans Vandamme et al. (1991)
C. showae Humans Etoh et al. (1993)
C. sputorum bv. faecalis Cattle, humans, sheep, swine Vandamme and On (2001)
C. sputorum bv. paraureolyticus Cattle, humans, sheep, swine
C. sputorum bv. sputorum Cattle, humans, sheep, swine
C. subantarcticus Gray-headed albatrosses, black-browed Debruyne et al. (2010a,b);
albatrosses, gentoo penguins
C. ureolyticus Cats, swine, canines, humans Han et al. (1991)
C. upsaliensis Dogs, cats, poultry, humans Goossens et al. (1990)
C. volucris Black-headed gulls Debruyne et al. (2010a,b)

The Encyclopedia of Food and Health, (2016), vol. 1, pp. 596-601

 Author's personal copy
598 Campylobacter: Health Effects and Toxicity
C. jejuni Enteritis and Associated Post-infectious
Manifestations
C. jejuni affects human health by causing an infection that is
known as Campylobacter enteritis or human campylobacterio-
sis. This infection is a foodborne disease that is characterized
by the following clinical symptoms: fever, abdominal pain,
watery or sometimes bloody diarrhea, headache, dizziness,
nausea, and vomiting. These symptoms usually start 2–4 days
after ingestion of C. jejuni and may clear after 5–7 days. The
C. jejuni minimal infectious dose is above 500 viable bacteria.
Although this disease is self-limiting, post-infectious manifes-
tations, namely, Guillain–Barré syndrome (GBS), reactive
arthritis (ReA), and inflammatory bowel disease (IBD), can
arise after recovery. Below is a brief description of each post-
campylobacteriosis manifestation:
(a) GBS: GBS is an autoimmune disorder in which the body’s
immune system ‘mistakenly’ attacks human GM
gangliosides – lipids found in the central nervous system
– leading to acute neuromuscular paralysis and consecu-
tive muscle weakness. There are four types of GBS, namely,
Miller Fisher syndrome (MFS), acute motor axonal neu-
ropathy (AMAN), acute inflammatory demyelinating poly-
radiculoneuropathy (AIDP), and acute motor and sensory
axonal neuropathy (AMSAN). C. jejuni is the leading cause
of GBS and has been linked to triggering MFS, AMAN, and
AMSAN, but not AIDP. It triggers these autoimmune dis-
orders because its cell wall surface contains lipooligosac-
charides (LOSs) that resemble ganglioside structures on
the surface of the Schwann cells and the coat of the nerve
axons. As a consequence of this molecular mimicry, the
immune system releases autoantibodies leading to neuritis
and axonal degeneration. GBS usually develops 3 weeks
after recovery from Campylobacter enteritis and is charac-
terized by slow recovery and severe residual disability.
(b) ReA: ReA is a spondyloarthropathic syndrome character-
ized by inflammation of the joints and tendons occurring
after gastrointestinal infections with C. jejuni as well as
Shigella dysenteriae, Salmonella enterica, Yersinia
enterocolitica, and Yersinia pseudotuberculosis or genitouri-
nary infections especially with Chlamydia trachomatis. The
mechanism of ReA is poorly understood. However,
interleukin IL-1, IL-6, and TNF-a have been implicated in
C. jejuni-associated ReA. In some cases, ReA occurs
together with an inflammation of the eye’s conjunctiva
or uvea, as well as of the urethra (and rarely additionally
of the uterine cervix in women). This inflammatory triad is
called Reiter’s syndrome.
(c) IBD: IBD is established when a gastrointestinal tract
immunologic disorder leads to chronic recurrent inflam-
mation of the colon and small intestine. Gut host cells and
gut commensal microflora continuously communicate cre-
ating a sustained normal gut homeostasis. The diversity
and load of the human normal gut microbiota are influ-
enced by the individual’s genetics and diet. It mostly
comprises Bacteroides spp. and Prevotella spp. A disruption
of the normal gut homeostasis by factors including smok-
ing, diet, drugs, geography, social stress, and psychological
elements leads to changes in the diversity of the gut
The Encyclopedia of Food and Health, (2016), vol. 1, pp. 596-601
microflora. This in turn promotes intestinal epithelial inva-
sion by C. jejuni and S. enterica and gut commensals, which
are recognized by nucleotide-binding oligomerization
domain (NOD) proteins and Toll-like receptors. Sensing
of these receptors stimulates the mucosa-associated
immune system leading to intestinal inflammation.
(d) Other possible C. jejuni-associated diseases: Besides the
above-mentioned clinical manifestations, campylobacter-
iosis was also associated with the postinfectious irritable
bowel syndrome, celiac disease, and potentially with the
so-called immunoproliferative small intestinal disease.
Pathogenesis of C. jejuni
The clinical features of campylobacteriosis are a result of the
interaction between C. jejuni bacterial cells and the enterocytes
of the host. This section looks at the Campylobacter virulence-
associated factors and counteracting enterocytal factors:
C. jejuni interaction with both the host microbiome and the
innate immune system.
Campylobacter Virulence-Associated Factors
The environment in the lower intestinal tract is hostile for
colonization with C. jejuni. In the process of adjusting its
metabolic systems in response to this unfavorable
environment, C. jejuni ends up secreting proteins, which lead
to the disruption of the intestinal epithelium. This epithelial
irritation results in clinical symptoms such as diarrhea. Also,
certain C. jejuni surface structures interact with enterocytes
contributing to their disruption. These secreted proteins and
surface structures are collectively termed Campylobacter
virulence-associated factors. They include the following:
(a) Flagella, motility, and chemotaxis: Motility helps bacteria to
effectively colonize their environment. C. jejuni’s flagella
and 11 different types of chemoreceptors allow it to
migrate within the mucosa in search for a suitable envi-
ronment. Interestingly, C. jejuni migrates to certain areas of
the mucosa that have energy sources, like carboxylic acids,
amino acids, and L-fucose. In addition to motility, the
flagellin A (flaA) and flagellin B (flaB) subunits undergo
phase variation, hence playing a role in evasion of the host
immune response.
(b) Toxin: C. jejuni produces a toxin known as cytolethal dis-
tending toxin (CDT). This toxin is made up of three sub-
units: CdtA, CdtB, and CdtC. The CdtB subunit has a
DNase 1-like activity; hence, it randomly cuts DNA of
enterocytes to release 50 -phosphorylated di-, tri-, and oli-
gonucleotide fragments leading to enterocyte cell cycle
arrest, disrupting cell protecting structures such as the
cell wall and eventually death of enterocytes. The subunits
CdtA and CdtC are binding proteins for delivering CdtB
into the cytoplasm of enterocytes. C. jejuni CDT is essential
for invasion and mucosal inflammation.
(c) Adhesion factors: Attachment of C. jejuni to the epithelial
cell surface is an important step in invasion of the mucosa
and in some situations for evasion of the immune
response. Unlike similar Gram-negative enteric pathogens
 Author's personal copy
such as E. coli and S. enterica, adherence of C. jejuni to
enterocytes is not mediated by pili or fimbriae. It is medi-
ated by structures that are found on the cell surface of
C. jejuni. These structures include the following: (i) CadF
binds to fibronectin bound to the surface of enterocytes
and is required for invasion of the epithelium. (ii) The
fibronectin domain-containing lipoprotein FlpA
(Cj1279c) also binds to fibronectin. (iii) The surface-
exposed lipoprotein JlpA binds to heat shock protein 90
(Hsp90). (iv) Further examinations have shown that lipo-
protein Cj0091; periplasmic adhesion protein Cj0268c;
fibronectin/fibrinogen-binding protein Cj1349; the auto-
transporter proteins CapA and CapB; flagellin A (FlaA);
hemolysin TlyA/Cj0588; the major antigenic peptides
PEB1, PEB3, and PEB4; and p95 adhesin play a role in
C. jejuni adherence. Their binding sites on enterocytes and
the outcome of their binding to enterocytes are under
investigation.
(d) Invasion factors: The process of C. jejuni internalization into
enterocytes and associated factors has been a focus of
research over the last 20 years. To date, it has been estab-
lished that (i) internalization of C. jejuni into enterocytes
is an energy-dependent process and (ii) the bile salt, deox-
ycholate, present in the lower intestinal tract stimulates
C. jejuni to synthesize and secrete a set of proteins termed
as Campylobacter invasion antigens (Cia) which play a role
in internalization. C. jejuni synthesizes and excretes at least
eight Cia proteins, but presently, only four, namely, CiaB,
CiaC, CiaD, and CiaI, have been functionally character-
ized. In addition, some other C. jejuni proteins and host
cell factors like actin have been shown to play a role in
C. jejuni internalization.
(e) Survival strategies within host cells: Upon internalization,
C. jejuni survives and multiplies within enterocytes in
membrane-bound compartments that are commonly
referred to as Campylobacter-containing vacuoles (CCV).
Poor nutrition, low pH, and antibacterial molecules includ-
ing superoxide, hydrogen peroxide, halogenated oxygen
molecules, and lysosomal enzymes characterize the CCV.
Therefore, C. jejuni must have strategies to survive and
multiply in this hostile microenvironment. Currently,
three survival strategies have been identified. Firstly,
C. jejuni synthesizes Cia proteins, which enable it to survive
within enterocytes. For example, CiaI deviates CCV from the
canonical endocytic pathway, thus avoiding union of CCV
with lysosomes. Secondly, within enterocytes, C. jejuni
undergoes a significant metabolic downshift leading to the
downregulation of several metabolic pathways. Thus,
amino acid biosynthesis and biosynthesis pathways associ-
ated with prosthetic groups, fatty acids, lipids, pentose
phosphate, purine, and pyrimidine are downregulated, as
well as catabolic pathways associated with degradation and
utilization of amino acids and C1 compounds and path-
ways involved in the transport of nutrients, metal ions, and
amino acids. Thirdly, within eukaryotic cells, C. jejuni
changes its mode of respiration from a mode that uses
many terminal electron acceptors including oxygen, nitrate,
fumarate, nitrite, trimethylamine N-oxide (TMAO), and
dimethylsulfoxide (DMSO) to a mode that uses only the
readily available fumarate as the terminal electron acceptor
The Encyclopedia of Food and Health, (2016), vol. 1, pp. 596-601
Campylobacter: Health Effects and Toxicity 599
(fumarate respiration). However, its survival strategy against
toxic molecules remains unclear because unlike other intra-
cellular pathogens such as Salmonella typhimurium, catalase
does not make a contribution to its survival within epithe-
lial cells.
(f) Glycolipids: Glycolipids are lipids with covalently attached
carbohydrates whose function is to provide energy and
serve as markers for cellular recognition. C. jejuni has two
kinds of glycoproteins or lipid-bound polysaccharides:
lipooligosaccharides (LOSs) and capsular polysaccharides.
LOSs form a major part of the C. jejuni outer membrane.
They contain a terminal structure similar to the human
gangliosides GM1a and GM2, and in response to the
microenvironment in the enterocytes, LOSs undergo
phase variation with the terminal b-1,3-linked galactose
residue (Gla) being switched on or off creating diverse
strains in a population. LOSs play the following roles in
pathogenicity: (i) LOS phase variation promotes C. jejuni’s
ability to adapt to the enterocyte’s hostile environment, (ii)
LOSs mediate adherence and invasion, (iii) structural sim-
ilarity to human gangliosides GM1a and GM2 and phase
variation help in evasion of host immune response, and,
(iv) as explained in the section on C. jejuni enteritis and
postinfectious manifestations, LOS’s similarity to human
gangliosides GM1a and GM2 plays a role in the pathoge-
nesis of GBS.
The polysaccharide capsule is an external structure of
C. jejuni. Like LOSs, it undergoes phase variation, hence
playing a role in adherence, invasion, and evasion of the
host immune response. Also, it is important for the survival
of C. jejuni outside its natural host.
(g) Glycoproteins: Glycoproteins are proteins with carbohy-
drate residues that are covalently attached to the hydroxyl
(dOH) group of the R group of serine or threonine or the
amino group (dNH2) in the R group of asparagines in a
process called glycosylation. The former is known as
O-linked while the latter is known as N-linked. Proteins
may undergo glycosylation during or after translation.
C. jejuni has both glycosylation systems. The O-linked
system is diverse and adds pseudaminic acid and related
sugars to the immunodominant flagellin. As a result of its
association with the flagella, it is essential for adaptation to
changing host environment and evasion of host immune
response. The N-linked system is conserved and adds the
bacillosamine-containing heptasaccharide to over 30 pro-
teins. It plays a role in adherence, invasion, and enhance-
ment of the stability of virulence-associated proteins.
Host Defense
The human gastrointestinal tract poses two defenses against
Campylobacter invasion. These are the following:
(a) Microbiota barrier: The human gastrointestinal tract harbo-
rs a diverse group of genetically different commensal
microbial species. This group of microorganisms is collec-
tively referred to as microbiota. The dominant species in
microbiota of a healthy individual are from the following
genera: Lactobacillus, Veillonella, Bacteroides, Peptococcus,
Escherichia, Peptostreptococcus, Bifidobacterium, Eubacterium,
 Author's personal copy
600 Campylobacter: Health Effects and Toxicity
Fusobacterium, and Clostridium. However, these species vary
from one healthy individual to another due to age, genet-
ics, diet, and environment. These microorganisms live in
the lumen, the outer mucus layer, within intestinal crypts
and on the surface of the mucosal epithelial cells. Micro-
biota benefit the host in the following ways: breaking
down complex nonabsorbable compounds into simple
absorbable molecules, maturation of the immune system,
and maturation of the intestinal mucosa. In addition, the
microbiota plays an important role of defending the host
against invasion by all invading pathogens including
C. jejuni using the following strategies: first, competing
for niches and nutrients and, second, secreting bactericidal
metabolic by-products including reactive oxygen species,
short-chain fatty acids, and bacteriocins. This phenome-
non is known as colonization resistance or microbiota
barrier.
(b) Immune barrier: The human gastrointestinal tract is pro-
tected with both the adaptive and innate immune systems,
which complement each other. The adaptive immune sys-
tem is triggered when the presence of C. jejuni stimulates
the synthesis of interleukin 8 (IL-8). Consequently, IL-8
activates the maturation of macrophages, T-cells, and
B-cells, which clear the invading C. jejuni. The innate
immune responses are initiated when C. jejuni’s cell wall
structures are detected by nucleotide-binding oligomeriza-
tion domain-containing protein 1 (NOD1) or Toll-like
receptors (TLRs). The interaction of C. jejuni cell wall
structures and NOD/TLR activates nuclear factor kappa B
(NF-kB), which stimulates the production of various cyto-
kines that mediate maturation of dendritic cells (DCs) into
antigen-presenting cells (APCs). The APCs capture C. jejuni
and present them to the mature T-cells for elimination.
Current Model of Disease Pathogenesis
The process of campylobacteriosis establishment starts when
C. jejuni gets an opportunity to adhere onto enterocytes upon
the disruption of the microbiota barrier by diet or chemicals
such as antibiotics. For instance, studies that have been carried
out in humanized gnotobiotic mice to determine which com-
mensal microorganisms promote C. jejuni invasion have
shown that eating a typical Western diet such as pizza, cheese,
French fries, and burgers elevates the dominance of Escherichia
coli, Clostridium innocuum, Eubacterium dolichum, Catenibacter-
ium mitsuokai, and Enterococcus spp. and reduces the levels of
Bacteroides spp. and Prevotella spp. leading to campylobacter-
iosis. Once C. jejuni adheres to enterocytes, the flagellar type-
III-homologue secretion system releases Cia proteins that
facilitate C. jejuni internalization through M cells. The internal-
ization process is unique because it shares the characteristics of
both trigger and zipper mechanisms. Once internalized,
C. jejuni survives and multiplies in vacuoles avoiding clearance
by lysosomes. In response to the vacuolar environment,
C. jejuni synthesizes several proteins that damage the host
cells. During internalization, C. jejuni releases CDT, which
damages the DNA of the host cell leading to cell death and
activates the adaptive immune response. At the same time,
NOD and TLR recognize C. jejuni and activate the innate
immune response. The activities of both the adaptive and
The Encyclopedia of Food and Health, (2016), vol. 1, pp. 596-601
innate immune responses lead to local inflammation. While
the activities of Cia damage tight junctions leading to diarrhea.
Treatment
Usually, campylobacteriosis is a self-limiting disease that
requires no interventional treatment. In most cases, campylo-
bacteriosis patients are treated with fluid and electrolyte sub-
stitution (especially potassium). However, in severe cases
especially immunosuppression or HIV infection, patients
should be treated with antibiotics immediately if laboratory
results indicate a C. jejuni or C. coli infection. C. jejuni is usually
sensitive to macrolides, tetracyclines, aminoglycosides, carba-
penems, and chloramphenicol but increasingly resistant to
cotrimoxazole and fluoroquinolones. In spite of a wide range
of antibiotics available for the treatment of campylobacteriosis,
the macrolide erythromycin remains the antibiotic of choice.
See also: Campylobacter: Properties and Occurrence; Campylobacter:
Species Detection; Diarrheal Diseases; Escherichia coli and Other
Enterobacteriaceae: Food Poisoning and Health Effects; Escherichia
coli and Other Enterobacteriaceae: Occurrence and Detection;
Salmonella: Detection; Salmonella: Properties and Occurrence;
Salmonella: Salmonellosis; Yersinia enterocolitica: Properties and
Occurrence; Yersinia enterocolitica: Detection and Treatment;
Zoonoses.
Further Reading
Backert S, Boehm M, Wessler S, and Tegtmeyer N (2013) Transmigration route of
Campylobacter jejuni across polarized intestinal epithelial cells: paracellular,
transcellular or both? Cell Communication and Signaling 11(72): 1–15.
Bell C and Kyriakides A (2009) Campylobacter – a practical approach to the organism
and its control in foods, 1st ed. Hoboken: Wiley-Blackwell.
Benjamin J, Leaper S, Owen RJ, and Skirrow MB (1983) Description of Campylobacter
laridis, a new species comprising the nalidixic acid resistant thermophilic
Campylobacter (NARTC) group. Current Microbiology 8(4): 231–238.
Dasti JI, Tareen AM, Lugert R, Zautner AE, and Groß U (2010) Campylobacter jejuni: a
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Relevant Websites
http://www.bfr.bund.de/en/campylobacter-54347.html – Bundesinstitut für
Risikobewertung (English page).
http://www.cdc.gov/nczved/divisions/dfbmd/diseases/campylobacter/ – Centers for
Disease Control and Prevention – National Center for Emerging and Zoonotic
Infectious Diseases: Campylobacter.
http://chemweb.calpoly.edu/cbailey/377/PapersW03/Kileen/index.htm –
Campylobacter jejuni: The Most Common Cause of Food Poisoning by Kileen
Mershon.
http://www.efsa.europa.eu/en/topics/topic/campylobacter.htm – European Food Safety
Authority: Campylobacter.
http://www.fda.gov/Food/FoodborneIllnessContaminants/CausesOfIllnessBadBugBook/
default.htm – US Food and Drug Administration: Bad Bug Book (2nd ed.).
http://www.patient.co.uk/health/campylobacter – Patient.co.uk.