genus campylobacter jenjuni and coli for

camp

1. Genus Campylobacter

2. General Characters
Campylobacter species are Gram negative,
slender (0.2 to 0.5 um wide), curved, motile
rods.
Gram-negative curved rods with comma, S, or
“gull-wing” shapes.
Daughter cells which remain joined have a
characteristic gull-winged appearance and
long spirals formed by joined cells also occur.
Motile, with a single polar flagellum
These microaerophilic organisms grow best
on enriched media in an atmosphere of
increased C02 and decreased oxygen tension.
Many Campylobacter species grow on
MacConkey agar.
They are non-fermentative and oxidase-
positive and have variable catalase reactions.
No spore and no capsule
C fetus subspecies fetus and C fetus subspecies
venerealis are structurally unusual as they
possess a S Layer /Microcapsule.
Campylobacter:
Corkscrew-like
motility/Darting
motility
Vibrio:
Rapid darting
(“Shooting
Star”) motility
Listeria:
Tumbling and
rotating

3. Usual Habitat
Campylobacter species are found in the intestinal and genital
tracts of domestic animals and are widely distributed
geographically.
The principal disease conditions associated with infection are
either intestinal, presenting as diarrhoea, or genital, causing
infertility or abortion.
Campylobacter species were previously classified in the genus
Vibrio, and the term 'vibriosis' has been retained for some of
the disease conditions which they cause.
Three species, namely C. fetus subspecies venerealis, C. fetus
subspecies fetus and C. jejuni subspecies jejuni are recognized
pathogens of veterinary importance.
A number of other species, some of which have been assigned
to the genus Arcobacter, have been isolated from domestic
animals and from humans.
The pathogenicity of these species has not been clearly
established.

4. Usual habitat
Many Campylobacter species are commensals in the intestinal
tracts of warm-blooded animals.
Campylobacter jejuni and C. lari (formerly C. laridis) colonize the
intestines of birds, which can result in faecal contamination of
water courses and stored food.
A number of Campylobacter species are excreted in the faeces
of pigs.
Campylobacter fetus subspecies venerealis appears to be
adapted principally to bovine preputial mucosa.

5. Important Veterinary Pathogens

6. Species of less importance

7. Differentiation of Campylobacter species
Campylobacter species are strictly microaerophilic, requiring an
atmosphere of 5 to 10% oxygen and 1 to 10% C02 for growth.
A selective enriched medium such as Skirrow agar is usually used
for primary isolation.
Differentiation of isolates is based on colonial morphology and
certain cultural, biochemical and antibiotic-susceptibility
characteristics.
Colonial morphology:
Campylobacter fetus subspecies venerealis and C. fetus
subspecies fetus have small, round, smooth, translucent colonies
with a DEWDROP APPEARANCE.
Campylobacter jejuni produces small, flat, grey colonies with a
SPREADING, WATERY APPEARANCE.
Colonies of some Campylobacter species, which may
contaminate clinical specimens, can be slightly pigmented.
Because Campylobacter species do not ferment carbohydrates,
other metabolic activities of these organisms must be used for
identification.

8. Pathogenesis and pathogenicity
Campylobacter fetus subspecies venerealis and C. fetus
subspecies fetus are structurally unusual in that they possess a
microcapsule or S layer, which consists of highmolecular-weight
proteins arranged in a lattice formation.
This S layer confers resistance to serum-mediated destruction
and phagocytosis (Blaser and Pei, 1993) and enhances survival in
the genital tract.
Virulence factors attributed to C. jejuni include soluble
components with enterotoxin-like activity and poorly defined
mechanisms for attaching to and invading host enterocytes.
The contribution of heat stable endotoxin to the pathogenesis of
campylobacteriosis is uncertain.

9. Toxins of C jejuni
Enterotoxins:
 C. jejuni secrete a toxin with similar activity to cholera toxin and
Heat labile toxin (LT) of E. coli
This toxin increase intracellular cAMP levels and cause
cytoskeletal rearrangements
Both toxins immunologically related
Binds to the same ganglioside (GM1) on target cell surfaces
C. coli & C. lari produce toxins with cytotonic & cytotoxic activity
Cytotoxins:
•A heat and trypsin labile protein of 70 Kda in size
•70 Kda cytotoxin neutralized by antibodies to Shiga like toxin
•Cia, 73 Kda protein inserted into target epithelial cell allowing
subsequent invasion of the cell
•A protein active on Vero tissue culture cells
•A cytolethal distending Toxin which increases intracellular cAMP
followed by cell death
•A protein having haemolytic activity (Haemolysin)
•A protein that induce Hepatitis in Mice (Hepatotoxin)

10. Growth characteristics
Colonies of C. fetus subspecies fetus and C fetus subspecies venerealis –
DEW DROP APPEARANCE
Colonies of C. jejuni – SPREADING WATERY APPEARANCE
Campylobacters require microaerophilic conditions for growth
Commercially available generators supply 6% O2, 10% CO2 & 84% N2
Most pathogenic species grow optimally at 37oC
C. jejuni require 5 days at 42C for optimal growth
Colonies of C jejuni – Spreading watery appearance

11. Growth requirements
Enrichment broth:
Bolton broth
Preston broth
Thioglycollate broth also used
Blood added to most of the enrichment media
FBP (Ferrous sulphate, Na metabisulphite, Na pyruvate)
supplement used if blood not available
Selective media used are
Skirrow’s selective medium
Butzler’s selective medium
Blaser-Wang selective medium

12. Campylobacter species differentiation

13. Specimen Collection and Processing:
Feces refrigerated and examined within few hours
Rectal swabs in semisolid transport medium
Blood drawn for C. fetus
Care to avoid oxygen exposure
Selective isolation by filtration of stool specimen
Enrichment broth and selective media
Filtration: pass through 0.45 μm filters
Microscopy:
Gull-wing appearance in Gram stain
Darting motility in fresh stool (rarely done in clinical lab)
Fecal leukocytes are commonly present
Identification:
Growth at 25
o
, 37
o, or 42-43
o
C
Hippurate hydrolysis (C. jejuni is positive)
Susceptibility to nalidixic acid and cephalothin
Laboratory Identification

14. Diagnostic procedures
Irrespective of the source of specimens for bacterial isolation,
certain general principles relating to culture techniques apply.
Campylobacter species require microaerophilic conditions for
growth, usually supplied by commercially-available generator
envelopes which deliver 6% oxygen, 10% carbon dioxide and 84%
nitrogen.
Although most pathogenic species grow optimally at 37
0
C, C.
jejuni requires up to 5 days at 42°C for optimum growth.
Smears from cultures and from clinical specimens should be
stained with dilute carbol fuchsin (DCF) for 4 minutes. This
method stains the organisms more intensely than the Gram
method.
Identification criteria for isolates:
Growth only under microaerophilic conditions
Colonial morphology
Cell morphology in smears stained with DCF or by
immunofluorescence
Metabolic characteristics and antibiotic susceptibility pattern.

15. Clinical infections
The most
important
consequences of
infections with
organisms in this
group are
infertility in
cattle due to C.
fetus subspecies
venerealis and
abortion in ewes
caused either by
C. fetus
subspecies fetus
or by C. jejuni.

16. Bovine genital campylobacteriosis
Campylobacter fetus subspecies venerealis, the principal cause of bovine genital
campylobacteriosis, is transmitted during coitus to susceptible cows by
asymptomatic carrier bulls.
The bacteria survive in the glandular crypts of the prepuce and bulls may
remain infected indefinitely.
The disease is characterized by temporary infertility associated with early
embryonic death, return lo oestrus at irregular periods and, occasionally, by
sporadic abortion.
About one-third of infected cows become carriers.
Campylobacter fetus subspecies venerealis persists in the vagina of carrier
cows, a feature attributed to antigenic shifts in the immunodominant
antigens of the S layer proteins.
Extension of infection to the uterus with the development of endometritis
and salpingitis can occur during the progestational phase of the oestrus cycle
when both the numbers and the activity of neutrophils decline.
The infertile period following uterine invasion can last for 3 to 5 months, after
which natural immunity may develop.
IgA antibodies, which predominate in the vagina, limit spread of the infection.
IgG antibodies produced in the uterus opsonize the pathogens, facilitating
phagocytosis by neutrophils and mononuclear cells.
This natural immunity may last for up to 4 years.
Campylobacter fetus subspecies fetus, an enteric organism acquired by
ingestion, can cause sporadic abortions in COWS.

17. Diagnosis
Investigation of the breeding records and vaccination history of an
affected herd may suggest campylobacteriosis.
Campylobacter spp. can be detected by fluorescent antibody test in
sheath washings from bulls or cervico-vaginal mucus from cows.
Isolation and identification of C. fetus subspecies venerealis from
preputial or vaginal mucus is confirmatory.
Specimens of mucus should be placed in special transport medium
(Amies Medium/ Cary Blair medium).
Vaginal mucus agglutination test detects about 50% of infected,
infertile cows on a herd basis.
An ELISA can be used to demonstrate IgA antibodies in vaginal
mucus after an abortion.
A PCR has been developed as a rapid screening test for detection
of C. fetus subspecies venerealis in bull's semen.
Infertility due to C. fetus subspecies venerealis must be
differentiated from other causes of infertility in cows.
Campylobacter sputorum biovar sputorum, a commensal which is
sometimes isolated from preputial washings, is of no clinical
significance in cattle.

18. Treatment and control
Dihydrostreptomycin, administered either systemically or
topically into the prepuce, is used for treating bulls.
Intrauterine administration of dihydrostreptomycin can be used
therapeutically.
Vaccination with bacterins in an oil emulsion adjuvant is used
therapeutically and prophylactically in problem herds.

19. Ovine genital campylobacteriosis
Campylobacteriosis in ewes may be caused by either C. fetus
subspecies fetus or C. jejuni.
The disease is worldwide in distribution and is one of the most
common causes of ovine abortion in some countries.
Campylobacter fetus subspecies fetus is found in the faeces of cattle
and sheep and C. jejuni may be present in the faeces of a wide range
of birds and mammals.
Transmission Of Both Of These Organisms Is By The Faecal-oral
Route.
During pregnancy, localization in the uterus of susceptible ewes
may occur following bacteraemia. The subsequent necrotic
placentitis may result in abortion late in pregnancy, stillborn lambs
or weak lambs.
Round, necrotic lesions up to 2 cm in diameter with pale raised rims
and dark depressed centres are evident on the liver surface in some
aborted lambs.
Aborting ewes are major sources of infection for susceptible
animals in a flock.
Up to 20% of ewes in a susceptible flock may abort.
Recovered ewes are immune for at least 3 years and flock fertility
in subsequent breeding seasons is usually good.

20. Diagnosis
Typical hepatic lesions in aborted lambs are PATHOGNOMONIC.
A presumptive diagnosis is made by demonstrating the organisms in
foetal abomasal contents or birth fluids.
Isolation and identification of C. fetus subsecies fetus or C. jejuni is
confirmatory.
These pathogens should be differentiated from other causes of
abortion in ewes .
Treatment and control
Aborting ewes should be isolated and placentae and aborted foetuses
promptly removed.
The remainder of the flock should be moved to clean pasture.
Vaccination of ewes with a C. fetus ssp fetus bacterin, after
confirmation of the disease in a flock, is reported to reduce the
number of abortions.
Routine vaccination of ewes with a bacterin is usually carried out
immediately before or after mating, with a booster after the second
month of gestation and annually thereafter.
There is no cross-protection between C. fetus subspecies fetus and C.
jejuni.
Chlortetracycline administered daily in feed has been used to control
outbreaks of abortion.

21. Intestinal campylobacteriosis in dogs
Diarrhoea in dogs and other domestic animals has been
attributed to infection with Campylobacter species, particularly
C. jejuni.
Confirmation is difficult because healthy animals may shed
Campylobacter species in their faeces.
However, the presence of large numbers of campylobacter-like
organisms in DCF-stained faecal smears or rectal scrapings from
dogs with diarrhoea may be indicative of infection.
Campylobacter species may contribute to the severity of enteric
disease in dogs infected with other enteropathogens such as
enteric viruses, Giardia species and helminths.
Young, debilitated or immunosuppressed animals are
particularly at risk.
Enrofloxacin is usually effective in eliminating faecal shedding
of Campylobacter species.
Dogs shedding C. jejuni are a potential source of human infection.

22. Avian vibrionic hepatitis
Birds commonly harbour C. jejuni in their intestinal tracts and
shed the organisms in their faeces.
Chicks acquire infection from feed, water and litter when they
are first introduced into contaminated premises.
Infection in chickens and turkeys is usually asymptonlatic and its
principal importance is as a source of infection for humans
following carcass contamination at slaughter.
Outbreaks of disease, which are uncommon, are characterized
by a substantial drop in egg production in the flock.
Severely affected birds are listless and lose condition.
There may be haemorrhage and multifocal necrosis in livers.
A presumptive diagnosis is made by demonstrating curved rods
with darting motility in bile, using phase contrast microscopy.
Dihydrostreptomycin sulphate should he administered in the
food early in an outbreak of disease.

23. Intestinal campylobacteriosis in humans
C. jejuni is the main cause of human intestinal campylobacteriosis
and Campylobacter infection is the most frequent cause of food
poisoning in many countries.
Campylobacter coli and C. lari are sometimes implicated.
These zoonotic infections are usually food-borne.
Poultry meat is a major source of human infection.
Fever, abdominal pain and diarrhoea, sometimes with blood,
are the most common manifestations of this enteric infection.
In addition, antimicrobial resistance in campylobacters,
particularly to fluoroquinolones, is a major public health
concern.

24. Low incidence potential sequela
Reactive, self-limited, autoimmune disease
Campylobacter jejuni most frequent antecedent pathogen
Immune response to specific O-antigens cross-reacts with
ganglioside surface components of peripheral nerves
(molecular or antigenic mimicry)
Acute inflammatory demyelinating neuropathy (85% of cases)
from cross reaction with Schwann-cells or myelin
Acute axonal forms of GBS (15% of cases) from molecular
mimicry of axonal membrane
Guillain-Barre Syndrome (GBS)