Pasteurella multocida

in liver imprint from

chicken with acute FC
(note bipolarity).
Wright’s stain, 2500.
Acute FC; mucous
excretion from the
mouth contains
large numbers of
Pasteurella
multocida that can
contaminate feed
and water.
Chronic FC; swollen wattle
resulting from localized
infection.
Chronic FC; serous
inflammation of
conjunctiva.
A. Acute FC; subepicardial B. B. Acute FC; multiple
hemorrhages in a turkey. necrotic foci in turkey liver.
 C. Acute FC; turkey lung
with extensive
hemorrhage and patchy
areas of necrosis (arrow)
and emphysema.

D. Submassive necrosis
with fibrous exudate
on pleural surface.
 E. Acute FC; flaccid ovarian
follicle (arrow) with thecal
blood vessels less evident
than normal.

F. Chronic FC; caseous

exudate in sternal bursa
(A) and hock joint (B) of
a turkey.
 Pathogenicity
It is variable depending on the strain, host species, and
variation within the strain or host and conditions of
contact between the two.
The a ability of P.m to invade and reproduce in the
host is enhanced by the presence of capsule .loss of
ability of a virulent strain to produce the capsule
results in loss of virulence. Many isolates from cases
of FC have large capsules but are of low virulence.
Therefore virulence is apparently related to some
chemical substance associated with the capsule rather
than with its physical presence.
p. multocida usually enters tissues of birds through
mucous membranes of the pharynx or upper air
passages also may enter through the conjunction of
coetaneous wounds. So the portal of infection is the mm
of mouth and pharynx but not the esophagus, crop or
proventriculus also the Eustachian tube was suggested
as the most likely route of infection turkeys are more
susceptible than chickens. and mature chickens are
more susceptible than young ones. Heavy losses were
observed in mature chickens but no losses in birds up to
16 weeks age.
 Natural and experimental hosts
Most reported outbreaks of FC affected chickens
turkeys ,ducks. Or geese. However this disease also
affects other types of poultry , game birds raised in
captivity, companion birds, birds in zoos, and wild birds.
Among types of poultry turkeys are most affected. The
disease usually occurs in young mature turkeys, but all
ages are highly susceptible.
Death losses from FC in chickens usually occur in laying
flocks, because birds of this age are more susceptible than
younger chickens. Chickens less than 16 week of age
generally are quite resistant.
In ducks losses usually occur greater than 4 weeks age
and mortality many reach 50%
 Mode of infection and transmission
Chronically infected birds are considered to be a major
source of infection. The only limit to the duration of the
chronic carrier state is the life span of the infected bird.
Free – flying birds having contact with poultry may be a
source of FC organisms.
Transmission of the organism through egg is seldom
(pigs, dog, cat)
Most species of farm animals(pigs, dog, cat)
may be carriers of P. multocida
Contaminated crates, feed bags any equipments used
previously for poultry may serve in introducing FC into a
flock
Organisms are disseminated throughout the carcasses of
birds that die of acute FC and may serve as an infection
source, especially because birds tend to consume such
carcasses
Sparrows, pigeons, and rats could become infected with
P. multocida when exposed to chickens with FC and that
they in turn could infect susceptible chickens
Insects may serve as vectors of FC
Dissemination of P.mulbocida within a flock is primarily
by excretions from the mouth, nose and conjunctiva of
diseased birds that contaminate their environment
particularly feed and water. Feces seldom contain viable
P.multocida as P.multocida inactivated in proventriculus.
 .Signs and lesions
Acute: signs of infection in acute FC are often present
for only a few hours before death. Unless infected birds
are observed during this period, death may be the first
indication of disease. Signs that often occur are fever,
anorexia, ruffled feathers, mucous discharge from the
mouth, diarrhea and increased respiratory rate –
Cyanosis often occurs immediately prior to death and
most evident in unfeathered areas of head, such as comb
and wattles. Fecal material associated with the diarrhea
is initially watery and whitish in color but later become
greenish and contains mucus
Chronic FC may follow an acute stage of the disease or
result from infection with organisms of low virulence.
Signs generally are related to localized infections,
wattles, Sinuses, leg or wing joints, foot pads and
sternal bursas often become swollen. Exudative
conjunctiva pharyngeal lesions may be observed and
tarticollis sometimes occurs. Tracheal rales and
dyspnea may result from respiratory tract infection.
 Gross lesions
Lesions of FC are not constant but vary in type and
severity. The greatest variation is related to the course
of the disease
P.M of acute stage
When the course of the disease is acute, most of the P.
M lesions are associated with vascular disturbances,
general hyperemia usually occurs is most evident in
veins of the abdominal viscera. Petechial hemorrhages
are frequently found and may be widely distributed,
hemorrhages in the lung and abdominal fat, increased
amount of pericardial and peritoneal fluid.
livers may be swollen and usually contain multiple
small focal areas of coagulative necrosis.
Ovaries of laying hens are commonly affected, mature
follicles often appear flaccid; theacal blood vessels
which are usually easily observed are less evident.
Yolk material from ruptured follicles may be found in
the peritoneal cavity. Immature follicles and ovarian
stroma are often hyperemic
 Chronic
Chronic FC is characterized by localized infections. They
often occur in the respiratory tract and may involve any
part, including sinuses and pneumatic bones. Pneumonia
is an especially common lesions in turkeys. Infection of
the conjunctiva and adjacent tissues occurs and facial
edema may be observed
localized infection may also involve joints ,foot pods,
peritoneal cavity
chronic localized infection may include the middle ear
and cranial bones and have bean reported to result in
tortiticollis
chronic localized infection may also involve wattles
(wattle form) in which wattles are severely swallen and
edematous.
 Diagnosis
p. multocida can be isolated readily from viscera of birds
that die of acute FC and usually from lesions of chronic
cases. A tentative diagnosis of acute of stage can be
make by demonstrations of bipolar organism in livers
imprint using wright stain
Immunofluorescent microscopy can be used to identify
p.multocida in tissue or exudates
Bon marrow ,heart blood, liver meningens or localized
lesions are preferred for culturing , then to peptone broth
and streak on dextrose starch agar containing 5% chicken
serum also MacConkey agar or blood agar can be used
Inoculation of animals may be used as an aid in
isolation ,rabbits hamster or mice are inoculated slc or
intra peritoneal with 0.2 exudates or minced tissue ,if
p.m is present the animal usually dies within 24- 48
hours and the organism can be isolated in pure cultures
from heart, blood or liver.
serologic diagnosis of FC by rapid whole blood
agglutination; serum plate agglutination . agar diffusion
test or ELISA ,has limited value with the acute form of
the disease.
 Prevention and control

Unlike many bacterial diseases FC is not a disease of

the hatchery.
Infection therefore, occurs after birds are in the hands
of the producers, and consideration must be given to
the many ways that infection might be introduced into
a flock.
 Immunization
- Vaccination should be considered in areas where FC is
prevalent, but it should not be substituted for good
sanitary practice
- Commercially produced bacterins and live vaccines
are available. Bacterins usually contain whole cells of
serotypes 1.3 or 4 emulsified in an oil adjuvant.
Because bacterin will not provide protection against
FC challenge from a serotypes not contained in that
bacterin an autogenous whole cell bacterin containing a
locally isolated strain other than serotyps 1,3 and 4 may
be used.
Available live vaccines CU (clemson university), a
strain of low virulence ; m-9 a mutant strain of CU
vaccine very low in virulence and PM-1, a mutant of
CU strain and intermediate in virulence between CU
and M-9
-Vaccination of chickens and turkeys with these live p-
multocida vaccines induces protection against
heterologous serotype challenge
-There have been many successful vaccination protocols
for chickens breeders against FC. Bacterins, live vaccines
or both are used and usually, two doses are given: The
first at 8-10 weeks of age and second 18-20 weeks of age
some of the more commonly used vaccination programs
consist of administration of a live vaccine in the wins web
at 10-12 week of age yellowed by either live vaccine or
bacterin at 18-20weeks of age
-Vaccination with live vaccine produce protection against
multiple serotypes but it may induce chronic fowl cholera.
The use of bactein at 10-12 weeks and a live vaccine at
18-20 weeks of age just prior movement to the laying
house, gives protection against multiple serotypes and
minimizes live vaccine induced chronic FC.