Download Colibacillosis

BVMS, MSC, PHD
College of Veterinary Medicine
University of Mosul
Definition
Colibacillosis refers to any localized or
systemic infection caused entirely or
partly by avian pathogenic Escherichia
coli including:
- Colisepticemia
- Coligranuloma ( Hjarre’s disease )
- Air sac disease ( chronic respiratory
disease, CRD )
-
Swolen – head syndrome
Venereal colibacillosis
Coliform cellulitis ( inflammatory process )
Peritonitis
Salpingitis
Orchitis
- Osteomyelitis/ synovitis ( turkey osteomyelitis complex )
- Panophthalmitis
- Omphalitis/ yolk sac infection
- Enteritis
Colibacillosis in mammals is most often a
primary enteric or urinary tract disease,
whereas colibacillosis in poultry is
typically a localized or systemic disease
occurring
secondarily when host
defenses have been impaired or
overwhelmed by virulent E. coli strains.
Strains of E. coli that cause disease outside
the intestinal tract of any species share
common characteristics and are called
extraintestinal pathogenic E. coli (ExPEC).
Most APEC are ExPEC and share
characteristics with mammalian ExPEC.
Etiology
The etiology of colibacillosis is Escherichia coli.
Other infectious agents and noninfectious factors
usually predispose a bird to infection or contribute
to the severity of the disease.
Escherichia is the type genus of the family
Enterobacteriaceae, which is composed of
organisms that can grow aerobically or
anaerobically and utilize simple carbon and
nitrogen sources
Gram-negative , Rod (bacillus) shape, Non-sporeforming, on MacConkey agar.
Incidence and Distribution
E. coli likely occur in most mammals and birds
although healthy psittacines may be an exception.
It is a common inhabitant in the intestinal tracts of
poultry at concentrations up to 106 E. coli/gram of
intestinal contents.
Higher numbers are found in younger birds, birds
without an established normal flora, and in the
lower intestinal tract.
Among normal chickens, 10–15% of intestinal
coliforms may belong to potentially pathogenic
serotypes although intestinal strains may not be the
same serotype as those from extra-intestinal sites in
the same bird
Egg transmission of pathogenic E. coli is common and
can be responsible for high chick mortality.
Pathogenic coliforms are more frequent in the
intestine of newly hatched chicks than in the eggs
from which they hatched, suggesting rapid spread
after hatching.
The most important source of egg infection seems to
be fecal contamination of the egg surface with
subsequent penetration of the shell and membranes.
Coliform bacteria can be found in litter and fecal matter.
Dust in poultry houses may contain 105–106 E. coli/g.
Age of Host Commonly Affected
All ages are susceptible to colibacillosis, but
young birds are more frequently affected and
severity of disease is greater in young birds,
including developing embryos.
Outbreaks can occur in caged layers and
coliform salpingitis/peritonitis is a common
cause of mortality in breeders.
Host Susceptibility Factors
Normal, healthy birds with intact defenses are remarkably
resistant to naturally occurring E. coli exposure including
virulent strains.
- Infection occurs when skin or mucosal barriers are
compromised (e.g., unhealed navel, wounds, mucosal damage
from viral, bacterial, or parasitic infections, lack of normal flora, etc.).
- The mononuclear-phagocytic system is impaired (e.g., viral
infections, toxins, nutritional deficiencies)
- There is immunosuppression (e.g., viral infections, toxins)
- Exposure is overwhelming (e.g., environmental contamination,
poor ventilation, contaminated water ).
- And/or birds are exposed to abnormal stress or have an
inappropriate response to stress
Incubation Period
The time between infection and onset of clinical signs
varies with the specific type of disease produced by E.
coli.
The incubation period is short, generally between 1
and 3 days, in experimental studies in which birds are
exposed to high numbers of virulent organisms.
In the field it is more common to see colisepticemia
5–7 days after infection with a predisposing agent
such as infectious bronchitis virus in chickens or
hemorrhagic enteritis virus in turkeys.
Clinical Signs
Clinical signs vary from inapparent to total
unresponsiveness just prior to death depending on the
specific type of disease produced by E. coli.
Localized infections generally result in fewer and milder
clinical signs than systemic diseases.
Coliform cellulitis is typically not detected until the birds
are processed.
Lameness and retarded growth are seen in birds with
skeletal lesions that develop as a sequel to sepsis.
When joints or bones of one leg are affected, birds walk
with a characteristic hopping motion to keep weight off of
the affected leg.
When the thoracolumbar spine is affected, the birds
have an arched back, sit on their hocks, and bear little
or no weight on their feet.
Birds with chronic lameness have caking of droppings
around the vent and on abdominal feathers. Feces are
green with white to yellow urates as a result of
anorexia and dehydration.
Young birds with omphalitis and infected yolk sacs also
may have difficulty in walking because of abdominal
distention, which alters weight distribution and
impairs balance.
Birds with colisepticemia are often terminally
moribund and the flock may be inactive and not
eating.
Decreased water consumption is associated with a poor
prognosis.
Severely affected individual birds are unresponsive
when approached, do not react to stimuli, and are easily
caught and handled.
They sit with their eyes closed in a hunched position
with drooping of the head, neck, and wings.
The beak may be inserted into the litter to support the
head.
Morbidity and Mortality
Both morbidity and mortality are highly variable
depending on the type of disease produced by E. coli.
It is probable that most, if not all, commercial flocks
experience some degree of morbidity, mortality, or
condemnation due to E. coli infections.
Mortality occurring during the day indicates a more
severe disease outbreak than when birds are only found
dead in the morning.
A flock that appears clinically normal when examined
during the day, but has an excess number of dead birds
the following morning, is a common finding in mildly
affected flocks.
This pattern is typical for egg layer and breeder flocks
experiencing coliform salpingitis/peritonitis.
Localized Forms of Colibacillosis
Coliform Omphalitis/Yolk Sac Infection
Omphalitis is an inflammation of the navel (umbilicus).
In birds the yolk sac is usually involved too because of its
close anatomic relationship.
Infection follows contamination of the unhealed navel
with APEC. Fecal contamination of eggs is considered to
be the most important source of infection.
Bacteria may be acquired in ovo if the hen has oophoritis
or salpingitis or via contamination following artificial
insemination.
Yolk sac infections also can result from translocation of
bacteria from the chick’s intestine or from the
bloodstream. In these cases the navel is not affected.
Omphalitis
Yolk sac infection
Some embryos may die before hatching, particularly
late in incubation; whereas others die at or shortly after
hatching.
Surviving infected chicks can be a source of E. coli for
other chicks in the same hatch.
The incidence of birds with omphalitis increases after
hatching and declines after about 6 days with occasional
losses continuing up to 3 weeks.
When birds become infected with low virulent strains
there may be no embryo or chick mortality or some may
survive although hatchability, chick livability, and
relative yolk weights may be affected ; the only
pathologic finding being retention of infected yolk sacs
containing caseated yolk.
Swelling, edema, redness, and possibly small abscesses
characterize acute inflammation of the navel.
The abdomen is distended and blood vessels are
hyperemic.
In severe cases the body wall and overlying skin undergo
lysis and are wet and dirty. These birds are referred to as
“mushy” chicks or poults.
There may be other nonspecific changes such as
dehydration, visceral gout, emaciation, vent pasting, and
enlarged gall bladder.
The yolk sac is typically distended because yolk has not
been absorbed and inflammatory products have been
added. Yolk is abnormal in color, consistency, and smell,
and may contain visible exudate. Blood vessels of the yolk
sac are often prominent
Chicks or poults with infected yolk sacs that live more
than 4 days also may have pericarditis or perihepatitis,
indicating systemic spread of the organism from the
yolk sac.
Consequences of yolk sac infection include deprivation
of nutrients and maternal antibodies, absorption of
toxins, and spread of E. coli by extension into the body
cavity or systemically to produce colisepticemia.
Survivors are usually stunted and do poorly.
Coliform
Cellulitis
Swollen Head Syndrome
Swollen head syndrome (SHS) is an acute to subacute
cellulitis involving the periorbital and adjacent
subcutaneous tissues of the head
Swelling of the head is caused by inflammatory exudate
beneath the skin that accumulates in response to
bacteria, usually E. coli, following upper respiratory viral
infections (e.g. avian pneumovirus, infectious bronchitis
virus).
Ammonia aggravates the disease.
Swollen Head Syndrome
Diarrheal Disease.
Primary enteritis is a common manifestation of E. coli
infections in mammals including human beings, but is
considered rare in poultry.
Intestinal E. coli in poultry have been poorly studied, so
our knowledge of the role that E. coli may play in
intestinal disease is limited.
Coliform
Salpingitis/Peritonitis/Salpingoperitonitis
Inflammation of the oviduct caused by E. coli results in
decreased egg production and sporadic mortality.
It is one of the most common causes of mortality in
commercial layer and breeder chickens.
Accumulations of caseating exudate in the body cavity
resemble coagulated yolk, which is the reason for the
common name “egg peritonitis.”
Salpingitis and egg binding may occur concurrently.
They are often confused with each other because they
both result in an obstructive mass within the oviduct.
Yolk peritonitis is a mild to moderate diffuse peritonitis
that results from free yolk in the body cavity.
Coliform Orchitis/Epididymitis/Epididymoorchitis
An ascending E. coli infection of the male reproductive
tract, analogous to that resulting in salpingitis in the
hen, occurs infrequently in roosters.
Testicles are swollen, firm, inflamed, irregularly shaped,
and have a mosaic of necrotic and viable tissue when
opened.
Systemic Forms of Colibacillosis
Colisepticemia
Presence of virulent E. coli in the blood stream defines
colisepticemia.
Characteristic features of colisepticemia at necropsy are tissues
that develop a green discoloration following exposure to air
and a characteristic odor, possibly related to indole produced
by the organism.
The bursa of Fabricius is often atrophic or inflamed as a result
of colisepticemia.
Pericarditis is common and is a characteristic of colisepticemia.
It is usually associated with myocarditis.
Vessels in the pericardium become increasingly prominent
because of hyperemia and the pericardium becomes cloudy
and edematous.
Initially fluid and soft masses of pale exudate
accumulate within the pericardial sac followed by
fibrinous exudate.
As the disease progresses exudate increases, becomes
more cellular (fibrinoheterophilic), and undergoes
caseation.
The pericardial sac adheres to the epicardium with
chronicity.
Respiratory-Origin Colisepticemia
E. coli gains access to the circulation following damage
to the respiratory mucosa by infectious or noninfectious
agents.
Infectious bronchitis virus (IBV) and Newcastle disease
virus (NDV), including vaccine strains, mycoplasmas, and
ammonia, are the most common predisposing agents.
Severity of the resulting disease, which is commonly
referred to as air sac disease, chronic respiratory
disease (CRD), or multicausal respiratory disease , is
directly related to the number of agents that are
involved.
Lesions are prominent in respiratory tissues (trachea,
lungs, air sacs), pericardial sac, and peritoneal cavities
and are typical of the subacute polyserositis stage of
colibacillosis.
Infected air sacs are thickened and often have caseous
exudate on the respiratory surface.
Enteric-Origin Colisepticemia
Enteric-origin colisepticemia is most common in turkeys.
E. coli gain access to the circulation and tissues following
damage to the intestinal mucosa by infectious agents.
The most common predisposing agent is hemorrhagic
enteritis virus.
Lesions are typical of the acute septicemic stage of
colibacillosis. Affected birds are in good physical
condition and often have full crops containing feed and
water.
The most characteristic lesions are congestion or green
discoloration of the liver, marked enlargement and
congestion of the spleen, and congested muscles.
Neonatal Colisepticemia
Chicks are affected within the first 24–48 hours after
hatching.
Mortality remains elevated for 2–3 weeks and usually
totals 10–20%. Up to 5% of the flock may be stunted
and require culling.
Unaffected birds grow normally and the disease does
not appear to spread.
Initial lesions consist of congested lungs, edematous
serous membranes, and splenomegaly.
The proventriculus and lungs develop a dark color that
can approach black as the interval between death and
necropsy increases.
Layer Colisepticemia.
Colisepticemia is usually a disease of young birds, but
occasional outbreaks of acute E. coli infection
resembling fowl typhoid or fowl cholera occur in mature
chickens and turkeys.
Acute colibacillosis in layers is being seen with increasing
frequency. The majority of outbreaks are associated
with onset of egg production, but less frequently they
occur at an older age, or may continue as the flock ages
and potentially spread to older flocks on the same farm.
Death usually occurred suddenly without premonitory
signs although depression and/or dirty vents were
observed in some affected hens in approximately half of
the flocks.
Weekly mortality was significantly higher in affected
flocks than age-matched control flocks (0.26–1.71% vs.
0.07-0.30 %).
Cumulative mortality ranged up to 10% and mortality
remained elevated for 3–10 weeks.
Polyserositis (perihepatitis, pericarditis) and peritonitis
associated with free yolk in the peritoneal cavity were
present in most birds at necropsy.
Oophoritis and salpingitis occurred less frequently.
The pathogenesis of the disease is unknown, but stress
associated with onset of egg production is believed to
be an important contributing factor.
Panophthalmitis.
Involvement of the eye is uncommon, However, if it is
infected the resulting panophthalmitis is severe.
Typically there is hypopyon and hyphema, and infection
is unilateral. The eye is swollen, cloudy to opaque, and
may be hyperemic initially. Later the eye shrinks as it
undergoes atrophy.
Fibrinoheterophilic exudate and numerous bacterial
colonies are present throughout the eye. Inflammation,
especially adjacent to necrotic tissue, becomes
granulomatous with time. Varying degrees of retinal
detachment, retinal atrophy, and lysis of the lens also
may be seen.
Coligranuloma (Hjarre’s Disease).
Coligranuloma of chickens and turkeys is characterized by
multiple granulomas in liver, ceca, duodenum, and
mesentery, but not spleen.
Coligranuloma is an uncommon form of systemic
colibacillosis that usually occurs sporadically in individual
birds, but can cause mortality as high as 75% when a flock
is affected.
Serosal lesions resemble leukosis tumors.
Diagnosis
Isolation and Identification of Causative Agent
Differential Diagnosis
Acute septicemic diseases may result from pasteurellae,
salmonellae, streptococci, and other organisms.
Chlamydiophila, pasteurellae (Pasteurella,
Ornithobacterium, Riemerella), or streptococci
(Streptococcus, Enterococcus) sometimes cause pericarditis
or peritonitis and other bacteria, mycoplasmas, and
Chlamydiophila can cause airsacculitis.
Treatment
Antimicrobial Drugs
When selecting an antimicrobial to use for
treatment, it is important to determine the
susceptibility of the isolate involved in the disease
outbreak so that ineffective drugs can be avoided.
Even a highly effective drug may not result in improvement
of the flock if too little is used or it is incapable of
reaching the site of infection. Therefore, underdosing may
promote development of resistance.
Other Treatments
The declining use of antibiotics for prevention and
treatment of colibacillosis has stimulated interest in
alternative methods including prebiotics, probiotics,
enzymes, digestive acidifiers, vitamins, immune
enhancers, anti-inflammatory drugs, and other
antimicrobial products.
Essential oils often have substantial inhibitory effect on
E. coli in vitro and in the lower intestinal tract of
chickens.