Colibacillosis

• Avian collibacillosis first described in 1894

• Caused by Escherichia coli
• The species is the normal inhabitant of the
digestive tract of mammals and birds and most
strains are not pathogenic
• There rare 100s of serotypes of E.coli
• Only a few Escherichia coli are true pathogens
• These are classified on the basis of various surface
antigens which are
• O (somatic) antigen- endotoxin liberated
• K (capsular) antigen- polymeric acid present
on the surface
• H (flagellar antigen)
• F(fimbrial or pilus) antigen- involved in
attachment to cell
• Three serotypes: 01:K1(L); 02:K1(L);
078:K80(B) have been identified
 Epizootiology
• E. coli is present n the intestine of birds and
mammals and disseminated widely in faeces
• Birds are exposed through contaminated faeces,
water, dust and environment
• These are associated with enteric disease,
referred as enteropathogenic, enterotoxigenic or
enterotoxic
• They are important cause of diarrhoea in
humans, pigs, cattle , sheep and horses
 Diseases caused by E.coli
• Colisepticaemia
• Egg peritonitis
• Yolk sac infection(Omphalitis)
• Coligranuloma(Hjarre’s disease)
• Collectively grouped under colibacillosis
 Colisepticaemia
• The disease is usually seen in young growing
chickens especially broilers
• It is most serious form of colibacillosis
• Coccidiosis, viral infections, Ranikhet disease or
infectious bronchitis, infectious bursal
disease(IBD) Mycoplasma gallisepticum infection
and nutritional deficiencies predispose bird to
disease
• Mortality vary from 5-10% occasionally>50%
 Etiology
• E coli belonging to serogroups 01, 02, 035 and
078 especially strains 078:K80 and 02:K1
• Gram negative bacteria, 3 µ long, motile
• Ability to ferment lactose producing pink
colonies on MacConkey’s agar compare to
Salmonella
 Spread
• E. coli persist for long periods outside the
body in dry , dusty conditions
• Faecal contamination of the eggs may result in
penetration of E. coli throught the shell and is
most important source of infection
• Ovarian infection or salpingitis
• Associated with heavy mortality during hatch
and may give rise to yolk sac infection
 Pathogenesis
• E. coli found in digestive tract of poultry
• The infection occurs when pathogenic E.coli enters
through respiratory tract when mucosal barrier are
compromised
• eg. damaged from viral, bacterial or parasitic
infections, toxins, ammonia fumes, poor ventilation,
nutritional deficiencies, overcrowding, immuno
suppression, poor litter condition, extreme
temperature cause deciliation of upper respiratory
tract
 Clinical Signs
• Birds of 4-12 weeks of age are usually affected
• First sign is drop in feed consumption,
depression, dyspnoea
• Listless, ruffled feathers and develop laboured
breathing and making sharp sound- snicking
• Morbidity can be uto 50% and mortality vary
 Lesions
• Airsacculitis, cellulitis, peritonitis, enteritis, salpingitis
fibrinousperihepatitis, and pericarditis
• Air sac membrane become thicker and cloudy in
appearance
• Liver may show a thin covering of fibrinous exudate
• Pneumonia and pleuropneumonia
• omphalitis, & Salpingitis- The naval is swollen and
inflammed
• Peritonitis is characterized by acute mortality, fibrin and
free yolk
• Liver, spleen, lungs and kidneys are dark and
congested
• The air sacs are thickened, opaque, and with
caseous deposit
• A fibrinous pericarditis with pericardial sac
thickened
• The surface of liver is covered by thin layer of
fibrinous material
• Enteritis often with excessive mucus
Collibacillosis: PM Lesions
 Diagnosis
• PM examination- typical lesions
• Isolation and identification of organisms from
lungs, heart, liver and air sacs
• ELISA
• PCR
 Egg peritonitis
• A number of reproductive disorders of poultry
• Peritonitis, salpingitis(inflammation of oviduct)
• Impaction of oviduct
• Post mortem examination reveal egg debris,
inspissated yolk, caseous material, or milky
fluid in abdominal cavity
• Inflammation and distortion of the ovaries
• Rupture of oviduct wall
• Small number of death in layers
• Flock peritonitis may result from vent pecking
and egg peritonitis
 Yolk sac infection
• Mushy chick disease, omphalitis
• Most common cause of mortality in chicks during
the first week after hatching
• Yolk sac infection associated with inflammed
navel or multiplication of bacteria in hatching
eggs following faecal contamination of the shell
• Other bacteria like Bacillus cereus, Staphylococci,
Pseudomonas, Proteus and Clostridia can also
cause yolk sac infection
 Clinical Signs and lesions

• Affected chicks have distended abdomens and

tendency to huddle
• Navel visibly thickened, prominent and
necrotic
• Subcutaneous and yolk sac blood vessels
engorged and dilated
• Lungs congested
• Liver and kidneys dark and swollen
• Inflammed unabsorbed yolk sac
• Yolk being abnormal in colour and consistency
• Yolk may be yellow and inspissated or brown
green and watery with fetid, foul smelling
• Peritonitis with haemorrhages on the serosal
surfaces of intestines
 Coligranuloma(Hjarre’s disease)
• Caused by 04,08 and 016
• Nodules(granulomas) occur along the
intestinal tract, mesentery and in the liver
• Causes sporadic death in adult hens
• The clinical signs are nonspecific
• Affected birds are found dead or die after
depression and loss of condition
• Post mortem examination shows hard, yellow,
nodular granulomas in the mesentery and wall
of intestine particularly of caeca, small
intestines
• Microscopically caseous nodule in the centre
and lymphocytes and giant cells around
necrotic centre like in tubercular nodule
• Bumble foot
• Peritonitis
• Airsacculitis- Respiratory signs occur and vary inseverity,
may be associated with dusty litter, stress, poor ventilation,
thickened air sacs accompnaies with fibrinous pericarditis
and prihepatitis
• Synovitis and arthritis: Affected birds are lame or
recumbent, swelling of one ore more tendon sheaths or
joints
• Synovitis is caused by Reovirus, Mycoplasma, Staphylococci
and Salmonella
 Fowl cholera
• Avian pasteurellosis, avian cholera and avian
haemorrhagic septicaemia
• Infectious and Contagious disease affecting
domestic and wild birds
• Chickens, turkeys, geese, ducks, quails, wild
and zoo birds
• Identified as a disease of poultry for >200yrs
 Etiology

• It is caused by Pasteurella multocida, 16

serotypes identified
• Gram negative, capsulated, bipolar, nonmotile
bacteria
• Grows readily in blood agar
• Encapsulated strains are highly virulent
• P. multocida easily destroyed by many
disinfectants and by sunlight, heat and drying
• World wide in distribution, has been
recognized for more than 200 years
• Pasteur isolated the organisms 100 years ago
and used it in one of the first vaccines
• All species of birds are susceptible
• Ducks and geese are highly susceptible
• Adult birds and late growing stage are more
susceptible than younger stock
• Poultry, geese, ducks, turkeys, guinea fowl,
pigeons
• In peracute form it is most virulent and highly
infectious disease
 Spread

• Recovered birds remain as Carrier birds and

diseased birds can spread
• Excretions and carcasses of birds died of infection
• Rats are reservoir for P. multocida
• Airborne infection do occur between pens
• Spread through water and feed troughs,crates feed
bags shoes and equipments
• Oral, nasal, conjunctival routes and through
wounds
 Pathogenesis
• Depend on strain, host species and
environment condition
• Virulence is due to fimbriae, a polysacharide
capsule, , endotoxin(lipopolysacharide), and
leukotoxin
• P. multocida enters tissues through mucous
membranes of the pharynx, conjunctiva or
cutaneous wounds
 Clinical Signs
• Occurs in peracute, acute, chronic, and localized form
• In peracute form there is no warning signs and large no.
birds are found dead but in good bodily condition
• In acute form marked depression, anorexia, mucus
discharges from the orifices, rales, cyanosis of comb
and wattle, nasal and oral discharges and fetid(foul
smelling) green mucoid diarrhoea
• Mortality increases, laying chickens found dead on the
nest
• Fever prostration and drooling of saliva
• In chronic form oedema of comb, wattle, foot
pad and joint
• The chronic form occurs in birds which survive
from acute disease
• Over all clinical signs include depression,
conjuntivitis, dyspnoea and in few cases
swelling of the joints, lameness, torticollis and
swelling of wattles
Fowl cholera
 Lesions
• Gross lesions in peracute and acute forms include
marked congestion of the carcass, multiple
petechial and echymotic haemorrages throughout
viscera(gizzard muscle, heart, proventriculus and
serosa of intestines and abdominal fat)
• Enlargement and dark colouration and multiple pin
point necrotic foci in liver and spleen
• In laying hens, free yolk may be present in the body
cavity
• Enteritis is constant feature
• Lungs congested and pneumonia
• In subacute disease oedema of lungs, pneumonia and
perihepatitis are seen
• Chronic lesions include caseous arthritis of hock and
foot joints and wattles and comb with cheesy or thick
pus
• Swelling and induration of one or both wattles
• In histopathology congestion , bipolar organisms in
tissue sections and infiltration of heterophils
 Diagnosis
• Clinical observations
• PM examinatiuon
• Isolation and identification of P. multocida
• Impression smears of the liver heart show bipolar
organisms with methylene blue
• Animal inoculation in mice or rabbits death in 24-48
hrs
• ELISA
• PCR
 Infectious coryza(Fowl coryza)
• Infectious coryza is an acute, highly contagious
disease of the upper respiratory tract of
chickens, pheasants and guinea fowl
• The disease is limited to chickens
• Chickens of all ages are susceptible but older
birds react more severely
• Presence of capsule and haemagglutnitation
antigen are responsible for pathogenicity
 Etiology

• Avibacterium paragallinarum
Haemophilus paragallinarum
3 common serotypes A,B and C
• B strains most pathogenic
•Gm –ve , bipolar staining nonmotile rod with a
tendency toward filament formation
•H.pargallinarum is present in sinus exudate and
is easily demonstrated in stained smears
•It can persist outside of the host for only a few
days
•Easily destroyed by many disinfectants and by
environmental factors
•Organism is present in sinus exudate
•Broiler breeder suffer with 2-3% drop in egg
production
 Spread
• Carrier birds are main source and readily
transmitt the agent in susceptible chickens
• Spread by drinking water contaminated by
nasal discharge or by inhalation
• Direct contact and air borne droplets
 Pathogenesis
• After entry of organisms first adhere to the ciliated
mucosa of upper respiratory tract
• The capsule and the haemaglutination antigen play
important role in the colonization
• Toxic substances released from the organism during
proliferation are associated with production of lesions
in the mucosa and appearance of clinical signs
• The capsule acts as a natural defence substance
against the bactericidal power of complement
• Haemophilus. paragallinarum is a non invasive
organism with a strong tropism for ciliated
cells
• It migrates into lower respiratory tract(lungs,
air sacs) only after synergistic interaction with
other infectious agents
 Clinical Signs
• The disease is characterized by rapid spread, high
morbidity and low mortality
• Feed consumption and egg production are reduced
noticeably
• Incubation period is 1-3 days after contact infection and
signs appear in 7-10 days
• If not complicated by other infections course is not more
than 10 days in mild form, 3 weeks in more severe form
• Acute inflammation around the eyes and upper
respiratory tract with swollen infraorbital sinus
• Seromucucoid nasal and occular discharge and facial
oedema with conjunctivitis
• Respiratory noises, sneezing and dyspnoea
• In severe cases marked conjunctivitis with closed eyes,
swollen wattles and difficulty in breathing
• Decrease in feed and water consumption
• Drop in egg production
• Increase in rate of culling
• Mortality low and secondary infections eg IB, ND, Mg, FC
 Lesions
• Chickens have catarrhal to fibrinopurulent
inflammation of the nasal passages and infra orbital
sinus with distension and conjunctiva
• Subcutaneous oedema of face and wattle
prominent
• Conjunctivitis , frequently with adherence of eye lids
• Tracheitis, pneumonia and airsacculitis
• Lungs and airsacs are affected only in chronic
complicated cases
• Microscopically loss of cilia(deciliation) and
microvilli, cell oedema ( cell swelling),
• Degeneration and desquamation of mucosal and
glandular epithelium
• Infiltration of leukocytes and deposition of
mucopurulent substances
• Air sas show oedematous thickening,
mesotelialhyperplasia and heterophillic
infiltration
 Diagnosis
• The history of rapidly spreading disease
• Clinical signs and lesions
• Isolation and identification of organisms from
swabs of ifraorbital sinus, swabs from the
trachea and airsacs
• Gm negative, pleomorphic, nomoyile organisms
• Serological tests- HA, HI and FAT
• Immunodiffusion test