Poultry disease slide, Credit: Prof. Dr. Upendra M Singh

1. Colibacillosis
• 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
• These are classified on the basis of various
surface antigens which are

2. • 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

3. • Only a few Escherichia coli are true pathogens
• These are associated with enteric disease,
referred as enteropathogenic, enterotoxigenic
or enterotoxic
• They are important cause of diarhoea in
humans, pigs, cattle , sheep and horses

4. Diseases caused by E.coli
• Colisepticaemia
• Egg peritonitis
• Yolk sac infection(Omphalitis)
• Coligranuloma(Hjarre’s disease)
• Collectively grouped under colibacillosis

5. 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%

6. 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

7. 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 salphingitis
• Associated with heavy mortality during hatch
and may give rise to yolk sac infection

8. 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

9. 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

10. Lesions
• Airsacculitis, cellulitis, peritonitis, perihepatitis,
and pericarditis
• Air sac membrane become thicker and cloudy in
appearance
• Liver may show a thin covering of fibrinous
exudate
• Pneumonia and pleuropneumonia
• omphalitis, & Salphingitis
• Peritonitis is characterized by acute mortality,
fibrin and free yolk

11. • 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

12. Collibacillosis

14. Diagnosis
• PM examination- typical lesions
• Isolation and identification of organisms from
lungs, heart, liver and air sacs
• ELISA
• PCR

15. Egg peritonitis
• A number of reproductive disorders of poultry
• Peritonitis, salphingitis(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

16. • Small number of death in layers
• Flock peritonitis may result from vent pecking
and egg peritonitis

17. 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

18. 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

19. • 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

20. Coligranuloma(Hjarre’s disease)
• Caused by 04,08 and 016
• Causes sporadic death in adult hens
• The clinical signs are nonspecific
• Affected birds are found dead or die after
depression and loss of condition

21. • 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

22. • Bumble foot
• Peritonitis
• Airsacculitis
• Synovitis and arthritis

23. Fowl cholera
• Avian pasteurellosis, avian cholera and avian
haemorrhagic septicaemia
• Contagious disease affecting domestic and
wild birds
• It is caused by Pasteurella multocida, 16
serotypes
• Gram negative, capsulated, bipolar, nonmotile
bacteria

24. • World wide in distribution
• All species of birds are susceptible
• Ducks and geese are highly susceptible
• Adult birds and late growing stage are more
susceptible than youger stock
• Poultry, geese, ducks, turkeys, guinea fowl,
pigeons
• In peracute form it is most virulent and highly
infectious disease

25. Spread
• Carrier birds, diseased birds
• 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
• Oral, nasal, conjunctival routes and through
wounds

26. 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

27. 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, cyanosis of
comb and wattle and fetid(foul smelling) green
mucoid diarrhoea
• Fever prostration and drooling of saliva
• In chronic form oedema of wattles and combs

28. • The chronic form occurs in birds which survive
from acute disease
• The clinical signs include depression,
conjuntivitis, dyspnoea and in few cases
swelling of the joints, lameness, torticollis and
swelling of wattles

29. Fowl cholera

32. Lesions
• Gross lesions in peracute and acute forms include
marked congestion of the carcass, multiple
petechiation throughout viscera(gizzard muscle,
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

33. • 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

34. 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

35. Infectious coryza(Fowl coryza)
• Infectious coryza is an acute, highly contagious
disease of the upper respiratory tract of chickens
• Avibacterium paragallinarum
Haemophilus paragallinarum
3 common serotypes A,B and C
• 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

36. Spread
• Carrier birds are main source
• Spread by drinking water contaminated by
nasal discharge
• Direct contact and air borne droplets

37. 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

38. • H. 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

39. Signs
• The disease is characterized by rapid spread, high
morbidity and low mortality
• 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
• Seromucucoid nasal and occular discharge and
facial oedemA

40. • 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

42. Lesions
• Chickens have catarrhal to fibrinopurulent
inflammation of the nasal passages and infra
orbital sinus and conjunctiva
• Subcutaneous oedema of face and wattle
prominent
• Upper trachea may be involved
• Lungs and airsacs are affected only in chronic
complicated cases

43. • Microscopically loss of cilia and microvilli, cell
oedema, degeneration and desquamation of
mucosal and glandular epithelium, infiltration
of leukocytes and deposition of mucopurulent
substances

44. 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
• Serological tests- HA, HI and FAT