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Fowl cholera
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Synonyms
Avian Cholera
Avian Pasteurellosis
Avian Hemorrhagic septicemia
Kolera Unggas (INA)
Cont. …
 Fowl cholera is a contagious, bacterial disease that affects
domestic and wild birds worldwide, caused by Pasteurella
multocida type A.
 It usually occurs as a septicemia of sudden onset with high
morbidity and mortality, but chronic and asymptomatic
infections also occur.
Cont. …
 Turkeys and waterfowl are more susceptible than chickens.
 Older chickens are more susceptible than young ones.
Cont. …
Pathogenic Pasteurella species are:
1. Pasteurella multocida type A
– Fowl Cholera in chicken.
2. Pasteurella multocida type B
– Septicemia epizootica or Hemorrhagic septicemia in ruminant.
3. Pasteurella haemolytica
– Pneumonia Pasteurellosis in Cattle.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Predisposing Factors
Fowl Cholera is closely related to some stress factor;
1. Change of weather, fluctuation of temp, humidity….ect.
2. Move to new cage.
3. Debeaking.
4. Alteration of food suddenly.
5. Exhaustion.
6. Over crowding.
7. Transport in long time with lack of drink.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Incidence & Distribution
 Fowl cholera occurs sporadically or enzootically in most
countries.
 It sometimes causes high mortality; at other times, losses are
nominal.
Cont. …
 Fowl cholera is more prevalent in late summer, fall, and
winter.
 Chickens become more susceptible as they reach maturity.
Cont. …
Acute from;
 Alberts and Graham reported a loss of 68% within 6 days in a
flock of 52 month old turkeys.
 Vaught et al. reported that more than 1,000 wild geese died
of FC in one night.
Chronic from;
 In studying the chronic respiratory form in chickens, Hall et al.
observed that mortality was low, but infection persisted for at
least 4 years.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Etiology
 The genus Pasteurella sensustricto includes at least 11
species.
 Only 7 species have been associated with avian hosts.
 Among these 7 species, P. multocida is considered the
causative agent of fowl cholera.
Cont. …
Pasteurella multocida
 Small, gram-negative.
 Non-motile rod with a capsule that may exhibit pleomorphism
(the ability of some bacteria to alter their shape or size in
response to environmental conditions) after repeated
subculture.
 The organism is susceptible to ordinary disinfectants, sunlight,
drying, and heat.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Transmission
Transmission occur through:
1. Oral
2. Inhalation
Cont. …
Indirect contact:
Through food/drink, tools/materials which were contaminated
by the agents, animals transmitted and wind.
Direct Contact:
Through discharges and feces.
Cont. …
 Chronically infected birds and asymptomatic carriers are
considered to be major sources of infection.
 Wild birds may introduce the organism into a poultry flock,
but mammals (including rodents, pigs, dogs, and cats) may
also carry the infection.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Clinical Signs
Clinical findings vary greatly depending on the course of disease:
1. Acute
2. Chronic
Cont. …
In acute fowl cholera,
1. Sudden surges in mortality, without previous signs.
2. Fever.
3. Loss of appetite.
4. Ruffled feathers.
5. Mucous discharge from the mouth.
6. Green watery diarrhea.
7. Respiratory difficulty.
8. Blue or purple coloration of skin and swelling of comb and
wattles.
9. Pneumonia is particularly common in turkeys.
Mucoid discharge
Swollen wattles
Blue/ purple coloration
Swollen wattles
Swollen wattles
Swollen wattles
Swollen face
Swelling
(infraorbital sinuses)
Swelling (ear)
Clinical Signs
Chronic fowl cholera,
1. Signs and lesions are generally related to localized infections
of wattles, joints, tendon sheaths, and footpads, which often
are swollen because of accumulated fibrinosuppurative
exudate.
2. There may be exudative conjunctivitis and pharyngitis.
3. Torticollis (abnormal, asymmetrical head or neck position)
may result when the meninges, middle ear, or cranial bones
are infected.
Torticollis
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Post Mortem Lesions
In per acute and acute forms;
1. The disease shows primarily vascular disturbances.
1. General passive hyperemia and congestion throughout
the carcass.
2. Petechial and ecchymotic hemorrhages are common,
particularly in subepicardial and subserosal locations.
2. Enlargement of the liver and spleen.
3. Increased amounts of peritoneal and pericardial fluids are
frequently seen.
Cont. …
In sub acute forms;
1. Multiple, small, necrotic foci may be disseminated
throughout the liver and spleen.
Cont. …
In chronic forms of fowl cholera;
1. Suppurative lesions may be widely distributed, often
involving the respiratory tract, the conjunctiva, and adjacent
tissues of the head.
2. Caseous arthritis and productive inflammation of the
peritoneal cavity and the oviduct.
3. Fibrinonecrotic dermatitis, includes caudal parts of the
dorsum, abdomen, and breast and involves the cutis,
subcutis, and underlying muscle has been observed in
turkeys and broilers.
4. Sequestered necrotic lung lesions in poultry should always
raise suspicion of cholera.
Petechiae in the heart of goose
(pasteurellosis, erysipelas, asphyxia)
Necrotic foci in the liver - goose
(pasteurellosis, erysipelas)
Liver - Multiple, small,
necrotic foci
Green feces in Fowl Cholera, nonspecific sign.
Many disease in fowl reveal defecating with green feces
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Diagnosis
Although the history, signs, and lesions may aid diagnosis, P
multocida should be isolated, characterized, and identified for
confirmation.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Treatment
A number of drugs will lower mortality from fowl cholera;
however, deaths may resume when treatment is discontinued,
showing that treatment does not eliminate P multocida from a
flock.
Cont. …
Sensitivity testing often aids in drug
selection and is important because
of the emergence of multi-resistant
strains.
Cont. …
 Sulfas should be used with caution in breeders because of
potential toxicity.
 Penicillin is often effective for sulfa-resistant infections.
 High levels of tetracycline antibiotics in the feed (0.04%),
drinking water, or administered parenteral may be useful.
 Norfloxacin administered via drinking water is also effective
against fowl cholera.
 In ducks, a combined injection of streptomycin and
dihydrostreptomycin can be effective.
Plan of Talk
 Introduction
 Predisposing factors
 Incidence and distribution
 Etiology
 Transmission
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
 Prevention
Prevention
Eradication of infection requires:
1. Depopulation, cleaning and disinfection of buildings and
equipment.
2. The premise should then be kept free of poultry for few
weeks.
3. High level of biosecurity.
4. Rodents, wild birds, pets, and other animals that may be
carriers of P multocida and must be excluded from poultry
houses.
Vaccination – Live Vaccines
 Attenuated live vaccines are available for administration:
1. In drinking water to turkeys.
2. By wing-web inoculation to chickens.
 Vaccination of chickens and turkeys with live P. multocida
vaccines induces protection against heterologous serotype
challenge.
Cont. …
Three live vaccines available for use in the United States are:
1. CU (Clemson University), a strain of low virulence
2. M-9, a mutant of CU with very low virulence
3. PM-1, a mutant of CU intermediate in virulence between CU
and M-9.
Cont. …
 The use of live FC vaccines stimulates an effective immune
response but has the disadvantage of potentially resulting in
mortality in the vaccinated birds.
 If the mortality post vaccination becomes excessive, it can be
reduced by the administration of an antibiotic.
This should be avoided, if possible, until at least 4 days
post-vaccination when there will be at least partial
immunity induced by the vaccine.
Vaccination – Killed Vaccines
 Commercially produced bacterins are available.
 Bacterins usually contain whole cells of serotypes 1, 3, and 4
emulsified in an oil adjuvant.

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Fowl Cholera Guide: Causes, Symptoms, Treatment

  • 2. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 3. Synonyms Avian Cholera Avian Pasteurellosis Avian Hemorrhagic septicemia Kolera Unggas (INA)
  • 4. Cont. …  Fowl cholera is a contagious, bacterial disease that affects domestic and wild birds worldwide, caused by Pasteurella multocida type A.  It usually occurs as a septicemia of sudden onset with high morbidity and mortality, but chronic and asymptomatic infections also occur.
  • 5. Cont. …  Turkeys and waterfowl are more susceptible than chickens.  Older chickens are more susceptible than young ones.
  • 6. Cont. … Pathogenic Pasteurella species are: 1. Pasteurella multocida type A – Fowl Cholera in chicken. 2. Pasteurella multocida type B – Septicemia epizootica or Hemorrhagic septicemia in ruminant. 3. Pasteurella haemolytica – Pneumonia Pasteurellosis in Cattle.
  • 7. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 8. Predisposing Factors Fowl Cholera is closely related to some stress factor; 1. Change of weather, fluctuation of temp, humidity….ect. 2. Move to new cage. 3. Debeaking. 4. Alteration of food suddenly. 5. Exhaustion. 6. Over crowding. 7. Transport in long time with lack of drink.
  • 9. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 10. Incidence & Distribution  Fowl cholera occurs sporadically or enzootically in most countries.  It sometimes causes high mortality; at other times, losses are nominal.
  • 11. Cont. …  Fowl cholera is more prevalent in late summer, fall, and winter.  Chickens become more susceptible as they reach maturity.
  • 12. Cont. … Acute from;  Alberts and Graham reported a loss of 68% within 6 days in a flock of 52 month old turkeys.  Vaught et al. reported that more than 1,000 wild geese died of FC in one night. Chronic from;  In studying the chronic respiratory form in chickens, Hall et al. observed that mortality was low, but infection persisted for at least 4 years.
  • 13. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 14. Etiology  The genus Pasteurella sensustricto includes at least 11 species.  Only 7 species have been associated with avian hosts.  Among these 7 species, P. multocida is considered the causative agent of fowl cholera.
  • 15. Cont. … Pasteurella multocida  Small, gram-negative.  Non-motile rod with a capsule that may exhibit pleomorphism (the ability of some bacteria to alter their shape or size in response to environmental conditions) after repeated subculture.  The organism is susceptible to ordinary disinfectants, sunlight, drying, and heat.
  • 16. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 18. Cont. … Indirect contact: Through food/drink, tools/materials which were contaminated by the agents, animals transmitted and wind. Direct Contact: Through discharges and feces.
  • 19. Cont. …  Chronically infected birds and asymptomatic carriers are considered to be major sources of infection.  Wild birds may introduce the organism into a poultry flock, but mammals (including rodents, pigs, dogs, and cats) may also carry the infection.
  • 20. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 21. Clinical Signs Clinical findings vary greatly depending on the course of disease: 1. Acute 2. Chronic
  • 22. Cont. … In acute fowl cholera, 1. Sudden surges in mortality, without previous signs. 2. Fever. 3. Loss of appetite. 4. Ruffled feathers. 5. Mucous discharge from the mouth. 6. Green watery diarrhea. 7. Respiratory difficulty. 8. Blue or purple coloration of skin and swelling of comb and wattles. 9. Pneumonia is particularly common in turkeys.
  • 31. Clinical Signs Chronic fowl cholera, 1. Signs and lesions are generally related to localized infections of wattles, joints, tendon sheaths, and footpads, which often are swollen because of accumulated fibrinosuppurative exudate. 2. There may be exudative conjunctivitis and pharyngitis. 3. Torticollis (abnormal, asymmetrical head or neck position) may result when the meninges, middle ear, or cranial bones are infected.
  • 33. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 34. Post Mortem Lesions In per acute and acute forms; 1. The disease shows primarily vascular disturbances. 1. General passive hyperemia and congestion throughout the carcass. 2. Petechial and ecchymotic hemorrhages are common, particularly in subepicardial and subserosal locations. 2. Enlargement of the liver and spleen. 3. Increased amounts of peritoneal and pericardial fluids are frequently seen.
  • 35. Cont. … In sub acute forms; 1. Multiple, small, necrotic foci may be disseminated throughout the liver and spleen.
  • 36. Cont. … In chronic forms of fowl cholera; 1. Suppurative lesions may be widely distributed, often involving the respiratory tract, the conjunctiva, and adjacent tissues of the head. 2. Caseous arthritis and productive inflammation of the peritoneal cavity and the oviduct. 3. Fibrinonecrotic dermatitis, includes caudal parts of the dorsum, abdomen, and breast and involves the cutis, subcutis, and underlying muscle has been observed in turkeys and broilers. 4. Sequestered necrotic lung lesions in poultry should always raise suspicion of cholera.
  • 37. Petechiae in the heart of goose (pasteurellosis, erysipelas, asphyxia)
  • 38. Necrotic foci in the liver - goose (pasteurellosis, erysipelas)
  • 39. Liver - Multiple, small, necrotic foci
  • 40. Green feces in Fowl Cholera, nonspecific sign. Many disease in fowl reveal defecating with green feces
  • 41. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 42. Diagnosis Although the history, signs, and lesions may aid diagnosis, P multocida should be isolated, characterized, and identified for confirmation.
  • 43. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 44. Treatment A number of drugs will lower mortality from fowl cholera; however, deaths may resume when treatment is discontinued, showing that treatment does not eliminate P multocida from a flock.
  • 45. Cont. … Sensitivity testing often aids in drug selection and is important because of the emergence of multi-resistant strains.
  • 46. Cont. …  Sulfas should be used with caution in breeders because of potential toxicity.  Penicillin is often effective for sulfa-resistant infections.  High levels of tetracycline antibiotics in the feed (0.04%), drinking water, or administered parenteral may be useful.  Norfloxacin administered via drinking water is also effective against fowl cholera.  In ducks, a combined injection of streptomycin and dihydrostreptomycin can be effective.
  • 47. Plan of Talk  Introduction  Predisposing factors  Incidence and distribution  Etiology  Transmission  Clinical signs  Post mortem lesions  Diagnosis  Treatment  Prevention
  • 48. Prevention Eradication of infection requires: 1. Depopulation, cleaning and disinfection of buildings and equipment. 2. The premise should then be kept free of poultry for few weeks. 3. High level of biosecurity. 4. Rodents, wild birds, pets, and other animals that may be carriers of P multocida and must be excluded from poultry houses.
  • 49. Vaccination – Live Vaccines  Attenuated live vaccines are available for administration: 1. In drinking water to turkeys. 2. By wing-web inoculation to chickens.  Vaccination of chickens and turkeys with live P. multocida vaccines induces protection against heterologous serotype challenge.
  • 50. Cont. … Three live vaccines available for use in the United States are: 1. CU (Clemson University), a strain of low virulence 2. M-9, a mutant of CU with very low virulence 3. PM-1, a mutant of CU intermediate in virulence between CU and M-9.
  • 51. Cont. …  The use of live FC vaccines stimulates an effective immune response but has the disadvantage of potentially resulting in mortality in the vaccinated birds.  If the mortality post vaccination becomes excessive, it can be reduced by the administration of an antibiotic. This should be avoided, if possible, until at least 4 days post-vaccination when there will be at least partial immunity induced by the vaccine.
  • 52. Vaccination – Killed Vaccines  Commercially produced bacterins are available.  Bacterins usually contain whole cells of serotypes 1, 3, and 4 emulsified in an oil adjuvant.