Understanding Pasteurellosis: A Bacterial Disease in Livestock

 
PASTEURELLOSIS
 
Genus – 
PASTEURELLA
                   
MANNHEIMIA
 
P. Multocida – Haemorrhagic Septicemia in cattle
                        - Fowl cholera in fowl
                        - Atropic rhinitis in  pig
                        - Snuffles in  Rabbit.
                        - 
Bubonic Plague – Man (Natural host – rat)
 Mannheimia haemolytica
– (
P. Haemolytica)
 
 shipping fever
in cattle, 
Arthritis – Calves, mastitis – Cows & Sheep
 
H.S
 
 
Colonies are small, non- hemolytic, translucent,
mucoid type.
They don’t grow in Mckonkcy’s agar.
 
Manniheimia Haemolytica – can grow in Mckonkcy’s
agar
 
H.S
 
Bio-chemical tests are done
.
They are oxidase + Ve , indole +Ve, catalase – Ve.
Nitrates will be reduced to nitrites, acid produces
without gas, citrate – Ve
 
H.S
 
They have both capsular (5) and somatic
antigens (16).
Capsular antigens – A, B, D, E, F: - H A test
Somatic Ag – I,--------XVI -  AGPT.
B : 2 is responsible for HS in India and S-E Asia.
E : 2 is found only Africa.
Fowl cholera – A: 1, A : 3,4, F : 4, D : 3.
A: 1  - more prevalent
 
HAEMORRHAGIC SEPTICAEMIA
 
Acute septacaemic disease with high fever,
respiratory distress, diarrhea. In less acute
case, oedema occurs at the brisket region.
Absent in buffalo, they usually occurs with in
2-4 days.
 
 
H.S
 
Synonym:
 Stockyards disease , Pasteurellosis,
Gala ghout.
 
Incidence
 
It is one of the important bacterial diseases of
cattle and rarely  buffaloes in India
Sheep and goat – Rarely affected
Swine and Fowls – May be affected
 
H.S
 
Transmission
Ingestion of contaminated feed, water etc.
The organism is found in the saliva of affected
animals
Droplet infection may occur
 
H.S
 
Pathogenesis
Organisms on entry into the system reaches
blood, proliferate and spread throughout the
body due to its septicaemic nature and
produces petechial and ecchymotic
haemorrhjages on serous  and mucous
menbranes in different organs. Hence it is
called as - “ 
HAEMORRHAGIC SEPTICAEMIA
 
 
Pathogenesis
 
The bacteria ( Bipolar) has capsule which
prevent its opsonization and Phagocytosis.
The bacteria comes in lymph through
pharyngeal tonsils and cause Bactermia.
The bacteria multiplies and produces
septicemia and produce toxins.
 
 
The toxins are –
A) Leukotoxin 
– it help in stabilizing bacteria &
prevent its Phagocytosis by destroying
monocyte, macrophages
B) Endotoxin 
– destroy endothelium of blood
vessels and cause intravascular permeability,
oedema & hemorrhage.
C) 
The toxin 
also activate macrophage to
release Cytokines.
 
H.S
 
Clinical signs
High temperature, dullness, dyspnoea, hot
painful swelling – head, dewlap and neck with
Inflammatory exudate in the subcutaneous
tissues.
 
H.S
 
H.S
 
Gross lesions
Petechiae on all serous and mucous
membranes especially on epicardium,
myocardium, pleura, peritoneum and
Gastrointestinal tract.
Lymph glands- Swollen and haemorrhagic
G.I tract is severely inflammed with contents
mixed with blood
 
Affected lungs
 
H.S
 
H.S
 
Microscopic lesions
In acute and subacute cases, the predominant
lesion is fibrinous bronchopneumonia
The organism is small ovoid rods the ends of
rods are more deeply stained than central
portion which gives them a bipolar
appearance.
In rabbits – Haemorrhagic tracheitis.
 
HS
 
H.S
 
Diagnosis
Examination of blood smear
A heart blood swab may be rubbed over the
scarified abdomen of a rabbit. It will die within
24 to 40 hours  showing haemorrhgaes,
especially haemorrhagic tracheitis is
pathognomonic lesion
 
JOHNE'S DISEASE
 
Synonym 
: Paratuberculosis
 
Chronic wasting illness of ruminants with
prolonged course, recurrent diarrhoea,
dehydration, emaciation and
 
 
Aetiology
Mycobaterium paratuberculosis - 
Three
strains:
Bovine strain
Ovine strain
Scottish strain
 
 
Incidence
The disease is of worldwide distribution and constitutes an
important economic problem in cattle
Susceptibility
Ruminants are usually affected. Horses and pigs may be
affected very rarely
2-3 year-old female in high milk production most
susceptible.
Cow – sub-clinical, organism abundantly in the milk – new
born animals highly susceptible.
Gut is the main target organ
It is less frequently encountered sheep and goats
 
 
Transmission
Infection is ingestion. Faeces containing the
organisms serve as the primary source of
infection
Incubation period : Long and protracted even
upto 2 years
 
 
Organisms enters the body through intestinal
mucosa, sets up bacteremia and settles in the
mucosa of intestine, mesenteric lymph nodes and
tonsil produce a chronic granulomatous
inflammation
 
Cell mediated immune response and followed by
humoral immune response initiated by the
release of bacteria by dying macrophages as the
disease progresses.
 
 
Immediate hypersensitivity – Mediates
diarrhea.
Delayed hypersensitivity – mediates
emaciation & anemia.
Failure of protein synthesis – mediates muscle
atrophy.
Cytotoxic – muscle atrophy & renal damage.
 
 
Clinical signs
Emaciation, hide and bound with dry coat
Normal appetite with increased thirst and
diarrrhoea
Sheep and goat – Diarrhoea is not common,
emaciation observed
 
 
Gross lesions
Carcass – Emaciation with gelatinous fat
Terminal part of ileum – Wall thickened and
oedematous
The mucosa is folded and showed Transverse
corrugation or rugae (like cerebral
convolution)
 
 
 
JD - corrugation of intestine
 
 
Microscopically – pronounced chronic
granulomatous enteritis with heavy
lymphocytic infiltration, typical Langerhans
type gaint cells & scattered granulomatas.
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Pasteurellosis, caused by organisms like Pasteurella and Mannheimia, affects various animals including cattle, fowl, pigs, and rabbits. The disease presents as haemorrhagic septicaemia in cattle, with symptoms like high fever and respiratory distress. It is an important bacterial disease in livestock, transmitted through contaminated feed or droplets. Pathogenesis involves organism proliferation in the body, leading to characteristic symptoms.


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  1. PASTEURELLOSIS Genus PASTEURELLA MANNHEIMIA P. Multocida Haemorrhagic Septicemia in cattle - Fowl cholera in fowl - Atropic rhinitis in pig - Snuffles in Rabbit. - Bubonic Plague Man (Natural host rat) Mannheimia haemolytica (P. Haemolytica) shipping fever in cattle, Arthritis Calves, mastitis Cows & Sheep

  2. H.S Colonies are small, non- hemolytic, translucent, mucoid type. They don t grow in Mckonkcy s agar. Manniheimia Haemolytica can grow in Mckonkcy s agar

  3. H.S Bio-chemical tests are done. They are oxidase + Ve , indole +Ve, catalase Ve. Nitrates will be reduced to nitrites, acid produces without gas, citrate Ve

  4. H.S They have both capsular (5) and somatic antigens (16). Capsular antigens A, B, D, E, F: - H A test Somatic Ag I,--------XVI - AGPT. B : 2 is responsible for HS in India and S-E Asia. E : 2 is found only Africa. Fowl cholera A: 1, A : 3,4, F : 4, D : 3. A: 1 - more prevalent

  5. HAEMORRHAGIC SEPTICAEMIA Acute septacaemic disease with high fever, respiratory distress, diarrhea. In less acute case, oedema occurs at the brisket region. Absent in buffalo, they usually occurs with in 2-4 days.

  6. H.S Synonym: Stockyards disease , Pasteurellosis, Gala ghout.

  7. Incidence It is one of the important bacterial diseases of cattle and rarely buffaloes in India Sheep and goat Rarely affected Swine and Fowls May be affected

  8. H.S Transmission Ingestion of contaminated feed, water etc. The organism is found in the saliva of affected animals Droplet infection may occur

  9. H.S Pathogenesis Organisms on entry into the system reaches blood, proliferate and spread throughout the body due to its septicaemic nature and produces petechial haemorrhjages on serous menbranes in different organs. Hence it is called as - HAEMORRHAGIC SEPTICAEMIA and ecchymotic and mucous

  10. Pathogenesis The bacteria ( Bipolar) has capsule which prevent its opsonization and Phagocytosis. The bacteria comes in lymph through pharyngeal tonsils and cause Bactermia. The bacteria multiplies and produces septicemia and produce toxins.

  11. The toxins are A) Leukotoxin it help in stabilizing bacteria & prevent its Phagocytosis by destroying monocyte, macrophages B) Endotoxin destroy endothelium of blood vessels and cause intravascular permeability, oedema & hemorrhage. C) The toxin also activate macrophage to release Cytokines.

  12. H.S Clinical signs High temperature, dullness, dyspnoea, hot painful swelling head, dewlap and neck with Inflammatory exudate in the subcutaneous tissues.

  13. H.S

  14. H.S Gross lesions Petechiae membranes myocardium, Gastrointestinal tract. Lymph glands- Swollen and haemorrhagic G.I tract is severely inflammed with contents mixed with blood on all serous and mucous especially pleura, on epicardium, peritoneum and

  15. Affected lungs

  16. H.S

  17. H.S Microscopic lesions In acute and subacute cases, the predominant lesion is fibrinous bronchopneumonia The organism is small ovoid rods the ends of rods are more deeply stained than central portion which gives appearance. In rabbits Haemorrhagic tracheitis. them a bipolar

  18. HS

  19. H.S Diagnosis Examination of blood smear A heart blood swab may be rubbed over the scarified abdomen of a rabbit. It will die within 24 to 40 hours showing haemorrhgaes, especially haemorrhagic pathognomonic lesion tracheitis is

  20. JOHNE'S DISEASE Synonym : Paratuberculosis Chronic wasting illness of ruminants with prolonged course, dehydration, emaciation and recurrent diarrhoea,

  21. Aetiology Mycobaterium paratuberculosis - Three strains: Bovine strain Ovine strain Scottish strain

  22. Incidence The disease is of worldwide distribution and constitutes an important economic problem in cattle Susceptibility Ruminants are usually affected. Horses and pigs may be affected very rarely 2-3 year-old female in high milk production most susceptible. Cow sub-clinical, organism abundantly in the milk new born animals highly susceptible. Gut is the main target organ It is less frequently encountered sheep and goats

  23. Transmission Infection is ingestion. Faeces containing the organisms serve as the primary source of infection Incubation period : Long and protracted even upto 2 years

  24. Organisms enters the body through intestinal mucosa, sets up bacteremia and settles in the mucosa of intestine, mesenteric lymph nodes and tonsil produce a inflammation chronic granulomatous Cell mediated immune response and followed by humoral immune response initiated by the release of bacteria by dying macrophages as the disease progresses.

  25. Immediate hypersensitivity Mediates diarrhea. Delayed hypersensitivity mediates emaciation & anemia. Failure of protein synthesis mediates muscle atrophy. Cytotoxic muscle atrophy & renal damage.

  26. Clinical signs Emaciation, hide and bound with dry coat Normal appetite with increased thirst and diarrrhoea Sheep and goat Diarrhoea is not common, emaciation observed

  27. Gross lesions Carcass Emaciation with gelatinous fat Terminal part of ileum Wall thickened and oedematous The mucosa is folded and showed Transverse corrugation or rugae (like cerebral convolution)

  28. JD - corrugation of intestine

  29. Microscopically granulomatous lymphocytic infiltration, typical Langerhans type gaint cells & scattered granulomatas. enteritis pronounced chronic heavy with

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