Salmonellosis
• Genus Salmonella consists of more than 2300
serologically distintinguishable varieties
• All species of salmonella except, S.pullorum,
S.gallinarum are usually motile and have long
flagellae
• These two sps are host specific for avian species.
• Pullorum disease is caused by S pullorum. It is an
acute disease of chicks and poults.
• Fowl typhoid is caused by S. gallinarum and it is a
acute or chronic septicaemic disease affecting
mature birds.
• The second group includes infection with
motile salmonella serotypes referred to
collectively as paratyphoid salmonellae
S.typhymurium and S.enteritidis
• Paratyphoid infections are important mainly
as a cause of food borne disease in humans.
• Mortality upto 100%, increases during stress
and immunocompromised flocks
Pullorum disease (Bacillary white
diarrhoea)
• Pullorum disease is caused by bacterium
Salmonella pullorum.
• It was previously known as bacillary white
diarrhoea or BWD.
• It is septicaemic disease affecting mainly
chickens and turkeys.
• S.pullorum is Gram negative, nonmotile rod
0.3-0.5 x 1.25 μm and has no flagellar or H
antigen
• Usually grow on direct culture on MacConkeys
agar as pale, non lactose fermenting colonies
• S. pullorum differs from S. gallinarum in its
inability to ferment dulcitol and maltose and
fermented by S. gallinarum
• Survive outside body for many months
• Mortality upto 60% in chicks ( mostly upto 3
wks of age) and 20% in adults
• Morbidity 1- 80% may reach upto 100%
Species affected
• Mainly domestic chicken
• Turkeys
• Ducks
• Pigeons
• Guinea fowl
• Pheasants
• sparrows
Spread:
• Horizontal and vertical(transovarian)
• The important method for spread is transovarian
transmission.
• A portion of infected birds become adult carriers with
S.pullorum persisting in the ovaries excreted in the ova.
• These birds become poor layers
• The fertility and hatchability of infected egg is also
below average.
• Contaminated feed, water and fluffs
• However viable chicks do hatch from such
infected eggs and remain as source of infection.
• Fluff from such chicks is heavily contaminated
with S.pullorum and it dries, the bacteria are
disseminated through the incubator or brooder.
• Pasty white in the vent area
• Both vertical snd horizontal transmission occurs.
Signs:
• Pullorum is seen in chicks under 3 weeks of age.
• First indication is excess numbers of dead in shell
chicks and death soon after hatching.
• Inappetence, depression, tendency to huddle,
respiratory distress(gasping), closed eyes, loud
chirping, white viscous droppings which adhere
to the feathers around the vent.
• The mortality can be 100%.
• A subacute form with lameness and swollen,
hock joints(arthritis) may be seen in growing
birds and result of poor growth rates.
• Many remain as carriers and disseminators of the
etiological agents
• Older birds may appear listless, depression and
have pale and shrunken combs with white
diarrhoea
• Reduced egg production may be the only sign of
the disease in adult birds.
Lesions:
• Chicks which die soon after hatching have
peritonitis with inflammed unabsorbed yolk
sac.
• Lungs may be congested, liver is dark and
swollen with haemorrhages. Necrotic foci
lungs, liver, spleen and heart
• In chicks which die after showing signs of
disease for 1-2 days, there may be typhlitis.
• The caeca are enlarged and distended with casts
of hard dry necrotic and cheesy material.
• Spleen enlarged
• Urates distended with urates
• Discrete small white necrotic foci in liver, lungs,
myocardium and gizzard wall.
• In adult birds abnormal ovary- ova are irregular,
discoloured, cystic, misshapen pedunculated with
prominent stalk
• Pericarditis peritonitis and arthritis
Salmonellosis
• In growers affected with arthritis. Hock joints
are enlarged.
• In chicks lesions area not constant.
• In adult birds abnormal ovary with irregular
cystic, misshapen, haemorrhagic, atrophic,
discoloured pedunculated with prominent
thickened stalks.
• Oviduct impaction, peritonitis and ascites
• Peritonitis and pericarditis is also common.
Diagnosis:
• Typical history, signs and lesions
• Isolation of the causal organisms
- Mckonkey’s Agar
- Xylose Lysin Deoxycholate(XLD) Agar
- Bismuth Sulphite Agar(BSA)
• Rapid plate agglutination test after 16 weeks of age -
>2min positive, within 30 sec positive
• Tube agglutination test
• ELISA
• PCR
Fowl typhoid
• Primarily of chicken and turkeys
• Most outbreaks occur in recently hatched
young birds
• Fowl typhoid is caused by S. gallinarum.
• A short bacillus 1-2 μm long and 1.5 μm broad
and don’t poses flagellae
• This organism shares many antigens with S.
pullorum
• Readily grows in blood agar and MacConkeys
agar as pale, non lactose fermenting colonies
• Ferments glucose , mannitol, maltose and
dulcitol but does not ferment lactose, sucrose,
and salicin
• It is septicaemic disease affecting mainly
chicks and growers or adult birds although
chicks can be infected.
• Morbidity 10- 100% and Mortality upto 100%
Spread:
• Vertical and horizontal
• Organisms are passed in droppings.
• Lateral spread is by ingestion of contaminated
food or water.
• Recovered birds remain carriers for long period of
time.
• Egg transmission also occurs.
• Transmission can occur by contact, attendant,
visitors and contaminated materials.
Signs:
• increase in mortality in chicks and continuous
mortality in adults (>50%)
• anorexia, drop in egg production.
• Watery mucoid yellowish diarrhoea and soiled
vent.
• Depression and ruffled feathers
• Reluctant to move
• Shrunken pale combs and wattle
• In sub cute outbreak sporadic mortality over a
long period.
• In chicks signs are similar to pullorum disease.
• Increase in dead in shell embryos and dead
chicks in hatching trays
Lesions:
• Swollen friable liver with multiple necrotic
foci.
• Surface has a characteristic coppery bronze
sheen.
• Spleen enlarged with necrotic foci and
enlarged kidney
• catarrhal enteritis.
• In chronic phase include emaciated and
intensely anaemic carcass with focal necrosis
in heart, intestine,liver heart.
• Necrotic foci in liver, lungs, myocardium and
gizzard.
• In laying bird rupture of yolk occurs.
Fowl Typhoid(Bronze coloured Liver)
Diagnosis:
• Bacerial culture, Isolation and identification of
organisms
• Rapid plate agglutination test
• Tube agglutination test
• ELISA
• PCR
Whole blood agglutination test
• Coloured pullorum antigen available
commercially
• Wing vein punctured
• One drop of blood transferred to a clean slide
(30 µl)
• 30 µl of coloured pullorum antigen mixed with
blood and mixed with the micro tips and by
rotating the glass slide for 2 min
• Observe for clumping
• Clumping in positive cases
Differential Diagnosis
Dextrose Mannitol Dulcitol &
Maltose
Litmus ilk
S.Pullorum Fermented
with gas
Fermented
with gas
Not fermented Little and in 18-
72 hrs
S.gallinarum Fermented
without gas
Fermented
without gas
Fermented Fast acid
production
Salmonellosis- Avian paratyphoid
• Food borne disease trnsmission to humans
• Salmonellosis, there are > 2300 serotypes isolated from
poultry.
• S.typhimurium
• S.hadar
• S.enteritidis
• S. Heidelberg
• S. montevideo
• S. kentucky
• It rarely cause clinical disease in chicks > 3 weeks of
age.
Pathogenesis:
3 type of toxins are reported
• Endotoxin- cell wall polysacharide(LPS)- fever,
liver and spleen lesions,
• Enterotoxin(heat labile)-Increased secretory
response in epithelial cells. Causes fluid
accumulation in the intestinal lumen.
• Cytotoxin(heat stable)- Structural damage to
epithelial cells.
Spread:
• It is spread by contaminated feed(animal protein,
fish meal, bone meal etc),
• animal and insect vectors( rats, mice, cockroach).
• It can be transmitted both by vertical
transmission and horizontal transmission.
• It is spread by contaminated faeces and water in
feed.
• S.enteritidis: Organisms enters as eggs get cooled
Signs:
• mortality of chicks >3 weeks of age
• Ruffled feather, droopy wings, diarrhoea and
pasty vent, dejection, closed eyes and loss of
appetite
• Ducklings, young turkeys. Mortality< 20% is
recorded. Diarrhoea, pasty vent is common.
Lesion:
• Dehydration and enteritis
• congestion and necrotic lesions in liver.
• Swollen liver, spleen and kidney.
• Unabsorbed yolk sac is common feature.
• Haemorrhagic enteritis
• Typhlitis is characteristic(cheesy core in Caeca).
• Distention of caeca with white necrotic cores.
• Peritonitis, enteritis and caecal coring are
pathognomonic.
Diagnosis:
• Isolation of organisms from liver, gall bladder,
yolk, and caecum( Brlliant green Agar and Mc
Conkeys.
• Whole blood agglutination tesi
• ELISA
• PCR
Salmonella colour antigen
Culture of Salmonella
Identification of salmonella by
Fermentation reactions
Lactose Maltose Dulcitol
Avian salmonellae No change Acid and gas Acid and gas
S.pullorum No change No change No change
S.gallinarum No change Acid Acid
E.coli Acid and gas Acid and gas Acid and gas

Salmonellosis

  • 1.
    Salmonellosis • Genus Salmonellaconsists of more than 2300 serologically distintinguishable varieties • All species of salmonella except, S.pullorum, S.gallinarum are usually motile and have long flagellae • These two sps are host specific for avian species. • Pullorum disease is caused by S pullorum. It is an acute disease of chicks and poults. • Fowl typhoid is caused by S. gallinarum and it is a acute or chronic septicaemic disease affecting mature birds.
  • 2.
    • The secondgroup includes infection with motile salmonella serotypes referred to collectively as paratyphoid salmonellae S.typhymurium and S.enteritidis • Paratyphoid infections are important mainly as a cause of food borne disease in humans. • Mortality upto 100%, increases during stress and immunocompromised flocks
  • 3.
    Pullorum disease (Bacillarywhite diarrhoea) • Pullorum disease is caused by bacterium Salmonella pullorum. • It was previously known as bacillary white diarrhoea or BWD. • It is septicaemic disease affecting mainly chickens and turkeys. • S.pullorum is Gram negative, nonmotile rod 0.3-0.5 x 1.25 μm and has no flagellar or H antigen
  • 4.
    • Usually growon direct culture on MacConkeys agar as pale, non lactose fermenting colonies • S. pullorum differs from S. gallinarum in its inability to ferment dulcitol and maltose and fermented by S. gallinarum • Survive outside body for many months • Mortality upto 60% in chicks ( mostly upto 3 wks of age) and 20% in adults • Morbidity 1- 80% may reach upto 100%
  • 5.
    Species affected • Mainlydomestic chicken • Turkeys • Ducks • Pigeons • Guinea fowl • Pheasants • sparrows
  • 6.
    Spread: • Horizontal andvertical(transovarian) • The important method for spread is transovarian transmission. • A portion of infected birds become adult carriers with S.pullorum persisting in the ovaries excreted in the ova. • These birds become poor layers • The fertility and hatchability of infected egg is also below average. • Contaminated feed, water and fluffs
  • 7.
    • However viablechicks do hatch from such infected eggs and remain as source of infection. • Fluff from such chicks is heavily contaminated with S.pullorum and it dries, the bacteria are disseminated through the incubator or brooder. • Pasty white in the vent area • Both vertical snd horizontal transmission occurs.
  • 8.
    Signs: • Pullorum isseen in chicks under 3 weeks of age. • First indication is excess numbers of dead in shell chicks and death soon after hatching. • Inappetence, depression, tendency to huddle, respiratory distress(gasping), closed eyes, loud chirping, white viscous droppings which adhere to the feathers around the vent. • The mortality can be 100%.
  • 9.
    • A subacuteform with lameness and swollen, hock joints(arthritis) may be seen in growing birds and result of poor growth rates. • Many remain as carriers and disseminators of the etiological agents • Older birds may appear listless, depression and have pale and shrunken combs with white diarrhoea • Reduced egg production may be the only sign of the disease in adult birds.
  • 10.
    Lesions: • Chicks whichdie soon after hatching have peritonitis with inflammed unabsorbed yolk sac. • Lungs may be congested, liver is dark and swollen with haemorrhages. Necrotic foci lungs, liver, spleen and heart • In chicks which die after showing signs of disease for 1-2 days, there may be typhlitis.
  • 11.
    • The caecaare enlarged and distended with casts of hard dry necrotic and cheesy material. • Spleen enlarged • Urates distended with urates • Discrete small white necrotic foci in liver, lungs, myocardium and gizzard wall. • In adult birds abnormal ovary- ova are irregular, discoloured, cystic, misshapen pedunculated with prominent stalk • Pericarditis peritonitis and arthritis
  • 13.
  • 14.
    • In growersaffected with arthritis. Hock joints are enlarged. • In chicks lesions area not constant. • In adult birds abnormal ovary with irregular cystic, misshapen, haemorrhagic, atrophic, discoloured pedunculated with prominent thickened stalks. • Oviduct impaction, peritonitis and ascites • Peritonitis and pericarditis is also common.
  • 16.
    Diagnosis: • Typical history,signs and lesions • Isolation of the causal organisms - Mckonkey’s Agar - Xylose Lysin Deoxycholate(XLD) Agar - Bismuth Sulphite Agar(BSA) • Rapid plate agglutination test after 16 weeks of age - >2min positive, within 30 sec positive • Tube agglutination test • ELISA • PCR
  • 17.
    Fowl typhoid • Primarilyof chicken and turkeys • Most outbreaks occur in recently hatched young birds • Fowl typhoid is caused by S. gallinarum. • A short bacillus 1-2 μm long and 1.5 μm broad and don’t poses flagellae • This organism shares many antigens with S. pullorum
  • 18.
    • Readily growsin blood agar and MacConkeys agar as pale, non lactose fermenting colonies • Ferments glucose , mannitol, maltose and dulcitol but does not ferment lactose, sucrose, and salicin • It is septicaemic disease affecting mainly chicks and growers or adult birds although chicks can be infected. • Morbidity 10- 100% and Mortality upto 100%
  • 19.
    Spread: • Vertical andhorizontal • Organisms are passed in droppings. • Lateral spread is by ingestion of contaminated food or water. • Recovered birds remain carriers for long period of time. • Egg transmission also occurs. • Transmission can occur by contact, attendant, visitors and contaminated materials.
  • 20.
    Signs: • increase inmortality in chicks and continuous mortality in adults (>50%) • anorexia, drop in egg production. • Watery mucoid yellowish diarrhoea and soiled vent. • Depression and ruffled feathers • Reluctant to move
  • 21.
    • Shrunken palecombs and wattle • In sub cute outbreak sporadic mortality over a long period. • In chicks signs are similar to pullorum disease. • Increase in dead in shell embryos and dead chicks in hatching trays
  • 22.
    Lesions: • Swollen friableliver with multiple necrotic foci. • Surface has a characteristic coppery bronze sheen. • Spleen enlarged with necrotic foci and enlarged kidney • catarrhal enteritis.
  • 23.
    • In chronicphase include emaciated and intensely anaemic carcass with focal necrosis in heart, intestine,liver heart. • Necrotic foci in liver, lungs, myocardium and gizzard. • In laying bird rupture of yolk occurs.
  • 24.
  • 25.
    Diagnosis: • Bacerial culture,Isolation and identification of organisms • Rapid plate agglutination test • Tube agglutination test • ELISA • PCR
  • 26.
    Whole blood agglutinationtest • Coloured pullorum antigen available commercially • Wing vein punctured • One drop of blood transferred to a clean slide (30 µl) • 30 µl of coloured pullorum antigen mixed with blood and mixed with the micro tips and by rotating the glass slide for 2 min • Observe for clumping • Clumping in positive cases
  • 27.
    Differential Diagnosis Dextrose MannitolDulcitol & Maltose Litmus ilk S.Pullorum Fermented with gas Fermented with gas Not fermented Little and in 18- 72 hrs S.gallinarum Fermented without gas Fermented without gas Fermented Fast acid production
  • 28.
    Salmonellosis- Avian paratyphoid •Food borne disease trnsmission to humans • Salmonellosis, there are > 2300 serotypes isolated from poultry. • S.typhimurium • S.hadar • S.enteritidis • S. Heidelberg • S. montevideo • S. kentucky • It rarely cause clinical disease in chicks > 3 weeks of age.
  • 29.
    Pathogenesis: 3 type oftoxins are reported • Endotoxin- cell wall polysacharide(LPS)- fever, liver and spleen lesions, • Enterotoxin(heat labile)-Increased secretory response in epithelial cells. Causes fluid accumulation in the intestinal lumen. • Cytotoxin(heat stable)- Structural damage to epithelial cells.
  • 30.
    Spread: • It isspread by contaminated feed(animal protein, fish meal, bone meal etc), • animal and insect vectors( rats, mice, cockroach). • It can be transmitted both by vertical transmission and horizontal transmission. • It is spread by contaminated faeces and water in feed. • S.enteritidis: Organisms enters as eggs get cooled
  • 31.
    Signs: • mortality ofchicks >3 weeks of age • Ruffled feather, droopy wings, diarrhoea and pasty vent, dejection, closed eyes and loss of appetite • Ducklings, young turkeys. Mortality< 20% is recorded. Diarrhoea, pasty vent is common.
  • 32.
    Lesion: • Dehydration andenteritis • congestion and necrotic lesions in liver. • Swollen liver, spleen and kidney. • Unabsorbed yolk sac is common feature. • Haemorrhagic enteritis • Typhlitis is characteristic(cheesy core in Caeca). • Distention of caeca with white necrotic cores. • Peritonitis, enteritis and caecal coring are pathognomonic.
  • 33.
    Diagnosis: • Isolation oforganisms from liver, gall bladder, yolk, and caecum( Brlliant green Agar and Mc Conkeys. • Whole blood agglutination tesi • ELISA • PCR
  • 34.
  • 35.
  • 36.
    Identification of salmonellaby Fermentation reactions Lactose Maltose Dulcitol Avian salmonellae No change Acid and gas Acid and gas S.pullorum No change No change No change S.gallinarum No change Acid Acid E.coli Acid and gas Acid and gas Acid and gas