SALMONELLA INFECTIONS OF

POULTRY

 1) PULLORUM DISEASE
 2) FOWL TYPHOID
 3) PARATYPHOID
 PULLORUM DISEASE
(Bacillary White Diarrhoea)
➢ An acute highly contagious disease of young
chicks (up to 3 weeks)
➢ Characterized by :
▪ Septicaemia
▪ White diarrhoea
▪ Respiratory distress
▪ High morbidity (10-80%)
▪ Up to 100% mortality
➢ In adults - localized and chronic infection
(brown-shell egg layers)
➢ Also infects turkeys, guinea fowls, sparrows,
parrots, ring doves, ostriches and peafowl
 ETIOLOGY

Salmonella pullorum
Family: Enterobacteriaceae
Characteristics:
▪ G –ve, rods with rounded ends
▪ Non motile
▪ Non spore forming
▪ Anaerobic
 TRANSMISSION
➢ Horizontal
▪ Infected Droppings
▪ Contaminated feed (animal proteins esp in mash feeds )
and water
▪ Salmonella can survive for two years in feed and at least
one year in dust in an empty poultry house
▪ Contaminated poultry houses
▪ Contaminated incubators and hatchers
▪ Cannibalism
▪ Insects including cockroaches, flies, and beetles can carry
salmonella in and out of the farm
▪ Mice and rats have been important vector
▪ Wild birds carry salmonella and contact with wild birds or
their droppings is a risk factor for commercial poultry
▪ Humans can also be a source of salmonella transmissible
to poultry
 Vertical
▪ From parents to offspring (Transovarian)
▪ 10-15% eggs produced by infected hen
carry the organism
▪ Salmonella carried in or on eggs can be
spread extensively in the hatchery
▪ As chicks or poults pips through egg shells
salmonella are released into the air and
circulated around the hatching cabinets on
contaminated fluff and other hatching
debris
▪ The newly hatched birds lacking protecting
intestinal micro flora are highly susceptible
to intestinal colonization by salmonella
 CLINICAL SIGNS
CHICKS
➢ Incubation period (4 – 5 days)

➢ Large numbers of dead in-shell chicks or chicks

that die shortly after hatching with heavy losses
occurring within one week
➢ Loss of appetite and huddling together

➢ Sagging of wings & distorted body appearance

➢ Chalky white excreta (white diarrhea)

➢ Vent pasting

➢ Pot-bellied

➢ Laboured breathing or gasping

ADULTS
➢ Exhibit little or no symptoms
➢ Swollen hock joints & poor growth
 PATHOGENESIS
➢ Organism enters by:
▪ Ingestion
▪ Abrasions
➢ Leads to septicemia manifested by:
▪ Severe enteritis
▪ Respiratory symptoms
➢ Localizes in GIT and sex organs
➢ Vertical transmission occurs
PATHOGENESIS
After ingestion, the organisms colonize the ileum and
colon, invade the intestinal epithelium, and
proliferate within the epithelium and lymphoid
follicles

The mechanism by which salmonellae invade the

epithelium involves an initial binding to specific
receptors on the epithelial cell surface followed by
invasion

Invasion occurs by the organism inducing the

enterocyte membrane to undergo "ruffling" and
thereby to stimulate pinocytosis of the organisms
PATHOGENESIS
After invading the epithelium, the organisms
multiply intracellularly and then spread to
mesenteric lymph nodes and throughout the
body via the systemic circulation; they are
taken up by the reticuloendothelial cells

The reticulo endothelial system confines and

controls spread of the organism
PATHOGENESIS
After invading the intestine, most salmonellae
induce an acute inflammatory response,
which can cause ulceration. They may
elaborate cytotoxins that inhibit protein
synthesis

However, invasion of the mucosa causes

the epithelial cells to synthesize and
release various pro-inflammatory
cytokines, including: IL-1, IL-6, IL-8, TNF-2,
IFN-U, MCP-1, and GM-CSF
PATHOGENESIS
These evoke an acute inflammatory
response and may also be responsible
for damage to the intestine

Because of the intestinal inflammatory

reaction, symptoms of
inflammation such as fever, chills,
abdominal pain, leukocytosis, and
diarrhea are common
PATHOGENESIS
Salmonella escape from the basal side of
epithelial cells into the lamina propria

Systemic spread of the organisms can occur,

giving rise to enteric fever

Invasion of the intestinal mucosa is followed by

activation of mucosal adenyl cyclase;
the resultant increase in cyclic AMP induces
secretion
PATHOGENESIS
It may involve local production of
prostaglandins or other components of
the inflammatory reaction

In addition, salmonella strains elaborate

one or more enterotoxin-like
substances which may stimulate
intestinal secretion
PATHOGENESIS
This increase intestinal secretions, acute
inflammation, ulceration, increased
intestinal motility and decreased feed
digestion & absorption, leads to
diarrhea
 POST MORTEM LESIONS
Sudden death
➢ Liver enlarged, congested and hemorrhagic
Septicaemic form;
➢ Small areas of necrosis in liver, heart and
lungs
➢ Intestinal or caecal inflammation and
caecal cores
Chronic cases;
▪ Yellowish or blood stained yolk sac
▪ Delayed yolk absorption
▪ Enlarged spleen & congested kidney
▪ Thickened intestinal wall and peritonitis
▪ Abscess formation in hock joint
▪ Necrotic foci/abscesses on cardiac
muscles, liver, lungs and gizzard
Common diagnostic lesions
Unabsorbed yolk sacs
Classic gray nodules in the liver, spleen,
lungs, heart, gizzard, and intestine
Firm, cheesy material in the ceca (cecal
cores)
Raised plaques in the mucosa of the
lower intestine
 DIAGNOSIS

➢ Typical lesions & gram stained specimen

examination
➢ Isolation & identification of organism
▪Sample sites: Liver, spleen, heart, heart
blood, ovary & yolk sac
▪ Primary isolation:
a. Brilliant green agar supplemented with
sulfapyridine or McConkey agar
b. Colonies are transparent pink to deep
fuchsia, surrounded by a reddish medium
➢ Serological identification
Rapid Serum Plate Test or Tube Agglutination
Test
PLATE AGGLUTINATION TEST

Figure 1—Results of the rapid whole-blood

plate agglutination test for pullorum are
positive (top left), suspect (top right), and
negative (bottom)
 DIFFERENTIAL DIAGNOSIS

➢ Liver lesions resemble other salmonella

infections
➢ Lung lesions resemble Aspergillus
infection
➢ Joint lesions resemble Mycoplasma
Synoviae infection
➢ Pericardium and ovary lesions resemble
Coliform, Staphylococci and Micrococci
infection
 CONTROL
➢ Good management
➢ Serological testing of flock and
removal of infected breeder birds
➢ Proper sanitation and disinfection
of farm and premises
➢ Control of rodents

➢ Focus on egg hygiene

➢ Proper hatchery sanitation

➢ Use of antibiotics (ciprofloxacin)

Sagging of wings & distorted
body appearance
Vent pastings
Nodular lesions on cardiac
muscles
Large abscesses in the lungs
Swelling of the joint and synovitis
Swelling of the joint and synovitis
Nodular lesions can be observed
in the heart
Nodular lesions can be observed
on the liver
Ulceration and plaque like
accumulation of necrotic tissue in the
duodenum : Caecal cores
 Gross lesions associated with Salmonella pullorum (A–F)
infection in chickens.
 A. Enlarged liver showing congestion and small
 necrotic foci (Glass).
 B. Heart from young chick with white nodules representing
 myocarditis. Such nodules can be confused for tumors, such
 as Marek’s disease (Chin).
 C. Nodular lesions in the heart; note the thickened yellowish
pericardium (reflected).
 D. Swollen hock joint containing yellow viscous fluid
(Peckham).
 E. Ovarian lesions and salpingitis.
 F. Lungs with pyrogranulomatous pneumonia due to pullorum
 disease in a chick (Peckham).
 G. Turkey poult with exudate in the anterior chamber of the
eye due to arizonosis.
FOWL TYPHOID
FOWL TYPHOID
 Acute septicemic disease which affects growers
and adults. Sometimes seen in young chicks as
well
 Many signs and lesions resembling Pullorum
disease
 Characterized by profuse bright sulphur yellow
diarrhea and later anemia
 Broiler parents and brown-shell egg layers are
especially susceptible
 Disease affects chicken, turkeys, ducks, parrots,
sparrows and wild birds
ETIOLOGY
 Salmonella gallinarum;
Gram negative rod
Non-motile
Non spore forming
Non capsulated
 Killed by phenol (1:1000), KMnO4 (1%) in
3 minutes and Formalin (2%) in 1 minute
 Environmental sources of the organism
include water, soil, insects, factory
surfaces, kitchen surfaces, animal faeces,
raw meats, raw poultry, and raw seafoods
TRANSMISSION
Horizontal;
▪ Droppings contaminating feed and water
▪ Cannibalism
▪ Vectors
▪ Carrier birds

Vertical; (Trans-ovarian)
 80-90% eggs laid are infected
CLINICAL SIGNS
 Watery bright yellow diarrhea
 Rapid respiration
 Marked thirst, listlessness, muscular weakness
 Anemia
 Comb pale and shrunken due to anemia
 After 5-6 days Mucoid greenish yellow droppings
along with pasting around vent
 Mortality 4-50%
 Arthritis in some cases
PATHOGENESIS
 Infection through oral route
 Invade intestinal lining
 Bacteremia after 3 hrs
 Multiplication of bacteria in spleen & liver
 Bacteria lodges in the reticulo-endothelial
cells in intestinal wall, liver and spleen and
further multiplies
 Death with in 5-9 days or the sick bird
recovers as carriers
POSTMORTEM LESIONS
ACUTE:
 Liver; enlarged, congested, friable and on
exposure to air bronze coloration or a
bronze sheen on the surface. (unexcreted
bile) with small necrotic foci
 Spleen; swollen, mottled and brittle
 Kidneys enlarged
 Intestines; catarrhal enteritis of anterior
small intestine along with ulceration
POSTMORTEM LESIONS
CHRONIC:
 Heart; white to grey nodular masses
scattered through out myocardium (pin
head to pea size) which bulge out from
surface; later pericarditis
 Intestines; irregular and lumpy gray
nodules along the length
 Ovary; follicles inflamed in laying hens,
broken egg yolks in peritoneal cavity,
misshapen eggs
 Lungs; congested edematous and peculiar
yellowish brown in color
DIAGNOSIS
 Field; clinical signs and postmortem
lesions
 Isolation and identification of S.gallinarum
from liver and spleen and in chronic case
from heart
 Agglutination test (Tube and Plate)
especially to identify carriers
 ELISA and FAT
 PCR
Colonies are transparent pink to deep fuchsia,
surrounded by a reddish medium
PLATE AGGLUTINATION TEST

Figure 1—Results of the rapid whole-blood

plate agglutination test for salmonella are
positive (top left), suspect (top right), and
negative (bottom)
DIFFERENTIAL DIAGNOSIS
 Fowl cholera
 Pullorum disease
 Coli-septicaemia
CONTROL
➢ Good management and sound biosecurity
➢ Serological testing of flock and removal of infected breeder
birds
➢ Proper sanitation and disinfection of farm and premises
with Compounds that contain phenol, quaternary
ammonium compounds and iodophores may be used
➢ Heat treatment, formalin, dichloride of mercury and
potassium permanganate can also inactivate these
organisms
➢ Salmonella free feed (crumbs)
➢ Control of rodents, free wild birds ( carriers)
➢ Focus on egg hygiene
➢ Proper hatchery sanitation use disinfectants like virus snip,
virkon-S and CID 20
➢ Use of antibiotics
Liver enlarged, pale and shows focal
necrosis (Acute) Right
Nodular lesions on Myocardium
(Chronic)
Nodular lesions on Myocardium
Liver Bronze Coloration
Liver Bronze
Enlarged and bronze greenish tint of
liver
Enlarged liver is mottled with multiple
miliary necroses
Acute fowl typhoid, the size of liver
necroses varies from miliary to spots
with a diameter of 1 - 2 cm
Spleen; swollen, mottled
Spleen is 2-3 times bigger, sometimes
with greyish-whitish nodules
prominating on the surface
Anterior part of small intestine,
Enteritis with ulcerations
Characteristic brown colour with
necroses
PARATYPHOID
(SALMONELLOSIS)
PARATYPHOID
 Acute or chronic infections of poultry causing enteritis
and septicaemia in young birds whereas birds older
than 1 month usually show subclinical disease
 The Infection Of Small Chickens Occurs By
Penetration Of Microorganisms Into The Egg After
Faecal Contamination
 Caused by any one of a large group of salmonellae
that are not host specific
 Young are most frequently and severely affected
 P.T. salmonellae are agents of food-borne disease
transmission to human
 Worldwide in distribution
PUBLIC HEALTH
IMPORTANCE
 Much more importance for public health
than for economic losses, common
zoonotic diseases causing acute
gastro-enteritis
 Poultry meat and eggs are consistently
identified as important sources of
salmonellae that cause illness in human.
 Between 1985 and 1991, 82% of S.
enteritidis outbreaks in the USA were
associated with eggs
ETIOLOGY

 Salmonella typhimurium
 Salmonella enteritidis

Characteristics:
 Not host specific/adapted
 Gram –ve rods, Non-spore-forming
 Motile by flagella
 Contain endotoxin, enterotoxin & cytotoxin which are
responsible for it’s pathogenic properties
 Killed in 5 minutes by heating at 60oC
 Highly susceptible to the lethal effects of irradiation
 May survive up to 13 months on poultry carcasses quickly
frozen at –37oC and then stored at –21oC
 Susceptible to most disinfectants and to fumigation with
formaldehyde gas
TRANSMISSION

 Direct ovarian transmission is uncommon

(10%)
 Faecal contamination of eggshell during
laying or from contaminated nests or floor &
subsequent penetration by the organism
 Contaminated incubator, hatcher and brooder
 Contaminated feed, particularly those
containing animal proteins (Meat And Bone
Meal Etc.)
 Biologic vectors: insects, mice & wild birds
 Human contact and human waste products
 Direct bird-to- bird contact
PATHOGENESIS

 Affinity for epithelial cells of ceca and ileocecal

junction
 Intestinal colonization leading to persistent shedding
to salmonellae in the faeces
 Invasion beyond to G.I.T. and result in Salmonella
multiplication in reticuloendothelial tissue of the
liver and spleen
 Dissemination to colonize a variety of internal tissue
sites
 Extensive bacteremia occurs
PREDISPOSING FACTORS

 Prior infection with several species of coccidian

increase the ability of salmonella to colonize the
intestinal tracts of chicken
 Infection of poultry with immunosuppressive
viruses or bacteria e.g. IBD virus &
Corynebacterium
 Exposure to stressful conditions e.g. lowered
brooding temperature, water deprivation, forced
molting by feed deprivation
 Young age: Newly hatched chicks are highly
susceptible but become resistant as age advances.
Age-associated decrease in susceptibility is largely
due to protective intestinal microflora
CLINICAL SIGNS

 Signs of disease are rarely observed after the first 2

weeks of life
 In acute cases, when death occur in incubator or
during first few days of life, no signs may be noted
 Progressive state of somnolence, with closed eyes,
dropping wings & ruffled feathers
 Marked anorexia & emaciation
 Shiver & huddle near heat sources
 Profuse watery diarrhoea followed by dehydration
 Pasting or wetting of vent area
 Occasionally blindness and lameness
 Acute outbreaks in semi-mature & adult birds under
natural conditions are rare
POST MORTEM LESIONS

 Severe outbreaks show no lesions

 Congested organs
 Swollen & congested with hemorrhagic streaks or
necrotic foci in liver, heart and spleen
 Severe enteritis with focal necrotic lesions in the
mucosa of small intestine
 Cheesy caecal casts
 Unabsorbed and coagulated yolk material
 Chronically infected adults frequently exhibit no
lesions
DIAGNOSIS

 Clinical symptoms and lesions

 Isolation & identification of organism
 Sample sites:
Caudal ileum, Caecal contents, Caecal tonsils, Crop
 Primary isolation:
 a. Brilliant green agar supplemented with
sulfapyridine
 b. Colonies are transparent pink to deep fuchsia,
surrounded by a reddish medium
 PCR
 Serological identification:
 Whole-blood plate, serum plate, tube agglutination
 ELISA
CONTROL

 Salmonella status of poultry & their environment should be

monitored by frequent testing
 Bacteriologic monitoring of environment
 Serologic monitoring of birds
 Culturing of tissues from selected birds
 Egg culturing
 PT positive breeder flocks should be disposed off & should not
be used as a source of hatching eggs
 Hatchery sanitation
 Proper disinfection of hatching eggs & use of only clean eggs
for hatching purposes
 Feed prepared from known salmonella-free animal bye-
products should be used
 Rodents, wild birds and insects control
 Use of antibiotics, competitive exclusion treatments to reduce
the susceptibility of birds to Salmonella
 Competitive exclusion treatments involve administering defined or
undefined bacterial cultures to poultry in order to diminish intestinal
colonization by salmonellae___ called probiotics
Enlarged liver with focal necrosis
Necrotic Foci In The Liver
Cheesy plugs in the ceca
Caeca Are Filled With Gelatinous,
Fibrinous, Cheese-Like Exudate. This Is A
Finding, Characteristic For Salmonellosis
The Inflammatory Fibrinous Exudate In
Caeca Often Forms Casts With The Shape
Of Mucosal Folds
Button type lesions in the
intestine
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