Avian Salmonellosis

Salmonella is a group of closely related organisms belongs to Genus Salmonella responsible for a
variety of acute and chronic diseases in poultry. These are intercellular organisms. With a dominant
vertically transmission pattern. The diseases occur with salmonella in chicken are economic
concern lead to severe losses to the industry. These are also one of the very important zoonotic
diseases. Salmonella consists of more than 2500 serologically distinguishable variants
Salmonellae in poultry can be grouped into three categories
Two nonmotile serovars (host-specific)
S. pullorum
S. gallinarum
One motile serovars (non-host specific member)
Paratyphoid (PT)

Type of diseases by Salmonella

Pullorum disease
Caused by S. pullorum, is an acute systemic disease of young chicks or poults. With a
severe septicemia and a major mortalities.
Fowl typhoid
Caused by S. gallinarum, is an acute or chronic septicemic disease that most often
affects mature birds.
Paratyphoid (PT).
S. enterica subspecies enterica serovars typhimurium.
It is a major food-borne disease in humans. Paratyphoid infections of poultry are very
common, they seldom cause acute systemic disease except in highly susceptible
young birds.

Etiology
Salmonellae are
Facultative anaerobic , Gram-negative rod- shaped bacteria. Its Size 2–5 microns
long by 0.5–1.5 microns wide. The organisms are either motile by peritrichous flagella
Others are non-motile too.
There is a range of different media for the growth of salmonella species. Among those;
Non-selective Media: Buffered Peptone
Selective Media: Salmonella shagella (SS) agar, selenite-F
Selective Agar: Brilliant green Agar

Growth characteristics
S. pullorum
Very small colorless colonies
S. gallinarum
2-3mm dome shape colonies with black precipitation
Survival outside Host
Salmonella survive well and are able to multiply outside the body. Can maintain virulence at
least 14 months in soil and it rapidly multiplies in egg stored at 20 C. Organism can be killed in 5
minutes at 60C. it may survive up to 13 months on poultry carcass and can easily kill by normal
disinfectants like phenols

Susceptible Hosts
Very vast host range include Domestic animals, birds, rodents, snakes, lizards and man.
Chicken are most commonly affected (broiler parent and brown shell egg layers), also infect
turkey, guinea fowl and ducks, pheasants, Wild birds, sparrows, parrots, pigeons etc.

Transmission
1- Horizontal
a) Between Flock
Contaminated feedstuff (fish meal, poultry byproducts, blood meal)
Rodents (rats and mice)
Direct contact with clinically affected and carrier birds)
Indirect contact with contaminated shoesm equopments, liter etc
Scavenger animals (dog, cats)
Flies potential source
Beetles
b) Within Flock

Droppings contaminate the environment and major source

Cannibalism
Egg eating of other birds

2- Vertical Transmission
a) Direct Trans ovarian
b) Directly from breeder to egg to chick
Contaminated eggs
Hatchery borne diseases

Factor Effect the Susceptibility

i- Age
Under 5 days of age highly susceptible. Meanwhile severe losses occur in 2nd week.
Losses are very less in birds of more than 6 week of age. In pullets susceptibility
increases from 3 month age to day of lay
ii- Sex
S. pullorum is more common in female than male.
Genetic Resistance play an important role
Light breeds (Leghorns) are more resistant than heavy breeds (Rhodes Island Red and
Light Sussex). Free range birds are more affected than control housed b9rids
Stress Factors
Overcrowding, inadequate feed and malnutrition, concurrent diseases are major
contributing factors.Chilling temperature and moisture help the long survival of bird.
 Pullorum Disease
Caused by S. pullorum, is an acute systemic disease of young chicks or poults. With a
severe septicemia and a major mortalities.
Pathogenesis
 Incubation period
o Young chicks 4-5 days
o Adult birds 16-21 days
 Organism enter through
 ingestiions
 inhalation
 adhesin (via naval card)
 lead to septicemia
 manifested as
 severe enteritis
 respiratraty signs
 lesins in the visceral organs
Clinical signs
1- Young chicks:
Under 3 wks suffer with highly fatal disease outbreaks. Severe white urates vent
pasting is common.
Chick hatched may be found dead mortality reached at peak within 7 days. Weakness and
sleepiness in the young chicks is very common. In the brooder peak mortality between
2nd and 3rd week. Head hanging and sleepy appearance common,. Bird look like dipped in
water. Pot belly appearance is common in acute septicemic cases. Bird cry while
defecating. Labored breathing also observed.
Rare signs
Arthritis and lameness
Blindness
Morbidity 10-80 percent
Mortality start at hatching and extend up to 21 days, generally 2-50 percent. In severely
immune compromised birds may reach up to 90%
2- Mature Birds
Mostly resistant (only sub clinical disease)
Depression, listlessness, pale comb, diarrhea, and increased thirst

Gross Lesion
Liver
Enlarged, congested and a streak of hemorrhage
In acute septicemia small area of necrosis (pin point peas size observed on Liver,
Heart, and lungs. Omphalitis is also common
Chronic case Delayed yolk absorption along with White nodular areas in muscle, heart,
gizzard and in the wall of intestines. Multiple nodules in the lung. Splenomegaly also
observed. Kidney congested and anemic may also filled with urates. Hock joint swelled
it may contain pus
In adult Birds
Mostly gross lesions are not present
In layers
Misshapen ovaries along with Ova contain oily or cheesy material
Endo and myocarditis
Grayish nodule on heart
Greyish miliary necrosis on liver
Kidney filled with urates

Microscopic Lesions
Intestine
Hyperemia and hemorrhages of mucosa
Liver
Hemorrhages and focal necrosis

Lungs
Congestion and hemorrhages, later stages contain nonnuclear cell infiltration

Fowl Typhoid
Acute septicemic disease, mostly effect adult and grower birds. Disease is characterized by
Sleepiness, Profuse sulphur yellow diarrhea and varying degree of anemia.
Pathogenesis
 Incubation period 4-6 days
 Entry through oral route
 Invade intestinal lining
 Transient bacteremia after 3 hours
 Bacteria increase in spleen and liver
 Bacteremia last for 3 days
 Localization of bacteria in reticuloendothelial cells transfer the bacteria into
 Intestinal wall
 Live rand supply and rapidly multiply here.
 In acute cased death occurs with 48 hrs
 In chronic cases proliferative lesions develop death with irregular intervals
 Survived animals become carrier

Clinical Signs
 Few watery, bright yellow splashes (urates).
 Increased temperature first 2 days 107 F then 110-111 F.
 Marked thirst and listlessness.
 Mucoid yellow droppings.
 Anemia with hemolysis (PCV 30%).
 Comb become congested in acute cases and anemic in chronic cases.
 Arthritis.
 Mortality: 4-50%.
 Egg production decreased
Gross Lesions
Acute Case
 Vent pasted with liquid greenish to yellowish droppings
 Skeletal muscle congested, Carcass may show jaundice like appearance
 Liver enlarged dark red and friable (Bronze Liver due to unexcreted bile)
 Swollen spleen.
 Catarrhal enteritis
Chronic Cases
 Emaciated and anemic carcass
 Oophoritis in laying hens (degenerated and misshapen ova)
 White to gray nodule on heart (pea size)
 Nodule In the small intestine
 Lungs are congested, edematous
 Acute myocardial necrosis
 Brown color lungs with nodular formation
 Characteristic Bronze color liver
 Mottled liver with multiple necrosis
 Miliary and spot necrosis of the liver
 Hypertrophied spleen
 Sever ulcer and hemorrhages in anterior small intestine
Microscopic Lesions
Diffused paranchymatous hepatitis
Myocardium show fibrinoid necrosis
Proliferative cellular reaction in pancreas and intestine

Paratyphoid
A large group of acute and chronic infection caused by many salmonella species Caused by
motile Salmonella (S. entertidis and s.typhimurium). Mostly it cause local infection however it
can cause septicemic changes as well.

Clinical Signs
a) In young chicks
 Huddling around heat source with lower head and close eyes
 Drowsy chicken
 Increased chirping sounds
 Increases thirst
 Stunting growth is common\
 Causes up to 3 percent loses during first 2 wks.
 Most acute disease occur in less than 4 wk age
 b) Adult Birds
 No specific sigs
 Mortality less than 10%
 Drowsy chicken

Gross Lesions
 Dehydration and emaciation
 Liver congested sometimes
 Enteritis is common
 Caseous cast in the cecum (cream to yellow color)
 Small intestine contain button like lesions
 Pericarditis and myocardial necrosis
 Arthritis and swollen joints
 Ceca filled wth gelatinous cheesy material
 Cast of cheesy material in ceca
 Pale necrotic foci on the liver
Diagnosis
A definitive diagnosis of salmonellosis requires the
Isolation and identification
A tentative diagnosis, however, can be made based on
 flock history
 clinical signs
 Mortality
 Specific lesions.
Motility based test could also performed for the differentiation of motile and non-motile
salmonella species.

Identification of Cultures

The colonies of S. Pullorum may appear small, smooth, and translucent on nutrient media after
24 hours of incubation.
S. Gallinarum, colonies are smooth, blue-gray, moist, circular,and entire. TSI agar slants for
preliminary differentiation.
S. Pullorum and S. Gallinarum produce a red slant with a yellow butt that shows delayed
blackening from H2S production.

Serology
 Serologic tests to detect PD and FT and PT include
 Macroscopic tube agglutination (TA) test,
 Rapid serum (RS) test,
 Stained antigen whole blood (WB) test,
 Microagglutination (MA) test.
 Enzyme-linked immunosorbent assays (ELISA) for detecting S. Pullorum and S.
Gallinarum antibodies have been developed
Differential Diagnosis
The clinical signs and lesions produced by PD or FT are not pathognomonic.
 Aspergillus or other fungi may produce similar lesions in the lungs.
 S. Pullorum and S. Gallinarum can localize in major joints and tendon sheaths of chicks.
Such signs and lesions resemble those produced by organisms such as Mycoplasma
synoviae, Staphylococcus aureus, Pasteurella multocida.
 Sometimes the white nodules in the heart of young chicks may resemble Marek’s disease
tumors
 Those in the liver resemble those produced by Yersinia pseudotuberculosis.

Vaccination
Not normally used; however possibilities are there
S. pullorum: no general vaccine available
S. gallinarum
Killed and live attenuated vaccine used
Rough strain 9R
Smnooth Straiins 9S
S. enteritidis
Live modified vaccine

Other Approaches
Incorporation of commercial formic acid preparations in the feed has been found to
significantly reduce the infection
Competitive exclusion using gut flora of useful bacteria compete the paratyphoid organism to
attach and penetrate the mucosal wall of epithelium

Treatment
Necessary to stop mortality However, It does not prevent to birds to become carrier. It can
prolong carrier state of birds
Choose the drugs on the basis of sensitivity on a culture medium
Use each antibiotic minimum for 5 days.
Furazolidone 400g/ton for two weeks
 Sulphonamides (Sulphamerazine (0.4% in drinking water OR 0.5% in mash
 Sulfadiazine and sulfapyrazine 0.5% in feed.
 Tetracycline and Oxytetracycline hydrochloride 250g/ton feed.
 Chlortetracycline 2g/kg feed
 Chloramphenicol 0.5% in feed for 10 days (reduce mortality)
 VitB complex level should enhanced
