Salmonellosis

Etiology:
- Family : Enterobacteriaceae .
- Genus: Salmonella ---2200 serotypes .
- S. typhi ,S.paratyphiA and Cwhich affected only man .
- S. Dublin ----- Cattle .
- S. abortus –equi --------horse .
- S. abortusovis --------sheep.
- S. choleraesuis -------swine .
- S. typhimurium -------- man and animals .
- Cattle -: S. typhimurium ,S. Dublin ,S.newport .
- Sheep and Goat : S.typhimurium,S.dublin ,S. Newport ,S. anatum .
- Pig : Styphimurium ,S.choleraesuis .
- Horse : S.typhimurium ,S. anatum ,S. Newport ,S. enteritidis ,S.heidelberg
Epidemiology:
- Morbidity rate in outbreak 50% ,mortality rate 100%
- Spread occur by direct and indirect .
- Infected animal are the source of the organism excret direct or indirectly by
contamination of environment ,feed ,water supplies.
- Farm animal may be infected in many way :
- Animal to animal transmission .
- Contaminated animal feed and contaminated environment ( soil, birds, rodents , insects,
water supplies ) .
- The excretion of the organism increase by stress .
- During slaughter ,fecal contamination of the carcass.
- Milk can be contaminated directily by excreted organism from udder .
- All infected adult become carriers but calves rarely become carriers in sheep and cattle
,the carrier state may persist for as long as 10 weeks and in horse up to 14 months .
- Pathogenesis :
Oral infection then invasion intestinal wall in ileum ,cecum, mesentrc L N.------then
development of the disease .
- And it depend on –immun status ,Age of host ,Stress , Virulence of Strain .
Clinical Finding :
1- Septicemia :characteristic form in newborn foals and calves and ayoung pig up
to 4 month old , depression ,dullness ,prostration ,high fever and death within
24-48 hours .
2- Acute enteritis :
-common form in adult animals of all species . ,high fever .anorexia .
- sever fluid diarrhea , some time dysentery with tenesmus ,feces have a putrid smell
and contain mucus ,some times blood ,fibrinous casts .
-puls rate is rapid, respiration is rapid and shallow .
-pregnant animal abort ( invasion to fetus ).
- dehydration and toxemia,recumbent and animal die in 2-5 days.
-polyarthritis or pneumonia complicate the recovery phase .
3- Chronic Enteritis :
-occur in cattle and adult horse .
-intermittent or persistent diarrhea with spots of blood ,mucus and firm fibrinous
casts.
-intermittent moderate fever and loss of weight .
Clinical Pathology :
- Bacterial culture ( isolationof organism from blood and feces) .
- Biopsy of rectal mucosa .
- Serological test .
Necropsy Finding :
- Septicemia : submucosal,subserous petechial hemorrhage .
- Acute enteric form : inflammation of larg and small intestine .
 Submucosal petechialtion ,diffuce hemorrhage enteritis
Sever necrotic enteritis in ileum ,lymph node enlargement.
- Chronic form : discrete area of necrosis wall of cecum ,colon the wall is thick and
covered with yellow-gray necrotic material overlying a red granular surface .-salmonella
present in heart blood ,spleen,liver ,bile mesenteric Lymph node and intestinal contents
in both septicemia and acute stage .
Differential Diagnosis :
-Septicemic form in calves resemble:
1- septicemia due to E coli .bacterial isolation ,salmonella has strong tendency for occur
during second and third weeks of life ( colibacillosis occur at first week) ,
2-Acute enteric form confused with Coccidiosis and Acute abdominal pain (acute
intestinal obstractionthere is profuse diarrhea,dysentery ).
3-Winter dysentery occur in explosive outbreak .
4-Mucosal disease .
5-Bracken fern poisoning .
6- Arsenic poisoning .
7-Lead poisoning .
Chronic form ;
1-Johnes Disease.
2-Chronic molybdenum poisoning .
3-massive stomach fluke infestation.
In sheep :
1-Coccidia
2-Compylobacter spp.
3-Parasitic infestation.
Treatment :
Rx use proad spectrum antibiotic and sulfonamides and antibacterial therapy.
1-Trimethoprim-sullfadoxine,parenterally daily until clinical recovery .
2-Ampicillin and amoxicillin orally .
3-Sulfadimidine .
4-Gentamicine 250mg i/v twice daily .
5-Ampicillin 1gm every 6hr.i/m .
6-Astringent and fluid orally or parenterallyto replace lost of electrolyte and fluid .
Control:
1- Prevention of introduction ( carrier animal and contaminated food stuffs ).
2- Guaranten for animal and disinfection .
3- Vaccination use killed bacterin and live attenuated vaccine use prenatal vaccine to
provid passive immunization of newborn for 6 weeks or use
Auto genus vaccine.
4- Identify the carrier animal cull or isolation and treatment and rechecked .
5- The prophylactic use of antibiotic( Oxytetracyclin in feed ) at rate of 10 gm /tone.
 Haemorrhagic Septicemia
Etiology :
The disease is presumed to be primary pasturellosis caused by Pasturella
multocida type 1 ( or B ) and occasionally type 4 ( D ) and type E ( 1 , 2 ) .

Epidemiology :
◙ Host range .
♦ Cattle and water buffaloes are the principal hosts . Septicemia and its
widely considered that buffaloes are the more susceptible .
♦ Haemorrhagic Septicemia have been reported in sheep and swine . It is
not a frequent or significant disease .
♦ Cases have been reported in deer , elephants , and yaks .
♦ There is no evidence of a reservoir of infection outside the principal
hosts .

◙ Mode of transmission .
♦ The disease is spread by direct or indirect contact .
♦ The source of infection is infected animals or carriers .
♦ Outbreaks of disease are often associated with wet humid weather
during the rainy seasons .
♦ Spread occurs by ingestion of contaminated foodstuffs .
♦ The disease may be transmitted by ticks or biting insects .

Pathogenesis :
♦ The portal of entry of infection is thought to be tonsils .
♦ A fulminating septicemia occurs which associated with the capsular
material of organism . .

1
 ♦ The effect of the septicemia are more severe in the respiratory tract ,
heart and gastrointestinal tract .
P multocida are common commensal organisms of the tonsils and
nasopharynx of healthy animals.
In order for these organisms to cause infection, a combination of stressors including heat,
overcrowding, exposure to inclement weather, poor ventilation, handling, and
transportation leaves sheep and goats susceptible to respiratory viral infections.
Parainfluenza 3, adenovirus type 6, respiratory syncytial virus, possibly bovine adenovirus
type 2, ovine adenovirus types 1 and 5, and reovirus type 1 .
-The combination of stressors and primary infections are thought to break down the
mucosal barrier integrity of the lower respiratory tract allowing bacteria to colonize,
proliferate and induce significant tissue damage.
The virulence of P is mediated by the action of several factors, including .
-endotoxin, leukotoxin, and capsular polysaccharide, that afford the bacteria advantages
over host immunity.
The leukotoxin is particularly important in the pathogenesis because it is specifically toxic
to ruminant leukocytes resulting in fibrin deposition in lungs and on pleural surfaces.
-The lipopolysaccharide endotoxin contributes to adverse reactions in the lungs and also
leads to systemic circulatory failure and shock.
The capsular polysaccharide prevents the phagocytosis of the bacteria and assists in
attachment to the alveolar epithelial surface.
Survival of the acute phase of pneumonic pasteurellosis is dependent on the
extent of lung involvement and damage in the lower respiratory tract.
♦ The portal of entry of infection is thought to be tonsils .
♦ A fulminating septicemia occurs which associated with the capsular
material of organism . .
♦ The effect of the septicemia are more severe in the respiratory tract ,
heart and gastrointestinal tract .
Incubation period .
Cattle or buffaloes artificially inoculated subcutaneously with lethal dose
show clinical signs within a few hours and succumb within 18 – 30 hours .

2
Clinical findings
♦ Sudden onset of fever ( 41 – 42 C ) , profuse salivation , sub mucosal
petechiation , severe depression and death in about 24 hours ( acute septicemia
).
♦ On range lands , animals may be found dead without any clinical signs .
♦ Localization may occur in subcutaneous tissue resulting in the
development of warm , painful swelling about the throat , dewlap ,
brisket or perineum and severe dyspnea may occur if the respiration is
obstructed .
♦ In the later stage of the outbreak , some affected animals develop signs of
pulmonary or alimentary involvement .

Clinical pathology .
♦ Culture and detection of bacteria : -
 The organism can be cultured from the blood or nasal swabs from
the animals within few hours of death .
 From older carcasses a long bones is used for culture from the bone
marrow .
 Samples of blood are injected into mice which will die in 24 -36
hours . Smear from the mouse blood will reveal the organism .
♦ Serology .
Necropsy findings .
♦ The gross findings are usually limited to generalized petechial
heamorrhage particularly under the serosa and edema of the lungs
and lymph nodes.
♦ Subcutaneous infiltration of gelatinous fluid may be present .

3
 ♦ There are lesions of early pneumonia and haemorrhagic
gastroenteritis.
♦ Varying degree of lung involvement range from generalized
congestion to patchy or extensive consolidation . Thickening of
interlobular septa may be prominent .
♦ Lymph nodes in thoracic region are enlarged and haemorrhagic .
♦ Isolation of causative agent is best attempted from heart blood and
spleen .

Differential diagnosis .
♦ Anthrax .
♦ Black leg .
♦ Acute leptospirosis .

Treatment :
♦ Oxytetracycline in Pigs .
♦ Sulfonamides in Cattle .

Control :
Vaccination with killed vaccine resulting in long lasting immunity .
The vaccination repeated annually