Salmonellosis (Paratyphoid) in Animals

Salmonellosis (Paratyphoid) is an acute, chronic and contagious disease of all species of animals, birds and human beings characterised by the development of severe dysentery and gastroenteritis.

Salmonellosis (Paratyphoid) causes the most important zoonotic problem in human beings.

Etiology

Until recent times more than 2500 salmonella serotypes have been identified and all of which may be considered potentially pathogenic.

The causative agent is a gram negative, non-sporing and rod shaped organism. It is killed by drying, sunlight and heat. But they may remain alive in soil for 7 months in water, feces and pasture. In moist soil they may remain viable for 12 months or more.

The organism can be destroyed at 60° C for 20 minutes. some of the important salmonella species are as follows.

• Salmonella enterica – the type species
• S. bongori
• S. enterica subsp. enterica is again classified as four serotypes
• S. enteritis
• S. typhimurium
• S. typhi
• S. cholerasuis
• S. tyhphi, S. paratyphoic – Human
• S. typhimurium – cattle, sheep and goats, pig and horses
• S. dublin – Cattle
• S. cholerasuis – Pigs
• S. abortivo equina – Horse
• S. aborus ovis – sheep

Epidemiolgy

Prevalence of infection

The disease is world wide in distribution however, almost it has been reported from all the tropical countries.

In India, many states have reported the prevalence of salmonellosis, despites various steps taken at national and international levels by the direction of the FAO and WHO human salmonellosis and has been increasing in the recent years.

The disease has got economic importance as it causes high morbidity and mortality.

Sources of infection

Animal may contract the infection from human sources.

Carrier states can exists. Carrier animals excrete the causative agents through their feces. Besides domestic animals, deer, elk, raccoons, possums may remain spread the infection to cattle.

Contaminated water is an important source of transmission.

Transmission

• The infection is transmitted horizontally by direct exposure of the susceptible animals from the infected population.
• Infection is directly spread by means of ingestion
• Cattle acquire infection from infected cattle or pigs or horse or sheep or dogs or poultry and pigeon.

Host Affected

• Salmonellosis is prevalent in cattle, sheep, human, rodents, horse and dogs.
• Most animals are affected by specific salmonella species.

Pathogenesis

Infection is spread by ingestion through oral route followed by reaching the distal ileum, caecum and from there invade the mucosa, where in they replicate in submucosa and payers patches.

In young animals and adults those have decreased immunity the organism spread beyond mesenteric lymph node and establishes the infection in reticulo-endothelium cells of liver followed by rapid entry into the blood circulation.

Invasion of the organism in the blood stream causes pyrexia in 24-48 hours and acute infection in 5-9days. It is a rapidly fatal condition. If invasion is sufficient to cause only a bacteremia, acute enteritis may develop and abortion is a final sequelae in sheep and cattle.

Many animals may survive out of infection and the organism localized in the mesenteric lymphnode, liver, spleen, particularly in gall bladder.

In chronic cases, organism shed intermittently from gall bladder and causes the foci of infection in the intestinal wall into the feces and occasionally into milk.

Enteritis: Develop at first time in carrier animals. The enteric salmonellosis much more complex than cholera, involving an increase in mucosal cell cyclic AMP content and prostaglandin concentration and inflammatory response to invading bacteria. Within a minute following infection in ileal loops in calves, salmonella can be seem to enter both M cells and enterocytes that process to over lie the domed villi associated with lymphoid follicles and absorptive villi. The organism must invade the intestinal mucosal epithelium to cause disease.

S. typhimurium requires a function of type III secretions system encoded by salmonella pathogenecity island (SPII) to cause diarrhoea. SPII secretions system direct the secreted effector protein into target epithelial cells. This effector proteins are virulent factor required for invasion and the induction of fluid secretion inflammatory response.

Virulent factors: Adhesion pili, flagella, cytotoxin, enterotoxin, LPS, and inflammatory response that they initiate in the intestinal wall. S.cholerasuisIn pigs it in 36 hours causes erosion, edema of caecal mucosa.

• In 64 hours, intestinal wall is thickened, diffuse and caseation overlying the erosions.
• In 96-128 hours, necrotic membrane sloughs and lose all function.
• In 176 hours, whole intestine is inflamed and obliteration of muscular coat occurs.

Colon is majorly affected in S.typhimurium can cause either local or diffuse colitis.

Organism proliferates in intestine, invade the epithelium and reaches the mesenteric lymph node. S.cholerasuis invade enterocytes by penetration of the brush border epithelium, results in local loss of microvilli and the bacteria endocytosed in to membrane bound vacuoles.

Clinical Signs

• Septicemic form New born foals, calves, young pigs upto 4 months old are highly susceptible.
• Prominent depression.
• Dullness and prostration.
• High fever 40.5-42 °C and death occurs in 24-48 hours
• Acute enteric  form Adult animals are highly affected.
• High fever
• Severe fetid diarrhoea, dysentery and occasional tenesmus.
• Feces with putrid odor and contains mucus, blood, fibrinous casts, complete tubular casts of intestine.
• Intestinal mucosa in casts or sheets.
• Complete anorexia and increase thirst.
• Increase heart and respiration rate and congestion noticed.
• Pregnant animals abort.
• Severe dehydration, toxaemia, loss of weight, weakness, recumbent, and death in 2-5 days.
• Chronic enteric  form A severe outbreak.
• Occasional in cattle and horses.

Calves

• Intermittent or persistent diarrhoea.
• Occasional spots of blood, mucus and firm fibrous casts present.
• Loss of weight and emaciation.

Cattle

• Septicemic form
• Depression, toxaemia, fever, dyspneoa  and  weakness.
• Nervous signs: incoordination and nystagamus.
• Diarrhoea and dysentery.
• Acute enteric form Abortion in pregnant cows.
• Polyarthritis in calves .
• Dysentery with large blood clots.
• Complete agalactiae, abdominal pain, with kicking of abdomen, rolling, crackling, groaning and looking at the flanks are more common features.
• Rectal examination at this stage creates severe distress. Chronic enteric form Inappetance, decrease weight gain, unthriftiness, acute enteritis.

Pigs

• Dark purple discolouration of skin in abdomen and ear. Subcutaneous petichial hemorrhages.
• Nervous signs: Tremor, weakness, paralysis, convulsion and fatality 100%.
• In four weeks old, meningitis, prostration, clonic convulsion and encephalitis.
• Enteritis and pneumonia.

Horses

• Sporadic occurrence.
• Asymptomatic animals shed organism.
• Subacute enteric form in adult horses (Endemic form): Fever, depression, neutropenia –left shift, acute fulminating enteritis and diarrhoea.

Necropsy Findings

• Lesions in the brain, neuro encephalitis, polyarthritis and fatal meningo encephalitis.
• S. agona in 7 days old foals causes head tilt, seizures and diarrhoea.
• In gastric mucosa develops haemorrhage and edema.
• In intestinal mucosa hyperaemia necrosis and ulcers.
• Caecum, zebra markings produced.
• Liver is enlarged with necrotic foci.
• Spleen is enlarged and become pulpy.
• Mesenteric lymph glands are haemorrhagic.
• In Lungs and pleura, pleural adhesion and abscess present.
• Pericardial and sub pericardial haemorrhage occurs.
• Skin becomes discolored in pigs.

Diagnosis

• Based on clinical signs and necropsy findings.
• Isolation and identification of organism through culture, and FAT.
• Most of the serological tests are lacking both sensitivity and specificity.
• Bacterial culture and detection of antigen.
• Antigen Capture Elisa.
• PCR and DNA probe test.

Sample Collection

• Feces
• Blood
• Serum
• Milk
• Body fluid and tissues

Differential Diagnosis

• Coccidiosis
• Pasteurellosis
• Liver fluke infestation
• Poisoning
• Colibacillosis
• Paratuberculosis

Treatment

Ruminants

• Ceftiofur: 5mg/kg 1/m 24 hours is  effective. Concentration should be maintained above MICs.
• Amoxicillin, ampicllin, Trimethoprim, sulphadiazine, sulfadimidine, Framycetin and Nitrofurazone can be used.

Horses

• Genetamycin (3mg/kg), Combined with ampicillin 20 mg/kg bw I/V 8-12 hours intervals.
• Trimethoprim and sulfonamide twice daily i/v combine dose 30 mg/kg bw.
• Combined sulfadoxin, sulfadiazine and sulfamethaxazole can be used in combined dose.

Foals

• Trimethoprim and sulfadoxine.
• Supportive therapy 5% Sodium bicarbonate solution 5-8 L/400 kg bw I/V over a 2 hours period.
• Potassium chloride 30g in 8 L water twice daily.

Prevention

• To prevent the human infection the following measures may be adopted.
• Effective pasteurization of milk is to be made.
• Proper refrigeration of food is required.
• Sterilisation of animal food liable to contamination.
• High standards of abattoir hygeine required.
• Proper handling of fish has to be made.

Control

• Calving should be kept  in a hygienic place.
• Calves should be allowed to have colostrum following their birth.
• Calves should not be exposed to adverse weather (too hot or too cold environment).
• Overcrowding of animals should be avoided.
• Animals should be provided with pure wholesome water.
• Animal should not be allowed to drink water from sewage or staganant water.
• Other susceptible animals like horse, sheep pigs, birds should be placed away from cattle shed.
• Affected animals should be brought under immediate treatment.