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salmonella causes

Causes enteric or systemic disease
• 2 species: S. enterica and S. bongori
• S. enterica: 6 subspecies and 2000 serovar


host adapted salmonella

Host adapted serovars produce systemic infections (not diarrhea). In horses, host adapted Salmonella serovar Abortus‐equi causes abortion (not present in
the US)


non host adapted salmonella

typically produce colitis and
diarrhea. Can produce systemic disease in neonates


Salmonella epidemiology

Source of Infection: difficult to identify feed
already consumed, many infected animals, etc
• Route of infection: oral water, feed, feces,
worker contaminated hands, etc • Outbreaks in hospitalized animals
• Horses and cattle can shed the bacteria and
infect other horses • Horses shed more in summer than winter
Salmonella can persist in fecal matter inenvironment for months‐years.
• Feed: commercial equine feeds are manufacturedusing GMP (good manufacturing procedures), butnone is certified Salmonella free.
– Study shows that up to 40% of concentrate was positive for Salmonella. Contaminated feed given to broodmares shed bacteria, infect foals
– Pelleting can destroy Salmonella
Other sources of contamination of feed:
rodents’ and birds’ feces, bodies of insects
• Pasture contamination: organic fertilizers orbone meals, runoff from neighboring farms,contaminated water is used in irrigation or sprinkling
• Horses can shed the bacteria without clinicalsigns.


prevalence of salmonella

Prevalence in general equine population is
• Study: horses presenting diarrhea: 18% were
positive for Salmonella
• Normal intestinal flora and motility make
horses more resistant to Salmonella


salmonella risk factors

• Stress
– Transportation – Surgery – Change in feed (change in flora) – Antibiotics (change in flora) – Colic (diminished motility)
• Deworming • High environment temperatures (Summer)


salmonella pathogenesis

Transmitted by fecal‐oral route • Infection depends on bacterial load • Salmonella invades the intestinal epithelial cells
• Large inflammatory response: neutrophils releaseinflammatory mediators and is responsible forepithelial cell destruction and loss of epithelial
barrier functions
• Inflammation and epithelial necrosis result in lossof serum protein into the lumen, leading to
hypoproteinemiaRelease of endotoxins: effects on cardiacfunction (decreased coronary blood flow),fever, leukopenia, coagulopathies,
hypotension • Can also cause septicemia


salmonella clinical signs

ilent carriers
• Mild Infection: fever, decreased feed intake, loosestools. Differential diagnosis with mild respiratory
• Severe acute diarrhea: fever, colic, anorexia, fluidand electrolyte losses, dehydration, can lead to
liver and kidney damage and laminitis • Septicemia • Abortion
• Death


salmonella diagnosis and treatment

False‐positive and false‐negative are possible • Bacterial isolation • Fecal culture: difficult
• Treatment:
– Antibiotic is controversial: use only in animals at risk forsepticemia or persistent fever. Fluoroquinolones (IM) in
adult horses and Cephalosporines in foals – Fluids – Banamine – Corticosteroids are contra‐indicated – Nursing care


prevention of salmonella

Quarantine of new arrivals, especially those
coming back from hospital • Cleanliness • Avoid overcrowding of pastures • Pelleted feeds
• Control insect, rodent and bird access to horse
housing • No vaccine available • Zoonosis


lawsonia epidemiology and etiology

Obligate intracellular bacteria • Isolated and identified in the mid 1990s • Produces proliferative enteropathy
• Worldwide distribution, causes disease in many
• Source of infection not yet identified in foals
– Many potential reservoirs: deer, foxes, wolves, etc
• Trans‐species transmission has been
experimentally demonstrated • Fecal‐oral transmission


lawsonia pathogenesis

everity of disease depends on load of bacteria
ingested and immune status of horse • Pathogenesis not yet described in horse
• Bacteria invade dividing intestinal cells. Infectedcells continue to divide even if heavily infected.
• PE develops as a progressive proliferation ofimmature epithelial cells, invaded with
intracellular bacteria
• Lesions reduce intestinal digestive and absorptive
capabilities diarrhea and weight loss


lawsonia clinical signs

Age: 3‐13 months
• Depression, fever, anorexia, weight loss,
diarrhea, colic • Poor body condition • Rough coat • Pot‐bellied


lawsonia pathological findings

Emaciation, subcutaneous edema
• Thickening of intestinal mucosa, lesions
generally on duodenum and ileum • Muscular hypertrophy of intestinal wall • Histology: hyperplasia of epithelium


lawsonia diagnosis

Differential: common GI diseases intestinalobstruction, sand impaction, parasites, ulcers,Salmonella, Rhodococcus, Clostridium, PHF,etc
• Clinical signs, exclusion of other entericdiseases, abdominal ultrasound thickening of intestinal wall, serology


lawsonia treatment

Antibiotics: able to enter the cell as organism
is obligate intracellular • Erythromycin PO, TID, for 3 weeks • Chloramphenicol and tetracyclines also useful
• Penicillin, SMZ‐TMP, gentamicin does not
treat disease • Omeprazole • Fluids


lawsonia prevention

Epidemiology is not very understood, so effective
methods of prevention is not known • Isolation of infected foals
• Disinfection of barn and stalls: paraquat,
• Humans: L. intracellularis is not considered azoonotic disease yet, but the disease has beendescribed recently in primates. People may besusceptible to infection.