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Flashcards in salmonella and lawsonia Deck (17)
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1

salmonella causes

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

2

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)

3

non host adapted salmonella

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

4

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.

5

prevalence of salmonella

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

6

salmonella risk factors

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

7

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

8

salmonella clinical signs

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

9

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

10

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

11

lawsonia epidemiology and etiology

Obligate intracellular bacteria • Isolated and identified in the mid 1990s • Produces proliferative enteropathy
• Worldwide distribution, causes disease in many
species
• 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

12

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

13

lawsonia clinical signs

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

14

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

15

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

16

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

17

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,
povidone‐iodine
• Humans: L. intracellularis is not considered azoonotic disease yet, but the disease has beendescribed recently in primates. People may besusceptible to infection.