Salmonella
Salmonella
Salmonella
- Subgroup 1
- S. cholerae-suis
- S. typhi
- S. enteritidis
- subgroups 2-5
- cold-blooded animals
- environment
- Human Pathogens
- Salmonella typhi
- Salmonella paratyphi
S. cholerae-suis: Transmission
- Humans and animals to animal feeds
Incidence in Ontario
salmonellosis 1003 639 581
Salmonella: Clinical Syndromes
- Bacteremia: followed by gastroenteritis
- Asymptomatic colonization
Salmonella: Gastroenteritis
- nausea, vomiting, diarrhea, fever, abdominal cramps, myalgia, headache
- 2 days - 1 week: usually spontaneous resolution
Mechanism of Pathogenicity Gastroenteritis
- absorbed to brush border of epithelial cells of small intestine and colon
- migrate to lamina propria, ileocaecal
- multiply in lymphoid follicles
- reticulendothelial hyperplasia and hypertrophy
Hyperplasia vs Hypertrophy
- Hyperplasia : abnormal increases in the number of normal cells (organ swells)
- Hypertrophy : increase in size of an organ
Salmonella:Bacteremia
Gram negative bacteremia is non-suppurative
Enteric Fever: S. typhi
- intraluminal multiplication
- mononuclear response (macrophages)
- 2nd week - lymphoid hyperplasia (mesenteric lymph nodes)
S. typhi
- found in stool - enteric media and selenite enrichment
Mechanism of Fluid Secretion Stimulation
- Arachidonic acid with the enzyme cyclooxygenase stimulates the production of prostaglandin which then causes an increase in cAMP (cyclic adenosine monophosphate) and stimulates fluid secretion.
Reduction of Fluid Secretion
- aspirin - non-steroidal, anti-inflammatory
- inhibits cyclo-oxygenase which is necessary to
- produce prostaglandins
The End