food poisoning Flashcards
Symptoms of Microbial food poisoning due to
1-invasion of intestinal mucosa e.g. E coli, Salmonella,
Shigella, Lesteria (fever, faecal leucocytosis)
2-toxin production in the GIT by bacteria and virus
(mild –self limiting )
Toxigenic
I.P.
Duration of illness
< 6 hours
Self limited<24 h
Toxogenic C/P: Vomiting Diarrhoea Abdominal pain Fever Bloody stool
Prominent Profuse and watery \++++ -ve -ve
Toxigenic
Pus cells in stools
Treatment
-ve
Fluid replacement
No antibiotics
Invasive
I.P.
Duration of illness
> 8-24 h
Several days
Invasive C/P: Vomiting Diarrhoea Abdominal pain Fever Bloody stool
Less prominent Mucoid and bloody \+ve \+ve \+ve
Invasive
Pus cells in stools
Treatment
+ve
I.V. fluids
Antibiotics are indicated
Diagnosis of food poisoning
History of food consumption. Possibly within a group
C/P of food poisoning
Investigations of food poisoning
a) CBC: (leucocytosis in invasive type)
b) Stool analysis and culture(for epidemiologic concern).
c) Pus cells indicates bacterial invasion of the wall of intestine)
d) Serum electrolytes, blood glucose and renal function tests
Complications of food poisoning
1-In neglected cases with severe vomiting: -Dehydration -Hypotension -Pre-renal failure 2-Rarely with enteroinvasive: -Haemorrhagic colitis -Haemolytic- uremic syndrome -Septicaemia -Peritonitis.
Treatment
1-Fluid replacement by I.V. saline (oral rehydration if possible).
2-Antiemetic
3-Antispasmodics
4-Antibiotics for enteroinvasive (bacterim, quinolone) then according to stool culture and sensitivity.
Food poisoning with Muscle weakness (Botulism) Caused by:
Clostridium botulinum toxin
Epidemiology of Botulism :
- Ingestion of preformed toxin by the bacteria in improperly preserved food (canned , fermented or smoked).
- In outbreaks with consumption of the salted fish ( fesikh)
Botulism How it is formed
1-Spores of clostridium botulium
2-Germination and release of botulinum toxin
(if anaerobic medium)
3- The toxin is very potent but heat labile
Botulism How it works
The toxin binds irreversibly to peripheral neuromuscular junction so prevents the release of ACh and produces block. The toxin does not cross the blood brain barrier