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
C/P of botulism
Incubation period: few hours to 8 days
Initially nausea, vomiting, abdominal pain
Anticholinergic manifestations
Neurological: Progressive paralysis of cranial nerves ( squint , ptosis, dysarthria—dysphagia)
Descending paralysis may involve resp. ms.
No sensory effect or coma (does not cross B.B.B.)
How to confirm diagnosis of botulism
History
Presenting picture( dry throat, squint or ptosis, gastro -enteritis)
Investigation:
1-Toxin assay by mouse neutralization test: suspected samples are inoculated in rat peritoneal cavity, test is +ve if the rat develops paralysis
2-Anaerobic culture of serum, stool, vomitus, consumed food)
Treatment of botulism
I.Emergency measures (ABC) : Maintain an open airway and assist ventilation if necessary.
II.Antidote:
-Botulinum antitoxin (trivalent ABE) is given.
-One vial /4 hours for at lease 4-6 vials
-Most effective when given in first 24 h
-It can only bind with the circulating toxin.
-It prevents further deterioration of the condition. Does not reverse already existing neurological complications)
III. Decontamination: gastric lavage and activated charcoal in asymptomatic patients shortly after the consumption of contaminated food.
IV. Symptomatic treatment
V. Notification of health authorities.
A. Infant botulism
It is not caused by ingestion of spore-contaminated food consumption with subsequent in vivo bacterial germination and toxin elaboration in the immature infant gut (which lacks gastric and bile acids).
The disease is characterized by hypotonia, constipation, tachycardia, difficulty in feeding, head lag, and diminished gag reflex.
It is rarely fatal, and infants usually recover strength within 4–6 weeks.
Treatment consists mainly of respiratory support.
B. Wound botulism
-It Occurs in crush injuries where the wound is dirty
and in intravenous drug abusers .
-Treatment consists of botulinum antitoxin, antibiotic
(penicillin) and wound debridement and irrigation.
C. Therapeutic botulism
- This is either botulinum toxin type A (Botox) or type B (Myobloc) which is injected in muscles to induce temporary weakness
- It is used to treat cases of blepharospasm, facial nerve disorders, torticollis and to eliminate frown lines.
-The affected muscles then weaken by atrophy over a 3-week period, but recover within 2–4 months as nerve transmission is restored through new nerve endings and functional connections at motor endplates.
Ciguatera poisoning
Ciguatoxin is produced by
tiny organisms eaten by small fish then eaten by larger fish, the toxin is concentrated in their flesh and fat tissue.
The toxin does not harm the
fish, or change its smell or colour
Mostly large sized fish are affected
Clinical picture of Ciguatera poisoning
-Incubation Period: 2-6 hours
-The typical patient presents with gastrointestinal then 2–24 hours later develops neurologic symptoms.
Other symptoms as can be present but not usual
-GIT manifestations: Nausea, vomiting, abdominal pain, watery diarrhea
-Neurological manifestations(mainly sensory):
numbness in the mouth and limbs, reversed sensation of heat (feels cold) and cold (feels electric), ataxia
-Cardiovascular manifestations: Hypotension and bradycardia
Treatment of Ciguatera poisoning
- Mainly supportive treatment.
- Charcoal administration within 4 hours of ingestion.
- Toxin-specific measures: mannitol to reverse the acute neurologic symptoms of ciguatera poisoning
Scombroid Cause
Scombrotoxin (histamine and histamine like compound)
Bacteria on the skin of the fish produce enzymes decomposes histidine in flesh of the fish not refrigerated (Tuna and Mackerel)
Scombroid
Time delay
C/P
Treatment
Time delay: minutes to 3 hours.
C/P:Headache and erythema of the head &chest flushing,itching and bronchospasm
Treatment : antihistaminic
