Food poisoning and Dysentry (internal medicine).pptx

Food poisoning and dysentery

1. Food poisoning And Dysentery Dr: Nashwan Mansoor

2. Food poisoning Bacillus cereus food poisoning :- Ingestion of the pre-formed heat-stable exotoxins of B. cereus. Presents with ;- Rapid onset of vomiting and some diarrhea within hours of food consumption. Resolves within 24 hours. Fried rice and freshly made sauces are frequent sources. The organism grows and produces enterotoxin during storage. Viable bacteria are ingested and toxin formation takes place within the gut lumen. Dr: Nashwan Mansoor

3. Food poisoning Bacillus cereus food poisoning :- The incubation period is longer (12–24 hours). Watery diarrhea and cramps, without vomiting are the predominant symptoms. The disease is self-limiting but can be quite severe. Rapid and judicious fluid replacement and appropriate notification of the public health authorities are all that is required. Dr: Nashwan Mansoor

4. Food poisoning Staphylococcal food poisoning :- Staph. aureus is transmitted via the hands of food handlers to foodstuffs. Inappropriate storage of these foods allows growth of the organism and production of one or more heat-stable enterotoxins that cause the symptoms. Nausea and profuse vomiting develop within 1–6 hours. Diarrhea may not be marked. abdominal cramping, usually without fever. The toxins that cause the syndrome act as ‘super-antigens’ and induce a significant neutrophil leukocytosis that may be clinically misleading. Dr: Nashwan Mansoor

5. Food poisoning Staphylococcal food poisoning :- Most cases settle rapidly but severe dehydration can occasionally be life-threatening. Antiemetics and appropriate fluid replacement are the mainstays of treatment. Suspect food should be cultured for staphylococci and demonstration of toxin production. Dr: Nashwan Mansoor

6. Food poisoning Clostridium perfringens food poisoning :- Spores of C. perfringens are widespread in the guts of large animals and in soil. C. perfringens spores germinate and viable organisms multiply, If contaminated meat products are incompletely cooked and stored in anaerobic conditions, . Subsequent reheating of the food causes release of enterotoxin. Symptoms (diarrhea and cramps) without vomiting or fever occur some 6–12 hours following ingestion. The illness is usually self-limiting. Dr: Nashwan Mansoor

7. Food poisoning Clostridium perfringens food poisoning :- Clostridial enterotoxins are potent and most people who ingest them will be symptomatic. ‘Point source’ outbreaks, a number of cases all become symptomatic following ingestion. Clostridial necrotizing enteritis (CNE) or pigbel is an often-fatal type of food poisoning caused by a β-toxin of C. perfringens, type C. The toxin is normally inactivated by certain proteases or by normal cooking. Pigbel is more likely in protein malnutrition or in the presence of trypsin inhibitors, either in foods such as sweet potatoes or during infection with Ascaris sp. roundworms. Dr: Nashwan Mansoor

8. Dysentery Dr: Nashwan Mansoor

9. Dysentery Dysentery means diarrhea with blood The most common causes of dysentery :- Bacteria ; Shigella (bacillary dysentery ). Enterohaemorrhagic toxin producing E, coli. Campylobacter. Non- typhoidal salmonella. Yersinia enterocolitica. Parasite:- Amoebic. Dr: Nashwan Mansoor

10. Dysentery Bacillary Dysentery (shigellosis) :- Shigella are Gram-negative rods, closely related to E. coli , invade the colonic mucosa. Four main groups: Sh. dysenteriae , flexneri , boydii and sonnei. In the tropics, bacillary dysentery is usually caused by Sh. Flexneri . Shigella are often resistant to multiple antibiotics, especially in tropical countries. Only infects humans and its spread is facilitated by its low infecting dose of around 10 organisms. Dr: Nashwan Mansoor

11. Dysentery Bacillary Dysentery (shigellosis) :- Spread may occur via:- Contaminated food or flies. Person to- person transmission by unwashed hands after defecation is the most important factor. Outbreaks occur in psychiatric hospitals, residential schools and other closed institutions, and dysentery is a constant accompaniment of wars and natural catastrophes, which bring crowding and poor sanitation in their wake. Shigella infection may spread rapidly among men who have sex with men. Dr: Nashwan Mansoor

12. Dysentery Bacillary Dysentery (shigellosis) :- Clinical features :- Varies from mild Sh. sonnei infections to more severe Sh. flexneri infections, while those due to Sh. dysenteriae may be fulminating and cause death within 48 hours. In a moderately severe illness, the patient complains of:- Diarrhea. Colicky abdominal pain. Tenesmus. Stools are small, and after a few evacuations contain blood and purulent exudate. Fever. Dehydration. Weakness. Tenderness over the colon. Reactive arthritis or iritis may occasionally complicate bacillary dysentery. Dr: Nashwan Mansoor

13. Dysentery Bacillary Dysentery (shigellosis) :- Complications :- Intestinal (e.g., toxic megacolon, intestinal perforation, rectal prolapse). Metabolic (e.g., hypoglycemia, hyponatremia). Shiga toxin produced by S. dysenteriae type 1 is linked to HUS in developing countries but is rare in industrialized countries. Diagnosis :- Stool culture. PCR. EIA. Dr: Nashwan Mansoor

14. Dysentery Bacillary Dysentery (shigellosis) :- Management and prevention :- Oral rehydration therapy if diarrhea is mid or moderate. Intravenous replacement of water and electrolyte loss is necessary, if diarrhea is severe. Zinc and vitamin A. Antibiotic therapy is with ciprofloxacin. Azithromycin and ceftriaxone are alternatives but resistance occurs to all agents. The use of antidiarrheal medication should be avoided. The prevention of fecal contamination of food and milk. The isolation of cases may be difficult, except in limited outbreaks. Hand-washing is very important . Dr: Nashwan Mansoor

15. Dysentery Escherichia coli infection :- Many serotypes of E. coli constitute part of the human gut microbiome . Clinical disease requires either colonization with a new or previously unrecognized strain, or the acquisition by current colonizing bacteria. Travel to unfamiliar areas of the world allows contact with different strains of endemic E. coli and the development of travelers' diarrhoea. Enteropathogenic strains may be found in the gut of healthy individuals and, if these people move to a new environment, close contacts may develop symptoms. At least five different clinico-pathological patterns of diarrhoea are associated with specific strains of E. coli with characteristic virulence factors. Dr: Nashwan Mansoor

16. Dysentery Escherichia coli infection :- Enterotoxigenic E. coli :- Enterotoxigenic E. coli (ETEC) is the most common cause of travelers' diarrhoea. The organisms produce either a heat-labile or a heat-stable enterotoxin, causing marked secretory diarrhoea and vomiting after 1–2 days’ incubation. The illness is usually mild and self-limiting after 3–4 days. Antibiotics are of questionable value. Other causes of travelers' diarrhoea:- • Shigella spp. • Campylobacter jejune. • Salmonella serovars • Plesiomonas shigelloides. • Non-cholera Vibrio spp. Dr: Nashwan Mansoor

17. Dysentery Escherichia coli infection :- Entero-invasive E. coli :- Illness caused by entero -invasive E. coli (EIEC) is very similar to Shigella dysentery. Caused by invasion and destruction of colonic mucosal cells. No enterotoxin is produced. Acute watery diarrhoea, abdominal cramps and some scanty blood-staining of the stool are common. The symptoms are rarely severe and are usually self-limiting. Dr: Nashwan Mansoor

18. Dysentery Escherichia coli infection :- Enteropathogenic E. coli :- Enteropathogenic E. coli (EPEC) organisms are very important in infant diarrhoea. They are able to attach to the gut mucosa, inducing :- A specific ‘attachment and effacement’ lesion. Causing destruction of microvilli. Disruption of normal absorptive capacity. The symptoms vary from mild non-bloody diarrhoea to quite severe illness, but without bacteraemia. Dr: Nashwan Mansoor

19. Dysentery Escherichia coli infection :- Entero-aggregative E. coli :- Entero-aggregative E. coli (EAEC) strains:- Adhere to the mucosa. Produce a locally active enterotoxin. Demonstrate a particular ‘stacked brick’ aggregation to tissue culture cells when viewed by microscopy. Associated with prolonged diarrhoea in children. Dr: Nashwan Mansoor

20. Dysentery Escherichia coli infection :- Enterohaemorrhagic E. coli :- E. coli O157:H7 is perhaps the best known of these verotoxin-producing E. coli (VTEC). The incidence of enterohaemorrhagic E. coli (EHEC) is considerably lower than that of Campylobacter and Salmonella infection, it is increasing in the developing world. The reservoir of infection is in the gut of herbivores. The organism has an extremely low infecting dose (10–100 organisms). Runoff water from pasture lands where cattle have grazed, which is used to irrigate vegetable crops, as well as contaminated milk, meat products, lettuce, radish shoots and apple juice have all been implicated as sources. Dr: Nashwan Mansoor

21. Dysentery Escherichia coli infection :- Enterohaemorrhagic E. coli :- The incubation period is between 1 and 7 days. Initial watery diarrhoea becomes uniformly blood-stained in 70% of cases and is associated with severe abdominal pain. There is little systemic upset, vomiting or fever. Enterotoxins have both a local effect on the bowel and a distant effect on particular body tissues, such as glomerular apparatus, heart and brain. Dr: Nashwan Mansoor

22. Dysentery Escherichia coli infection :- Enterohaemorrhagic E. coli :- The potentially life-threatening hemolytic uraemic syndrome occurs in 10–15% of sufferers from this infection, arising 5–7 days after the onset of symptoms. It is most likely at the extremes of age, may be induced, particularly in children, by antibiotic therapy. HUS is treated by dialysis if necessary and may be averted by plasma exchange. Antibiotics should be avoided since they can stimulate toxin release. Dr: Nashwan Mansoor

23. Dysentery Campylobacter jejuni infection :- Transmission to humans occurs via contact with or ingestion of raw or undercooked food products or direct contact with infected animals. An incubation period of 2–4 days (range, 1–7 days) . Clinical features:- A prodrome of fever, headache, myalgia, and/or malaise. Within the next 12–48 h:- Colicky abdominal pain may be severe and mimic acute appendicitis or other surgical pathology. Nausea, vomiting and significant diarrhoea , frequently containing blood, are common features. Complications:- include Reactive arthritis (particularly in persons with the HLA-B27 phenotype). Guillain-Barre syndrome (in which campylobacters are associated with 20–40% of cases). Approximately 1% of cases will develop bacteraemia and possible distant foci of infection. Dr: Nashwan Mansoor

24. Dysentery Campylobacter jejuni infection :- Diagnosis The diagnosis is confirmed by cultures of stool, blood, or other specimens on special media. Tretment :- The majority of Campylobacter infections affect fit young adults and are self-limiting after 5–7 days. Fluid and electrolyte replacement is the mainstay of therapy. About 10–20% will have prolonged symptomatology, occasionally meriting treatment with a macrolide, most often azithromycin, as many organisms are resistant to ciprofloxacin. Dr: Nashwan Mansoor

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