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Acute infectious diarrhea

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Acute infectious diarrhea

Seminar Prepared by :-
Mohammed Musa
Mohammed Saadi
Hussein Jassam
Mahmoud Ahmed
Meran Salih

Internal Medicine
College of Medicine - University of Kirkuk

Publicado en: Salud y medicina
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Acute infectious diarrhea

  1. 1. Acute infectious diarrhea Prepared by :- Mohammed Musa Mohammed Saadi Hussein Jassam Mahmoud Ahmed Meran Salih
  2. 2. Learning Objectives 2 ▰ Define acute infectious diarrhea ▰ Create a differential diagnosis for acute diarrhea ▰ Investigation and Clinical assessment ▰ Discuss treatment options including symptom management
  3. 3. 3 1 Definition
  4. 4. Diarrhoea 4 ▰ Diarrhoea is defined as the passage of more than 200g of stool daily and measurement of stool volume is helpful in confirming this. ▰ The most severe symptom in many patients is urgency of defecation, and faecal incontinence is a common event in acute and chronic diarrhoeal illnesses
  5. 5. Acute diarrhea 5 ▰ This is extremely common and is usually caused by faecal–oral transmission of bacteria or their toxins, viruses or parasites. ▰ Infective diarrhoea is usually short-lived and patients who present with a history of diarrhoea lasting more than 10 days rarely have an infective cause. ▰ A variety of drugs, including antibiotics, cytotoxic drugs, PPIs and NSAIDs, may be responsible.
  6. 6. 6 ▰ Acute diarrhoea, sometimes with vomiting, is the predominant symptom in infective gastroenteritis. ▰ Acute diarrhoea may also be a symptom of other infectious and non-infectious diseases. ▰ Stress, whether psychological or physical, can also produce loose stools.
  7. 7. 7 2 Pathophysiology of Diarrhea
  8. 8. Secretory Diarrhea 8 ▰ Large volumes of water are normally secreted into the small intestinal lumen, but a large majority of this water is efficiently absorbed before reaching the large intestine. ▰ Diarrhea occurs when secretion of water into the intestinal lumen exceeds absorption.
  9. 9. Secretory Diarrhea 9 ▰ Many millions of people have died of the secretory diarrhea. associated with cholera. The responsible organism, Vibrio cholerae, produces cholera toxin, which strongly activates adenylyl cyclase, causing a prolonged increase in intracellular concentration of cyclic AMP within crypt enterocytes. ▰ This change results in prolonged opening of the chloride channels that are instrumental in secretion of water from the crypts, allowing uncontrolled secretion of water. Additionally, cholera toxin affects the enteric nervous system, resulting in an independent stimulus of secretion.
  10. 10. Secretory Diarrhea 10 ▰ Exposure to toxins from several other types of bacteria (e.g. E. coli heat-labile toxin) induce the same series of steps and massive secretory diarrhea that is often lethal unless the person is aggressively treated to maintain hydration. ▰ In addition to bacterial toxins, a large number of other agents can induce secretory diarrhea by turning on the intestinal secretory machinery, including: ▰ some laxatives, hormones, drugs, certain metals, organic toxins, and plant products (e.g. arsenic, insecticides, mushroom toxins, caffeine) ▰ In most cases, secretory diarrheas will not resolve during a 2-3 day fast.
  11. 11. Inflammatory and Infectious Diarrhea 11 ▰ The epithelium of the digestive tube is protected from insult by a number of mechanisms constituting the gastrointestinal barrier, but like many barriers, it can be breached. ▰ Disruption of the epithelium of the intestine due to microbial or viral pathogens is a very common cause of diarrhea in all species. ▰ Destruction of the epithelium results not only in exudation of serum and blood into the lumen but often is associated with widespread destruction of absorptive epithelium. ▰ In such cases, absorption of water occurs very inefficiently and diarrhea results.
  12. 12. Inflammatory and Infectious Diarrhea 12 ▰ Examples of pathogens frequently associated with infectious diarrhea include: ▻ Bacteria: Salmonella, E. coli, Campylobacter ▻ Viruses: rotaviruses, norovirus ▻ Protozoa: Giardia, Cryptosporium,
  13. 13. Inflammatory and Infectious Diarrhea 13 ▰ The immune response to inflammatory conditions in the bowel contributes substantively to development of diarrhea. ▰ Activation of white blood cells leads them to secrete inflammatory mediators and cytokines which can stimulate secretion, in effect imposing a secretory component on top of an inflammatory diarrhea. ▰ Reactive oxygen species from leukocytes can damage or kill intestinal epithelial cells, which are replaced with immature cells that typically are deficient in the brush border enyzmes and transporters necessary for absorption of nutrients and water. In this way, components of an osmotic (malabsorption) diarrhea are added to the problem.
  14. 14. Osmotic diarrhea 14 It is the diarrhea that occurs due to the ingestion of poorly absorbed osmotically active substances that cause shifting of the water into the intestinal lumen ▻ If you stop oral feeding the diarrhea will stop. ▰ Can be Occur in: 1.ingestion of high CHO diet. 2-Congenital Lactase deficiency (primary) 3.infection with rotavirus or Salmonella, Enter hemorrhagic E.coli causes severe shedding of villi that contains Disaccharidases enzyme (secondary lactase deficiency).
  15. 15. Dysmotility/Functional diarrhea 15 ▰ Gut dysmotility may cause increased intestinal and colonic transit time as well as decrease contact time with intestinal absorptive mucosa. ▰ Functional syndromes such as irritable bowel syndrome (IBS) include a pain component as well as a change in bowel habits.
  16. 16. 16 3 Epidemiology
  17. 17. Epidemiology 17 ▰ Diarrhoeal disease is the second leading cause of death in children under five years old. It is both preventable and treatable. ▰ The World Health Organisation (WHO) estimates that there are more than 1.7 billion cases of acute diarrhoea annually globally. ▰ Each year diarrhoea kills around 760 000 children under five. ▰ In developed countries, diarrhoea remains an important problem, with the elderly being most vulnerable.
  18. 18. 18 4 Etiology
  19. 19. 19 Causes of Acute infectious diarrhea
  20. 20. 20
  21. 21. ▰ Gram –ve bacillus ▰ Normal commensal in human gut Virulent types- ▰ Enterotoxigenic - leading cause of watery diarrhea, most common cause of travellers’ diarrhea ▰ Enteropathogenic- diarrhea with mucus ▰ Enteroinvasive- profuse diarrhea with fever ▰ Enterohemorrhagic - dysentery, can cause HUS Enteroaggregative- watery diarrhea 21 Escherichia coli
  22. 22. ▰ Caused by bacteria Vibrio cholerae Primarily affects small-intestine ▰ People with O blood group more affected, carriers of cystic fibrosis are protected?? ▰ Toxin leads to cAMP activation causing secretion of water, Na, K, Cl & HCO3 ▰ Causes profuse diarrhea (rice water), ▰ with abdominal pain, ± vomiting 22 Cholera
  23. 23. 23 Cholera
  24. 24. 24 Cholera
  25. 25. 25 ▰ A gram –ve bacillus ▰ Causes diarrhea with mild fever or TYPHOID- enteric fever ▰ Stages- each lasting ~1 week Salmonella typhi
  26. 26. WIDAL TEST 26
  27. 27. 1 Mild fever, relative bradycardia, malaise, leucopenia, blood culture +ve, Widal test –ve 2 High fever, Rose spots on trunk, delirium, bradycardia, diarrhea (occasionally constipation), HSmegaly, blood culture/Widal test +ve 3 High fever, delirium, complications- hemorrhage, perforation, peritonitis, cholecystitis, metastatic abscess 4 Resolution/Defervescence 27 Salmonella typhi
  28. 28. 28 Salmonella typhi
  29. 29. Campylobacter ▰ Typically caused by Campylobacter jejuni ▻ or C. coli; it is largely a foodborne disease. ▰ Primarily uncooked poultry ▰ Diarrhea (bloody ~10%), abdominal pain
  30. 30. 30 Campylobacter
  31. 31. 31 • Fever with chills • Abdominal cramps • Diarrhea often with blood and mucus • Headache, malaise • Direct person-to-person spread • Tx Trimethoprim- ▻ sulfamethoxazole, ciprofloxin, levofloxacin, ampicillin • Increasing resistance to antibiotics noted • Azithromycin, 500mg orally on day 1 and 250mg orally one time a day for 4 days, may be an effective alternative treatment for resistant strains Shigellosis
  32. 32. 32 • Clostridium difficile • 20% chance after completing broad spectrum antibiotic • The A and B toxins produced by C. difficile can cause severe diarrhea, pseudomembranous colitis, or toxic megacolon. • High risk pts: nursing home residents and employees, hospitalized pts and employees • metronidazole (250mg orally four times a day or 500mg orally three times a day for 10 days) CLOSTRIDIUM DIFFICILE
  33. 33. 33 CLOSTRIDIUM DIFFICILE
  34. 34. 35 5 Clinical assessment
  35. 35. Clinical assessment 36 ▰ The history should address foods ingested, duration and frequency of diarrhoea, presence of blood or steatorrhoea, abdominal pain and tenesmus, and whether other people have been affected. ▰ Fever and bloody diarrhoea suggest an invasive, colitic, dysenteric process. ▰ An incubation period of less than 18 hours suggests toxin-mediated food poisoning, and longer than 5 days suggests diarrhoea caused by protozoa or helminthes. ▰ Person-to-person spread suggests certain infections, such asshigellosis or cholera.
  36. 36. Foods associated with infectious illness, including gastroenteritis 37
  37. 37. Foods associated with infectious illness, including gastroenteritis 38
  38. 38. Clinical assessment 39 ▰ Examination includes assessment of the degree of dehydration. ▰ Assessment for early signs of hypotension, such as thirst, headache, altered skin turgor, dry mucous membranes and postural hypotension, is important, particularly in tropical regions where dehydration progresses rapidly. ▰ Signs of more marked dehydration include supine hypotension and tachycardia, decreased urinary output, delirium and sunken eyes. ▰ The blood pressure, pulse rate, urine output and ongoing stool losses should be monitored closely.
  39. 39. 40
  40. 40. Clinical assessment 41 ▰ The severity of diarrhoea may be assessed by reference to the Bristol stool form scale (Bristol stool chart), which allows an objective assessment of stool consistency by providing a verbal and visual reference scale. ▰ The Bristol stool form scale was developed in the 1990s to monitor patients with irritable bowel syndrome, but its main use (at least in UK hospitals) is to monitor hospital inpatients with loose stool to assist in decisions on stool sampling and infection prevention precautions, especially in relation to C. difficile.
  41. 41. Bristol stool chart ▰ The stool is given a ‘score’ of 1–7 by ▰ reference to the verbal and visual description. ▰ This is recorded on a chart (usually known as a ‘Bristol stool chart’) or in a patient monitoring database. 42
  42. 42. Bristol stool chart 43
  43. 43. Investigations 44 These include stool inspection for blood and microscopy for leucocytes, and also an examination for ova, cysts and parasites if the history indicates residence or travel to areas where these infections are prevalent. ▰ Stool culture should be performed and C. difficile toxin sought. ▰ FBC and serum electrolytes indicate the degree of inflammation and dehydration. ▰ Where cholera is prevalent, examination of a wet film with dark-field microscopy for darting motility may provide a diagnosis. ▰ In a malarious area, a blood film for malaria parasites should be obtained.
  44. 44. 45
  45. 45. Investigations 46 ▰ Blood and urine cultures and a chest X-ray may identify alternative sites of infection, particularly if the clinical features suggest a syndrome other than gastroenteritis.
  46. 46. Investigations 47 ▰ Structural examination by sigmoidoscopy, colonoscopy, or abdominal computed tomography (CT) scanning (or other imaging approaches) may be appropriate in patients with uncharacterized persistent diarrhea to exclude IBD or as an initial approach in patients with suspected noninfectious acute diarrhea such as ischemic colitis, diverticulitis, or partial bowel obstruction.
  47. 47. 48 6 Management
  48. 48. Management 49 ▰ All patients with acute, potentially infective diarrhoea should be appropriately isolated to minimise person-to-person spread of infection. ▰ If the history suggests a food-borne source, public health measures must be implemented to identify the source and to establish whether other linked cases exist.
  49. 49. Fluid replacement 50 ▰ Replacement of fluid losses in diarrheal illness is crucial and may be life- saving. ▰ Although normal daily fluid intake in an adult is only 1–2 L, there is considerable additional fluid movement in and out of the gut in secretions. ▰ Altered gut resorption with diarrhea can result in substantial fluid loss; for example, 10–20 L of fluid may be lost in 24 hours in cholera. ▰ The fluid lost in diarrhea is isotonic, so both water and electrolytes need to be replaced.
  50. 50. 51 Fluid homeostasis in the gastrointestinal tract. • Absorption of electrolytes from the gut is an active process requiring energy. • Infected mucosa is capable of very rapid fluid and electrolyte transport if carbohydrate is available as an energy source.
  51. 51. Fluid replacement 52 ▰ Oral rehydration solutions (ORS) therefore contain sugars, as well as water and electrolytes. ▰ ORS can be just as effective as intravenous replacement fluid, even in the management of cholera. ▰ In mild to moderate gastroenteritis, adults should be encouraged to drink fluids and, if possible, continue normal dietary food intake. ▰ If this is impossible – due to vomiting, for example – intravenous fluid administration will be required.
  52. 52. ▰ In very sick patients or those with cardiac or renal disease, monitoring of urine output and central venous pressure may be necessary. 53 Fluid replacement
  53. 53. Fluid replacement 54 The volume of fluid replacement required should be estimated based on the following considerations: ▰ Replacement of established deficit ▰ Replacement of ongoing losses ▰ Replacement of normal daily requirement
  54. 54. Fluid replacement 55 Replacement of established deficit ▰ After 48 hours of moderate diarrhoea (6–10 stools per 24 hrs), the average adult will be 2–4 L depleted from diarrhoea alone. Associated vomiting will compound this. ▰ Adults with this symptomatology should therefore be given rapid replacement of 1–1.5 L, either orally (ORS) or by intravenous infusion (normal saline), within the first 2–4 hours of presentation. ▰ Longer symptomatology or more persistent/severe diarrhoea rapidly produces fluid losses comparable to diabetic ketoacidosis and is a metabolic emergency requiring active intervention.
  55. 55. Fluid replacement 56 Replacement of ongoing losses ▰ The average adult’s diarrheal stool accounts for a loss of 200 mL of isotonic fluid. ▰ Stool losses should be carefully charted and an estimate of ongoing replacement fluid calculated. ▰ Commercially available rehydration sachets are conveniently produced to provide 200 mL of ORS; one sachet per diarrhoea stool is an appropriate estimate of supplementary replacement requirements.
  56. 56. Fluid replacement 57 Replacement of normal daily requirement ▰ The average adult has a daily requirement of 1–1.5 L of fluid in addition to the previous calculations. ▰ This will be increased substantially in fever or a hot environment.
  57. 57. Antimicrobial agents 58 ▰ In non-specific gastroenteritis, routine use of antimicrobials does not improve outcome and may lead to antimicrobial resistance or side- effects. ▰ They are usually used where there is systemic involvement, a host with immunocompromise or significant comorbidity. ▰ Evidence suggests that, in Enterohaemorrhagic Escherichia coli (EHEC) infections, the use of antibiotics may make the complication of haemolytic uraemic syndrome (HUS) more likely due to increased toxin release. Antibiotics should therefore not be used in this condition.
  58. 58. Antimicrobial agents 59 ▰ Conversely, antibiotics are indicated in Shigella dysenteriae infection and in invasive salmonellosis – in particular, typhoid fever. ▰ Antibiotics may also be advantageous in cholera epidemics, reducing infectivity and controlling the spread of infection.
  59. 59. Antidiarrhoeal, antimotility and antisecretory agents 60 ▰ These agents are not usually recommended in acute infective diarrhoea. ▰ Loperamide, diphenoxylate and opiates are potentially dangerous in dysentery in childhood, causing intussusception. ▰ Antisecretory agents, such as bismuth and chlorpromazine, may make the stools appear more bulky but do not reduce stool fluid losses and may cause significant sedation. ▰ Adsorbents, such as kaolin or charcoal, have little effect.
  60. 60. 61 7 Prevention
  61. 61. ▰ Good hygiene, hand washing, safe food preparation, and access to clean water are key factors in preventing diarrheal illness. ▰ Vaccine development remains a high priority for disease prevention. ▰ Effective and safe vaccines exist for rotavirus, typhoid fever, and cholera, and are under investigation for Campylobacter, enterotoxigenic E. coli, and Shigella infections. 62 Prevention
  62. 62. 63 Take Home Message ▰ Infectious diarrhoea is due to faeco–oral transmission of viruses, bacteria, bacterial toxins or parasites. ▰ Most cases are self-limiting and a pathogen is rarely identified. ▰ Viruses and toxins causes large-volume watery diarrhoea. ▰ Invasive intestinal pathogens (cause bloody diarrhoea) ▰ Clostridium difficile infection (CDI) (cause hospital-acquired diarrhoea). ▰ Diarrhoea that persists for >10 days is unlikely to be infective. ▰ Consider protozoal infections in patients who are immunocompromised or have recently travelled to the tropics.
  63. 63. References: 64
  64. 64. Thank you 65

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