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Dr.Farzin khorvash. Dr Farzin Khorvash Dr.Farzin khorvash.

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Presentation on theme: "Dr.Farzin khorvash. Dr Farzin Khorvash Dr.Farzin khorvash."— Presentation transcript:

1 Dr.Farzin khorvash

2 Dr Farzin Khorvash Dr.Farzin khorvash

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4 Enteric Host Defenses Host species, genotype, and age Personal hygiene Gastric acidity and other physical barriers Intestinal motility Enteric microflora Specific immunity Phagocytic Humoral Cell–mediated Nonspecific protective factors and human milk Intestinal receptors Dr.Farzin khorvash

5 MICROBIAL FACTORS Toxins Attachment Invasiveness Dr.Farzin khorvash

6 Gastrointestinal infections exception of Helicobacter pylori gastritis noninflammatory ; syndromes of diarrhea or vomiting that tend to involve infection in the upper small bowel inflammatory infection in the colon. Other enteric infections and infestations cause predominantly systemic symptoms. Dr.Farzin khorvash

7 MECANISM (1) a shift in the delicate balance of bidirectional water and electrolyte fluxes in the upper small bowel by intraluminal toxins or minimally invasive organisms (2) inflammatory destruction of the ileal or colonic mucosa (3) penetration through an intact mucosa to the reticuloendothelial system. Dr.Farzin khorvash

8 Infectious Doses of Enteric Pathogens Shigella10 to 10 2 Campylobacter jejuni10 2 to 10 6 Salmonella10 5 Escherichia coli10 8 Vibrio cholerae10 8 Giardia lamblia10 to 10 2 cysts Entamoeba histolytica10 to 10 2 cysts Cryptosporidium parvum1 to 10 3 oocysts Dr.Farzin khorvash

9 ACUTE NONINFLAMMATORY DIARRHEA IN ADULTS Rotaviruses Norwalk-like viruses adenoviruses Coxsackieviruses toxigenic Clostridium difficile food poisoning such as Clostridium perfringens, Bacillus cereus, or Staphylococcus aureus cholera undercooked shellfish enterotoxigenic E. coli Dr.Farzin khorvash

10 ACUTE NAUSEA AND VOMITING (WINTER VOMITING DISEASE) acute nausea and vomiting “intestinal flu,” or “viral gastroenteritis” commonly occurs in winter months in temperate climates Dr.Farzin khorvash

11 Norwalk-like viruses (including Norwalk or Montgomery County agent and Hawaii, Snow Mountain, and Taunton agents) caliciviruses astroviruses enteroviruses (especially echovirus types 11, 14, and 18) enteric adenoviruses human coronaviruses Pestiviruses toroviruses Picobirnaviruse Dr.Farzin khorvash

12 DIFFERENTIAL DIAGNOSIS OF ACUTE NONINFLAMMATORY DIARRHEA osmotic diuresis nonabsorbable agents such as sorbitol, Ipecac fluid Heavy metal poisoning (with As, Sn, Fe, Cd, Hg, Pb) non–b-islet cell tumors, medullary carcinoma of the thyroid, carcinoid tumors, vasoactive intestinal polypeptide thyrotoxicosis and adrenal or parathyroid insufficiency lactase deficiency and pancreatic or biliary insufficiency HUS with or without enterohemorrhagic E. coli O157:H7 dermatitis herpetiformis Dr.Farzin khorvash

13 CHRONIC NONINFLAMMATORY DIARRHEA Giardiasis tropical spruelike syndromes syndromes of bacterial “overgrowth,” Cryptosporidium I. belli infection Dr.Farzin khorvash

14 ACUTE DYSENTERY fecal blood and pus have frequent, small bowel movements blood and mucus tenesmus pain on defecation an inflammatory invasion of the colonic mucosa resulting from bacterial, cytotoxic, or parasitic destruction. Dr.Farzin khorvash

15 Bacillary dysentery (Shigella dysenteriae, Shigella flexneri, Shigella sonnei, Shigella boydii; invasive Escherichia coli) Campylobacteriosis (Campylobacter jejuni) Amebic dysentery (Entamoeba histolytica) Ciliary dysentery (Balantidium coli) Bilharzial dysentery (Schistosoma japonicum, Schistosoma mansoni) Other parasitic infections (Trichinella spiralis) Vibriosis (Vibrio parahaemolyticus) Salmonellosis (Salmonella typhimurium) Typhoid fever (Salmonella typhi) Enteric fever (Salmonella choleraesuis, Salmonella paratyphi) Yersiniosis (Yersinia enterocolitica) Spirillar dysentery (Spirillum spp.) Proctitis Gonococcal (Neisseria gonorrhoeae) Herpetic (herpes simplex virus) Chlamydial (Chlamydia trachomatis) Syphilitic (Treponema pallidum) Other syndromes Necrotizing enterocolitis of the newborn Enteritis necroticans Pseudomembranous enterocolitis (Clostridium difficile) Diverticulitis Typhlitis Dr.Farzin khorvash

16 Syndromes without known infectious etiology Idiopathic ulcerative colitis Crohn's disease Radiation enteritis Ischemic colitis Allergic enteritis Dr.Farzin khorvash

17 Antibiotic-Associated Colitis Nearly 15% of hospitalized patients receiving b-lactam antibiotics develop diarrhea Clostridium difficile Staphylococcus aureus Candida Enterotoxigenic Clostridium perfringens Dr.Farzin khorvash

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19 CLINICAL MANIFESTATIONS after 5 to 10 days of antibacterial treatment or as late as 10 weeks after cessation of therapy may be brief and self-limited or cholera-like, resulting in more than 20 stools per day fever (30 to 50% of patients),leukocytosis (50 to 60%) and abdominal pain or cramping (20 to 33%) Nausea, malaise, anorexia, hypoalbuminemia, occult colonic bleeding, dehydration Infrequently, C. difficile colitis presents without diarrhea as an acute abdominal syndrome or toxic megacolon Dr.Farzin khorvash

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21 Autopsy the cecum of a patient with pseudomembranous colitis. Dr.Farzin khorvash

22 CHRONIC INFLAMMATORY PROCESSES Weight loss, fever, headache, and colicky abdominal pain,steatorrhea, malabsorption Enteropathogenic and Enteroaggregative Escherichia coliEnteropathogenic and Enteroaggregative Escherichia coli Syphilis Gastrointestinal Tuberculosis Gastrointestinal Mycosis Parasitic Enteritis Dr.Farzin khorvash

23 Parasitic Enteritis coccidiosis Isospora belli Cryptosporidium Cyclospora G. lamblia Dr.Farzin khorvash

24 differential diagnosis of chronic inflammatory diarrhea Idiopathic inflammatory bowel disease including regional enteritis, granulomatous colitis, and ulcerative colitis Sarcoidosis lymphoma Carcinoma Radiation enterocolitis ischemic colitis diverticulitis Dr.Farzin khorvash

25 Abdominal Symptoms with Fever (1) Enteric fever : fever, headache, abdominal pain, splenomegaly, bacteremia, and occasionally skin rash, is by several bacteria. A number of systemic bacterial, rickettsial, viral, fungal, and parasitic infections, such as malaria, may mimic enteric fever (2) Mesenteric adenitis, a syndrome that may mimic acute appendicitis, can be caused by several bacteria (3) Eosinophilia:abdominal cramps or diarrhea often accompanied by fever, parasites, usually helminths, several diseases of unknown cause, and neoplasms. Dr.Farzin khorvash

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28 MESENTERIC ADENITIS fever right lower quadrant pain vomiting diarrhea rebound tenderness Rectal tenderness Leukocytosis, polymorphonuclear leukocytes Sonographic, radiographic contrast studies or CT examination Stool cultures were positive in 56% Serologic confirmation Dr.Farzin khorvash

29 MESENTERIC ADENITIS Y. enterocolitica Y. pseudotuberculosis nontyphoidal Salmonella spp S. typhi infections tuberculous mesenteric lymphadenitis intestinal anthrax Penicillium marneffei infection hemolytic streptococci Staphylococcus aureus Bacteroides and Clostridium spp Dr.Farzin khorvash

30 Differential Diagnosis Tuberculosis nontyphoidal Salmonella infections Salmonella typhi infections Actinomycosis Mycobacterium avium-intracellulare infection P. marneffei infections parvovirus B19 Epstein-Barr virus Adenovirus infection Angiostrongylus costaricensis Dr.Farzin khorvash

31 chronic enteric inflammatory abdominal pain, weight loss, diarrhea, or malabsorption gastrointestinal mycoses Mycobacterioses bacterial infections certain parasitic infections such as coccidiosis. Dr.Farzin khorvash

32 SYNDROME OF ABDOMINAL PAIN OR DIARRHEA WITH EOSINOPHILIA NematodesStrongyloides stercoralis Ascaris lumbricoides small bowel)Visceral larva migrans (Toxocara canis, Toxocara cati Trichinella spiralis Anisakiasis Capillaria philippinensis Angiostrongylus costaricensis TrematodesSchistosoma spp Clonorchis sinensis Opisthorchis spp Metorchis conjunctus Fasciola hepatica Fasciolopsis buski Heterophyes heterophes Metagonimus yokogawi Nanophyetus salmincola CestodesEchinococcosis ProtozoaIsospora belli Dientamoeba fragilis causeEosinophilic gastroenteritis Polyarteritis nodosa and other forms of vasculitis Inflammatory bowel disease Malignancies Dr.Farzin khorvash

33 Etiology of Traveler's Diarrhea Enterotoxigenic Escherichia coli Shigella Salmonella Campylobacter jejuni Vibrio parahaemolyticus Rotavirus Dr.Farzin khorvash

34 DIARRHEA IN PATIENTS WITH AIDS Cytomegalovirus Cryptosporidium Microsporidium Entamoeba histolytica Giardia lamblia Salmonella spp. Campylobacter spp. Shigella spp. Clostridium difficile toxin Vibrio parahaemolyticus Mycobacterium spp. Isospora belli Cyclospora Blastocystis hominis Candida albicans Herpes simplex Chlamydia trachomatis Strongyloides Intestinal spirochetes Dr.Farzin khorvash

35 simple examination fresh stool specimen is mixed with a drop of methylene blue on a slide and examined for the presence of fecal leukocytes In most cases, no leukocytes are noted. This suggests a noninflammatory process in which diarrhea usually arises from the upper small bowel by the action of a true enterotoxin or agents such as Giardia or viruses. The presence of numerous polymorphonuclear leukocytes documents an inflammatory or invasive process that usually arises from the colon or distal small bowel. Dr.Farzin khorvash

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37 Of greatest importance in the treatment of microbial diarrhea, regardless of the cause or category, is fluid replacement (ORT). Dr.Farzin khorvash

38 degree of volume depletion examining the turgor of the skin and mucous membranes by noting the amount of lacrimation by obtaining a history of urinary output changes in pulse and blood pressure Dr.Farzin khorvash

39 Electrolyte losses in severe watery diarrhea are similar to the electrolyte composition of serum, and fluid replacement should contain approximately these concentrations of electrolytes Dr.Farzin khorvash

40 standard ORT regimen contains 3.5 g NaCl, 2.5 g NaHCO3, 1.5 g KCl, and 20 g glucose per liter of boiled water sodium 90, potassium 20, bicarbonate 30, chloride 80, and glucose 110 mmol/liter A similar solution may be prepared with 3 level tablespoons of sugar, ¾ teaspoon salt, ½ teaspoon sodium bicarbonate in 1 cup of orange juice to make up 1 liter (1.05 qt) in water. Dr.Farzin khorvash

41 Therapy IV Na + Cl – K+K+ HCO 3 – Glucose Intravenous solutions Ringer's lactate *0 Normal saline WHO ORS †111 Dr.Farzin khorvash

42 BRAT DIET Banana Rice Apple Tosted bread Dr.Farzin khorvash

43 ANTIMUTILITY AGENT Inflammatory infections: non use non Inflammatory infections:use Dr.Farzin khorvash

44 THERAPY OF ACUTE DYSENTERY shigellosis : fluoroquinolones Salmonella gastroenteritis :ciprofloxacin C. jejuni :ciprofloxacin or azithromycin E. histolytica :metronidazole is effective in eradicating hepatic amebiasis and may eradicate intestinal disease, the iodoquinol Schistosomal: Praziquantel Dr.Farzin khorvash

45 Therapy of Enteric Fever ampicillin, trimethoprim- sulfamethoxazole, and chloramphenicol Fluoroquinolones, such as ciprofloxacin or ofloxacin Third-generation cephalosporins, such as ceftriaxone aztreonam Dr.Farzin khorvash

46 Therapy OF MESENTERIC ADENITIS self-limited Y. enterocolitica : trimethoprim- sulfamethoxazole, second- and third- generation cephalosporins, ciprofloxacin and other fluoroquinolones, piperacillin, imipenem, tetracycline, and chloramphenicol Yersinia pseudotuberculosis : tetracycline, cephalosporins, aminoglycosides and chloramphenicol Dr.Farzin khorvash

47 Treatment of Clostridium difficile– Associated Diarrhea and Colitis 1. discontinue the offending antibiotic and/or modify the regimen to include an agent less commonly associated with C. difficile disease 2. Replace fluid and electrolyte losses 3. Avoid antiperistaltic agents 4. oral metronidazole, 250 mg qid for 10 days 5. Do treat asymptomatic patients colonized with C. difficile 6. Retreat first–time recurrences with the same regimen used to treat the initial episode 7. Avoid vancomycin use, if possible Dr.Farzin khorvash

48 Metronidazole 250 mg qid × 10 d 500 mg tid × 10 d Vancomycina 500 mg tid × 10 d 500 mg qid × 10 d 125 mg qid × 7 d 125 mg qid × 5 d Teicoplanin 400 mg bid × 10 d 100 mg bid × 10 d Fusidic acid 500 mg tid × 10 d Bacitracin 25,000 U qid × 10 d Dr.Farzin khorvash

49 SHIGELLOSIS acute infectious inflammatory colitis "bacillary dysentery," Dr.Farzin khorvash

50 ETIOLOGIC AGENT small, gram-negative, nonmotile bacilli family Enterobacteriaceae (S. dysenteriae, S. flexneri, S. boydii, and S. sonnei) on the basis of somatic O antigens and carbohydrate fermentation patterns. Dr.Farzin khorvash

51 EPIDEMIOLOGY high rate of secondary household transmission often symptomatic in children asymptomatic in adults Dr.Farzin khorvash

52 PATHOGENESIS AND PATHOLOGY extensive ulceration of the epithelial surface of the colonic mucosa exudate consisting of desquamated colonic cells, PMNs, and erythrocytes that may resemble a pseudomembrane Dr.Farzin khorvash

53 CLINICAL MANIFESTATIONS is typically a pediatric ambulatory disease presenting as a self-limited nonbloody but inflammatory watery diarrhea containing many neutrophils. over the first 24 to 48 h, one-fourth developed transient fever one-fourth had fever and self-limited watery diarrhea the remaining one-fourth had fever and watery diarrhea that progressed to bloody diarrhea and dysentery Dr.Farzin khorvash

54 In young children in particular fever 40° to 41°C sometimes resulting in generalized seizures Dr.Farzin khorvash

55 Severe dysentery due to S. dysenteriae type 1, occurs less commonly with S. flexneri, and is least likely with S. sonnei or S. boydii mild disease generally recover without specific therapy in a few days to a week Severe shigellosis can progress to toxic dilatation and colonic perforation Dr.Farzin khorvash

56 Endoscopy shows the mucosa to be hemorrhagic, with mucous discharge and focal ulcerations sometimes an overlying exudate resembling a pseudomembrane. The majority of lesions are in the distal colon Dr.Farzin khorvash

57 Mild dehydration is common severe dehydration is very rare protein-losing enteropathy can occur extraintestinal complications of shigellosis arise in patients in developing countries caused by S. dysenteriae type 1 and S. flexneri and to the poor nutritional state of the hosts. Dr.Farzin khorvash

58 HUS with S. dysenteriae type 1 STEC strains (such as E. coli O157:H7) usually develop toward the end of the first week of shigellosis, when dysentery is already resolving Oliguria and a marked drop in hematocrit (by as much as 10% within 24 h) are the first signs may progress to anuria with renal failure and to severe anemia with congestive heart failure Even with advanced therapy, 5 to 10% of patients with HUS die of the acute illness. Dr.Farzin khorvash

59 HUS Leukemoid reactions with leukocyte counts of <50,000/uL thrombocytopenia, with 30,000 to 100,000 platelets/uL, is common and in adults can lead to TTP profound hyponatremia and severe hypoglycemia may underlie central nervous system abnormalities such as seizures and altered consciousness. Dr.Farzin khorvash

60 Ikari syndrome S. flexneri is associated with a rare toxic encephalopathy that is manifested by bizarre posturing and lethal cerebral edema Dr.Farzin khorvash

61 Reactive arthritis with S. flexneri antigen HLA-B27 the full triad of Reiter's syndrome sometimes develops weeks to months after diarrheal illness Pneumonia, meningitis, vaginitis (in prepubertal girls), keratoconjunctivitis, and "rose spot" rashes are rare events Dr.Farzin khorvash

62 DIAGNOSIS AND LABORATORY FINDINGS The specific :culture of Shigella from the stool PCR have been developed but are not yet widely available enzyme immunoassay to detect Shiga-family toxins in stool : S. dysenteriae type 1 More than one differential selective medium should be used for culture— i.e., MacConkey and one other medium, such as Hektoen enteric or xylose-lysine-deoxycholate. Dr.Farzin khorvash

63 TREATMENT The mild to moderate dehydration in shigellosis is readily corrected with oral rehydration solutions Since S. sonnei infection is usually self- limited, culture results generally do not become available until the patient is better and there is little clinical need for further therapy. Dr.Farzin khorvash

64 Trimethoprim-sulfamethoxazole 10/50 mg/kg bid × 3-5 d Ciprofloxacin 15 mg/kg q12h × 3-5 d; 500 mg max/dose 500 mg bid × 3 d Azithromycin 12 mg/kg on day 1 (max, 500 mg), 6 mg/kg on days 2-5 (max,250 mg/d),1 g (single dose) Cefiximeb 8 mg/kg (max, 400 mg) once daily × 5 d,400 mg/d × 5 d Dr.Farzin khorvash

65 HUS often requires dialysis Dr.Farzin khorvash

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67 Cholera Dr.Farzin khorvash

68 VIBRIO 1. Aerobic, motile Gram negative rods 2.a profuse watery diarrhea that is potentially fatal Dr.Farzin khorvash

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70 Vibrio cholerae Microbiology: Gram stain Comma-shaped, curved Gram negative rod Can’t differentiate from other Gram negative rods Dr.Farzin khorvash

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72 LAB DIAGNOSIS Organism can be seen in stool by direct microscopy after gram stain and dark field illumination Organism can be seen in stool by direct microscopy after gram stain and dark field illumination Cholera can be cultured on special alkaline media like triple sugar agar or TCBS agar. Cholera can be cultured on special alkaline media like triple sugar agar or TCBS agar. Serologic tests are available to define strains, but this is needed only during epidemics to trace the source of infection. Serologic tests are available to define strains, but this is needed only during epidemics to trace the source of infection. Dr.Farzin khorvash

73 OTHER LAB FINDINGS Dehydration leads to high blood urea & serum creatinine. Hematocrit & WBC will also be high due to hemoconcentration. Dehydration leads to high blood urea & serum creatinine. Hematocrit & WBC will also be high due to hemoconcentration. Dehydration & bicarbonate loss in stool leads to metabolic acidosis with wide-anion gap. Dehydration & bicarbonate loss in stool leads to metabolic acidosis with wide-anion gap. Total body potassium is depleted, but serum level may be normal due to effect of acidosis. Total body potassium is depleted, but serum level may be normal due to effect of acidosis. Dr.Farzin khorvash

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81 Cholera: ‘Rice water’ stool Dr.Farzin khorvash

82 نقش مواد غذایی در انتقال ویبریوکلره:  استفاده از آب آلوده در پخت برنج  آب میوه رقیق شده با آب آلوده  شستشوی میوه و سبزی با آب آلوده  مواد غذایی دریایی (خرچنگ، میگو و ماهی خام)  گوشت خوک پخته نشده  فرنی گندم  غذاهای خیابانی  شیر نارگیل فریز شده Dr.Farzin khorvash

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85 CHOLERA Clinical manifestation & Assessment of dehydration Dr.Farzin khorvash

86 PATHOPHYSIOLOGY Non inflammatory Enterotoxin induced diarrhea Dr.Farzin khorvash

87 PATHOPHYSIOLOGY Infective dose Normal condition Abnormal condition Enterotoxin structure Component A Component B Dr.Farzin khorvash

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90 CLINICAL MANIFESTATION Depends on : biotype age number of bacteria status of immunity blood group O ? Dr.Farzin khorvash

91 CLINICAL MANIFESTATION Sub clinical Clinical : profuse, watery diarrhea “rice water” vomiting leg cramps convulsion,fever,hypoglycemia(children) sometimes “cholera sica” Dr.Farzin khorvash

92 LABORATORY FINDINGS Hemoconcentration Leuckocytosis Hyperglycemia Hypocalemia Increased protein, phosphate, lactate Increased BUN, Cr Metabolic acidosis Dr.Farzin khorvash

93 CLINICAL MANIFESTATION Dehydration some dehydration severe dehydration Dr.Farzin khorvash

94 CLINICAL MANIFESTATION Some dehydration Restlessness and irritability Sunken eyes Dry mouth and tongue Increased thirst Skin goes back slowly when pinched Dr.Farzin khorvash

95 CLINICAL MANIFESTATION Severe dehydration Lethargy or unconsciousness Very dry mouth and tongue Skin goes back slowly when pinched Weak or absent pulse Low blood pressure Dr.Farzin khorvash

96 ASSESSMENT OF DIARRHEA PATIENTS FOR DEHYDRATION SEVER DEHYDRATION SOME DEHYDRATION NO DEHYDRATION LETHARGIC OR UNCONSCIOUS,FLOPPY RESTLESS, IRRITABLEWELL,ALLERT CONDITION VERY SUNKEN AND DRY SUNKENNORMAL EYE ABSENT PRESENT TEARS VERY DRYDRYMOIST MOUTH&TONGUE DRINK POORLY OR NOT ABLE TO DRINK THIRSTY DRINK EAGERLY NOT THIRSTY DRINK NORMALLY THIRST GOES BACK VERY SLOWLY GOES BACK SLOWLYGOES BACK QUICKLY SKIN PINCH Dr.Farzin khorvash

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99 The goal of therapy to restore the fluid losses caused by diarrhea and vomiting Dr.Farzin khorvash

100 treatment of patients without severe dehydration is easy treatment of patients with severe dehydration requires experience and proper training. Dr.Farzin khorvash

101 Basic training in how to recognize the degree of dehydration how to select the proper intravenous solution how rapidly to rehydrate the patient is crucial Dr.Farzin khorvash

102 Guidelines to rehydrate cholera patients have been written and reviewed elsewhere Dr.Farzin khorvash

103 intravenous route should be restricted to patients with moderate dehydration who do not tolerate the oral route those who purge more than 10 to 20 ml/kg/hour patients with severe dehydration. Dr.Farzin khorvash

104 Rehydration should be accomplished in two phases rehydration phase maintenance phase Dr.Farzin khorvash

105 The purpose of the rehydration phase is to restore normal hydration status it should last no more than 4 hours Dr.Farzin khorvash

106 Intravenous fluids should be infused at a rate of 50 to 100 ml/kg/hour in severely dehydrated patients. Ringer's lactate solution is the most frequently recommended solution Dr.Farzin khorvash

107 Electrolyte Concentration of Cholera Stools and Common Solutions Used for Treatment Electrolyte and Glucose Concentration (mmol/L) Na + Cl – K+K+ HCO 3 – Glucose Cholera stool Adults Children Intravenous solutions Ringer's lactate *0 Normal saline WHO ORS †111 *Ringer's lactate does not contain HCO 3 – ; it has lactate instead. †Bicarbonate is replaced by trisodium citrate, which persists longer than bicarbonate in sachets. Abbreviation: WHO ORS, World Health Organization oral rehydration solution. Copyright © 2000, 1995, 1990, 1985, 1979 by Churchill Livingstone Dr.Farzin khorvash

108 Normal saline solution is not recommended because it does not correct the metabolic acidosis. Dr.Farzin khorvash

109 When intravenous access proves difficult nasogastric tubes or intraosseous catheters can be used Dr.Farzin khorvash

110 finishing the rehydration all signs of dehydration should have abated the patient should pass urine at a rate of 0.5 ml/kg/hour or greater Then starts the maintenance phase. Dr.Farzin khorvash

111 maintenance phase During this phase the objective is to maintain normal hydration status by replacing ongoing losses The oral route is preferred during this phase use of oral rehydration solutions at a rate of 500 to 1000 ml/hour is highly recommended Dr.Farzin khorvash

112 Oral rehydration therapy uses the principle of common transportation of solutes, electrolytes, and water by the intestine not affected by the cholera toxin People with diarrhea can undergo successful rehydration with simple solutions containing glucose and electrolytes that may be prepared at home. Dr.Farzin khorvash

113 Evaluation of rehydration status accurate recording of intake and output volumes are essential Patients without severe dehydration who tolerate the oral route can be rehydrated with oral rehydration solutions exclusively and discharged promptly from the health center Dr.Farzin khorvash

114 Discharge patients urine volume higher than 40 ml/hour diarrhea output below 400 ml/hour oral ingestion of rehydration solutions between 600 and 800 ml/hour Dr.Farzin khorvash

115 Case-fatality rate during epidemics may be reduced to values below 1% even in disaster situations, provided that adequate access to health care centers and proper management of patients can be ensured Figures as high as 10% have been reported in epidemic settings when patients had no access to health care or received improper treatment Dr.Farzin khorvash

116 Antimicrobial agents play a secondary role in the treatment of cholera patients with severe dehydration are given antibiotics duration of diarrhea is decreased volume of stool is reduced by nearly half Early discharge and lessened hydration decrease hospital expense These benefits are critical in epidemic conditions. Dr.Farzin khorvash

117 Oral tetracycline and doxycycline are the agents of choice in areas of the globe where sensitive strains predominate A single dose of doxycycline (300 mg) is the preferred regimen Tetracyclines are not safe in children younger than 7 years alternatives such as trimethoprim- sulfamethoxazole, erythromycin, and furazolidone are preferred over tetracyclines Pregnant women can be treated with erythromycin or furazolidone Dr.Farzin khorvash

118 In the last 2 decades the appearance of strains resistant to tetracyclines and other antimicrobial agents New agents :with quinolones being the most effective Ciprofloxacin has been more extensively studied than other quinolones. Dr.Farzin khorvash

119 Two regimens of ciprofloxacin a single dose of 1 g once-daily regimens of 250 mg for 3 days. Dr.Farzin khorvash

120 Therapy of Cholera 1.Evaluate the degree of dehydration on arrival 2.Rehydrate the patients in two phases: Rehydration phase: lasts 2–4 h Maintenance phase: lasts until diarrhea abates 3.Register output and intake volumes in predesigned charts and periodically review the data 4.Use the intravenous route only for Severely dehydrated patients during the rehydration phase, in whom an infusion rate of 50–100 ml/kg/h is advised Moderately dehydrated patients who do not tolerate the oral route High stool purgers (>10 ml/kg/h) during the maintenance phase 5.Use ORS for patients during the maintenance phase at a rate of 800– 1000 ml/h, matching ongoing losses with ORS 6.Discharge patients to the treatment center if the following conditions are fulfilled: Oral tolerance,  1000 ml/h Urine volume,  40 ml/h Stool volume,  400 ml/h Dr.Farzin khorvash

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122 Prevention V. Cholerae is spread through contaminated food and water, therefore, prevention depends upon the interruption of fecal-oral transmission Anti-biotic prophylaxis, vaccines and surveillance of new cases are the answer to preventing the spread of disease. Dr.Farzin khorvash

123 Cholera is not transmissible person- to-person, but can easily be spread through contaminated food and water Dr.Farzin khorvash

124 Sari Cloth Filtration: Preventative Measure Using Sari cloth to filter Water Dr.Farzin khorvash

125 Vaccines Two types of cholera vaccines are currently approved for use in humans. –Killed-whole-cell formulation: killed bacterial cells from both biovars of serovar 01 and purified B subunit of the cholera toxin. Provides immunity to only 50% of adult victims and to less than 25% of child victims. –Live-attenuated vaccine, genetically engineered Provides >90% protection against classical biovar and 65-80% agaisnt E1Tor biovar. Dr.Farzin khorvash

126 Vaccines: Problems The live vaccine is associated with certain problems: Side Effects: Cause mild diarrhea, abdominal cramping and slight fever Possible virulence of live strain Upon infection of the vaccine strain by cholera toxin Dr.Farzin khorvash

127 Chemoprophylaxis of household contacts published data do not support this concept More recently it has been shown that when transmission of the disease is low, as occurs in endemic areas, the utility of chemoprophylaxis is not significant Prophylaxis with antibiotics might be considered in situations in which the rate of transmission of the disease is high, along with other measures to curtail transmission Dr.Farzin khorvash

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