به نام خدا Dr.Farzin khorvash.

به نام خدا Dr.Farzin khorvash

Dr Farzin Khorvash Dr.Farzin khorvash

Dr.Farzin khorvash

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

MICROBIAL FACTORS Toxins Attachment Invasiveness Dr.Farzin khorvash

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

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

Infectious Doses of Enteric Pathogens
Shigella 10 to 102 Campylobacter jejuni 102 to 106 Salmonella 105 Escherichia coli 108 Vibrio cholerae Giardia lamblia 10 to 102 cysts Entamoeba histolytica Cryptosporidium parvum 1 to 103 oocysts Dr.Farzin khorvash

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

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

enteroviruses (especially echovirus types 11, 14, and 18)
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

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

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

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

Campylobacteriosis (Campylobacter jejuni)
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

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

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

Dr.Farzin khorvash

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

Dr.Farzin khorvash

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

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

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

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

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

Dr.Farzin khorvash

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

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

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

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

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

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

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

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

Dr.Farzin khorvash

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

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

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

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

Therapy IV Na+ Cl– K+ HCO3– Glucose Intravenous solutions
Ringer's lactate 130 109 4 28* Normal saline 154 WHO ORS 90 80 20 30† 111 Dr.Farzin khorvash

BRAT DIET Banana Rice Apple Tosted bread Dr.Farzin khorvash

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

HUS often requires dialysis Dr.Farzin khorvash

Dr.Farzin khorvash

Cholera Dr.Farzin khorvash

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

Dr.Farzin khorvash

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

Dr.Farzin khorvash

LAB DIAGNOSIS 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. Serologic tests are available to define strains, but this is needed only during epidemics to trace the source of infection. Dr.Farzin khorvash

OTHER LAB FINDINGS 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. Total body potassium is depleted, but serum level may be normal due to effect of acidosis. Dr.Farzin khorvash

Dr.Farzin khorvash

Cholera: ‘Rice water’ stool
Dr.Farzin khorvash

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

Dr.Farzin khorvash

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

PATHOPHYSIOLOGY Non inflammatory Enterotoxin induced diarrhea
Dr.Farzin khorvash

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

Transmission: contaminated food and water
Dr.Farzin khorvash

Dr.Farzin khorvash

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

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

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

Dehydration some dehydration severe dehydration Dr.Farzin khorvash

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

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

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

Dr.Farzin khorvash

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

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

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

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

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

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

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

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

Electrolyte and Glucose Concentration (mmol/L)
Electrolyte Concentration of Cholera Stools and Common Solutions Used for Treatment Electrolyte and Glucose Concentration (mmol/L) Na+ Cl– K+ HCO3– Glucose Cholera stool Adults 130 100 20 44 Children 90 33 30 Intravenous solutions Ringer's lactate 109 4 28* Normal saline 154 WHO ORS 80 30† 111 *Ringer's lactate does not contain HCO3–; 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. Dr.Farzin khorvash Copyright © 2000, 1995, 1990, 1985, 1979 by Churchill Livingstone

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

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

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

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

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

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

urine volume higher than 40 ml/hour diarrhea output below 400 ml/hour
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

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

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

A single dose of doxycycline (300 mg) is the preferred regimen
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

New agents :with quinolones being the most effective
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

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

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, ³1000 ml/h Urine volume, ³40 ml/h Stool volume, £400 ml/h Dr.Farzin khorvash

Dr.Farzin khorvash

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

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

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

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

The live vaccine is associated with certain problems: Side Effects:
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

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

پایان Dr.Farzin khorvash

به نام خدا Dr.Farzin khorvash.

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