gastroenteritis and food poisining meral sÖnmezoĞlu, md yeditepe university hospital associate...

GASTROENTERITISAnd

FOOD POISINING Meral SÖNMEZOĞLU, MDYeditepe University HospitalAssociate ProfessorDepartment of Infectious Diseases and Microbiology

Learning Objectives

– Describe and classify of gastroenteritis and food poisoning

– Explain the epidemiology of gastroenteritis and possible etiologic agents in various clinical settings

– Know the pathophysiology of gastroenteritis– Develop an information on diagnosis and

management plan for gastroenteritis

• With the exception of Helicobacter pylori gastritis, the term gastroenteritis is applied to syndromes of diarrhea or vomiting that tend to involve noninflammatory infection in the upper small bowel or inflammatory infection in the colon

• Risk of acquiring a gastrointestinal infection varies greatly with age, living conditions, personal and cultural habits, and group exposures

• The second epidemiologic determinant of risk for enteric infection is where you are

• The third determinant of risk is when you are there. The majority of enteric illnesses in temperate climates occur during winter months. The opposite is true in tropical countries, where distinct summer peaks of illnesses are common. The role of rainfall is uncertain, and some adjacent areas with similar monsoon climates have opposite seasons of major diarrheal illnesses, as illustrated by the peak seasons for cholera

Host defense factors

• Gastric acidity• Intestinal motility• Intestinal microflora• Mucus• Systemic and local immune

mechanisms• Others (e.g. breast feeding)

Bacterial virulence factors

• Adherence• Enterotoxin production• Cytotoxin production• Mucosal invasion

Mechanisms of infection

• Ingestion of preformed toxin (food poisoning)

• Fecal-oral contamination – Food, flies, fingers, feces, and fomites– Contaminated food

• Animal reservoir• Fecal-oral contamination of food

– Infectious dose varies (~100 to 109)

Infectious Doses of Enteric Pathogens

  Shigella 10 to 102

  Campylobacter jejuni 102 to 106

  Salmonella 105

  Escherichia coli 108

  Vibrio cholerae 108

  Giardia lamblia 10 to 102 cysts  Entamoeba histolytica 10 to 102 cysts  Cryptosporidium parvum 1 to 103 oocysts

DIARRHEA

• Alteration in a normal bowel movement• Characterized by an increased in the water

content, volume, or frequency of stools• >3 or more stools and at least 200 gr• Decrease in consistency (soft or liquid) and

an increase in frequency of bowel movement to >3 stools per day

INFECTIOUS DIARRHEA

• 3-5 billion episodes yearly• Major cause of worldwide morbidity and

mortality• 5 million deaths yearly, 80% < 1 year of age• Major cause of work/school absenteeism• Major economic burden, especially in

developing countries

INFECTIOUS DIARRHEA• Due to an infectious etiology • Accompanied by symptoms of nausea,

vomiting, or abdominal cramps.• Acute diarrhea is an episode of diarrhea

of <14 days in duration• Persistent diarrhea is of >14 days in

duration• Chronic diarrhea lasts >30 days

INFECTIOUS DIARRHEA

• Second leading cause of morbidity and mortality worldwide

• More than 2 million deaths annually• Some causes of infectious diarrhea

result in serious long term sequelae (HUS-STEC,G-B Campylobacter)

Etiology of Diarrhea

Infective Non infective

Viruses Bacteria

Parasites Fungi

Allergic

Symptomatic Inappropriate feeding

Food intolerance Climate

Major PathogensBacterial infection Campylobacter, Shigella, and

Salmonella

Protozoal infection Cryptosporidium species, Giardia lamblia, Isospora belli, Entamoeba histolitica, Microsporidium species

Toxin induced E. coli and Clostridium difficile

Mycobacterial infection M. tuberculosis, M. Avium complex

Helminthic infection Strongyloides stercoralis

Fungal infection Candida species (seldom a cause of diarrhea)

Etiology of Infectious Diarrhea

(in (((8developed countries)

• 70-80% is viral • 10-20% is bacterial– Bacterial are responsible for most severe cases• < 10% is parasitic

Infectious Causes – Foodnet 2005

• 44.5 million persons (15% of the US pop.)

• Laboratory confirmed infections – 16,614

Microorganism

# Incidence

(per 100,000

)

Salmonella 6,471 14.55

Campylobacter

5,655 12.72

Shigella 2,078 4.67Cryptosporidium

1,313 2.95

STEC 0157 473 1.06

Yersinia 159 0.36

STEC non-0157

146 0.33

Listeria 135 0.3

Vibrio 119 0.27

Cyclospora 65 0.15

Salmonella SubtypesTyphimurium 19%

Enteritidis 18%

Newport 10%

Heidelberg 6%

Javiana 5%

Mechanisms of infection

• Ingestion of preformed toxin (food poisoning)

• Fecal-oral contamination – Food, flies, fingers, feces, and fomites– Contaminated food

• Animal reservoir• Fecal-oral contamination of food

– Infectious dose varies (~100 to 109)

Host defense factors

• Gastric acidity• Intestinal motility• Intestinal microflora• Mucus• Systemic and local immune mechanisms• Others (e.g. breast feeding)

Defense Barriers of the Enterocytes

1. Physical barrier: mucus 2. Bacteriological (flora) 3. Immunological: Secretory IgA

1 2

3

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Morphology of Intestinal Mucosa

Villicovered mainly (90%) by tall columnar absorptive cells (Enterocytes) having a micrevillar brush border

Crypts of lieberkuhnCovered mainly by short columnar secretory cellsGoblet cellswithout brush border

Bacterial virulence factors

• Adherence• Enterotoxin production• Cytotoxin production• Mucosal invasion

Diarrhea

• Non-inflammatory– Watery diarrhea, no blood or mucus or pus in stool, no fever or

systemic signs– Secretory or osmotic mechanism– Dehydration may occur– Generally self-limited and more benign– Therapy generally supportive

• Inflammatory– Frequent lower volume stool, mucoid, bloody, or purulent. Often

with fever or systemic signs, tenesmus, urgency– Exudative mechanism– Dehydration rare– Less benign

Osmotic Diarrhea

• Interferes with absorption of water• Solutes are ingested

– Magnesium sulfate or citrate or magnesium containing antacids

– Sorbitol– Malabsorption of food

• Lactase deficiency• Celiac sprue• Variety of infectious organisms (particularly viruses)

Definition: Increased amounts of poorly absorbed, osmotically active solutes in gut lumen

Secretory Diarrhea

• Excess secretion of electrolytes and water across mucosal surface

• Usually coupled with inhibition of absorption• Clinical features

– stools very watery– stool volume large– fasting does not stop diarrhea

Secretory Diarrhea

• Bacterial or viral enterotoxins– Cholera, enterotoxigenic E. coli, B. cereus, S.

aureus, Rotavirus, Norwalk virus• Hormonal secretagogues• Certain laxatives (castor oil, senna)

Exudative Diarrhea

• Intestinal or colonic mucosa inflamed and ulcerated– Leakage of fluid, blood, pus– Impairment of absorption– Increased secretion (prostaglandins)

• The extent of bowel involved determines– Severity of diarrhea– Systemic signs and symptoms (abdominal pain,

fever, etc)

Exudative Diarrhea

• Infectious, invasive organisms– Shigella, Campylobacter, Yersinia, E.

histolytica, EHEC, C diff• Idiopathic inflammatory bowel disease

– Crohns disease– Ulcerative Colitis

• Ischemia

Associated Signs & Symptoms

••

•Systemic illness/fever – invasive pathogen involvement• Vomiting as predominant symptom– likely viral organism or food poisoning• Abdominal pain– inflammatory process (Shigella, Campylobacter, EHEC)• Persistent abdominal pain and fever: Yersinia

When to Consider ABX

Most cases of diarrhea resolve spontaneously and do not require treatment with antibiotics. Antibiotic therapy may be considered however, in the following circumstances:– When signs and symptoms include:• Fever• Bloody stools• Presence of fecal leukocytes or occult blood;– To reduce fecal excretion and environmental contamination by a highly infectious agent like Shigella;– For persistent or life-threatening diarrheal infections such as cholera;– For immunocompromised patients.

Antibiotics

• Most helpful for:– Shigella, ETEC, ameobiasis, Giardia, cholera, S. typhi•May help for:– non-typhi Salmonella & Camplyobacter• Can prolong fecal shedding, use only if severe case • Not useful for viral, EIEC• Can be harmful in EHEC (O157:H7)• Multi-Drug resistance is a rapidly growing problem

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Acute infectious diarrhea

• Bacterial infection• Common nonbacterial infection • HKO antigens• Common among population – particular day care

centers• Developing countries – serious health effects, fatal• In the U.S., 1/3 due to contaminated food

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HKO antigens

• H = flagellar antigen• K= capsular antigen• O= cell wall antigen• Ex. E. coli O157:H7

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Bacterial

• Salmonella• Shigella• Shiga-toxin producing Escherichia coli• Non-shiga-toxin E. coli• Campylobacter• Yersinia• Clostridium difficile• Vibrio cholerae

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Acute Diarrhea in ChildrenThe most important infective causes of acute diarrhea in

developing countries in children are:• Rotavirus• Enterotoxigenic escherichia coli• Shigella• Campylobacter jejuni• Salmonella typhimurium

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Salmonella

• Contaminated animal products • Salmonellosis - mild• Typhoid fever – severe• Normal flora in animals

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Cases of typhoid fever and salmonelloses.

Fig. 22.10 Data on the prevalence of typhoid fever andother salmonelloses

Nontyphoidal Salmonella

• Salmonella typhimurium and enteritidis• Clinical syndromes

– Gastroenteritis and colitis– Bacteremia and endocarditis– Enteric fever (typhi and paratyphi)– Localized tissue infection– Carrier state (> 1 year)

• Food-borne illness (poultry, meat, eggs)

Bacterial infection: Salmonella

• Clinical Symptoms may evolve• Fever; general malaise • Sometimes no GI symptoms• If there are GI symptoms, will see:

• Bloody diarrhea• Abdominal pain• Weight loss

Presenting Signs and Symptoms

Salmonellosis• Fever, cramping, abdominal pain, and diarrhea within 8-48

hours after ingestion of infective dose (contaminated poultry, shell eggs, dairy products, beef, exotic pets such as reptiles)

• Inflammatory (neutrophilic) enteritis most typically involving the small bowel mucosa, occasional cause of colitis with crypt abscesses and erosive ulceration of colonic mucosa (Salmonella serotype Typhimurium)

• Moderate number of fecal neutrophils, usually fewer than in shigellosis except colitis with blood and pus in stool

Complications of Salmonellosis

• Diarrhea usually self-limited (3-7 days), if persists >10 days another microbial etiology likely

• Occasional dehydration requiring hospitalization• Bacteremia (1-4% immunocompetent cases) (persistent

bacteremia suggests endovascular infection site such as atherosclerotic plaques and aneurysms)

• After resolution of diarrhea mean duration of carriage in stool is 4-5 weeks

• Stool culture

• Salmonella bacilli may be found in

stool/blood cultures

• Serology: positive Widal test with

increased titers

Bacterial infection: Salmonella Diagnostics

Management and Treatment

• TMP/SMX 960 mg bid or• Chloramphenicol 250 mg qid for 3 weeks• In case of sepsis, IV therapy is necessary • Shorter regimens are:

• ciprofloxacin 500 mg bid or ofloxacin 400 mg bid or ceftriaxone 2 g IV for 7-10 days

• Many patients often relapse after treatment and chronic maintenance therapy (TMP/SMX 1 DD daily) is sometimes necessary.

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Shigella

• Primarily a human parasite• Infects the large intestine• No perforation of intestine• Dysentery• Exotoxin (shiga-toxin)• Enterotoxin

Shigella

Presenting Signs and Symptoms

• Clinical Symptoms may evolve

• High fever• Abdominal pain• Bloody diarrhea

Shigella

• dysenteriae, flexneri, boydii, sonnei• Watery or bloody diarrhea• May be complicated by reactive arthritis and

rarely HUS• Very infectious ( ~100 organisms cause

disease)

• Stool microscopy— fresh examination and after concentration

• Multiple stool samples may be necessary

• Shigella bacillus found in stool

Shigella- Diagnostics

ShigellaManagement and Treatment

TMP/SMX 960 mg bid x 5 days or amoxicillin 500 mg tid x 5 days

• If resistant to the above, give • or • norfloxacin 400 mg bid x 5 days • or• nalidixic acid 1 g qid x 10 days • ciprofloxacin 500 mg bid

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Infection of the large intestine by Shigella dysenteriae.

Fig. 22.11 The appearance of the large intestional mucosaIn Shigella dysentery.

© University of Alabama at Birmingham, Dept. of Path.

Shigella colitis (Campylobacter or Salmonella would look much the same.)

Diarrhea of Shigella – WBCs & RBCs

CDC

E. coli

Type Clinical Features Complications

ETEC (Enterotoxigenic) Watery diarrhea, travelers diarrhea

rare

EHEC (Enterohemorrhagic )

Bloody diarrhea Hemolytic uremic syndrome, TTP (mostly 0157:H7)

EIEC (Enteroinvasive) watery diarrhea or bloody diarrhea

rare

EAEC (Enteroaggregative)

watery diarrhea or bloody diarrhea

rare

EPEC (Enteropathogenic) Watery diarrhea or bloody diarrhea, mainly in children

May be protracted

Enterohemorrhagic Escherichia coli

• Non-sorbitol fermenting Escherichia coli (Escherichia coli 94% + for sorbitol fermentation)

• Majority of enterohemorrhagic strains positive for somatic O157 and flagellar H7 antigens (O104 and O111 strains have caused outbreaks in the US)

• Bacteriophage-mediated production of Shiga-like toxin (Stx1 or Stx2) which are cytotoxic (verotoxin)

• Accounts for 15% to 36% of cases of bloody diarrhea

Enterohemorrhagic Escherichia coli

• Abdominal cramps and watery diarrhea 3 to 8 days following ingestion of contaminated food (undercooked beef, raw milk, fresh produce) or water

• Shiga toxin absorbed from intestine and damages vascular endothelial cells (intestinal mucosa and kidney)

• Watery diarrhea followed by grossly bloody diarrhea• Uncomplicated illness lasts 1 to 12 days• Use of antibiotics contraindicated (phage-mediated

production of Shiga toxin enhanced by ampicillin, norfloxacin, and other antibiotics)

Complications of Hemorrhagic Escherichia coli Colitis

• Fever and neutrophilic leukocytosis herald hemolytic uremic syndrome (HUS) (thrombocytopenia, oliguria, hematuria, microangiopathic hemolytic anemia)

• HUS in 8% of infections in children with a 3% to 5% mortality

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Shiga-toxin (E. coli)

• O157:H7 • Enterohemorrhagic E. coli (EHEC)• Serious manifestations – hemolytic uremic

syndrome, neurologic symptoms• Shiga-toxin gene present on bacteriophage

genome• Type III secretion system

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The Type III secretion is a complex bridge formed by the bacteria, enabling binding to the host cell, thereby allowing the bacteria to insert its products in the host cell.

Fig. 22.12 Type III secretion system.

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Non-shiga-toxin (E. coli)

• Enterotoxigenic – traveler’s diarrhea• Enteroinvasive – no exotoxin• Enteropathogenic – similar to EHEC• Enteroaggregative – chronic diarrhea

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Campylobacter

• Most common bacterial cause of diarrhea• Related to Guillain-Barre syndrome (GBS) –

paralysis

Campylobacter

• Mainly C. jejuni• Transmission from infected animals or food

products, fresh or salt water• Watery diarrhea or dysentery• May be complicated by Guillain-Barré and

IPSID (Immunoproliferative small intestinal disease)

Bacterial infection: Campylobacter

• Clinical Symptoms may evolve• Fever and general malaise, sometimes

without GI symptoms

• When present, GI symptoms include bloody diarrhea, abdominal pain and weight loss.

Presenting Signs and Symptoms

Campylobacter jejuni…

• Spirilla morphology

• Gram Negative Stain

• Motile

• Role as an Enteric Pathogen

© 2007 Aichi Prefectural Institute of Health

• Relatively fragile

• Microaerophilic organism.

• Seems to be well adapted to birds

Campylobacter jejuni

Campylobacteriosis

• Known as campylobacter enteritis or gastroenteritis.

• Infection causes watery or sticky diarrhea, which contain blood and fecal leukocytes.

• Other symptoms include: fever, abdominal pain, nausea, headache and muscle pain.

• Erythromycin 500 mg bid x 5 days (1st choice) • Fluoroquinolones are also effective, but resistance rates of

30-50% have been reported in some developing countries

CampylobacterManagement and Treatment

Complications of Campylobacteriosis

• Enteritis usually self-limiting (1 day to 1 week or longer)

• Guillain-Barré syndrome (structural homology of LPS O-antigen with human nerve gangliosides)

• Post-infectious reactive arthritis (associated with HLA-B27)

• Bacteremia (rate of 1.5/1,000 intestinal infections)

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Campylobacter jejuni has a unique S-shaped and spiral morphology, and is closely related to H. pylori.

Fig. 22.13 Scanning micrograph of Campylobacter jejuni, Showing comma, S, and spiral forms.

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Yersinia

• High degree of abdominal pain• Mistaken for appendicitis• Infects the small intestine• Some can affect the lymphatic system

(intracellular)

Yersinia enterocolitica• Fermentative, rod-shaped or coccoid gram-negative bacteria,

non-motile and metabolically inactive at 37oC but motile and metabolically active at 22-30oC

• Enteropathogenic strains cytotoxic by penetratating human epithelial cells

• Infection results in inflammatory ileitis (generally) and colitis (occasionally involving ascending colon) with mixed neutrophilic and mononuclear cell response

• Necrosis of Peyer’s patches, mesenteric lymph node enlargement, and in severe cases thrombosis of mesenteric blood vessels with intestinal necrosis and hemorrhage

Yersinosis

• Febrile diarrhea with abdominal pain 16 to 48 hours following ingestion of an infectious inoculum

• Duration of illness ranges from 1 day to a prolonged diarrhea of 4 weeks

Complications of Yersinosis

• Can simulate acute appendicitis (mesenteric lymphadenitis)

• Bacteremic dissemination with hepatic and splenic abscess formation

• Reactive arthritis associated with HLA-B27 histocompatibility antigen (10-30%)

• Exudative pharyngitis (8% of infections accompanied by fever but no diarrhea)

Treatment

• Safe food handling• Y. enterocolitica is suscestible to amg,chloram,

tetra, TMP/SMZ,pip, cipro, • ß lactamase, resis to pen, ampi, 1. gen. ceph.• Patients with septicemia should receive antb.• Y. pseudotuberculosis usually not require antb,

but with septicemia ampi or tetra

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Clostridium difficile

• Pseudomembranous colitis or antibiotic associated colitis

• Capable of superinfecting the large intestine due to drug treatments

• Enterotoxins

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A mild and more severe case of antibiotic-associated colitis.

Fig. 22.14 Antibiotic-associated colitis.

• Pseudomembranes:

Irregular yellow plaques of necrotic debris (black arrow) with intervening edematous bowel mucosa (white arrow) in an 87-year-old woman. These findings are consistent with pseudomembranes caused by Clostridium difficile infection.

Schroeder, 2005

♦ Pathogenesis• Accountable for 15-25% of antibiotic-associated

diarrhea.

• Fecal-oral route transmission.

• Three steps to C. Difficile diarrhea:

Alteration of the normal fecal flora↓

Colonic colonization of C. difficile↓

Growth and production of its toxins

LaMont, 2006Poutanen & Simor, 2004

Pathogenesis of C. difficile infection

Uncolonized patient↓

Antibiotic exposure↓

Disruption of colinic microflora↓

C. Difficile ingestion & colonization ↓ ↓ Good IgG Poor IgG ↓ ↓ Asymptomatic carrier Production of toxins ↓ Colonic mucosal damage ↓ Clinical Disease

Schroeder, 2005

♦ Risk Factors

• Antibiotics – fluoroquinolones, cephalosporins, clindamycins, penicillins

• Medications:– Proton pump inhibitor– Histamine-2 receptor blockers– Non-steroidal anti-inflammatories (except aspirin)– Laxatives– Narcotics– Antiperistaltic drugs

• Advanced age ( ≥ 65yrs.)• Chemotherapy

• Medical/Surgical procedures– Gastrointestinal surgery– Enemas– Enteral tube feedings– Endoscopy

• Underlying illness and its severity– Inflammatory bowel disease– Diabetes mellitus/Hyperthyroidism– Leukemia/Lymphoma– Liver/Renal failure

• History of C. difficile associated diarrhea• Prolonged hospital stay/Nursing home resident

Louie & Meddings, 2004McDonald, Owings, & Jernigan, 2006

Melillo, 1998Poutanon & Simor, 2004

• Toxic Megacolon

LaMont, 2006

♦♦ Diagnostic Testing

LaMont, 2006

♦ Treatment

• Discontinue the offending agent– If unable:

• Choose an antibiotic less frequently associated with antibiotic-associated diarrhea (aminoglycosides, sulfonamides, macrolides, vancomycin, tetracyclines)

• Prescribe Metronidazole 500mg PO TID throughout the needed course of antibiotic therapy and for 7 days after.

LaMont, 2006Schroeder, 2005

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Vibrio cholerae

• Cholera• Unique O and H antigens• Cholera toxin (CT) – A-B toxin• Bacteria never enter host cells• Heavy lost of fluid “rice-water stool”• Untreated cases can be fatal

85

Vibrio cholerae has a unique curved shaped and single polar flagellum.

Fig. 22.15 Vibrio cholerae

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Common nonbacterial

• Cryptosporidium• Rotavirus

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Cryptosporidium

• Protozoan infection• Zoonotic• Oocysts• Intracellular• AIDS patients are at risk• Associated with fresh water outbreaks

89

A SEM of Cryptosporidium shows attachment to the intestinal epithelium, prior to intracellular invasion.

Fig. 22.16 Scanning electron micrograph of Cryptosporidium

90

Acid-fast staining enables oocysts to be identified, as they stain red or purple.

Fig. 22.17 Acid-fast stain in Cryptosporidium

91

Rotavirus

• Responsible for most morbidity and mortality from diarrhea

• Babies lacking maternal antibodies are at risk • Unique morphological appearance

92

A feces sample containing Rotavirus, which has a unique “spoked-wheel” appearance.

Fig. 22.18 Rotavirus visible in a sample of feces from A child with gastroenteritis.

• Acute diarrhea is an episode of diarrhea of <14 days in duration

• Persistent diarrhea is of >14 days in duration• Chronic diarrhea lasts >30 days

94

Features of acute diarrhea.

Checkpoint 22.5 Acute diarrhea

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Acute diarrhea with vomiting

• Food poisoning - toxin– Staphylococcus aureus– Bacillus cereus– Clostridium perfringens

Classic Syndromes: Acute food poisoning

• Similar illness in 2 or more persons• Epidemiologic evidence of common food source• Onset of symptoms typically within 6 hours of ingestion• Nausea and vomiting prominent• Preformed toxin of S. aureus or B. cereus• Longer incubation periods for C. perfringens

97

Features of acute diarrhea with vomiting.

Checkpoint 22.6 Acute diarrhea with vomiting

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Chronic diarrhea

• Enteroaggregative (EAEC) E. coli• Cyclospora cayetanensis• Giardia lamblia• Entamoeba histolytica

99

EAEC E. coli can be identified by its ability to adhere to human cells in aggregates.

Fig. 22.19 Enteroaggregative E. coli adhering to epithelial cells.

100

The protozoan Cyclospora can be identified by the acid-fast stain, in which large cysts stain pink to red and have a wrinkled outer wall.

Fig. 22.20 An acid-fast stain of Cyclospora in a human Fecal sample.

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The protozoan Giardia is typically transmitted by its cysts, which eventually germinates into the trophozoite and damages the jejunum.

Fig. 22.21 The “face” of a Giardia lamblia trophozoite.

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Entamoeba histolytica have different cellular forms, which includes a trophozoite that contains a karyosome and hosts cells (rbc) and bacteria, and a mature cyst which undergoes excystment.

Fig. 22.22 Cellular forms of Entamoeba hystolytic

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Features of chronic diarrhea.

Checkpoint 22.7 Chronic diarrhea.

History

• Onset and duration of diarrhea• Timing of exposure to potential pathogens

– Travel, ingestion history, environment, recent medications, age

• Character of stool– Volume, presence of blood, mucus, or pus

• Associated symptoms and signs– Abdominal pain, fever, vomiting, dehydration

Physical examination

• Vital signs: Fever, tachycardia• Abdominal tenderness or pain• Signs of dehydration• Blood in stool

Evaluation of Infectious Diarrhea

• Stool studies– fecal leukocytes and RBC/blood– Bacterial culture

• Include C. difficle toxin assay• May need to request EHEC screen

• Endoscopic evaluation may be useful in some– especially for bloody diarrhea or chronic

diarrhea

Laboratory investigations

Stool WBC may be

ABSENT PRESENT VARIABLE

V. cholerae

Enterotoxigenic

E. coli

Virus

E. Histolytica

Food poisoning

Shigella

Campylobacter

Invasive E. coli

Salmonella

Non-cholera

vibrio

Yersinia

C. difficile

Laboratory investigation Not routinely indicated

• Low yield 1.5 -2.4%

• Not useful in initial management

• More sensitive and specific in stool with WBC

Fecal PMNs

• Common in Shigella, Campylobacter, EHEC, EIEC, C. diff

• Rare in Salmonella, Yersinia, ETEC, EAEC

MANAGING INFECTIOUS DIARRHEA• Initial rehidration• Perform thorough clinical and

epidemiological evaluation• Perform selective fecal studies• Institute selective therapy for

– Traveler’s diarrhea– Shigellosis– Campylobacter infection

• Avoid administering antimotilty agents• Selectively administer available vaccines

Oral rehydration solutions

Components WHO Ricelyte Pedialyte

Na (mEq/L) 90 50 45

K (mEq/L) 20 25 20

Cl (mEq/L) 80 45 35

Citrate (mEq/L) 30 34 30

Glucose (g/L) 20 30 25

Treatment of Diarrhea

• Treatment of specific etiology• Non-specific treatment

– hydration– Absorptions (Kaopectate®)– Bismuth – Antiperistaltics/opiate derivatives– Fiber supplementation