Mcphs Viral And Bacterial Gastroenteritis

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Gastrointestinal GI infx are problematic for:

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children, travelers, campers, immunocompromised patients, chornic care facility residents, military personnel assigned oversease

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Definition of gastroenteritis:

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syndromes of diarrhea or vomiting that tend to involve noninflammatory infection of the upper small bowel or inflammatory infection in the colon.

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Likelihiood of exposure and risk of disease with exposure is affected by:

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-personal hygiene
-living conditions
-ingestion of contaminated foods/beverages
-where you are (home vs. vacation)

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Route of acquiring GI infections:

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oral route (fecal-to-oral transmission via ingestion of contaminated foods/beverages)

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Susceptibility for young children:

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-Particulary susceptible to rotaviral infections and enteropathogenic E. coli (EPEC)
-Relatively immune to C. difficile

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Gastric acidity:

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-forms acid barrier that prevents most pathogens from reaching the intestinal tract
-at normal pH; 99.9% of coliform bacteria are killed w/in 30 minutes
-w/ high pH (no acid) no reduction in bacterial inoculum is seen at 1 hour

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Normal Enteric Microflora:

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-99.9% are anaerobes
-effective in resisting colonization w/ potentially pathogenic organisms

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One dose of Streptomycin:

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will reduce the infecting dose of Salmonella typimurium by 100,000 fold

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Intestinal immunity contains:

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-phagocytic, humoral, and cell mediated elemnts
-maintain a state of "physiologic inflammation"

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Enteric pathogenicity is determined by:

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organisms ability to produce toxins, adhere to the intestinal mucosa, and its ability to invade the intestinal mucosa

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Neurotoxins

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-ingested as preformed toxins
-act on the CNS rather than having a direct effect on intestinal mucosa

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Enterotoxins

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-have direct effect on the intestinal mucosa to elicit a net fluid secretion

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Cytotoxins

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-have a direct effect on the intestinal mucosa
-responsible for the mucosal destruction that often results in an inflammatory colitis

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Pathogen attachment

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-pathogenicity is enhanced by an organism's ability to adhere to and colonize the mucosa

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Adhesins

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binding substances on the surface of the organism

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Invasiveness

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organisms that invade and destroy epithelial cells cause inflammatory diarrhea

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Microbe-host interactions cause an alteration of the normal intestinal physiology in 3 ways

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1) Shift in the balance of bidirectional water and electrolyte flow in the upper small bowel by intraluminal toxins (all types)

2) Inflammatory destruction of the ileal or colonic mucosa (Type 2,3)

3) Penetration through an intact mucosa and enter the lymphatic system (Type 3)

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Type 1 Interactions

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-Noninflammatory
-Proximal small bowel
-Water diarrhea
-No fecal leukocytes

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Type 1 Interaction Organisms

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-ET E. coli
-Clostridium perfringens
-Bacillus cereus
-Staph aureus
-Rotavirus
-Norwalk virus
-Norwalk-like virus

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Type 2 Interactions

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-Inflammatory
-Colon
-Dysentery
-Fecal leukocytes present

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Type 2 Interaction Organisms

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-Shigella
-Non-typhoid Salmonella
-Clostridium difficile
-Campylobacter jejuni
-EH E. coli

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Type 3 Interaction

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-Penetrating
-Distal small bowel
-Enteric fever
-Fecal leukocytes present

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Type 3 Interaction Organisms

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-Salmonella typhi

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Dysentery:

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GI infection characterized by severe diarrhea which contains mucous (leukocytes) and blood

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Method to assess extent of water loss

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Determine acute weight loss:
Mild = 3-5% loss
Moderate = 6-9% loss
Severe = > 10% loss

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Treatment of Mild-Moderate Fluid Loss

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-Glucose-based oral rehydration therapy (ORT)
-Reverses dehydration in nearly all patients (3-6% failure)

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ORT

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-inexpensive
-noninvasive
-no hospitalization
-driven by thirst (less problem with overhydration)
-does not alter time course, just hydration

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Treatment of Severe Fluid Loss or in patient unable to take PO

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-IV fluid replacement required
-Normal saline or Ringer's lactate
-IV for 1-2 days followed by ORT

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ORT Essential components

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- Glucose <5%
- Electrolytes Na (40-60mEq), K, Cl
- H2O
- Low-osmolarity products better (250mOsm/L)

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Fluids to avoid:

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Colas, juices, chicken broth, sports beverage

b/c too much sodium, glucos or high-osmolality

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Acute Viral Gastroenteritis

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-Virus are most common etiologic agent
-Common in winter months in temperate climates

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Acute Viral Gastroenteritis for Children b/t 3 and 24 months

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-Rotavirus
-Manifestations: N/V/D and fever
-Incubation: 48 hours
-Duration: 1-9 days

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Acute Viral Gastroenteritis for older Children and Adults

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-Norwalk virus and Norwalk-like viruses
-Manifestations: N/V/D and fever
-Vomiting more common symptom in children
-Diarrhea more common symptom in adults
-Incubation: 48 hours
-Duration: 1-3 days

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Treatment of Acute Viral Gastroenteritis

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-Supportive
-Fluids

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Traveler's Diarrhea

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-Most cases start 5-15 days after arrival and also upon return

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Traveler's Diarrhea Manifestations

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-Common: malaise, anorexia, abdominal cramps water diarrhea (>3 loose stools/24 hrs)
- Less common: (10-30%) nausea/vomiting, fever, and bloody stools
- Can be self-limited (3-5 days)

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Traveler's Diarrhea Bug

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-Enterotoxigenic E. coli (ETEC) is most commonly implicated single organism (30-50% of cases)
-Other bugs: Salmonella, Shigella, Campylobacter, and viruses are less frequently implicated
-Occurs in someone who normally resides in an industrialized region and travels to a developing country
-

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Traveler's Diarrhea Treatment

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-Supportive, fluids
-Bismuth subsalicylate (BSS)
-Loperamide

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BSS dose

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524 mg (15-30ml or 2 tablets) every 30-60 minutes; up to 8 doses/day x 1-2 days

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Loperamide dose

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4 mg follwed by 2 mg after each loose stool; max of 16 mg in 24 hours x 1-2 days

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Loperamide benefits over BSS

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-Longer 1st dose effect
-Loose stools resolve sooner
-Fasier subjective relief
-Easier to administer

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Loperamide drawlbacks vs. BSS

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-Loperamide may prolong illness due to organisms other than ETEC
-Loperamide SE

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Traveler's Diarrhea Abx Tx

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-Reduce symptoms from 3-5 days to 1-2 days

-TMP/SMX
-Fluoroquinolones
-Rifaximin

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Traveler's Diarrhea Abx Tx Concerns

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-FQ = photosensivity
-TMP/SMX = rash and photosensitivity
-Drug interactions
-Infections caused by Salmonella

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Traveler's Diarrhea Tx
TMP/SMX

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-more effective when used in combo w/ loperamide
-resistance is common, less in central Mexico
-poor activity against other causes of traveler's diarrhea

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Traveler's Diarrhea Abx Tx
TMP/SMX Dosing

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-1DS tablet q12h x 3 days

OR

-2 DS tablets then 1 DS q12h for 5 more doses (more effective regimen)

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Traveler's Diarrhea Abx Tx
Fluroquinolones

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-active against most enteric pathogens causing traveler's diarrhea
-unclear if patients benefit from addition of loperamide

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Traveler's Diarrhea Abx Tx
Fluroquinolone Dosing

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-Ciprofloxacin 500mg BID x 3 days
-Norfloxacin 400mg BID x 3 days

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Traveler's Diarrhea Abx Tx
Rifaximin

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- 200mg po tid

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Traveler's Diarrhea
Prophylaxis 1st line

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-prevention is best achieved by avoiding consumption of potentially infectious sources
-water, fresh vegetables, and fruits

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Traveler's Diarrhea
Prophylaxis Pharm

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BSS - 62-65%
TMP/SMX - 70-80%
Fluoroquinolones - >90%
Rifaximin - 72%

Started on 1st day in country and continue for 1-2 days after leaving; max tx 3 weeks

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Traveler's Diarrhea
Prophylaxis Concerns

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-side effects and drug interactions
-promotion of resistance
-is it necessary when tx is effective and illness is self-limited
-what to do if prophylaxis fails
-provides a false sense of security

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Traveler's Diarrhea
Prophylaxis for Specific Pop

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-important underlying health conditions that increase risk for diarrhea or in whome the consequences of diarrhea are severe (IBS, conditions requiring antacids, DM, cardiac dx, AIDs, immunodeficiency)
-whose trip absolutely can't be interupted by an illness
-whose preference is to use prophylaxis
-who is unwilling to follow dietary restrictions

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Food Poisoning
Staphylococcus aureus

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-preformed toxin in food
-salad, pastries, ham, poultry
-TX = fluids, supportive

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Food Poisoning
Bacillus cereus

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-preformed toxin in food or in vivo
-meats, vegetables, fried rice
-TX = fluids, supportive

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Food Poisoning
Clostridium perfringens

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-in vivo toxin production
-meat, poultry
-TX = fluids, supportive

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Inflammatory gastroenteritis =

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-Acute dysentery
-Stool examinations reveals sheets of polymorphonuclear leukocytes in clumps

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Clostridium difficile diarrhea

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-accounts for 20-30% of Abx-associated diarrhea
-almost all Abx have been associated with the disease
-Most common agents are cephalosporins, aminopenicillins, and clindamycin

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C. diff steps in pathogenesis

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-disruption of normal colonic flora (Abx or antineoplastics)
-colonization with C. difficile
-acid-resistant spores survive passage through the stomach and convert to vegetative forms in the small bowel on exposure to bile acid
-elaboration of toxin A (enterotoxin) and toxin B (cytotoxin) which cause intestinal fluid secretion, mucosal injury, and inflammation
-disease acquisition more consistent with scenario B below

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Disease acquisition for C. diff

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-2 theories
-Abx tx allows for C. diff colonization which produces asymptomatic and symptomatic pts (more consistent)
-C. diff is acquired before Abx tx but Abx tx causes symptomatic infx

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Clostridium difficile
Clinical Manifestations

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-asymptomatic carriage (3-8% in healthy; 20% in hospital)
-diarrhea may be brief and self-limited or cholera-like
-fever (30-50%), leukocytosis (50-60%), abdominal pain and cramping (20-33%)

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Clostridium difficile
Time Course

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-onset typically after 5-10 days of Abx tx
-range between 1 day of Abx and 10 weeks after d/c of Abx
-resolution in 15-25% of cases

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Clostridium difficile
Diagnosis

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-clinical presentation
-history of Abx use
-presence of fecal leukocytes
-detection of toxin

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Clostridium difficile
Specific treatment

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-continued symptoms after w/drawal of Abx (S&S should resolve w/in 48-72hrs)
-require continued Abx therapy
-are elderly or debilitated
-severe C. diff disease (fever, pronounced leukocytosis, severe abdominal pain)

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Clostridium difficile
Metronidazole

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-PO 250mg QID or 500mg TID x 7-10 days
-1st line
-Established efficacy
-relatively inexpensive vs. vancomycin
-concerns with promoting enterococcus resistance (VRE) with vancomycin exposure

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Clostridium difficile
Vancomycin

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-PO 125mg-500mg QID x 7-10 days
-considered by some to be 1st line for patients with severe or life-threatening disease
-consider use for older patients with fever/high WBC (>15k) or documented pseudomembranous colitis or those in the ICU
-concerns with promoting enterococcus resistance (VRE) w/ use

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Clostridium difficile
Metronidazole vs. Vancomycin

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-milder forms of disease, similar response (90-95%)and relapse rates (15-30%)
-response seen within 2-4 days

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Clostridium difficile
Relapse

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-usually not due to resistance
-may be due to failure to eradicate the organism or reinfection
-spores are hard to kill
-initial relapses can be treated with same agent as the initial course of therapy

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Other GI pathogens that cause inflammatory gastroenteritis

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-Shigella sonnei and S. flexneri
-Campylobacter jejuni
-Entero-hemorrhagic E.coli 0157:H7

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Inflammatory Gastroenteritis
Shigella sonnei and S. flexneri

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-salads, water, fecal-oral
-specific tx may not be needed but does decrease shedding and duration of illness

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Inflammatory Gastroenteritis
Shigella sonnei and S. flexneri
Abx

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3-5 days of tx
-TMP/SMX 1DS q12H (resistance concern)
-Ciprofloxacin 500mg BID
-Norfloxacin 400mg BID
-Azithromycin 500mg x1, 250mg x 4 days

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Inflammatory Gastroenteritis
Campylobacter jejuni

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-poultry, raw milk, water, fecal-oral
-specific treatment may not be needed but does shorten duration of bacterial excretion
-tx does not effect diarrhea unless started very early

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Inflammatory Gastroenteritis
Campylobacter jejuni
Abx

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5 days of:
-azithromycin 1000mg x1; 500mg x 4 days
-ciprofloxacin 500mg BID (resistance concern)

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Inflammatory Gastroenteritis
Entero-hemorrhagic E. coli 0157:H7

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-undercooked hamburger, fecal-oral
-TX = fluids, supportive only
-Abx increase risk for developing HUS

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HUS

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hemolytic uremia syndrome
-anemia
-thrombocytopenia
-acute renal failure

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Salmonellosis

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-source is contaminated foods and fecal-oral transmission (reptile)
-manifestations vary in severity and include acute (self-limiting) to bactermic disease (risk for metastatic infection)

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Salmonellosis
Acute
Organisms

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Usually not typhoid strains
-Salmonella paratyphi A
-Salmonella paratyphi B
-Salmonella paratyphi C
-Salmonella choleraesuis
-Salmonella enteritidis

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Salmonellosis
Acute Manifestations

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-Incubation: <72h; duration 1-5 days
-N/V
-abdominal cramps
-HA
-Fever
-Diarrhea (usually mucoid; rarely bloody)

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Salmonellosis
Acute
Treatment

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-AVOID antiperstaltics
-fluids, supportive
-Abx not needed for healthy adults

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Salmonellosis
Acute
Treatment: Pt needing Abx

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Those at risk for invasive disease and the complications of invasive disease
-children <6 months of age
-adults >50 years of age
-patients with valvular abnormalities or vascular grafts
-immunodeficient patients
-splenectomized patients
-severely symptomatic patients

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Salmonellosis
Acute
Abx Treatment

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1st line
-ciprofloxacin 500mg BID, norfloxacin 400mg BID
Alternative
-azithromycin 1gm PO x1; 500mg PO x 6 days

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Salmonellosis
Acute
Why not treat everyone

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-tx does not affect duration of symptoms or stool carriage
-treated patients have a greater likelihood of relapse
-treated patients have a higher rate of chronic carriage
-increases risk for development of Salmonella resistance
-disease is usually contained to the GI tract (<5% progress to bacteremia)

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Salmonellosis
Bacteremic Disease
Pathogenesis

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-Organisms are ingested and survive exposure to gastric acid before gaining access to the small bowel
-organisms penetrate the intestinal epithelium
-organisms multiply in intestinal lymphoid tissue and then disseminate via the lymphatic or hematogenous route

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Enteric Fever

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-Bacteremic disease
-Salmonella typhi is most common = Typhoid fever
-nontypoidal Salmonella = paratyphoid fever
--Salmonella paratyphi A
--Salmonella paratyphi B
--Salmonella paratyphi C

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Enteric Fever
Incubation
Duration

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-Incubation = 5-21 days
-Duration = typically 4 weeks

10% mortality without treatment

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Enteric Fever
Manifestations

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-typhoid and paratyphoid fever are clinically indistinguishable
-initially may resemble acute enteritis; however may present w/ constipation
-fever (initially remittent fever followed by sustained fever)
-HA in almost all patients
-rash - "rose spots"
-organism may be found in stool, blood, or urine
-fecal leukocytes in stool
-leukocytosis; leukopenia in 16-46% of pts

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Enteric Fever
Treatment

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-Ciprofloxacin 500mg BID x 10-14 days
-Azithromycin 1gm x 1 dose, then 500mg QD x 5 days
-Ceftriaxone 2 gm QD x 10-14 days

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Bacteremia with extraintestinal complications

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-occus in 5-10% of patients with Salmonella bacteremia
-endocarditis, meningitis, pneumonia, osteomyelitis, septic arthritis, pyelonephritis

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Salmonella Carrier State

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-persistence of salmonella in the stool or urine for >1 year after acute disease
-more common with S. typhi versus other salmonella species
-more likely in patients getting Abx therapy (lower for patients getting FQ)
-associated with an increased risk of biliary and GI carcinoma
-continued shedding is a public health concern