Infectious Disease · PANCE / PANRE

Salmonella, Shigella, Campylobacter, and Pathogenic E. coli (Bacterial Enteritis)

Acute inflammatory diarrhea from invasive enteric bacteria; supportive care is the backbone, antibiotics reserved for severe or high-risk cases (and avoided in EHEC).

Also known as: bacterial gastroenteritis, Salmonella, Shigella, Campylobacter, EHEC, STEC, O157:H7, dysentery, food poisoning

Overview

Acute infectious enteritis caused by invasive or toxigenic gram-negative bacilli that produce inflammatory diarrhea, typically with fever, abdominal cramps, and occasionally bloody stools. The four most board-relevant pathogens are nontyphoidal Salmonella, Shigella species, Campylobacter jejuni, and pathogenic Escherichia coli — particularly enterohemorrhagic (EHEC/STEC) O157:H7.

Epidemiology

Foodborne illness causes ~48 million US cases annually (CDC). Campylobacter and Salmonella are the most frequently confirmed bacterial enteric pathogens. Outbreaks linked to undercooked poultry (Campylobacter, Salmonella), eggs and reptiles (Salmonella), ground beef and leafy greens (EHEC), and person-to-person spread in daycares and institutions (Shigella).

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Question 1Infectious DiseaseMedium
A 6-year-old boy is brought to the emergency department with 3 days of severe crampy abdominal pain and visibly bloody diarrhea. He attended a family barbecue 4 days ago where he ate a hamburger. He is afebrile (temperature 37.1°C). Examination shows diffuse abdominal tenderness without rebound or guarding and mildly dry mucous membranes. A complete blood count and basic metabolic panel are pending. Which of the following is the most appropriate next diagnostic test?
  • AStool Shiga toxin EIA assay
  • BStool ova and parasite exam
  • CAbdominal and pelvic CT scan
  • DStool C. difficile toxin PCR
Reveal answer & full explanation
Correct answer: A — Stool Shiga toxin EIA assay
  • AStool Shiga toxin EIA assay
  • BStool ova and parasite exam
  • CAbdominal and pelvic CT scan
  • DStool C. difficile toxin PCR

Why Stool Shiga toxin EIA assay is correct

  • Bloody diarrhea without fever after eating ground beef is the classic presentation of enterohemorrhagic E. coli (EHEC/STEC O157:H7), which releases Shiga-like toxin.
  • IDSA guidelines recommend a stool Shiga toxin assay (EIA or PCR) on any patient with bloody diarrhea, because identifying STEC changes management: antibiotics and antimotility agents are avoided since they increase the risk of hemolytic-uremic syndrome.
  • Confirming EHEC also triggers monitoring of CBC and creatinine through about day 10 for HUS (microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury).

Why the others are wrong

  • Stool ova and parasite exam fits subacute, travel- or daycare-associated watery diarrhea from Giardia or Entamoeba; parasites rarely cause this acute, ground-beef-linked bloody illness.
  • Stool C. difficile toxin PCR is indicated with recent antibiotic or healthcare exposure and watery diarrhea, neither of which is present here.
  • Abdominal and pelvic CT scan is reserved for peritoneal signs, severe pain, or suspected toxic megacolon or perforation; this child has no peritoneal findings, so it is not the next step.
Question 2Infectious DiseaseMedium
A 6-year-old boy is brought in with 3 days of severe crampy abdominal pain and grossly bloody diarrhea that began after a backyard barbecue where he ate an undercooked hamburger. He is afebrile with a temperature of 37.1°C (98.8°F). Abdominal exam shows diffuse tenderness without peritoneal signs. A stool viral PCR panel is negative, fecal leukocytes are present, and a Shiga toxin assay returns positive. The clinician counsels the family that antibiotics will be withheld to reduce the risk of hemolytic-uremic syndrome. Which of the following best explains the findings?
  • AMolecular mimicry against neuronal gangliosides
  • BShiga-like toxin damage to vascular endothelium
  • CEnterocyte invasion via a type III secretion system
  • DDirect colonic epithelial invasion through M cells
Reveal answer & full explanation
Correct answer: B — Shiga-like toxin damage to vascular endothelium
  • AMolecular mimicry against neuronal gangliosides
  • BShiga-like toxin damage to vascular endothelium
  • CEnterocyte invasion via a type III secretion system
  • DDirect colonic epithelial invasion through M cells

Why Shiga-like toxin damage to vascular endothelium is correct

  • The vignette is classic enterohemorrhagic E. coli (EHEC/STEC, typically O157:H7): bloody diarrhea with a notably low-grade or absent fever after undercooked ground beef, plus a positive Shiga toxin assay.
  • EHEC adheres to colonic epithelium and releases Shiga-like toxin, which damages vascular endothelium to produce hemorrhagic colitis and, in children, hemolytic-uremic syndrome (microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury).
  • Antibiotics are withheld because they can increase toxin release and HUS risk; antimotility agents are also avoided.

Why the others are wrong

  • Enterocyte invasion via a type III secretion system is the mechanism of nontyphoidal Salmonella (invading enterocytes and Peyer patches, with bacteremia in immunocompromised or sickle cell hosts), not the toxin-mediated endothelial injury seen here.
  • Direct colonic epithelial invasion through M cells describes Shigella, which causes dysentery with high fever and tenesmus; this patient is afebrile and the Shiga toxin assay points to EHEC.
  • Molecular mimicry against neuronal gangliosides is the Campylobacter pathway linked to Guillain-Barre syndrome, an antecedent-infection complication, not the cause of HUS-prone hemorrhagic colitis.
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Risk factors

  • Ingestion of undercooked poultry, eggs, ground beef, unpasteurized dairy, or contaminated produce
  • Travel to areas with poor sanitation
  • Daycare attendance and crowded living (Shigella)
  • Reptile or amphibian exposure (Salmonella)
  • Immunocompromise, sickle cell disease (invasive Salmonella, osteomyelitis), age <5 or >65
  • PPI or H2-blocker use (reduced gastric acid barrier)

Pathophysiology

Salmonella invades enterocytes and Peyer patches via type III secretion, with potential bacteremia in immunocompromised hosts and sickle cell patients (osteomyelitis). Shigella invades colonic epithelium directly via M cells and produces Shiga toxin (S. dysenteriae type 1), causing dysentery. Campylobacter invades the distal small bowel and colon, sometimes triggering molecular mimicry against gangliosides (Guillain-Barré syndrome). EHEC adheres to colonic epithelium and releases Shiga-like toxin, damaging endothelium and producing hemorrhagic colitis and hemolytic-uremic syndrome (HUS).

Clinical presentation

Symptoms

  • Crampy abdominal pain, fever, and diarrhea developing 1-3 days after ingestion (longer incubation for Campylobacter)
  • Bloody or mucoid stools (dysentery pattern) more common with Shigella, EHEC, and Campylobacter
  • Nausea and vomiting more prominent with Salmonella
  • EHEC: severe abdominal cramps with bloody diarrhea and notably low-grade or absent fever

Signs / physical exam

  • Diffuse abdominal tenderness without peritoneal signs
  • Volume depletion: tachycardia, orthostasis, dry mucous membranes
  • Tenesmus and frequent low-volume stools with Shigella
  • HUS triad in children with EHEC: microangiopathic hemolytic anemia, thrombocytopenia, acute kidney injury (typically 5-10 days into illness)

Classic findings

Stool studies showing fecal leukocytes or elevated lactoferrin support invasive bacterial enteritis; absence does not exclude.

Differential diagnosis

  • Viral gastroenteritis (norovirus, rotavirus) — Watery diarrhea, vomiting, low-grade fever, brief duration (24-72 h), no blood in stool
  • C. difficile colitis — Recent antibiotic or healthcare exposure; watery diarrhea with leukocytosis; toxin/PCR positive
  • Parasitic diarrhea (Giardia, Entamoeba, Cryptosporidium) — Subacute course, travel or daycare exposure, stool O&P or antigen testing
  • Inflammatory bowel disease flare — Chronic course, extraintestinal manifestations, characteristic endoscopic findings
  • Ischemic colitis — Older adults with vascular disease, sudden abdominal pain followed by bloody diarrhea, watershed areas on imaging
  • Appendicitis with periappendiceal phlegmon — RLQ pain, fever, anorexia; CT distinguishes from terminal ileitis (which Yersinia and Campylobacter can mimic)

Diagnostic workup

Diagnostic criteria

Clinical syndrome of acute inflammatory diarrhea plus positive stool culture or PCR for the responsible pathogen.

Labs

  • Stool culture or multiplex GI PCR panel — preferred initial test; identifies Salmonella, Shigella, Campylobacter, STEC
  • Stool Shiga toxin assay (EIA or PCR) in any bloody diarrhea — essential to identify EHEC
  • CBC: leukocytosis with left shift in Shigella; falling platelets and rising creatinine raise concern for HUS
  • BMP for renal function and electrolytes
  • Blood cultures if febrile or immunocompromised (invasive Salmonella)

Imaging

  • Not routinely required
  • CT abdomen if severe pain, peritoneal signs, or toxic megacolon suspected

Treatment

First-line

  • Aggressive oral or IV rehydration with isotonic fluids and electrolyte replacement
  • Empiric antibiotics generally NOT indicated for routine community-acquired bacterial enteritis; reserve for severe disease, dysentery, immunocompromise, age extremes, or confirmed Shigella
  • Avoid antimotility agents (loperamide) in dysentery or suspected EHEC — increased risk of toxic megacolon and HUS

Shigella

  • Treat to shorten illness and reduce transmission
  • Fluoroquinolone — ciprofloxacin, levofloxacin (rising resistance; check susceptibilities)
  • Azithromycin alternative; ceftriaxone for severe or pediatric cases

Campylobacter

  • Macrolide — azithromycin preferred (rising fluoroquinolone resistance)
  • Treat severe illness, prolonged symptoms (>7 days), bacteremia, or immunocompromise

Nontyphoidal Salmonella

  • Supportive care for uncomplicated disease — antibiotics prolong carriage
  • Treat infants <3 months, age >50 with atherosclerosis, immunocompromise, sickle cell, prosthetic devices, or bacteremia
  • Fluoroquinolone, ceftriaxone, or azithromycin

EHEC / STEC (O157:H7)

  • Supportive care ONLY — antibiotics increase risk of HUS by promoting Shiga toxin release
  • Avoid antimotility agents
  • Monitor CBC and creatinine for HUS through day 10

Second-line / adjunct

  • Public health reporting required for Salmonella, Shigella, STEC, and Campylobacter
  • Probiotics may modestly shorten symptoms in select cases

Complications

  • Hemolytic-uremic syndrome (EHEC, occasionally Shigella dysenteriae type 1)
  • Guillain-Barré syndrome and reactive arthritis (Campylobacter)
  • Reactive arthritis and Reiter syndrome (Shigella, Salmonella, Campylobacter)
  • Bacteremia and metastatic infection — osteomyelitis in sickle cell disease (Salmonella), mycotic aneurysm in older adults
  • Toxic megacolon and intestinal perforation
  • Chronic carrier state (Salmonella typhi, gallbladder colonization)

PANCE pearls

  • Bloody diarrhea without fever = think EHEC. Do NOT give antibiotics or antimotility agents.
  • Bloody diarrhea WITH high fever and tenesmus = Shigella; treat empirically.
  • Campylobacter is the most common antecedent infection in Guillain-Barré syndrome.
  • Salmonella osteomyelitis is classic in sickle cell disease (though Staph aureus is still more common overall).
  • PPIs and H2 blockers raise risk by neutralizing the gastric acid barrier.

References

  • IDSA 2017 — IDSA Clinical Practice Guidelines for the Diagnosis and Management of Infectious Diarrhea (Shane et al., Clin Infect Dis 2017)
  • CDC — CDC Foodborne Diseases Active Surveillance Network (FoodNet) annual reports
  • AAP Red Book — American Academy of Pediatrics Red Book — Salmonella, Shigella, Campylobacter, E. coli chapters

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