INFECTIOUS SYNDROMES

Infectious Diarrhea

Etiology and risk factors

• Risks include contaminated food/water, travel, outbreak or sick contacts, animal exposure, antibiotics or healthcare exposure, sexual exposure, immune compromise, and age extremes (Fiske & Bloch, 2019; Norris, 2020).
• Bacteria, viruses, and parasites cause disease through preformed toxin, enterotoxin, adherence, mucosal invasion, or cytotoxin. Incubation and exposure narrow the organism list (Fiske & Bloch, 2019; Norris, 2020).

Pathophysiology

• Preformed toxins stimulate vomiting/diarrhea without invasion. Enterotoxins activate chloride/water secretion in small intestine, producing watery stool with limited inflammation (Fiske & Bloch, 2019; Norris, 2020).
• Invasive or cytotoxic pathogens injure ileal/colonic epithelium, producing neutrophilic inflammation, fever, pain, and blood. Fluid and electrolyte loss can cause hypovolemia, kidney injury, and shock (Fiske & Bloch, 2019; Norris, 2020).
• Toxin or immune-mediated sequelae include hemolytic uremic syndrome, reactive arthritis, and Guillain-Barre syndrome (Fiske & Bloch, 2019; Norris, 2020).

Clinical manifestations

• Watery or bloody stool, abdominal cramps, nausea/vomiting, fever, urgency/tenesmus, dehydration, or systemic toxicity. Small-bowel disease often produces large-volume watery stool; colitis produces frequent small-volume inflammatory stool (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Danger findings include orthostasis, oliguria, altered mentation, severe abdominal tenderness/distention, high fever, blood, sepsis, or neurologic weakness (Carbo & Smetana, 2012; Seller & Symons, 2018).

Findings that argue against or redirect

• A chronic course redirects toward inflammatory bowel disease, malabsorption, medication, endocrine, or functional disease, although persistent parasites and C. difficile remain possible (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Absence of fever or blood does not exclude infection. Stool leukocytes/lactoferrin/calprotectin cannot identify a specific pathogen (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Do not assume a positive multiplex result is causal without considering colonization, prolonged shedding, and clinical context (Carbo & Smetana, 2012; Seller & Symons, 2018).

Diagnostic evaluation

• Most mild, short, uncomplicated illness needs no testing. Test stool when fever, blood/mucus, severe pain, sepsis, immunocompromise, outbreak/public-health concern, persistent course, or important exposure is present (Carbo & Smetana, 2012; Fiske & Bloch, 2019).
• Use culture or multiplex molecular testing for bacterial pathogens; include Shiga toxin testing when STEC is possible. Test for C. difficile after relevant antibiotic/healthcare exposure and clinically significant diarrhea. Use ova/parasite or targeted antigen/PCR for persistent/travel/immunocompromised patterns (Carbo & Smetana, 2012; Fiske & Bloch, 2019).
• Assess electrolytes, renal function, CBC, lactate, and blood cultures when dehydration, HUS, or sepsis is possible (Carbo & Smetana, 2012; Fiske & Bloch, 2019).

Expected diagnostic and laboratory findings

• Secretory/noninflammatory: watery stool, limited fecal inflammatory evidence, often no gross blood. Inflammatory: blood, fecal leukocyte markers, fever, and colonic symptoms (Carbo & Smetana, 2012; Fiske & Bloch, 2019).
• Definitive etiology requires compatible organism/toxin detection. STEC concern rises with bloody diarrhea and abdominal pain, sometimes with little fever; falling hemoglobin/platelets and rising creatinine indicate HUS (Carbo & Smetana, 2012; Fiske & Bloch, 2019).
• C. difficile diagnosis requires compatible diarrhea plus toxin or toxigenic-organism testing interpreted through the local algorithm (Carbo & Smetana, 2012; Fiske & Bloch, 2019).

Differential diagnosis

• Inflammatory bowel disease: chronic/recurrent symptoms, weight loss, extraintestinal findings, endoscopic/histologic inflammation without an explanatory pathogen (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Ischemic colitis: abrupt pain and hematochezia in a vascular-risk patient; CT/endoscopy pattern (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Medication/osmotic diarrhea: temporal exposure and improvement with withdrawal/fasting pattern (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Irritable bowel syndrome: chronic pain related to defecation without fever, bleeding, dehydration, nocturnal symptoms, or inflammatory abnormalities (Carbo & Smetana, 2012; Seller & Symons, 2018).

Treatment and management

• Oral rehydration is preferred when feasible; use intravenous isotonic fluid and electrolyte/glucose correction for severe dehydration, shock, or inability to drink (Fiske & Bloch, 2019; Norris, 2020).
• Use antimicrobial therapy selectively according to pathogen, severity, host, and public-health guidance. Avoid antibiotics and antimotility agents when Shiga toxin-producing E. coli is suspected because of HUS risk (Fiske & Bloch, 2019; Norris, 2020).
• Use contact precautions and soap-and-water hand hygiene for suspected C. difficile; manage outbreaks and reportable disease with infection prevention/public health (Fiske & Bloch, 2019; Norris, 2020).

Additional complications and red flags

• New weakness or areflexia after diarrhea may indicate Guillain-Barre syndrome (Carbo & Smetana, 2012; Fiske & Bloch, 2019).

Clinical Reasoning Priorities

• Recognize first: Determine whether the patient has dehydration, hemodynamic instability, severe abdominal pain, bloody stool, high fever, altered mental status, or substantial vulnerability from age, pregnancy, or immunocompromise before pursuing an extended etiologic workup (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Reassess probability: Recent antibiotics or healthcare exposure, travel, untreated water, contaminated food, sick contacts, outbreaks, sexual exposure, and immune status meaningfully shift the differential. Brief, nonbloody, self-limited illness without fever is less suggestive of invasive bacterial disease (Carbo & Smetana, 2012; Fiske & Bloch, 2019).
• Do not miss: Severe dehydration, sepsis, toxic megacolon, hemolytic uremic syndrome, ischemic colitis, inflammatory bowel disease, and a surgical abdomen can present with diarrhea or develop as complications (Fiske & Bloch, 2019; Norris, 2020).
• Use decisive testing: Reserve stool molecular, culture, toxin, or ova-and-parasite testing for patients whose severity, duration, host factors, exposure history, outbreak implications, or treatment decisions make an etiologic result actionable. Assess electrolytes and kidney function when volume depletion or systemic illness is possible (Carbo & Smetana, 2012; Seller & Symons, 2018).
• Act on time-sensitive decisions: Begin oral or intravenous rehydration according to severity and correct electrolyte abnormalities. Use antimicrobials selectively rather than routinely, and avoid antimotility treatment when inflammatory diarrhea, toxic megacolon, or another invasive process is suspected (Fiske & Bloch, 2019; Norris, 2020).

Compare infectious diarrhea with the broader Diarrheal Disease differential, and review when symptomatic medications may be inappropriate in Antidiarrheals.

References

Carbo, A. R., & Smetana, G. W. (2012). Diarrhea. In M. C. Henderson, L. M. Tierney, Jr., & G. W. Smetana (Eds.), The patient history: An evidence-based approach to differential diagnosis (2nd ed., pp. 389–399). McGraw-Hill Medical.

Fiske, C. T., & Bloch, K. C. (2019). Infectious diseases. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed.). McGraw-Hill Education.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Seller, R. H., & Symons, A. B. (2018). Differential diagnosis of common complaints (7th ed.). Elsevier.