Select Gastrointestinal and Hepatobiliary Infections


Esophagitis is an inflammatory mucosal injury disorder that may be caused by infectious agents and local irritants. The inflammation may present with substernal pain, odynophagia, and occasionally dysphagia. The risk factors for esophageal inflammatory disorders may be iatrogenic (i.e., pill esophagitis, chemical injuries) or disease related. Infectious esophagitis often presents with odynophagia in the setting of immunosuppression, recent antibiotics, corticosteroids, or neutropenia. Most infectious esophagitis is viral or due to Candida .

  • Microbiology: Most commonly viral—herpes simplex virus (HSV) but can be due to cytomegalovirus (CMV) or fungal (Candida)

    • HSV—seen in immune compromised host (ICH); endoscopically ulcers, vesicles

    • Candida spp.—usually with oral thrush; one-third without—endoscopically, white plaques, hyphae on biopsy

  • Diagnostics: Endoscopic examination, histology (HSV—multinucleated giant cells; CMV—“owl’s eye,” Candida —hyphae), bacterial or fungal cultures or polymerase chain reaction (PCR) (HSV, CMV)

  • Treatment: Candida —fluconazole 200 mg/day for 14 days; HSV—acyclovir 5 mg/kg intravenous (IV) q8h for 14 to 21 days; CMV—ganciclovir 5 mg/kg IV q12h for 14 to 21 days


Gastritis and duodenitis are mucosal inflammatory disorders of the stomach and duodenum, most often due to Helicobacter pylori . Patients commonly present with epigastric pain, nausea, and vomiting without fever.

  • Microbiology: H. pylori —a urease-producing, curved, Gram-negative rod

    • Less common causes—Immunocompromised hosts—CMV

    • Granulomatous gastritis—syphilis, tuberculosis (TB), nontuberculous mycobacteria (NTM), Whipple disease, cryptococcus, anisakiasis, schistosomiasis

  • Chronic gastritis is common—usually asymptomatic

  • Symptomatic peptic ulcer disease (95% of duodenal ulcer and 70% gastric ulcer cases are associated with H. pylori ), gastric cancer, or mucosa-associated lymphoid tissue (MALT) lymphoma; idiopathic thrombocytopenic purpura (ITP) rarely

  • Diagnosis: Upper endoscopy when warning symptoms—biopsies, histopathology; urease (Campylobacter-like organism [CLO]) test on gastric tissue samples for H. pylori ; urea breath test for H. pylori ; fecal antigen test for H. pylori (both for diagnosis and eradication tests)

    • H. pylori serology is not useful for identifying active infection

    • Testing should be done off proton pump inhibitors (PPIs) or H 2 receptor blockers (H 2 Bs) for 2 weeks; off antibiotics for 4 weeks

  • Treatment: Assess risk for resistance to macrolides: prior exposure, high local resistance >15%

    • If no macrolide risk—triple therapy with macrolide: clarithromycin/amoxicillin/PPI

    • If penicillin allergy—clarithromycin-based triple therapy with metronidazole consists of clarithromycin, metronidazole, and a PPI

    • If resistance: bismuth quadruple therapy—bismuth, metronidazole, tetracycline, and a PPI

    • Treatment should be 14 days

  • For recurrent or refractory disease—obtain cultures and sensitivity; refer for infectious diseases (ID) consultation.

  • Test for cure at 6 to 8 weeks with stool antigen or urease breath test.

Infectious Diarrhea

Due to the numerous causes of both infectious and noninfectious diarrhea, development of a stepwise approach is critical to management. A simple six-step approach asks the following questions:

  • 1.

    Is it diarrhea?

  • 2.

    Is it acute, persistent, or chronic?

  • 3.

    Who is the host?

  • 4.

    What are the exposures?

  • 5.

    What is the severity?

  • 6.

    Is it inflammatory, noninflammatory, or invasive?

The first step is defining diarrhea—at least three loose stools a day. Use the Bristol Stool Scale (types 6 and 7).

Not all loose stool is diarrhea—fecal incontinence often mimics diarrhea.

Step 2: What is the duration?

  • Acute—acute gastroenteritis; lasts <14 days

  • Persistent diarrhea—lasts 14 to 30 days

  • Chronic diarrhea—lasts more than 30 days, rarely infectious

Step 3: Who is the host?

  • Healthy person

  • Returning traveler

  • Individual with food-borne illness

  • Individual with health care or institutional exposures

  • Pregnant woman

  • Elderly

  • Immunocompromised

    • HIV, transplant, hematologic malignancy, medications, asplenia, immune globulin deficient

Step 4: Determine the exposure risks.

  • Food and water ingestion

  • Water exposures/outdoor exposures

  • Daycare/institutional settings

  • Pools

  • Livestock/pets

  • Sexual practices

  • Health care exposures

Step 5: What is the severity?

  • Uncomplicated watery diarrhea

  • Invasive disease

  • Dysentery (bloody stools)

  • Severe volume-depleting diarrhea

Step 6: Is the diarrhea inflammatory, invasive, or noninflammatory?

Inflammatory diarrhea may be associated with small-volume, mucoid or bloody stools, tenesmus, cramps, and fever—usually involves the colon.

Invasive diarrhea may be associated with fever and periumbilical or right-lower-quadrant abdominal pain. Usually due to Salmonella, Campylobacter, Yersinia, or enteroinvasive Escherichia coli or Entamoeba histolytica .

Noninflammatory diarrhea may be associated with watery, large volume without fever. May be toxin mediated or directly related to the microorganism. These are often viral, parasitic, or toxigenic bacteria.

Tables 10.1 and 10.2 provide epidemiologic links and clinical clues to the etiologic diagnosis of infectious diarrhea. The algorithms illustrated in Figs. 10.1 to 10.3 illustrate approaches to diagnosis and management.

Table 10.1

Epidemiologic Considerations in Infectious Diarrhea: Who Is the Host?

Host Factors Potential Infectious Agents/Associations
Immune status
Cell-mediated immune deficiencies
Salmonella, Yersinia, Giardia (IgA deficiency)
Salmonella, Mycobacterium avium complex, Listeria , CMV, Adenovirus, Cryptosporidia, Cystoisospora, Cyclospora
Antimicrobial treatments C. difficile infection
International travel E. coli (mostly ETEC), Campylobacter, Salmonella, Shigella, Vibrio cholera, E. histolytica (prolonged diarrhea— Giardia , Blastocystis, Cyclospora, Cystoisospora, Cryptosporidia )
Food and water exposures Norovirus (work parties, cruise ships), Salmonella , C. perfringens, B. cereus, S. aureus (picnics, food poisoning), Campylobacter , ETEC, STEC (undercooked burgers, cider, veggies), Listeria (soft cheeses, cantaloupes), Shigella , Cyclospora (raspberries), Cryptosporidia (pools)
Yersinia (pork), Campylobacter (poultry), Trichinella (pork, bear, jerky),
C. perfringens (beef, poultry),
B. cereus (old pasta)
Brucella (goat cheese, milk)
Institutionalization—child care, long-term care Norovirus, rotavirus, C. difficile, Shigella
Health care exposure—hospitals, nursing facilities C. difficile , Norovirus
Sexual practices HSV, Chlamydia, N. gonorrhea, Salmonella, Shigella, Campylobacter, E. histolytica, Cryptosporidia
Adults vs. children Rotavirus, E. coli —children

CMV, Cytomegalovirus; ETEC, enterotoxigenic E. coli; HSV, herpes simplex virus; IgA, immunoglobulin A; STEC, Shiga toxin E. coli .

Table 10.2

Clinical Considerations in Infectious Diarrhea

Clinical Clues Infectious Agents
Acute-onset nausea and vomiting <24 hr Toxin-mediated— S. aureus, B. cereus
Acute-onset nausea and vomiting lasts >24 hr
Watery diarrhea for several days
Grossly bloody stool, severe abdominal pain (dysentery) Shigella , STEC, Salmonella, Campylobacter, Yersinia enterocolitica
Abdominal pain C. difficile, Salmonella, Shigella , STEC, Campylobacter jejuni, Y. enterocolitica
Persistent abdominal pain, fever
Mimics of appendicitis
Y. enterocolitica , pseudotuberculosis Salmonella typhi or paratyphi , Campylobacter
Persistent diarrhea >14 days Giardia lamblia, Cryptosporidia, Cyclospora, Cystoisospora, E. histolytica

STEC, Shiga toxin E. coli .

Fig. 10.1

Approach to empirical therapy and management of the adult with acute diarrhea.

From Riddle MS, DuPont HL, Connor BA. ACG Clinical Guideline: Diagnosis, treatment and prevention of acute diarrheal infections in adults. Am J Gastroenterol . 2016;111:602–622.

Fig. 10.2

Approach to the adult with persistent diarrhea. PCR, Polymerase chain reaction.

From DuPont HL. Persistent diarrhea: A clinical review. JAMA. 2016;315:2712–2723.

Fig. 10.3

Testing algorithm for infectious diarrhea in immunocompromised hosts. GI, Gastrointestinal.

From Liesman RM, Binnicker MJ. The role of multiplex molecular panels for the diagnosis of gastrointestinal infections in immunocompromised patients. Curr Opin Infect Dis . 2016;29[4]:359–365, Figure 1 .

Clostridoides difficile Infection

C. difficile has become an increasingly common cause of both community-onset and health care–associated diarrhea. Its spectrum of illness can range from mild self-limiting diarrhea to severe colitis, sepsis, and death. Community-onset C. difficile infection (CDI) tends to occur in younger persons with less antibiotic exposure versus health care–associated infections. Antibiotics are the major risk factor for CDI, especially second- and third-generation cephalosporins and fluoroquinolones. Clindamycin and antianaerobic penicillins have the greatest risk.

  • Diagnosis is made by testing of diarrheal (Bristol 5 to 7) stools when there are >3 loose stools/24 hours in the appropriate epidemiologic circumstances.

  • Current guidelines recommend a two-step C. difficile glutamate dehydrogenase antigen plus C. difficile toxin A and B enzyme immunoassay test or a molecular test using polymerase chain reaction (PCR) to the toxin B gene.

    • Repeat testing is not recommended if the initial test is negative.

    • Three to five percent of healthy adults are colonized with C . difficile.

    • Twenty to fifty percent of hospitalized or long-term care patients may be colonized.

    • Testing for cure is not indicated, as the test may remain positive despite clinical resolution.

  • Treatment of CDI is currently stratified by severity and the initial versus recurrent episodes.

    • First episode, nonsevere—treat with oral vancomycin 125 mg four times a day (QID) for 10 to 14 days or fidaxomicin 200 mg twice a day (BID) for 10 days

      • Recurrence occurs in 20% to 30% after the first episode

    • Fulminant CDI initial—vancomycin 500 mg QID oral or via nasogastric (NG) tube. If ileus, rectal vancomycin 500 mg QID as retention enema, plus IV metronidazole 500 mg three times a day (TID) for 10 days.

    • Second episode—treat with fidaxomicin 200 mg BID for 10 days if prior vancomycin or if prior fidaxomicin use, vancomycin 125 mg QID for 10 to 14 days followed by BID for 7 days, daily for 7 days, then every 2 to 3 days for 2 to 8 weeks.

    • Third or more episode—vancomycin pulse and taper or vancomycin 125 mg QID for 10 days followed by rifaximin 400 mg TID for 20 days or fecal microbiota transplant (investigational)

    • Bezlotuxumab (monoclonal antibody against the C. difficile toxin B) may be administered in a first episode or beyond in high-risk patients for recurrence.

Acute Appendicitis

Acute appendicitis is thought to result from luminal obstruction of the appendix by a fecalith, leading to distension, bacterial overgrowth, and increased intraluminal pressure followed by gangrene. Patients with acute appendicitis may present with bloating, periumbilical pain followed by anorexia, nausea/vomiting and right-lower-quadrant abdominal pain, fever, and an elevated white blood cell (WBC) count (seen in less than one-third of patients).

May 30, 2021 | Posted by in PUBLIC HEALTH AND EPIDEMIOLOGY | Comments Off on Select Gastrointestinal and Hepatobiliary Infections

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