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Select Gastrointestinal and Hepatobiliary Infections


Esophagitis

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 .

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

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

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

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    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)

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    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/Duodenitis

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.

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

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      Less common causes—Immunocompromised hosts—CMV

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

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    Chronic gastritis is common—usually asymptomatic

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    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

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    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)

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      H. pylori serology is not useful for identifying active infection

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      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

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

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

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

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

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      Treatment should be 14 days

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

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    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:

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    Is it diarrhea?

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    Is it acute, persistent, or chronic?

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    Who is the host?

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    What are the exposures?

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    What is the severity?

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    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?

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    Acute—acute gastroenteritis; lasts <14 days

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    Persistent diarrhea—lasts 14 to 30 days

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    Chronic diarrhea—lasts more than 30 days, rarely infectious

Step 3: Who is the host?

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    Healthy person

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    Returning traveler

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    Individual with food-borne illness

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    Individual with health care or institutional exposures

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    Pregnant woman

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    Elderly

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    Immunocompromised

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

Step 4: Determine the exposure risks.

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    Food and water ingestion

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    Water exposures/outdoor exposures

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    Daycare/institutional settings

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    Pools

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    Livestock/pets

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    Sexual practices

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    Health care exposures

Step 5: What is the severity?

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    Uncomplicated watery diarrhea

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    Invasive disease

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    Dysentery (bloody stools)

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    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
Hypogammaglobulinemia
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 		Norovirus
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.

Fig. 10.2, Approach to the adult with persistent diarrhea. PCR, Polymerase chain reaction.

Fig. 10.3, Testing algorithm for infectious diarrhea in immunocompromised hosts. GI, Gastrointestinal.

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.

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    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.

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    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.

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

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

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

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

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

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      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

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

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      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.

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      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.

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      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)

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      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).

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    Clinical risk scoring systems for appendicitis include the Alvarado score and Appendicitis Inflammatory Risk (AIR) ( Table 10.3 ).

    Table 10.3
    Clinical Risk Scoring Systems for Suspected Acute Appendicitis
    Alvarado Score
    Clinical Feature Score
    Anorexia 1
    Nausea or vomiting 1
    Pain migration to right lower quadrant (RLQ) 1
    RLQ pain 2
    Rebound tenderness 1
    Temperature > 37.5° C 1
    White blood cell (WBC) count with left shift 1
    WBC > 10,000 2
    Total 10

    Appendicitis Inflammatory Risk Score (AIR)
    Clinical Feature Score
    Vomiting 1
    RLQ pain 1
    Mild rebound tenderness 1
    Moderate rebound tenderness 2
    Severe rebound tenderness 3
    Temperature > 38.5° C 1
    Polymorphonuclear (PMN) 70%–84% 1
    PMN > 85% 2
    WBC 10,000–14,999 1
    WBC > 15,000 2
    C-reactive protein (CRP) 10–49 1
    CRP > 50 2
    Total maximum points 12

    Appendicitis Risk Alvarado AIR
    Low 1–4 1–4
    Moderate 5–6 5–8
    High 7–10 9–12

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    Classical signs—Tenderness at McBurney point, psoas sign (retrocecal), obturator sign

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    Helical multislice spiral computed tomography (CT) scan is preferred diagnostic test

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      Enlarged >6 cm, thickened wall of the appendix, fecalith, periappendiceal stranding

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    Microbiology—Enteric Gram-negatives— E. coli, Klebsiella, Enterobacter, Proteus spp.

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      Late prolonged symptoms and rupture—anaerobes, Pseudomonas aeruginosa

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    Mimics— Yersinia enterocolitica, Campylobacter jejuni , Salmonella , Crohn disease, gynecologic disease/pregnancy

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    Treatment—Two approaches:

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      Antibiotics first and observe

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        Ampicillin–sulbactam 3 g IV q6h, piperacillin–tazobactam 3.375 g IV q6h, ceftriaxone 1g q24h plus metronidazole 500 mg q6–8h for 7 to 10 days if no surgery

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        Twenty-five to thirty percent of patients treated with antibiotics first will eventually need appendectomy

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        Risk for complications (peritonitis, abscess, wound infection) no different with delayed surgery

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        Predictors of antibiotic failure or recurrence: appendicolith seen on imaging

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        Predictors of success with antibiotics-first approach: C-reactive protein (CRP) <60, WBC <12,000, age <60

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      Surgical treatment—laparoscopic or open appendectomy

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        Recent advances in endoscopic retrograde appendicitis therapy with irrigation, appendicolith removal, and stent placement

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    Postappendectomy antibiotics

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      Simple appendicitis—not needed postoperatively

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      Complicated, perforated appendicitis—3 days if clinically improving

Diverticulitis

Diverticulitis is a common gastrointestinal (GI) inflammatory disorder that occurs in 1% to 5% of those with diverticulosis; 20% of those have recurrent disease within 10 years. Recent theories suggest that prolonged fecal stasis may alter the colonic microbiome leading to an increased ratio of Firmicutes/Bacteroidetes and increased Proteobacteria resulting in a chronic inflammatory state.

These patients often present with acute or subacute left-lower-quadrant abdominal pain, malaise, fever, elevated WBC, and CRP. A CT scan abdomen with IV and oral contrast is the preferred diagnostic test for diverticulitis.

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    Microbiology—colonic flora, principally enteric Gram-negatives, anaerobes, and aerobic and anaerobic streptococci.

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    May be uncomplicated or complicated—12% of cases; modified Hinchey criteria may help ( Table 10.4 )

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      Complications—abscess, peritonitis, obstruction, or fistulae; sepsis

    Table 10.4
    Modified Hinchey Classifications for Diverticulitis
    Modified Hinchey Stage Definition Clinical Classification
    0 Clinically mild diverticulitis
    Diverticula with wall thickening on CT     		Uncomplicated
    Ia Colonic wall thickening with Inflammation in pericolonic fat (phlegmon) Uncomplicated
    IIb Pericolonic or mesenteric abscess proximal to the inflamed tic (diverticular abscess) Complicated
    II Distant intraabdominal abscess Complicated
    III Purulent peritonitis Complicated
    IV Feculent peritonitis Complicated
    CT, Computed tomography.

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    Treatment:

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      Uncomplicated inflammatory disease—may not require antibiotics; supportive management with pain medicines, IV fluids, nothing by mouth (NPO)

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        Probiotics, rifaximin, mesalamine, and nut avoidance of no value to prevent recurrence

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        High-fiber diet and avoidance of nonsteroidal antiinflammatory drugs (NSAIDs) may be helpful in prevention

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      Complicating factors: severe disease, sepsis, immunosuppression, multiple comorbidities—may benefit from antibiotics

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        Four to seven days of antibiotics if source controlled—mild disease

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        Amoxicillin/clavulanate 875/125 mg q12h or if penicillin allergy

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        Ciprofloxacin 750 mg q12h plus metronidazole 500 mg q8h

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        Trimethoprim–sulfamethoxazole (TMP-SMX) 160/800 mg q12h plus metronidazole 500 mg q8h

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    Inpatient admission—failure of outpatient treatment for 48 to 72 hours; complicated disease, inability to take oral medicines, complicated morbidities

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    Inpatient—mild to moderate disease

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      Ertapenem 1g daily

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      Moxifloxacin 400 mg IV daily

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      Ceftriaxone 1g q 2h IV plus metronidazole 500 mg IV q8h

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      Levofloxacin 750 mg IV plus metronidazole 500 mg IV q8h

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    Complicated diverticulitis: IV antibiotics, IV fluids, and NPO

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      Meropenem 1 g IV q8h

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      Piperacillin–tazobactam 3.375 g q6h IV

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      Cefepime 2 g IV q8h plus metronidazole 500 mg IV q8h

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      Levofloxacin 750 mg IV q24h plus metronidazole 500 mg IV q8h

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    Diverticular abscesses

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      Abscess < 3 cm—antibiotics and bowel rest

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      Abscess > 3 cm—antibiotics and drainage by CT

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      Indications for surgery: Failure of medical management, persistent sepsis, peritonitis

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      In perforated diverticulitis, surgical resection is preferred over laparoscopic lavage

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        Colonoscopy recommended 6 to 8 weeks after recovery

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