Chapter 133: Acute Infectious Diarrheal Diseases And Bacterial Food Poisoning PDF

University of the Philippines ­ Manila Acc...

University of the Philippines ­ Manila Access Provided by: Harrison's Principles of Internal Medicine, 21e Chapter 133: Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning Richelle C. Charles; Regina C. LaRocque INTRODUCTION Diarrheal disease mortality has decreased substantially in the past three decades. Nevertheless, acute diarrheal disease is still a leading cause of illness globally and is associated with an estimated 1.7 million deaths per year. Among children 2 weeks is generally defined as chronic; in such cases, many of the causes of acute diarrhea are much less likely, and a new spectrum of causes needs to be considered. 2. Fever often implies invasive disease, although fever and diarrhea may also result from infection outside the gastrointestinal tract, as in malaria. 3. Stools that contain blood or mucus indicate ulceration of the large bowel. Bloody stools without fecal leukocytes should alert the laboratory to the possibility of infection with Shiga toxin–producing enterohemorrhagic Escherichia coli. Bulky white stools suggest a small­intestinal process that is causing malabsorption. Profuse “rice­water” stools suggest cholera or a similar toxigenic process. 4. Frequent stools over a given period can provide the first warning of impending dehydration. 5. Abdominal pain may be most severe in inflammatory processes like those due to Shigella, Campylobacter, and necrotizing toxins. Painful abdominal muscle cramps, caused by electrolyte loss, can develop in severe cases of cholera. Bloating is common in giardiasis. An appendicitis­like syndrome should prompt a culture for Yersinia enterocolitica with cold enrichment. 6. Tenesmus (painful rectal spasms with a strong urge to defecate but little passage of stool) may be a feature of cases with proctitis, as in shigellosis or amebiasis. 7. Vomiting implies an acute infection (e.g., a toxin­mediated illness or food poisoning) but can also be prominent in a variety of systemic illnesses (e.g., malaria) and in intestinal obstruction. 8. Asking patients whether anyone else they know is sick is a more efficient means of identifying a common source than is constructing a list of recently eaten foods. If a common source seems likely, specific foods can be investigated. See text for a discussion of bacterial food poisoning. 9. Current antibiotic therapy or a recent history of treatment suggests Clostridium difficile diarrhea (Chap. 134). Stop antibiotic treatment if possible and consider tests for C. difficile toxins. Antibiotic use may increase the risk of chronic intestinal carriage following salmonellosis. 10. See text (and Chap. 124) for a discussion of traveler’s diarrhea. (From RL Guerrant, DA Bobak: Bacterial and protozoal gastroenteritis. N Engl J Med 325:327, 1991. Copyright © 1991 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.) Downloaded 2024­8­4 6:42 A Your IP is 49.147.196.41 Chapter 133: Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning, Richelle C. Charles; Regina C. LaRocque Page 4 / 13 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility difficile diarrhea (Chap. 134). Stop antibiotic treatment if possible and consider tests for C. difficile toxins. Antibiotic use may increase the risk of University of the Philippines ­ Manila chronic intestinal carriage following salmonellosis. 10. See text (and Chap. 124) for a discussion of traveler’s diarrhea. (From RL Guerrant, DA Bobak: Access Provided by: Bacterial and protozoal gastroenteritis. N Engl J Med 325:327, 1991. Copyright © 1991 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.) History The answers to questions with high discriminating value can quickly narrow the range of potential causes of diarrhea and help determine whether treatment is needed. Important elements of the narrative history are detailed in Fig. 133­1. Physical Examination The examination of patients for signs of dehydration provides essential information about the severity of the diarrheal illness and the need for rapid therapy. Mild dehydration is indicated by thirst, dry mouth, decreased axillary sweat, decreased urine output, and slight weight loss. Signs of moderate dehydration include an orthostatic fall in blood pressure, skin tenting, and sunken eyes (or, in infants, a sunken fontanelle). Signs of severe dehydration include lethargy, obtundation, feeble pulse, hypotension, and frank shock. Diagnostic Approach After the severity of illness is assessed, the clinician must distinguish between inflammatory and noninflammatory disease. Using the history and Downloaded epidemiologic2024­8­4 features of6:42 theAcase Your as IP is 49.147.196.41 guides, the clinician can then rapidly evaluate the need for further efforts to define a specific etiology and for Chapter 133: Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning, Richelle C. Charles; Regina C. LaRocque Page 5 / 13 therapeutic intervention. Examination of a stool sample may supplement the narrative history. Grossly bloody or mucoid stool suggests an ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility inflammatory process. A test for fecal leukocytes (preparation of a thin smear of stool on a glass slide, addition of a drop of methylene blue, and examination of the wet mount) can suggest inflammatory disease in patients with diarrhea, although the predictive value of this test is still debated. A dehydration include an orthostatic fall in blood pressure, skin tenting, and sunken eyes (or, in infants, a sunken fontanelle). Signs of severe University of the Philippines ­ Manila dehydration include lethargy, obtundation, feeble pulse, hypotension, and frank shock. Access Provided by: Diagnostic Approach After the severity of illness is assessed, the clinician must distinguish between inflammatory and noninflammatory disease. Using the history and epidemiologic features of the case as guides, the clinician can then rapidly evaluate the need for further efforts to define a specific etiology and for therapeutic intervention. Examination of a stool sample may supplement the narrative history. Grossly bloody or mucoid stool suggests an inflammatory process. A test for fecal leukocytes (preparation of a thin smear of stool on a glass slide, addition of a drop of methylene blue, and examination of the wet mount) can suggest inflammatory disease in patients with diarrhea, although the predictive value of this test is still debated. A test for fecal lactoferrin, which is a marker of fecal leukocytes, is more sensitive and is available in latex agglutination and enzyme­linked immunosorbent assay formats. Causes of acute infectious diarrhea, categorized as inflammatory and noninflammatory, are listed in Table 133­1. TABLE 133­2 Postdiarrhea Complications of Acute Infectious Diarrheal Illness COMPLICATION COMMENTS Chronic diarrhea (diarrhea lasting >4 weeks) Occurs in ~1% of travelers with acute diarrhea Lactase deficiency Protozoa account for approximately one­third of cases Small­bowel bacterial overgrowth Malabsorption syndromes (tropical and celiac sprue) Initial presentation or exacerbation of inflammatory bowel May be precipitated by traveler’s diarrhea disease Irritable bowel syndrome Occurs in ~10% of travelers with traveler’s diarrhea Reactive arthritis Particularly likely after infection with invasive organisms (Shigella, Salmonella, Campylobacter, Yersinia) Hemolytic­uremic syndrome (hemolytic anemia, Follows infection with Shiga toxin–producing bacteria (Shigella dysenteriae type 1 and thrombocytopenia, and renal failure) enterohemorrhagic Escherichia coli) Guillain­Barré syndrome Particularly likely after Campylobacter infection Postdiarrhea Complications Chronic complications may follow the resolution of an acute diarrheal episode. The clinician should inquire about prior diarrheal illness if the conditions listed in Table 133­2 are observed. EPIDEMIOLOGY TRAVEL HISTORY Of the several million people who travel from temperate industrialized countries to tropical regions of Asia, Africa, and Central and South America each year, 20–50% experience a sudden onset of abdominal cramps, anorexia, and watery diarrhea; thus, traveler’s diarrhea is the most common travel­ related infectious illness (Chap. 124). The time of onset is usually 3 days to 2 weeks after the traveler’s arrival in a resource­poor area; most cases begin within the first 3–5 days. The illness is generally self­limited, lasting 1–5 days. The high rate of diarrhea among travelers to underdeveloped areas is related to the ingestion of contaminated food or water. The organisms that cause traveler’s diarrhea vary considerably with location (Table 133­3), as does the pattern of antimicrobial resistance. In all areas, enterotoxigenic and enteroaggregative strains of E. coli are the most common isolates from persons with the classic secretory traveler’s diarrhea syndrome. Infection with Campylobacter jejuni is especially common in areas of Asia. Downloaded 2024­8­4 6:42 A Your IP is 49.147.196.41 Chapter 133: Acute Infectious Diarrheal Diseases and Bacterial Food Poisoning, Richelle C. Charles; Regina C. LaRocque TABLE 133­3 Page 6 / 13 ©2024 McGraw Hill. All Rights Causes of Traveler’s Diarrhea Reserved. Terms of Use Privacy Policy Notice Accessibility begin within the first 3–5 days. The illness is generally self­limited, lasting 1–5 days. The high rate of diarrhea among travelers to underdeveloped areas University of the Philippines ­ Manila is related to the ingestion of contaminated food or water. Access Provided by: The organisms that cause traveler’s diarrhea vary considerably with location (Table 133­3), as does the pattern of antimicrobial resistance. In all areas, enterotoxigenic and enteroaggregative strains of E. coli are the most common isolates from persons with the classic secretory traveler’s diarrhea syndrome. Infection with Campylobacter jejuni is especially common in areas of Asia. TABLE 133­3 Causes of Traveler’s Diarrhea ETIOLOGIC AGENT APPROXIMATE PERCENTAGE OF CASES COMMENTS Bacteria 50–75 Enterotoxigenic Escherichia coli 10–45 Single most important agent Enteroaggregative E. coli 5–35 Emerging enteric pathogen with worldwide distribution Campylobacter jejuni 5–25 More common in Asia Shigella 0–15 Major cause of dysentery Salmonella 0–15 — Others 0–5 Including Aeromonas, Plesiomonas, and Vibrio cholerae Viruses 0–20 Norovirus 0–10 Associated with cruise ships Rotavirus 0–5 Particularly common among children Parasites 0–10 Giardia lamblia 0–5 Affects hikers and campers who drink from freshwater streams Cryptosporidium 0–5 Resistant to chlorine treatment of water sources Entamoeba histolytica 24 h. Not all food poisoning has a bacterial cause. Nonbacterial agents of short­incubation food poisoning include capsaicin, which is found in hot peppers, and a variety of toxins found in fish and shellfish (Chap. 460). LABORATORY EVALUATION Many cases of noninflammatory diarrhea are self­limited or can be treated empirically, and in these instances, the clinician may not need to determine a specific etiology. Potentially pathogenic E. coli cannot be distinguished from normal fecal flora by routine culture, and tests to detect enterotoxins are not available in most clinical laboratories. In situations in which cholera is a concern, stool should be cultured on selective media such as thiosulfate–citrate–bile salts–sucrose (TCBS) or tellurite–taurocholate–gelatin (TTG) agar; rapid diagnostic tests are also available. A latex agglutination test has made the rapid detection of rotavirus in stool practical for many laboratories, while reverse­transcriptase polymerase chain reaction (PCR) and specific antigen enzyme immunoassays have been developed for the identification of norovirus. Stool specimens should be examined by immunofluorescence­based rapid assays, or PCR or (less sensitive) standard microscopy for Giardia cysts or Cryptosporidium if the level of clinical suspicion regarding the involvement of these organisms is high. All patients with fever and evidence of inflammatory disease acquired outside the hospital should have stool evaluated for Salmonella, Shigella, and Campylobacter. Salmonella and Shigella can be selected on MacConkey agar as non­lactose­fermenting (colorless) colonies or can be grown on Salmonella–Shigella agar or in selenite enrichment broth, both of which inhibit most organisms except these pathogens. Evaluation of nosocomial diarrhea should initially focus on C. difficile; stool culture for other pathogens in this setting has an extremely low yield and is not cost­effective. Toxins A and B produced by pathogenic strains of C. difficile can be detected by rapid enzyme immunoassays, latex agglutination tests, or PCR (Chap. 134). Isolation of C. jejuni requires inoculation of fresh stool onto selective growth medium and incubation at 42°C in a microaerophilic atmosphere. In many laboratories in the United States, E. coli O157:H7 is among the most common pathogens isolated from visibly bloody stools. Strains of this enterohemorrhagic serotype can be identified in specialized laboratories by serotyping but also can be identified presumptively in hospital laboratories as lactose­fermenting, indole­positive colonies of sorbitol nonfermenters (white colonies) on sorbitol MacConkey plates. If the clinical presentation suggests the possibility of intestinal amebiasis, stool should be examined by a rapid antigen detection assay or by (less sensitive and less specific) microscopy. Multiplex nucleic acid amplification methods for detection of many stool pathogens (viral, bacterial, and parasitic) are increasingly being used in clinical microbiology laboratories to decrease the time to detection of a pathogen. Although these tests may be more sensitive and rapid than standard culture methods, the lack of a microbial isolate prevents determination of antimicrobial susceptibility and typing of strains by public health authorities in order to detect and respond to common­source outbreaks. For this reason, the Centers for Disease Control and Prevention suggests that diagnosis of an enteric bacterial infection by a nucleic acid amplification method should be followed by attempted isolation of the pathogen by culture. TREATMENT OF INFECTIOUS DIARRHEA OR BACTERIAL FOOD POISONING In many cases, a specific diagnosis is not necessary or not available to guide treatment. The clinician can proceed with the information obtained from the history, stool examination, and evaluation of dehydration severity. Empirical regimens for the treatment of traveler’s diarrhea are listed in Table 133­5. TABLE 133­5 Treatment of Traveler’s Diarrhea on the Basis of Clinical Featuresa CLINICAL SYNDROME SUGGESTED THERAPY Watery diarrhea (no blood in Oral fluids (oral rehydration solution, Pedialyte, Lytren, or flavored mineral water) and saltine crackers stool, no fever), 1 or 2 unformed stools per day without distressing enteric symptoms Watery diarrhea Downloaded 2024­8­4 (no6:42 bloodAinYour IPBismuth subsalicylate (for adults): 30 mL or 2 tablets (262 mg/tablet) every 30 min for 8 doses; or loperamideb: 4 mg is 49.147.196.41 Chapter 133: Acute Infectious Diarrheal stool, no fever), 1 or 2 unformed Diseases and initially followed byBacterial 2 mg after Food passagePoisoning, Richelle of each unformed C. Charles; stool, Regina not to exceed C. LaRocque 8 tablets Page 10 / 13 (16 mg) per day (prescription ©2024stools McGraw Hill. All Rights per day with distressing Reserved. Terms of Use Privacy Policy Notice Accessibility dose) or 4 caplets (8 mg) per day (over­the­counter dose); drugs can be taken for 2 days. Antibacterial drugc can be enteric symptoms considered in selected circumstances. TREATMENT OF INFECTIOUS DIARRHEA OR BACTERIAL FOOD POISONING University of the Philippines ­ Manila In many cases, a specific diagnosis is not necessary or not available to guide treatment. The clinician can proceed with the information obtained from Access Provided by: the history, stool examination, and evaluation of dehydration severity. Empirical regimens for the treatment of traveler’s diarrhea are listed in Table 133­5. TABLE 133­5 Treatment of Traveler’s Diarrhea on the Basis of Clinical Featuresa CLINICAL SYNDROME SUGGESTED THERAPY Watery diarrhea (no blood in Oral fluids (oral rehydration solution, Pedialyte, Lytren, or flavored mineral water) and saltine crackers stool, no fever), 1 or 2 unformed stools per day without distressing enteric symptoms Watery diarrhea (no blood in Bismuth subsalicylate (for adults): 30 mL or 2 tablets (262 mg/tablet) every 30 min for 8 doses; or loperamideb: 4 mg stool, no fever), 1 or 2 unformed initially followed by 2 mg after passage of each unformed stool, not to exceed 8 tablets (16 mg) per day (prescription stools per day with distressing dose) or 4 caplets (8 mg) per day (over­the­counter dose); drugs can be taken for 2 days. Antibacterial drugc can be enteric symptoms considered in selected circumstances. Dysentery (passage of bloody Antibacterial drugc stools) or fever (>37.8°C) Vomiting, minimal diarrhea Bismuth subsalicylate (for adults; see dose above) Diarrhea in infants (24 h, bloody stools, or diarrhea lasting more than several days aAll patients should take oral fluids (Pedialyte, Lytren, or flavored mineral water) plus saltine crackers. If diarrhea becomes moderate or severe, if fever persists, or if bloody stools or dehydration develops, the patient should seek medical attention. bLoperamide should not be used by patients with fever or dysentery; its use may prolong diarrhea in patients with infection due to Shigella or other invasive organisms. cThe recommended antibacterial drugs are as follows: If the level of suspicion is low for fluoroquinolone­resistant Campylobacter: Adults: (1) A fluoroquinolone such as ciprofloxacin, 750 mg as a single dose or 500 mg bid for 3 days; levofloxacin, 500 mg as a single dose or 500 mg qd for 3 days; or norfloxacin, 800 mg as a single dose or 400 mg bid for 3 days. (2) Azithromycin, 1000 mg as a single dose or 500 mg qd for 3 days. (3) Rifaximin, 200 mg tid or 400 mg bid for 3 days (not recommended for use in dysentery). Children: Azithromycin, 10 mg/kg on day 1, 5 mg/kg on days 2 and 3 if diarrhea persists. If fluoroquinolone­resistant Campylobacter is suspected (for example, following travel to Southeast Asia): Adults: Azithromycin (at above dose for adults). Children: Same as for children traveling to other areas (see above). Source: After DR Hill et al: The practice of travel medicine: Guidelines by the Infectious Diseases Society of America. Clin Infect Dis 43:1499, 2006. The mainstay of treatment is adequate rehydration. The treatment of cholera and other dehydrating diarrheal diseases was revolutionized by the promotion of oral rehydration solution (ORS), the efficacy of which depends on the fact that glucose­facilitated absorption of sodium and water in the small intestine remains intact in the presence of cholera toxin. The use of ORS has reduced cholera mortality rates from >50% (in untreated cases) to