How can I be sure that the patient has an intestinal infection?
Signs and symptoms usually found
Diarrhea is defined as acute (lasting less than 14 days), persistent (14 days to 1 month), and chronic (>1 month). Most infectious diarrheas are self-limited. Infectious diarrheas can generally be divided into small intestinal or colonic pathogens, with differing clinical presentations.
Small intestinal infectious diarrheas tend to cause mild to moderate symptoms, including large volume, watery diarrhea with diffuse abdominal pain or cramping. Colonic infections tend to be more severe infections, leading to small volume stools, which can be associated with blood or mucus, with lower abdominal cramps and tenesmus. Both types of infections can lead to dehydration, although this tends to be more profound in small intestinal infections and can have associated malabsorption. Table I describes clinical features of mild, moderate, and severe diarrheas.
A tabular or chart listing of features and signs and symptoms
See Table I.
Noninfectious etiologies of acute diarrhea should also be considered, including medications and toxins (magnesium, proton pump inhibitors, caffeine, theophylline, opiates, lactulose, cholchicine, metformin, digitalis, iron, methyldopa, hydralazine, sorbitol, quinidine, fructose, mannitol, arsenic, cadmium, mercury, and mushrooms), irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), food allergies, lactase deficiency, ischemic bowel disease, and early symptoms of any other cause of chronic diarrhea.
Many different organisms can cause acute infectious diarrhea. The most common infectious etiologies of acute diarrhea are listed in
Table II, with common epidemiologic features and risk factors. Generally, small intestinal infections are noninvasive and will cause mild to moderate disease, whereas ileocolonic infections tend to be invasive pathogens that cause more severe illness. HIV positive and other immunosuppressed patients are at risk for other infectious agents. These organisms are included in Table II, but evaluation and treatment can be complex and is out of the scope of this chapter.
How can I confirm the diagnosis?
The utility of screening for the presence of infectious diarrheas with fecal leukocytes or stool lactoferrin, a by-product of leukocytes, is debatable. Both fecal leukocytes and stool lactoferrin are unable to differentiate between infections versus inflammatory bowel disease. Additionally, both have high false-positive and false-negative rates. The sensitivity of fecal leukocytes is only between 42% to 72% of culture-positive infectious diarrheas. Stool lactoferrin is more sensitive but still no more specific. The author would not recommend sending either of these tests as part of the routine diagnostic work-up of acute diarrheas.
Stool culture is indicated as part of the diagnostic evaluation, when the patient presents with moderate to severe diarrhea. This includes relevant patient history (e.g., travel to endemic areas, known sick contacts, on-going outbreaks, immunosuppression, or recent hospitalization or antibiotic use) or clinical exam findings (bloody dysentery, fever, severe abdominal pain, tenesmus, or severe dehydration). Routine stool culture for enteric pathogens will detect Shigella, Salmonella, and Campylobacter. Special media or testing is required for several organisms, including Yersinia (cold-enrichment medium), Shiga toxin E. coli O157:H7 (sorbitol-MacConkey agar), Vibrio cholera (thiosulfate-citrate-bile salts medium), and Clostridium difficile (requires identification of Toxins A and/or B by PCR or ELISA).
Testing for stool ova and parasites is recommended for all patients with persistent diarrhea. Ideally, three stool specimens should be sent for evaluation for parasites.
Additional testing may be warranted for patients who are immunocompromised or HIV positive, but it is out of the scope of this chapter and will not be addressed.
|A diagnostic algorithm for acute diarrhea|
|Evaluate severity and duration of acute diarrhea|
|If pregnant with headache, meningitis, sepsis (no diarrhea)|
|If recent antibiotics use in last 2 mons or recent hospitalization|
|Mild symptoms (3-5 BM daily)|
|Moderate to severe diarrhea|
|If persistent (duration 2-4 wk): Examine for ova and parasites; consider stool lactoferrin and fecal leukocytes to evaluate|
|for inflammatory diseases|
|Send stool for C. difficile toxin A and B EIA or PCR.|
|Likely, viral gastroenteritis.|
|Likely, preformed toxin-mediated (S. aureus, B. cereus).|
|Most likely antibiotic-associated diarrhea|
|Start treatment (Table III).|
|Continue symptomatic treatment with ORT.|
|Can also consider K. oxytoca, MRSA toxin, or enterotoxin-producing C. perfringens.|
|DO NOT GIVE antibiotics or antidiarrheals to children due to risk of HUS.|
|If suspected STEC (R-sided abdominal pain, afebrile, bloody diarrhea),|
|send for stool culture for STEC O157 and Shiga toxin.|
|Moderate to severe diarrhea|
|Screen history for|
|1. Travel to endemic areas (Africa, SE Asia, parts of Central and South America)|
|2. Exposure to sick contacts|
|4. On-going epidemic/outbreak|
|Evaluate physical examination|
|2. Abdominal tenderness|
|3. Blood or mucus in stools|
|Continue symptomatic treatment with ORT.|
|If symptoms persist >48 hrs|
|If YES to any of above:|
|Send stool culture.|
|Start appropriate antibiotic therapy (Table III).|
|Consider empiric therapy (Table III).|
|Continue symptomatic treatment with ORT.|
|Symptoms persist or worsen.|
What other diseases, conditions, or complications should I look for in patients with intestinal infections?
What is the diagnostic approach if this initial evaluation fails to identify the cause?
Most cases of infectious diarrheas are self-limited and do not warrant additional endoscopic evaluation. However, if the diagnosis is in question or if a patient is severely ill, then colonoscopy or flexible sigmoidoscopy with colonic biopsies may be helpful for differentiating between acute bacterial infectious colitis versus IBD. In some cases, the gross appearance of the colon on endoscopy may not be able to differentiate between infectious colitis and IBD; however, histopathology may be useful.
Colorectal biopsies from patients with infectious colitis will typically have normal colonic architecture and acute inflammation within the lamina propria (including crypt abscesses), whereas IBD is more commonly associated with distorted architecture and chronic inflammation (particularly basilar lymphoid aggregates and basilar plasmacytosis). Microgranulomas are nonspecific and can be associated with some infectious organisms, including tuberculosis, schistosomiasis, histoplasmosis, and Yersinia, as well as Crohn’s disease.
What other diseases, conditions, or complications should I look for in patients with acute diarrhea?
The most common complication of acute diarrhea is dehydration and, therefore, initial therapeutic efforts should be targeted toward fluid rehydration as discussed below. Other complications of acute infectious diarrhea, particularly with C. difficile colitis and Shigellosis, can lead to abdominal distention, toxic megacolon, and colonic perforation, with all the associated complications, including death. It is important to monitor for abdominal distention and developing megacolon as patients undergo treatment.
Other common complications of acute diarrhea include post-infectious IBS, reactive arthritis (formerly called Reiter’s Syndrome, which is particularly associated with Campylobacter but can also be seen following Shigella, Salmonella, and Yersinia), TTP, and HUS, which can be seen following Shigellosis or STEC. Campylobacter can cause Guillain-Barré syndrome. Yersinia can also be complicated by mesenteric adenitis and erythema nodosum.
What is the right therapy for the patient with an intestinal infection?
Most patients with acute diarrheal illness do not require clinical intervention or additional diagnostic evaluation since symptoms will usually self-resolve quickly (<24 hrs). However, when indicated, the initial clinical evaluation of infectious diarrhea should focus on the patient history and physical exam to assess disease severity and volume status, as well as clinical and epidemiologic features of the illness. Clinical history should include evaluation of symptom duration, onset (acute vs. gradual), stool frequency and volume, small intestinal versus colonic infection, associated symptoms (nausea, vomiting, fever, abdominal pain, etc.), and pertinent epidemiologic findings (see Table II).
Evaluation should begin with assessment of patient volume status, which is done primarily by physical examination. Indicators of hypovolemia include postural dizziness, resting tachycardia, orthostatic increase in heart rate above 30 bpm, dry mucus membranes or axilliae, skin turgor, decreased urine output, confusion, weakness, or sunken eyes.
The abdominal exam should assess for tenderness, distention, and bowel sounds. Serum chemistries, including serum creatinine and blood urea nitrogen and urine electrolytes, can also assist in the initial evaluation of volume status. A complete blood count should be obtained to assess for leukocytosis.
Oral rehydration therapy (ORT) or IV fluids should be initiated in patients with evidence of dehydration. ORT can be made with the following recipe: ½ tsp salt, ½ tsp baking soda, and 4 tbsp sugar in 1 L of water. The World Health Organization (WHO) now recommends using a low-osmolar rehydration solution in cases of noncholera diarrheal illness. In cases of severe illness, intravenous fluids may need to be administered.
Severe diarrheal illness is defined by prolonged illness, volume depletion, more than 6 loose stools per day, bloody stools, fever, weight loss, or severe abdominal pain. Patients with severe illness or other risk factors, including recent antibiotic use or hospitalization, elderly, immunocompromised state (including HIV/AIDS, post-transplant, chemotherapy, and diabetes mellitus), suspected outbreaks, persons at high risk to spread infection (food handlers, health-care workers, caregivers, day-care workers or attendees, institutionalized patients) warrant additional diagnostic evaluation as described above.
Most antidiarrheal agents, including bismuth subsalicylate and loperamide, can be given safely to most patients with infectious diarrhea, and have been shown to have benefit for traveler’s diarrhea. However, antimotility agents can be risky in certain situations as they can lead to toxic megacolon and prolonged systemic illness. Antidiarrheals should be avoided in children, adults with severe or bloody diarrhea, or known C. difficile colitis or possible STEC.
Antimicrobial agents should generally be initiated only when an etiologic agent has been identified so as to avoid risks and unnecessary side effects of antibiotics. This includes risk of precipitating TTP/HUS in setting of Shigellosis or STEC, increasing development of antibiotic resistance, and development of super-infections when normal colonic flora is disrupted. However, there are several exceptions to this rule. Initiation of antimicrobial therapy is recommended in the following situations: empiric treatment of traveler’s diarrhea, severe diarrhea requiring hospitalization, suspected C. difficile colitis, elderly or immunosuppressed patients, and suspected Giardia infection causing persistent diarrhea.
Most cases of acute infectious diarrhea are self-limited and will resolve completely. However, approximately 20% of patients with C. difficile infection will have recurrence of symptoms within 1 month of completion of successful antibiotic treatment of initial infection. There is no difference in recurrence rates between patients treated with metronidazole or vancomycin. Fidaxomicin, a macrocyclic antibiotic, is a new drug that seems to have equal efficacy as vancomycin for the treatment of mild to moderate disease. Preliminary studies suggest that fidaxomicin may have decreased rate of recurrence than vancomycin due to a reduced effect on colonic microflora.
Risk factors for recurrent C. difficile infection (RCDI) include personal history of prior RCDI; elderly patients; continued use of antibiotics not for treatment of C. difficile infection; IBD; renal disease; and stomach acid suppression using antacids, H2 antagonists, and proton pump inhibitors.
Treatment of RCDI usually involves high doses of oral vancomycin (500 mg p.o. q6 hr) for 14 days, with a gradual tapering off (125 mg p.o. b.i.d. x 5 days, then every other day for a week, then every third day for a week, until the patient is only taking vancomycin p.o. every 10 days before it is stopped). Rifaximin has also been used as pulse therapy for 2 weeks for RCDI, following the initial 14 days of oral vancomycin. This method has shown some preliminary promise, but data is limited by small sample size.
Other treatment modalities that are being evaluated are cholestyramine or colestipol hydrochloride to bind to C. difficile toxin; fidaxomicin as alternative to vancomycin; tigecylcine as alternative to metronidazole; passive immunization with intravenous immunoglobulin (IVIG); probiotic administration of Saccharomyces boulardii; anti-Clostridium whey protein from cows immunized against C. difficile; and fecal microbiota transplant. Vaccination development is underway against toxins A and B.
What is the most effective initial therapy?
See Table III.
Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy.
See Table III.
How should I monitor the patient with acute diarrhea?
All patients should be monitored clinically for evidence of dehydration and development of abdominal distention that can lead to toxic megacolon or colonic perforation.
For patients with known mild to moderate C. difficile colitis who are not clinically improving within 3 days of initiation of metronidazole, treatment should be switched to oral vancomycin. There is no role for repeat stool testing for C. difficile after completion of antibiotic treatment since the toxins can remain in the stool for several weeks despite successful treatment with clinical resolution of diarrhea.
What's the evidence?
Guerrant, RL, Van Gilder, T, Steiner, TS, Thielman, NM. “IDSA Guidelines: Practice Guidelines for the Management of Infectious Diarrhea”. Clin Infect Dis. vol. 32. 2001. pp. 331-50.
Surawicz, CM, Waye, JD, Rex, DK, Williams, CB. “Infections and other noninflammatory bowel disease colitides”. 2009. pp. 659-74.
Guerrant, RL, Bobak, DA. “Bacterial and protozoal gastroenteritis”. NEJM. vol. 325. 1991. pp. 327-40.
Kelly, CR, Kahn, S, Kashyap, P. “Update on Fecal Microbiota Transplantation 2015: Indications, Methodologies, Mechanisms, and Outlook”. Gastroenterology. 2015. pp. 149-223.
Newton, JM, Surawicz, CM, Guandalini, S, Varizi, H. “Infectious gastroenteritis and colitis”. 2010.
Cohen, SH, Gerding, DN, Johnson, S. “SHEA-IDSA Guidelines: Clinical Practice Guidelines for Clostridium difficile Infection in Adults: 2010 update by the Society for Healthcare Epidemiology of America (SHEA) and the Infectious Diseases Society of America (IDSA)”. ICHE. vol. 31. 2010. pp. 431-55.
Surawicz, CM, Alexander, J. “Treatment of refractory and recurrent Clostridium difficile infection”. Nat Rev Gastroenterol Hepatol. 2011.
De la Cabada Bauche, J, Dupont, HL. “New developments in traveler’s diarrhea”. Gastroenterol Hepatol (N Y). vol. 7. 2011. pp. 88-95.
Gorkiewicz, G. “Nosocomial and antibiotic-associate diarrhoea caused by organisms other than Clostridium difficile”. Int J Antimicrob Agents. vol. 33. 2009. pp. S37-S4.
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- How can I be sure that the patient has an intestinal infection?
- A tabular or chart listing of features and signs and symptoms
- How can I confirm the diagnosis?
- What other diseases, conditions, or complications should I look for in patients with intestinal infections?
- What is the right therapy for the patient with an intestinal infection?
- What is the most effective initial therapy?
- Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy.
- How should I monitor the patient with acute diarrhea?