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Bacterial Infections of the Bowel

Bacterial Infections of the Bowel

Bacterial gastroenteritis may result from the ingestion of a preformed bacterial toxin present in the food at the time of ingestion, by the production of a toxin or toxins in vivo, or by invasion and infection of the bowel mucosa by the bacterial pathogen. In this chapter, the most common bacterial pathogens affecting immunocompetent hosts are discussed.

Toxigenic bacteria

In general, toxigenic bacteria produce watery diarrhea without systemic illness. There may be low-grade fever in some patients. Some microorganisms can produce other toxins in addition to an enterotoxin, for example, neurotoxins that can cause extraintestinal manifestations. The stools contain no blood or fecal leukocytes, which helps to distinguish these diseases from diarrheas caused by tissue-invasive organisms. Table SOME ETIOLOGIC AGENTS FOR TOXIGENIC DIARRHEA lists some of the common causes of toxigenic diarrhea.

Bacterial Infections of the BowelStaphylococcus aureus

  • Epidemiology. Staphylococcal food poisoning is the most frequent cause of toxin-mediated vomiting and diarrhea encountered in clinical practice. All coagulase-positive staphylococci can produce enterotoxins. Staphylococci are introduced into food by the hands of food-handlers. The organisms multiply and produce the toxin if the food is kept at room temperature. The foods most commonly implicated are coleslaw, potato salad, salad dressings, milk products, and cream pastries. Food contaminated with staphylococci is normal in odor, taste, and appearance.
  • Clinical disease. Staphylococcal food poisoning is manifested by an abrupt onset of vomiting within 2 to 6 hours after ingestion of the contaminated food. The diarrhea is usually explosive and may be accompanied by abdominal pain. Fever is usually absent. The diagnosis is usually suspected from the history. In most instances, the organism can be cultured from the contaminated food.
  • Treatment. Gastroenteritis resolves with supportive care within 12 to 24 hours. Antimicrobial therapy is not indicated.

Bacillus cereus

  • Epidemiology. Bacillus cereus is a common gram-positive, spore-forming organism found in soil. Contamination of food occurs before cooking. Vegetative growth continues at temperatures of 30В° to 50В°C, and spores can survive extreme temperatures. The spores of the organism germinate and produce toxins during the vegetative stage.

B. cereus is a frequent cause of food poisoning from many sources but is usually associated with contaminated rice or meat from Chinese restaurants.

TABLE . SOME ETIOLOGIC AGENTS FOR TOXIGENIC DIARRHEA
Staphylococcus aureus Other toxigenic diarrheas
Bacillus cereus Scrombrotoxin poisoning
Vibrio cholerae Paralytic shellfish poisoning
Enterotoxigenic Escherichia coli Neurotoxic shellfish poisoning
Vibrio parahaemolyticus Ciguatoxin poisoning
Clostridium perfringens Tetrodotoxin poisoning
  • Clinical disease. B. cereus intoxication manifests as two distinct clinical syndromes. The «emesis syndrome» is caused by the thermostable toxin and mimics staphylococcal food poisoning. Within 2 to 6 hours after ingestion of the contaminated food, the patient has severe vomiting and abdominal pain with or without diarrhea. There is no accompanying fever or systemic manifestations. Illness is self-limited and lasts 8 to 10 hours. The «diarrhea syndrome» is caused by the thermolabile enterotoxin and occurs after 8 to 16 hours of ingestion of the contaminated food. It is characterized by a foul-smelling, profuse watery diarrhea, usually accompanied by nausea, abdominal pain, and tenesmus. Most of the symptoms resolve in 12 to 24 hours.
  • Diagnosis is made by history and stool cultures demonstrating the organism.
  • Treatment is supportive.

Vibrio cholerae

  • Epidemiology. V. cholerae is a mobile, gram-negative bacterium with a single flagellum and is easily recognizable by a fecal Gram’s stain. It produces a thermostable enterotoxin, which stimulates the adenylate cyclase in small-intestinal crypt cells, especially in the jejunum, resulting in profuse secretory diarrhea. V. cholerae is seen occasionally in the United States, especially along the Gulf coast. Any fecally contaminated water or food has the potential to cause cholera, but contaminated saltwater crabs and freshwater shrimp are responsible for most instances seen in the United States.
  • Clinical disease. The incubation period is 1 to 3 days after ingestion. Cholera is characterized by an abrupt onset of profuse, large-volume, watery diarrhea. The stools are isotonic and do not contain blood or mucus. There is usually no associated fever, abdominal pain, vomiting, or tenesmus. Hypotension, shock, and death may result if volume depletion is not adequately treated.
  • Diagnosis. Organisms may be demonstrated by dark-field microscopy of the stool and by stool cultures.
  • Treatment. The mainstay of therapy is volume repletion intravenously or orally with fluids that contain glucose and electrolytes. If dehydration is adequately reversed, patients recover in 7 to 10 days without antimicrobial therapy. The duration of the disease may be shortened to 2 to 3 days with oral tetracycline 500 mg four times daily (q.i.d.) or doxycycline 300 mg in a single dose. In resistant instances, alternative antimicrobials are furazolidone 100 mg q.i.d., erythromycin 250 mg q.i.d., or trimethoprim/sulfamethoxazole 160/800 mg twice daily (b.i.d.) for 3 days.

EnterotoxigenicEscherichia coli

  • Epidemiology. Enterotoxigenic E. coli (ETEC) can cause diarrhea by tissue invasion or via its enterotoxin. The enterotoxin is thermolabile and produces diarrhea by the same mechanism as the cholera enterotoxin. The organism is transmitted from contaminated water and food by the fecal oral route. Even though it may cause outbreaks in the United States, ETEC is the most common traveler’s pathogen. A large inoculum is required for disease. The incubation period is 1 to 3 days. The clinical disease is similar to cholera. The watery diarrhea is profuse and lasts 3 to 5 days. There may be accompanying mild abdominal pain.
  • The diagnosis is by history and clinical observation. Serotyping of E. coli is available only in research settings.
  • Treatment. Most patients require no antimicrobial therapy. Intravenous or oral volume replacement with glucose-electrolyte solutions is usually adequate. Severe instances may be treated with tetracycline, trimethoprim/sulfamethoxazole, or ciprofloxacin.

Vibrio parahaemolyticus

  • Epidemiology. V. parahaemolyticus is a gram-negative bacillus that survives in water with a high salt content. It is recognized as an important pathogen in the Far East and more recently in the United States. It is most common in the summer and least common in the winter months because the bacterial populations in the ocean are temperature-dependent. It is associated with acute diarrheal disease after the ingestion of contaminated raw or cooked fish or shellfish. The organism produces a variety of toxins. The incubation period is 12 to 48 hours after ingestion.
  • Clinical disease. The illness is characterized by explosive watery diarrhea. Headaches, vomiting, and abdominal cramps are common. Low-grade fever and chills occur in 25% of the patients. Bloody diarrhea may occur in some instances. The stools are not as profuse as in V. cholerae, but hypotension and shock have been seen. The illness is usually self-limiting and resolves within 1 to 7 days.
  • Diagnosis. The diagnosis is by stool culture on thiosulfate-citrate-bile salt – sucrose agar.
  • Treatment is supportive with fluid repletion. Complicated instances may be treated with oral tetracycline.

Clostridium perfringens

  • Epidemiology. Clostridium perfringens is a gram-positive, spore-forming obligate anaerobe found in soil and in the gastrointestinal tract of humans and animals. It produces 12 toxins. The thermolabile exotoxin is an important cause of toxigenic diarrhea. The toxin is a structural component of the spore’s coat and is formed during sporulation. Most of the toxin is synthesized before ingestion. Additional toxin is produced in the gastrointestinal tract after ingestion of contaminated beef, beef products, or poultry. The pathogenesis of infection requires the food to be inadequately precooked and then reheated before it is served. The toxin has its maximal activities in the ileum. It inhibits glucose transport and activates adenylate cyclase of small-intestinal crypt cells stimulating intestinal secretion. Outbreaks may occur in institutions or after large gatherings.
  • Clinical disease. Watery diarrhea with severe, crampy abdominal pain usually occurs 8 to 24 hours after the ingestion of contaminated food. Vomiting, fever, chills, and headaches are not seen. The stools are usually foul smelling. The disorder is self-limited and resolves within 24 to 36 hours.
  • The diagnosis is by history.
  • Treatment is supportive.

Bacterial Infections of the BowelClostridium botulinum

  • Epidemiology. C. botulinum is a gram-positive, anaerobic, spore-forming bacillus. Three exotoxin types, A, B, and E, have been associated with C. botulinum intoxication. Types A and B are associated with improperly prepared home-canned fruits and vegetables. Type E outbreaks are associated with smoked freshwater fish and are most frequent in the Great Lakes region. The contaminated foods may not appear, taste, or smell spoiled, thereby inciting no suspicion of their contamination. The exotoxin is neurotoxic and thermolabile. It can be inactivated by boiling in water for 15 minutes.
  • Clinical disease. C. botulinum is responsible for one third of the deaths from food-borne diseases. The intoxication results in acute cranial nerve dysfunction, dysarthria, diplopia, blurred vision, dysphagia, and a symmetric descending weakness without a sensory component. Dilated pupils occur in 15% of patients. Respiratory muscle insufficiency may occur. The neurologic disease may last for months and can result in death.  The diagnosis is made by history and culture or toxin assay from the contaminated food or the patient’s blood or stool. Electromyography may be used to differentiate the disease from Guillain-Barr syndrome.
  • Therapy. When intoxication is suspected, therapy should be started immediately with administration of the polyvalent antitoxin and penicillin. Gastrointestinal lavage with orally administered solutions, e.g., GoLYTELY or Colyte, may help to eliminate the toxin from the gastrointestinal tract. Guanidine hydrochloride may be used to reverse the motor weakness. Some patients may require ventilatory support.

Bacteria causing «enteric» infection. The resulting diarrhea may be watery or bloody. Although watery diarrhea is often associated with infections with viruses, protozoa, and toxin-producing bacteria such as Vibrio cholerae and enterotoxigenic E. coli, invasive bacteria can also cause watery diarrhea (Table Infectious organisms that result in watery diarrhea). The diarrhea is usually greater than 1 liter/day. Systemic symptoms such as fever, headache, myalgia, and arthralgias are usually absent.

Bloody diarrhea, or dysentery, is usually accompanied by abdominal pain, tenesmus, nausea, vomiting, and systemic symptoms such as fever and malaise. Bacteria that result in bloody diarrhea are listed in Table INFECTIOUS ORGANISMS THAT RESULT IN BLOODY DIARRHEA. These enteric infections cannot be distinguished easily from one another clinically. Diagnosis must be based on the identification of the infectious agent by appropriate cultures.

Campylobacter jejuni and Campylobacter fetus

Epidemiology. C. jejuni is the most common bacterial pathogen that causes bloody diarrhea in the United States. It is implicated in infections in underdeveloped countries also. The organism is a microaerophilic, gram-negative curved rod transmitted to humans from contaminated pork, lamb, beef, milk and milk products, and water, and from exposure to infected household pets. The organism is destroyed by appropriate cooking, pasteurization, and water purification. The incubation period is 1 to 7 days.

Histopathology. The bacterial endotoxin causes mucosal inflammation in the small and large intestine that resembles the lesions seen in ulcerative colitis and Crohn’s disease and those seen with Salmonella and Shigella infections. The infection is usually more severe in the colon than in the small bowel.

TABLE. Infectious organisms that result in watery diarrhea
Viruses Protozoa
Rotavirus
Norwalk and related viruses
Adenovirus
Bacteria
Vibrio cholerae
Escherichia coli (enterotoxigenic)
Giardia lamblia
Cryptosporidium
TABLE. INFECTIOUS ORGANISMS THAT RESULT IN BLOODY DIARRHEA
Campylobacter Escherichia coli 0157:H7
Escherichia coli
(enteropathogenic and invasive)
Shigella
Salmonella
Yersinia
Vibrio parahaemolyticus
Clostridium difficile
Entamoeba histolytica

Clinical disease

Enterocolitis

Bowel infections with C. jejuni and rarely C. fetus cause a diarrheal illness resembling enteritis from Salmonella and Shigella. Occasionally there is a prodrome of headache, myalgia, and malaise for 12 to 24 hours, followed by severe abdominal pain, high fever, and profuse watery and then bloody diarrhea. The diarrhea is usually self-limited and in most instances resolves in 7 to 10 days; however, in one-fifth of the instances, the diarrhea has a protracted or a relapsing course.

  • Systemic infection. C. fetus and rarely C. jejuni may cause a systemic infection, especially in elderly, debilitated patients, and in those with alcoholism, diabetes mellitus, and malignancies. Bacteremia may be transient or may lead to localized infection such as endocarditis, meningitis, cholecystitis, and thrombophlebitis. There may or may not be clinically evident enterocolitis.
  • Complications. Campylobacter infection may be complicated by Reiter’s syndrome, mesenteric adenitis, terminal ileitis (resembling Crohn’s ileitis), and rarely an enteric feverlike illness.
  • Diagnosis is made by stool and blood cultures. Stool Gram’s stain may show the organism with its characteristic «gull wings» In dark-field/ phase-contrast microscopy, the organism shows «darting motility» Fecal leukocytes are present in 75% of instances.
  • Treatment. In mild cases supportive therapy is given. In cases with bloody diarrhea, erythromycin 250 mg per os (p.o.) q.i.d. for 5 to 7 days or ciprofloxacin 500 mg p.o. b.i.d. for 3 to 7 days is effective.

Salmonella

  • Epidemiology. The three primary species of Salmonella (Salmonella typhi, Salmonella choleraesuis, and Salmonella enteritidis) may cause disease in humans. S. enteritidis is a common cause of infectious diarrhea. There are 1,700 serotypes and variants of Salmonella, which are classified into 40 groups. Ninety percent of Salmonella organisms that are pathogenic for human beings are in groups B, C, and D. The organism is transmitted from fecally contaminated foods and water with fecal-oral contact. Poultry and poultry products coinstitute the major reservoir for the bacteria. A large inoculum (> 105 organisms) is required to produce infection. Thus, the incidence is relatively low despite the widespread contamination of commonly ingested foods.
  • Pathology.Salmonella elaborates an enterotoxin, which is responsible for the watery diarrhea. The organism also adheres to the mucosal surface and invades the epithelium, resulting in colitis and bloody diarrhea.
  • Clinical disease. Salmonella invades the mucosa of the small and large intestine and produces an enterotoxin that causes a secretory diarrhea. Watery diarrhea is more common, but bloody diarrhea may occur. Patients complain of headache, malaise, nausea, vomiting, and abdominal pain within 6 to 48 hours after ingesting the contaminated food. The disease is usually self-limited and resolves in 7 days. Fever and bacteremia occur in less than 10% of patients. Immunosuppression, malignancy, hemolytic states, liver disease, achlorhydria, and chronic granulomatous disease of children predispose patients to progressive salmonellosis with bacteremia, with localized infection in joints, bones, meninges, and other sites. In 5% of patients, the bacteria may localize in the reticuloendothelial system and may cause an enteric fever (especially S. typhi). A carrier state also exists in some patients, with bacteria carried in the gallbladder or in the urinary tract.

The diagnosis is made by history and stool and blood cultures. A fourfold rise in serum O and H agglutinin titers 3 to 4 weeks after infection confirms the diagnosis.

Treatment is supportive in most instances. Antimicrobial therapy is contraindicated for most patients because it can increase the carrier state. However, antimicrobial agents such as ampicillin, chloramphenicol, trimethoprim/sulfamethoxazole, ciprofloxacin hydrochloride, or third-generation cephalosporins can be used in young children or in patients who are susceptible to bacteremia and prolonged salmonellosis (Table TREATMENT OF COMMON ACUTE ENTERIC INFECTIONS ). Patients with bacteremia, enteric fever, and metastatic infection should be treated with antimicrobial therapy. Also, patients with underlying acquired immunodeficiency syndrome (acquired immunodeficiency syndrome), hemolytic states, lymphoma, and leukemia, and neonates, the elderly, and chronic carriers should receive antimicrobials. Anticholinergic agents and opiates should not be used because they can prolong the excretion of the bacteria.

TABLE. TREATMENT OF COMMON ACUTE ENTERIC INFECTIONS
Organism Antimicrobial Therapy
Campylobacter Erythromycin 250 mg PO q.i.d. for 5-10 d or ciprofloxacin 500 mg PO b.i.d. for 5 d
Shigella Trimethoprim/sulfamethoxazole DS PO b.i.d. for 5 d or tetracycline 500 mg PO q.i.d. for 5 d or ciprofloxacin 500 mg PO b.i.d. for 5 d
Salmonella (severe disease) Ampicillin or amoxicillin 1 gm PO t.i.d. or q.i.d. for 14 d or chloramphenicol 1 gm PO or intravenous q8h for 14 d or trimethoprim/sulfamethoxazole DS PO b.i.d. for 10 d or a third-generation cephalosporin or ciprofloxacin 500 mg PO b.i.d. for 5 d
Enterotoxigenic Escherichia coli, E. coli 1057:H7, and traveler’s diarrhea Trimethoprim/sulfamethoxazole DS PO b.i.d. for 5 d or ciprofloxacin 500 mg PO b.i.d. for 5 d or ofloxacin 300 mg PO b.i.d. for 5 d or norfloxacin 400 mg PO b.i.d. for 5 d
Giardia lamblia Quinacrine hydrochloride 100 mg PO t.i.d. for 7 d or metronidazole 250 mg PO t.i.d. for 7 dor furazolidone 100 mg q.i.d. for 7 d
Entamoeba histolytica Diloxanide furoate 500 mg PO t.i.d. for 10 d plus diiodohydroxyquin 650 mg PO t.i.d. for 20 d
Yersinia enterocolitica Trimethoprim/sulfamethoxazole DS PO b.i.d. for 7 d or tetracycline 250-500 mg PO for 7 d
Vibrio cholerae Tetracycline 500 mg PO q.i.d. for 3 d or trimethoprim/sulfamethoxazole DS PO b.i.d. for 3 d
Noncholera Vibrio Tetracycline 250 mg PO q.i.d. for 7 d
Clostridium difficile
Mild disease
Severe disease
Cholestyramine 4 gm PO t.i.d. for 7 d or metronidazole 250 mg PO t.i.d. for 7 d
Metronidazole 250 mg PO t.i.d. for 7 d or vancomycin 125-500 mg PO q.i.d. for 7 d
Trimethoprim/sulfamethoxazole DS, trimethoprim 160 mg/sulfamethoxazol 800 mg; PO, by mouth; q.i.d., four times a day; b.i.d., twice a day; t.i.d., three times a day.

Shigella

  • Epidemiology. There are four major groups: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei. S. dysenteriae causes the severest form of dysentery. In the United States, 60% to 80% of instances of bacillary dysentery are caused by S. sonnei with a seasonal preference for winter. In tropical countries, S. flexneri dysentery is more common especially in the late summer months. It is transmitted by the fecal-oral route. Human beings are the only natural host for this organism. Enteric infections with Shigella are most commonly seen in children 6 months to 5 years old, although persons of all ages can become infected. Clinical shigellosis is highly contagious and can be caused by a very small inoculum: less than 200 organisms. Food, water, and milk can be contaminated, which can result in epidemics. Incidence of the disease increases in crowded, unsanitary conditions.
  • Pathophysiology. Shigella elaborates an enterotoxin that is responsible for the watery diarrhea. The organism also adheres to the mucosal surface and invades the epithelium, resulting in colitis and bloody diarrhea.
  • Clinical disease. The incubation period is 1 to 3 days. In most individuals, the disease starts as lower abdominal pain and diarrhea. Fever is present in less than half of the patients. In many patients, there is a biphasic illness that begins as fever, abdominal pain, and watery diarrhea. In 3 to 5 days, rectal burning, tenesmus, and small-volume bloody diarrhea characteristic of severe colitis develop. Toxic megacolon and colonic perforation may recur. Extraintestinal complications include conjunctivitis, seizures, meningismus, Reiter’s syndrome, thrombocytopenia, and hemolytic uremic syndrome.

The course of shigellosis is variable. In children, it may resolve in 1 to 3 days and in most adults in 1 to 7 days. In severe instances, it may last longer than 3 to 4 weeks with associated relapses. It may be confused with idiopathic ulcerative colitis. A minority of patients become chronic carriers.

The diagnosis of shigellosis is made by identification of the gram-negative bacillus in the stool. Sigmoidoscopic findings are identical to those of idiopathic inflammatory bowel disease.

Treatment. Patients should receive supportive therapy with antipyretics and fluids. Antiperistaltic agents such as diphenoxylate hydrochloride (Lomotil) or loperamide hydrochloride (Imodium) should be avoided. Antimicrobial therapy decreases the duration of fever, diarrhea, and excretion of the organisms in the stool. Trimethoprim/sulfamethoxazole, tetracycline, and ampicillin (but not amoxicillin) are all effective; however, resistance has been demonstrated. Ciprofloxacin and norfloxacin are also effective.

Escherichia coli.

In addition to ETEC, other serotypes of E. coli also cause diarrhea. These include enteroinvasive E. coli (EIEC), enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), diffuse adherence E. coli (DAEC), and enteroaggregating E. coli (E AGGEC). All of these bacteria possess plasmid-encoded virulence factors. They make specific interactions with the intestinal mucosa by way of bacterially derived adhesions. Some produce enterotoxins and cytotoxins. Transmission is fecal-oral.

Enteroinvasive E. coli

  • Epidemiology. EIEC is a traveler’s pathogen. Epidemics have been described resulting from imported cheese. The organism also causes epidemics in young children, 1 to 4 years of age.
  • Clinical disease. Similar to Shigella, EIEC invades and destroys the colonic mucosal cells and causes, first, watery diarrhea followed by a dysenterylike syndrome. The incubation period is 1 to 3 days. The fever and diarrhea last 1 to 2 days.
  • Diagnosis. Fecal leukocytes are present. Serotyping and enzyme-linked immunosorbent assay are available only in research settings.
  • Treatment is supportive. Bismuth subsalicylate, by decreasing colonic secretions, seems to decrease the diarrhea and other symptoms in all infections with E. coli species. The antimicrobials used in shigellosis are effective.

Enteropathogenic E. coli

Epidemiology. EPEC is a major cause of diarrhea in both economically developed and underdeveloped countries. It commonly causes outbreaks in nurseries affecting children up to 12 months of age. It may also cause sporadic diarrhea in adults. The bacteria adhere closely to the enterocyte membrane via an adherence factor with destruction of microvilli.

Clinical disease. Disease onset is with fever, vomiting, and watery diarrhea. Symptoms may continue for longer than 2 weeks and patients may relapse.

Diagnosis is by serotype analysis

Treatment. Nonabsorbable antibiotics such as neomycin, colistin, and polymyxin have been recommended. Ciprofloxacin hydrochloride, norfloxacin, and aztreonam are also effective and preferred.

Enterohemorrhagic E. coli

  • Epidemiology. EHEC, or E. coli: 157:07, and rarely E. coli: H11 have been detected in contaminated hamburger meat; outbreaks have occurred in nursing homes, daycare centers, and schools.
  • Pathogenesis and clinical disease. EHEC elaborates aShigella-like toxin (verotoxin 1) that is identical to the neuroenterocytotoxin of S. dysenteriae and to verotoxin 2 and an adherence factor encoded by a plasmid. Transmission is fecal-oral. Although the disease is more common in children, several outbreaks have occurred in adults from contaminated beef. The bloody diarrhea may be copious but may show no fecal leukocytes. It usually lasts 7 to 10 days but may be complicated by hemolytic uremia syndrome.
  • Diagnosis. Stool cultures and serotyping sorbitol-negative E. coli isolates may yield the organism.
  • Treatment. Symptomatic treatment and ciprofloxacin or norfloxacin may be used in severe illness. Supportive measures are recommended.

Diffuse adherence E. coli (DAEC) affects young children, especially in economically underdeveloped countries. Diarrhea is usually watery, lasts less than 2 weeks, and may become persistent.

Enteroaggregating E. coli (EAGGEC) has been recognized recently as a pathogen especially affecting the ileum and the terminal ileum. The aggregating bacteria gather around the villi and cause epithelial destruction. The pathogenesis is transferred by a plasmoid via fimbriae. It causes persistent diarrhea in children and is more common in economically underdeveloped countries. The management of the diarrheal illness is similar to that of other E. coli species strains.

Yersinia enterocolitica

  • Epidemiology. Y. enterocolitica can be found in stream and lake water and has been isolated from many animals, including dogs, cats, chickens, cows, and horses. It is transmitted to humans via contaminated food or water, or from human or animal carriers. It most commonly affects children and rarely causes disease in adults. It is found worldwide, especially in Scandinavia and Europe, and may result in epidemics.
  • Pathogenesis and clinical disease. Yersinia causes a spectrum of diseases ranging from gastroenteritis to invasive ileitis and colitis. The organism is invasive and elaborates a heat-stable toxin. These properties allow its invasion into and through the distal small-bowel mucosa and subsequent infection of the mesenteric lymph nodes. The incubation period is 4 to 10 days. The disease normally lasts several weeks but can be prolonged for many months.
  • The manifestation of Yersinia infection is variable. In infants and young children less than 5 years, it may be febrile gastroenteritis lasting 1 to 3 weeks. In older children, it may mimic acute terminal ileitis, mesenteric adenitis, or ileocolitis. It may be confused with acute appendicitis. The enterocolitis presents with bloody diarrhea, fever, and abdominal pain accompanied by anorexia, nausea, and fatigue. The diarrhea usually lasts 1 to 3 weeks but may be protracted (> 3 months). Polyarthritis, erythema multiforme, and erythema nodosum occasionally develop 1 to 3 weeks after the onset of diarrhea. Bacteremia is rare but may be seen in immunosuppressed patients and may result in hepatosplenic abscess, meningitis, and infections of other organs. Metastatic foci may occur in joints, lungs, and bones.
  • Diagnosis can be made by stool and blood cultures using special media and culture conditions. The laboratory should be notified. Serologic tests have been useful in Europe and Canada. The serotypes found in the United States do not give reliable serologic results.
  • Treatment in most instances is supportive. Antimicrobials such as tetracycline, chloramphenicol, and trimethoprim/sulfamethoxazole may be used in severe illness.

Aeromonas hydrophila

  • Epidemiology. A. hydrophila is a member of the Vibrionaceae family. It is transmitted from contaminated food and water, especially in the summer months.
  • Pathogenesis and clinical disease. Aeromonas produces several toxins. The heat-labile enterotoxin and the cytotoxin are implicated in the intestinal infection. The disease commonly follows ingestion of untreated water just before the onset of symptoms and consists of fever, abdominal pain, watery diarrhea, and vomiting lasting about 1 to 3 weeks in children and 6 weeks or longer in adults. In 10% of instances, diarrhea is bloody and mucoid. Chronic diarrhea and choleralike presentation have also been described. In immunocompromised patients and patients with hepatobiliary disease, bacteremia may occur.
  • Diagnosis. Stool cultures are diagnostic. Fecal leukocytes may be present in one third of instances.
  • Treatment is supportive in mild instances. In severe illness and with chronic diarrhea, antibiotics may shorten the duration of the disease. Aeromonas is resistant to beta-lactam antibiotics. Trimethoprim/sulfamethoxazole, tetracycline, and chloramphenicol have been effective.

Plesiomonas shigelloides

  • Epidemiology. Plesiomonas is another member of the Vibrionaceae family that causes sporadic diarrheal disease affecting travelers to Mexico, Central America, and the Far East after ingestion of raw shellfish. It produces a choleralike toxin but also has invasive potential.
  • Clinical disease. Diarrhea is usually watery, but in one third of the patients it is bloody. Abdominal pain is usually severe. Vomiting and fever may be present. Although the disease is usually over in 1 week, it may last longer than 4 weeks.
  • Diagnosis is by stool culture. Fecal leukocytes may be present.
  • Treatment is supportive. The organism has the same microbial sensitivity as Aeromonas.

Clostridium difficile

  • Epidemiology. C. difficile is a spore-forming obligate anaerobe. It is found as «normal flora» in 3% of adults, 15% of hospitalized patients, and 70% of infants in pediatric wards. It may cause disease in people of all ages, but it most frequently affects elderly and debilitated patients. The transmission is usually fecal-oral; however, it may be transmitted environmentally by spores carried on fomites or on contaminated hands of health care workers. The disease usually follows antibiotic use with disruption of the normal colonic flora. All antimicrobial agents with the exception of vancomycin and parenterally administered aminoglycosides have been linked with C. difficile enterocolitis. In most instances, the ingestion of the antimicrobial agent is within 6 weeks of the onset of the diarrhea. Case reports of C. difficile disease in patients who have not received antibiotics include patients with neutropenia or uremia, those undergoing cancer chemotherapy, and homosexual males.
  • Pathogenesis and clinical disease. C. difficile produces two major toxins. Toxin A is an enterotoxin, and toxin B is a cytotoxin used in commercial latex agglutination testing for detection of the infection. Toxin A binds to receptors on the colonic mucosal surface and causes severe inflammatory changes. The toxigenic effect is catalyzed by previously present trauma or injury to the mucosal cells. The severity of the disease varies from watery diarrhea to severe pseudomembranous colitis with bloody diarrhea, fever, and systemic toxicity.
  • Diagnosis is made by stool cultures or by the demonstration of the presence of the associated cytopathic toxin produced by C. difficile in stool samples. Fecal leukocytes may be absent in 50% of instances. Toxin assay may be negative in 10% to 20% of instances. Sigmoidoscopy, colonoscopy, and histologic examination of the mucosal biopsies support the diagnosis. Pseudomembranes, if present, are most common in the rectum and distal colon. Occasionally, however, they are present only in the transverse colon or cecum.
  • Treatment. The strategies for treatment vary according to the severity of the symptoms. Unnecessary antibiotics should be stopped. Corticosteroids and antiperistaltic agents should be avoided because they may prolong C. difficile carriage and exacerbate the diarrhea. Patients with colitis may be treated with oral vancomycin 125 mg q.i.d. for 10 days or oral metronidazole 250 mg q.i.d. for 10 days. Cholestyramine may be used in mild disease to aid in binding the elaborated toxins. Relapse after antimicrobial therapy occurs in 20% of patients within 1 week after therapy. In such patients, the eradication of C. difficile may require vancomycin 250 to 500 mg q.i.d. for 1 month or pulsed doses of therapy for 5 days each time as long as necessary. Combining rifampin 600 mg with vancomycin produces a synergistic effect. Bacterial therapeutic agents such as Lactobacillus or Saccharomyces boulardii may add additional benefit.

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