Understanding fecal incontinence requires knowledge of the normal function of the anorectum. Anatomically, it consists of the internal anal sphincter surrounded by the external anal sphincter and puborectalis muscles. The internal anal sphincter consists of smooth muscle and is a continuation of the circular smooth muscle of the rectum. The external anal sphincter is made up of skeletal muscle and surrounds the internal anal sphincter, whereas the puborectalis (also consisting of skeletal muscle) is a large U-shaped muscle that wraps around the upper anal canal at the anorectal junction above the external anal sphincter and loops anteriorly to attach to the pubic bone. This creates an anatomical sling of muscle that pulls the anorectal junction forward when it tightens, thus closing the upper anal canal and creating the anorectal angle that is vital to the maintenance of fecal continence.

When stool (or gas or liquid) enters the rectum or sigmoid colon, a normal rectoanal inhibitory reflex (RAIR) or rectosphincteric reflex is initiated – that is, the internal anal sphincter relaxes and, if voluntary muscle action occurs, the rectum empties through the anal canal (Figure 2). Fecal continence is maintained by contraction under voluntary control of the striated-muscle sphincters – i.e., the external anal sphincter (EAS) and puborectalis (PR) – until the rectal pressure rise decreases and the resting tone of the internal anal sphincter is restored. Thus, the “voluntary” sphincters (i.e., the EAS and PR) have the ability to be maximally contracted for approximately one minute, beyond which fecal continence is lost as a result of fatigue in the muscle if the tone of the internal anal sphincter has not recovered.

The patient with fecal incontinence will often describe the problem as “diarrhea” rather than loss of control of bowel function. All patients with a complaint of diarrhea should be asked if they have lost control of stool, as this may indicate where the problem actually lies. Once fecal incontinence has been noted, it is then necessary to identify the frequency of the incontinence, whether both liquid and solid stool have been leaked and whether the individual has an urge to defecate before the leakage occurs. A history of previous anorectal trauma (surgical or otherwise) is important to note, as is the strength of voluntary anal canal tone on digital rectal exam.

Most patients presenting with fecal incontinence have “idiopathic” fecal incontinence, but recent investigations in females with this complaint indicate they have suffered damage to the pudendal nerves during childbirth and, with time, this has led to gradual striated-muscle anal sphincter weakness. Surgical trauma is the next most common cause of fecal incontinence; it should be remembered that surgery (e.g., a vaginal hysterectomy) can put excess stretch on the pelvic floor nerves and muscles, causing injury that may lead to weakness of the anal sphincters. Another common source of fecal incontinence is disruption of the internal anal sphincter, either during a lateral internal sphincterotomy to treat an anal fissure or, more commonly, with the older “Lord’s” procedure of forceful three-or four-finger dilation of the anal sphincter under anesthetic, where the extent of damage to the sphincters is not predictable. The finding of perineal descent can be noted on examination of the perineum when the patient is asked to strain and appears to be associated with weakness of the pelvic floor muscles as well as disruption of the normal anatomy. This gives rise to a mechanical disadvantage affecting the sphincter mechanism. Perineal descent may be associated with a rectocele or, in female patients, with a uterine prolapse. Rectal prolapse can also accompany weakness of the pelvic floor muscles and give rise to fecal incontinence.

Therapy of fecal incontinence has improved over the past decade, primarily because of the introduction of biofeedback training. This technique allows the patient to practice tightening of the striated-muscle portion of the anal sphincter, usually with a surface electromyography (EMG) plug electrode held in the anal canal with audio and visual feedback that the patient can see and hear to encourage maximal contraction of these muscles. Attention should also be given to increasing dietary fiber to help reduce the amount of liquid stool. Other drug therapy is limited, but loperamide has been shown to increase the resting tone of the anal sphincters and is a useful adjunct, especially if the stool frequency is increased (loperamide reduces this contributing factor). Cholestyramine may be useful when the patient has diarrhea or loose stool(s) since cholestyramine can make stool more solid (constipating effect). Surgery is sometimes required and is of greatest benefit in those patients who appear to have a mechanical problem such as rectal prolapse or disruption of the sphincter. Surgery to correct perineal descent is often less helpful, since the problem of muscle weakness that gives rise to the descent is not satisfactorily reversed by any of the surgical procedures currently used, and attempts to “suspend” the pelvic floor muscles cannot strengthen these muscles. Patients should refrain from excess straining if they have significant perineal descent, since this will serve only to worsen the pelvic floor muscle weakness.

In the approach to a patient with constipation, it is first necessary to define what the patient means by the term. Many definitions exist, but the best clinical definition is that over 95% of the North American population has a stool frequency from three times a day to three times a week: therefore, patients who have a bowel frequency less than three times a week would be defined as being constipated. Many patients will describe their stool as “constipated,” usually meaning that the stool is hard or in pellets (scybalous), while other patients may have a stool frequency that falls within the “normal” range yet feel that their bowels have not completely emptied. This latter symptom is a frequent complaint of the irritable bowel syndrome, and many patients with this disorder will describe a constipated bowel habit. Those constipated patients who have infrequent stool alternating with occasional diarrheal stool have the most common presentation of irritable bowel syndrome. Yet there are a great many patients, almost all female, who have infrequent stool passage, and this group must be considered as separate from the usual irritable bowel syndrome patient for they may be among those rare patients with a secondary cause of constipation.

In Western culture the most frequent cause of constipation is a lack of dietary fiber. The concept of “fiber” has become quite confusing to many patients with the increased emphasis on “oat fiber” for elevated cholesterol treatment. Many foods that patients consider to be high in fiber (e.g., salads, lettuce, tomatoes and celery) are in fact mainly water, and some vegetables may aggravate their symptoms. Fiber is complex carbohydrates that are incompletely digested by the small bowel and are then “digested” by colonic bacteria, liberating fermentation gases and short-chain fatty acids that may provoke and aggravate many of the associated abdominal symptoms (e.g., abdominal pain, “gas” and bloating). It should be emphasized that cereal grain fibers that have more insoluble fiber (as opposed to soluble oat bran fiber) are best to increase stool frequency, but should be added gradually over 8 to 12 weeks to a daily dose of about 30 g. Other fibers in the form of “bulk laxative” preparations containing psyllium, methylcellulose Sterculia or isphagula may be added to wheat bran fiber to accomplish this level of fiber without completely altering a patient’s diet. Many patients who are constipated continue to pass dry, hard stool despite an increase in dietary fiber because they do not increase the water content of their diet. Fiber works in the gut by holding onto water and keeping the stool soft; to achieve this effect, the intake of liquids must be increased. For a 30 g/day fiber diet, it is recommended that patients drink eight 8 oz. glasses (i.e., 2 L) of non–caffeine-containing beverages per day.

Secondary causes of constipation must be excluded. The patient with bowel obstruction can present with constipation, and this possibility should always be considered in a patient with the onset of constipation after the age of 40 years (when the incidence of colon cancer rises). A rarer cause of constipation is hypothyroidism; not infrequently, patients with an underactive thyroid will present with a primary symptom of constipation. Hypercalcemia rarely reaches levels that produce constipation but should always be considered, since it can be a life-threatening disorder; constipation in this setting is always resistant to therapy until the hypercalcemia is treated. Proctitis can present with a complaint of infrequent stool passage due to the functional obstruction caused by the inflammation of the rectum; the colon more proximally continues to produce formed stool, which cannot pass easily through the inflamed rectum. Proctitis will usually be associated with excess mucus production, with or without blood in the stool, and proctosigmoidoscopy will always diagnose this entity.

Another cause of constipation is diabetes mellitus, often as a result of impaired motility; dietary factors may also play a role, along with autonomic neuropathy of the enteric nervous system. A small proportion of these diabetic patients with constipation can go on to develop diarrhea, which again has been linked to the autonomic neuropathy seen with long-standing diabetes mellitus.

Inactivity from whatever cause seems to increase the likelihood of a patient’s complaining of a constipated bowel habit. This is presumed to be secondary to reduced colonic activity but could be aggravated by a low fiber intake in many of these patients. Severe cardiopulmonary diseases of whatever cause that limit activity can result in constipation. Neurologic disorders that cause the patient to have a reduced ability to ambulate can have constipation as a feature. Some patients with diseases of the nervous system may have impaired awareness of rectal distention to signal a need to defecate, and nerve dysfunction (both peripheral and central) may impair normal colonic propulsion. Finally, the elderly may develop problems with defecation, and although constipation with fecal impaction occurs they may complain of “diarrhea” or “soiling” due to overflow incontinence of stool from the fecal impaction of the rectum inhibiting the normal resting tone of the anal sphincter. Not surprisingly, many of these patients may respond to laxative therapy after the fecal impaction is removed, since this prevents the recurrence of the fecal impaction with overflow incontinence. Some patients can aggravate long-standing constipation with regular laxative abuse, and some theoretical concerns remain that this practice may indeed damage the normal innervation of the colon, rendering it atonic and nonfunctional.

The physical findings are often minimal in the majority of patients with constipation, but specific secondary causes must be looked for. Signs of hypothyroidism may be present; signs of dehydration should be sought, as this may be an early indicator of hypercalcemia. Thorough cardiopulmonary and neurologic examinations are necessary to pick out associated diseases that may be treated, thereby improving the patient’s overall health and thus improving bowel function. On abdominal examination, inspection for evidence of distention or hyperperistalsis or masses may point out the source of the impaired stool passage. Localized tenderness of the abdomen must be noted, along with any evidence of liver, spleen or renal enlargement. A complete rectal examination and proctosigmoidoscopy is required in any patient with constipation so that the presence or absence of a fecal impaction, dilation or enlargement of the rectum or the presence of proctitis can be determined.

When the rectum is enlarged, further investigations are required to exclude other causes, particularly Hirschsprung’s disease (Section 3.6.2). The majority of patients with constipation and a dilated rectum and/or colon at proctosigmoidoscopy or barium enema have idiopathic or acquired megarectum. A useful guideline for the diagnosis of a “megarectum” is a rectal diameter of greater than 6 cm on a lateral film at the level of the S2 vertebral body. These patients can often present in childhood (many of them presenting with encopresis) and in the elderly with a fecal impaction. The cause of the megarectum is unknown, but if the onset is in childhood it may be the result of chronic stool holding by the child, leading to progressive distention of the rectum and eventual loss of awareness of rectal distention. Once this has occurred the patient can no longer recognize when stool is present in the rectum; the distention of the rectum causes chronic inhibition of the resting tone of the internal anal sphincter. This leads to the loss of control of liquid or semisolid stool that passes by the fecal impaction without the patient being aware of it.

The majority of patients with this disorder present soon after birth or in early childhood. This is a lesion, present at birth, where variable lengths of distal colon have no myenteric plexus. The distal colon remains contracted and the normal proximal colon dilates as it fills with stool. Most of these patients present early in life with obstipation and colonic obstruction, and require surgery. However, a few patients have a very short segment of denervated distal colon, so that they can overcome the obstruction and force stool out of the rectum. They usually have lifelong constipation; the normal rectum proximal to the denervated segment dilates over time so that the patient presents with constipation and a “megarectum.” These patients rarely have fecal incontinence or fecal “soiling” as seen with idiopathic megarectum, since the internal anal sphincter and denervated distal rectum maintain a high resting tone. This condition can be diagnosed by anorectal manometry in that a normal rectoanal inhibitory reflex cannot be identified (Figure 2). However, a definite diagnosis requires deep rectal biopsy from the denervated segment, which will show absence of the myenteric plexus ganglion cells and hypertrophy of nerve fiber bundles. It should be added that an identical condition can be acquired with Chagas’ disease from South America, which attacks the myenteric plexus and other autonomic ganglion cells; patients with this condition can also present with achalasia or intestinal pseudo-obstruction as well as cardiac arrhythmias. These patients will also have an absent rectoanal inhibitory reflex if the disease involves the rectal myenteric plexus.

The majority of patients with constipation have a form of irritable bowel syndrome, but there is a small subgroup of patients who may have a specific disorder in colonic and/or anorectal function that produces constipation. These patients are almost all female, may have delayed colonic transit or present with anorectal dysfunction with impaired awareness to rectal distention (without a megarectum), or may demonstrate a phenomenon of rectal outlet obstruction due to inappropriate contraction of the voluntary anal sphincters during defecation. This has been termed pelvic floor dyssynergia or anismus. These patients can present major therapeutic dilemmas and warrant further investigation in specialized coloproctology units involved in the care of such patients.

3.7.1 SHIGELLA

This infectious diarrhea is the classic cause of “bacillary dysentery.” Typical presentation is with fever, abdominal cramping and watery diarrhea that usually becomes bloody within 24 to 48 hours of onset. The incubation period is from 36 to 48 hours. As the disease progresses the symptoms become typical of colonic dysentery, with small, frequent stools and cramping and tenesmus that may lead to rectal prolapse in some individuals with prolonged straining.

The causative organism is a gram-negative bacterium with only humans as its host. The organism is well adapted to causing disease in humans. As few as 200 organisms are needed to cause infection as compared with other enteric infections requiring 10⁶ organisms or more. It can persist in food for weeks and on contaminated body surfaces for several hours. Pathogenesis is through production of a cytotoxin called Shiga toxin or similar toxins that are both cytotoxic and neurotoxic, very similar to the toxin produced by E. coli 0157:H7 species. Shigella is a microinvasive bacterium that enters the host via the M cells in the intestine and then spreads laterally through the colonic mucosa to involve the basolateral membrane of the surrounding cells. It is seen mostly in travelers returning from endemic areas (tropical and subtropical). There is also a higher incidence in male homosexuals who practice oral–anal sex.

Treatment depends on the antibiotic resistance of the infecting strain of bacteria. Shigella species quickly develop antibiotic resistance; patients should be encouraged to complete their course of antibiotics to prevent this. Antibiotics shorten the duration of both symptoms and carriage of the organism. Fluoroquinolones are the antibiotics of choice because of the low incidence of resistance at present, but this may change. Ampicillin and trimethoprim-sulfamethoxazole are also effective against sensitive strains. If infection has been acquired overseas, a confirmed Shigella infection is best treated with a fluoroquinolone twice daily for 5 days, but there are reports of a single large dose eradicating infection. Antimotility agents such as loperamide, diphen-oxylate or narcotic analgesics are contraindicated with this infection because of the risk of a toxic colon. In general, antimotility agents should never be used in acute infectious diarrhea when bloody stool is present.

Infection with nontyphoidal strains of Salmonella results from ingesting foods contaminated with organisms. These bacteria are endemic to poultry and cattle populations. Large epidemics have resulted from undercooked eggs, and these bacteria are also frequently found in reptiles and amphibians. Salmonella contamination of marijuana can be an important infection source in young adults. The usual incubation period is from 8 to 48 hours after ingestion.

S. typhi, which causes typhoid fever, is found only in humans. It will not be discussed further other than to emphasize that all Salmonella species are related and therefore can cause systemic illness of similar severity, especially in patients who are immunocompromised and those at the extremes of age (i.e., those under 2 and the frail elderly).

Salmonella is an invasive bacterium that can cause septicemia after first multiplying in the mesenteric lymph nodes. Resistance to infection is first a result of the presence of gastric acid and then of the integrity of the intestinal flora and of motility. Increased infection is associated with the use of purgatives, antimotility agents and broad-spectrum antibiotics along with acid-suppression therapy. Bowel surgery will also increase the chance of symptomatic infection. Diseases that predispose to infection as a result of impaired host defenses include sickle cell disease, systemic lupus erythematosus (SLE) and AIDS.

Treatment is usually symptomatic. Antibiotics should be used only if the patient is showing signs of bacteremia; antibiotics often increase the development of a chronic carrier state. The antibiotics of choice are ampicillin and trimethoprim-sulfamethoxazole, but recently the fluoroquinolones and the third-generation cephalosporins (especially ceftriaxone with its high biliary excretion) have been shown to be very effective in patients who need antibiotic therapy. Treatment with antibiotics should normally be considered only for patients under the age of 2 years and elderly patients with vascular disease, as well as patients with metal implants in bones, lymphoproliferative disease, sickle cell disease or AIDS. The site of chronic infection is usually the biliary tract. Disease of the biliary tree, especially cholelithiasis, requires surgery to correct the disease followed by a two-week course of therapy, which often leads to resolution of the chronic carrier state.

This spore-forming anaerobic gram-positive bacterium is the commonest cause of infectious diarrhea in hospitalized patients. The organism is not invasive, but with reduction of the normal colonic bacterial flora it multiplies and produces two toxins, known as toxins A and B. Toxin A causes colitis. Toxin B is a cytotoxin that is often used as a diagnostic test for this infection.

Most commonly, infection is preceded by antibiotic therapy. Outbreaks in hospital frequently occur among the sickest patients, some not receiving antibiotics beforehand. Penicillins, cephalosporins and clindamycin are more likely to be associated with C. difficile infection, but all antibiotics, including metronidazole and vancomycin, have been associated with it. Other risk factors include agents that affect gut motility such as enemas and anti-diarrheal medications, and intensive chemotherapy. Patients with severe illnesses and advanced age are also more prone to manifest disease symptoms.

Diarrhea is the commonest symptom of presentation and is usually nonbloody, but with prolonged diarrhea some blood can result from local anorectal irritation. The typical appearance at endoscopy of the colon and rectum is of “pseudomembranes” or whitish plaques on the surface of the colonic mucosa with intervening areas of mucosa that appear almost normal. For this reason, infection is often called “pseudomembranous colitis” (PMC). Unfortunately, these characteristic changes may not be present in the rectum, so diagnosis is usually confirmed by the presence of cytotoxin in the stool placed on tissue culture. The clinician must be alert to the possibility of this infection in susceptible patients since in some patients, neither culture of C. difficile nor the presence of the cytotoxin in the stool is positive. A careful inventory of any antibiotic therapy in the last three months is crucial in considering this cause for diarrhea, as many patients will have taken the offending antibiotic several days to weeks before symptoms begin.

Metronidazole (FlagylŪ) treatment is preferred to vancomycin because both antibiotics show similar efficacy in treating this infection and metronidazole is about one-tenth the cost of vancomycin. Treatment is for 7 to 10 days, usually in a dose of 250 mg p.o. q.i.d. in the studies that have been reported. The vancomycin dosage is 125 mg p.o. q.i.d. but is effective only via the oral route, whereas metronidazole is also effective intravenously in the occasional patient with postoperative ileus. With both regimens there is a high relapse rate of infection, of up to 20%. The best method to prevent relapse is unknown, but relapsing symptoms may respond to retreatment of the infection with either metronidazole or vancomycin.

Entamoeba histolytica, the parasite that causes amebiasis infection, appears to be the only ameba that causes disease in humans. Other amebas are often found in the colon as normal commensals. E. histolytica is a cyst-forming parasite, but the cysts do not cause disease. The cysts are ingested and are protected by gastric acid; then the trophozoite develops in the colon from the ingested cyst. The cysts spread disease to others, and frequently unaffected carriers spread disease by excreting cysts. The trophozoites, which invade the colonic mucosa, cause disease, but trophozoites passed in the stool of symptomatic individuals cannot survive outside the body and rarely transmit infection. The disease is most prevalent in areas of the tropics where sanitation is poor.

The colon is the usual site of initial disease. Invasion of the mucosa by trophozoites is due to the production of an “amebapore” molecule that causes the lining colonocytes to lyze; the lyzed colonocytes are then ingested by the amebas, leading to ulceration of the colon and dissemination throughout the body. The amebas infect the colon and rarely the ileum, but the cecum is usually involved. E. histolytica is an invasive pathogen and can spread hematogenously to other organs, especially the liver.

Diagnosis is usually made by identification of E. histolytica on microscopic analysis of stool, but can also be made on identification of the ameba on histological diagnosis of colonic biopsies. There is a decreased yield on stool analysis after barium studies and if antibiotics or mineral oil is used prior to collection. At endoscopy the ulcers of the rectum and colon may appear characteristic with undermined edges, and sometimes the intervening mucosa looks normal in contrast to acute bacillary dysentery (see Section 3.7.1) and ulcerative colitis. Diagnosis can also be made by indirect hemagglutination and ELISA tests on serum to detect infection, but if the patient is a carrier with only cyst excretion these tests are often negative. Chronic infection of the cecum leads to a “coned” appearance on x-ray. Other colonic complications include perforation, ameboma (a granulomatous tissue reaction in the colon; the mass effect can lead to obstruction or be mistaken for colonic malignancy), pericolic abscess and fistulas. The liver is the commonest extraintestinal organ infected, but E. histolytica can also spread to the brain, lungs, pericardium and eyes. There is an increased risk of disseminated disease and abscess formation if the patient is on steroids, is pregnant or is immunocompromised.

Treatment is usually metronidazole 400–750 mg t.i.d. x 5–10 days for acute colitis. If the patient has chronic colonic disease with chronic shedding of cysts, diloxanide 500 mg t.i.d. x 10 days is the drug of choice. If this cannot be obtained, then iodoquinol 650 mg t.i.d. x 20 days can be used, but this is the maximal dose because it can cause optic neuritis. Patients with amebic liver abscess should first be treated with metronidazole for 10 days and then be given 10 days of diloxanide. All patients should be reassessed two to three months after treatment to ensure clearance of the parasite and that there is no chronic carrier state with cyst excretion.

A very large, ciliated protozoan that uncommonly causes an illness similar to amebic dysentery, B. coli is usually easy to identify in stool samples owing to its large size. It is acquired in tropical or subtropical countries from exposure to pigs, which frequently carry this organism without signs of illness. Treatment is with tetracycline 500 mg q.i.d. for 10 days. B. coli is also sensitive to ampicillin and metronidazole.

A yeast frequently found in asymptomatic individuals, recently B. hominis has been suggested as a cause of unexplained diarrhea in some patients found to have large numbers of this protozoan in the stool. Treatment appears to be with either metronidazole 750 mg t.i.d. x 10 days or iodoquinol 650 mg t.i.d. x 20 days. Iodoquinol may be more successful, but the best treatment has not been identified to date.

3.8.1 ROUNDWORM (ASCARIS LUMBRICOIDES)

Roundworm or ascaris, one of the more common nematodes found in humans, is most often found in the tropics. Usually eggs are ingested from contaminated foods or dirty hands. The eggs hatch in the intestine and spread by the blood to the liver and then to the lungs. An eosinophilic pneumonitis can develop and then the larvae migrate through the alveoli, up to the trachea and through the larynx where they are swallowed. They develop into adult worms in the small intestine. The adults can cause intestinal obstruction symptoms if large numbers are present, and can cause biliary symptoms if they migrate into the common bile duct.

Hookworm can infiltrate skin from contaminated earth and is prone to be found in areas with fecal contamination of the soil. A pruritic rash develops at the site of entry into the body. The filarial larvae then travel to the lungs, migrate through the alveoli and then up through the larynx where they are swallowed. After being swallowed, they cause nausea, diarrhea, vomiting, abdominal pain and flatulence. Many patients present with iron deficiency from a daily blood loss of 0.1–0.4 mL with each worm.

Whipworm can also cause iron deficiency if large numbers infect the GI tract. It primarily invades the colon. Bloody diarrhea develops with larger infestations. It is easily diagnosed by stool analysis looking for the typical eggs, but is increasingly diagnosed at colonoscopy during investigation of the bloody diarrhea, where the worms are easily seen if present.

Pinworm is probably the commonest nematode worldwide. It usually causes pruritus ani, often worse at night when the worms migrate onto the perianal skin and lay their eggs. Pinworm is probably the most common nematode encountered in Canada, especially in children. Diagnosis is by identification of the eggs from the perianal skin, usually collected in the early morning before defecation.

Strongyloides stercoralis is widely found in the tropics. It is the only nematode that can multiply and reproduce its entire life cycle within the human host, thus causing persistent reinfection over many years after the original infection. Larvae can penetrate intact skin or the eggs can be ingested. Filariform larvae that penetrate the skin travel hematogenously to the lungs and then, as with the other worms, travel into the airways and are swallowed. In the intestine the larvae become adult worms. When the eggs are ingested, they become filariform larvae in the intestine; then the larvae invade the blood vessels, thus reinfecting the host.

Symptoms of strongyloidiasis vary and may include abdominal pain, diarrhea, nausea and vomiting. With mostly intestinal involvement diarrhea can develop; especially in children, a syndrome similar to celiac disease with protein-losing enteropathy can develop. The majority of adult infections are asymptomatic or are only intermittently symptomatic. Recurrent urticaria can develop where the worms infiltrate the skin, particularly the perianal skin and gluteal areas.

Diagnosis can be confirmed by stool analysis but can be negative in up to 25% of cases, even after repeated stool analysis. The larvae look similar to hookworm. An ELISA test is useful for diagnosis, but there may be overlap with the presence of Filaria species. Eosinophilia is often present, even in asymptomatic individuals.

Thiabendazole is usually used to treat, 25 mg/kg twice daily to a maximum of 3 g daily for two days, or five days for disseminated disease. Albendazole or ivermectin may be used if the patient is unable to tolerate thiabendazole, but these drugs appear to be less effective against S. stercoralis. With the hyperinfection syndrome, when large numbers of the worms are present (often in association with immune suppression, as with steroid therapy), antibiotics are often needed to treat the septicemia that results if the intestinal damage allows secondary bacterial invasion.

A rare condition has been recognized increasingly in which the patient presents with usually painless diarrhea. Investigations often find signs of inflammation, but the colon appears normal on both radioscopic and colonoscopic examination. This condition is sometimes called “lymphocytic colitis” and may also be part of a spectrum of colitis conditions that include “collagenous colitis.” The natural history of these diseases is unclear at present, and no infective agent has been found. These disorders can be diagnosed only by colonoscopic biopsy. The colonic mucosa appears normal, yet on histological examination there is an increase in the inflammatory infiltrate of the lamina propria. In collagenous colitis the basement membrane of the colonic mucosa is thickened by a band of collagen. In most patients the disease appears to follow a benign course, but about half of patients continue to have significant diarrhea for more than two years. The disease is controlled by antimotility agents such as loperamide or by use of 5-aminosalicylic acid–based therapies directed at the colon (see Chapter 10, “Inflammatory Bowel Disease”), which often help to lessen the diarrhea. Glucocorticoids also control the diarrhea, but in view of the benign course of this illness in most patients, steroid therapy should be used only in severely symptomatic patients who cannot be controlled by other therapy.

Eosinophilic gastroenteritis is an uncommon inflammatory condition that affects primarily the upper GI tract and small intestine (see Chapters 5, 6 and 7). However, there have been recent reports of an apparently separate condition called “eosinophilic colitis” in which patients with connective tissue disease present with diarrhea of uncertain cause with negative stool investigations. These patients have all been diagnosed at colonoscopy by biopsy of essentially normal-looking mucosa, yet with increased eosinophils in the lamina propria. All patients respond to steroids, but it would appear that not all patients resolve over time and some may need prolonged steroid therapy.

RETURN to Part 1 of this subsection.