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Regional enteritis

Crohn's disease is a chronic inflammatory disease of the digestive tract and it can involve any part of it, from the mouth to the anus. more...

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It typically affects the caecum and/or the terminal ileum as well as demarcated areas of large bowel, with other areas of the bowel being relatively unaffected. It is often associated with auto-immune disorders outside the bowel, such as aphthous stomatitis and rheumatoid arthritis.

Crohn's disease should not be confused with a non-progressive and non-degenerative digestive disorder called irritable bowel syndrome (IBS), which is not an autoimmune disease. Ulcerative colitis is a sibling autoimmune disease to Crohn's but only impacts the colon while Crohn's can impact any part of the digestive tract. Furthermore, Crohn's tends to affect multiple layers of the bowel lining, which can lead to many additional and hard-to-treat complications.

Symptoms

Crohn's patients typically suffer from abdominal pain, chronic diarrhea and disrupted digestion, which may make it difficult for sufferers, particularly in the acute phase of the disease, to eat and/or digest food. The inflammation can be extremely painful and debilitating. Other common complications of Crohn's include fistulas of the colon, hemorrhoids, lipid absorption problems, and anemia. Bleeding is seen in 20% cases, against 98% cases in ulcerative colitis. Rectal bleeding may be serious and persistent, leading to anemia. Bruising of the shins, varying fever symptoms, varying levels of pain, and psychological damage is seen in many cases. Children with Crohn's disease may suffer delayed development and stunted growth.

Epidemiology

The disease typically first appears in young adults in their late teens and twenties, although it is not unknown for symptoms to first appear quite late in life. Additionally, there has been an increase in cases occurring in young children. Recent studies suggest that up to 30% of all newly diagnosed cases are in children and teens under the age of 18. Estimates suggest that up to 60,000 people in the UK (about 1 in 1200) and 1,000,000 Americans have the disease (around 1 in 300). Some ethnic groups (such as Ashkenazi Jews) have a significantly higher rate of prevalence than others. Increased rates of disease have also been noted in some families, leading to speculation of a possible genetic link (see below). Epidemiological research indicates that Crohn's belongs to the group of diseases of affluence. In other words, the incidence of the disease is much higher in industrialized countries than elsewhere. However, this finding may be associated with the fact that Crohn's symptoms are typically diagnosed over a long period of time, in order to establish a pattern; in countries where medical help is less available, it may be difficult to arrive at a diagnosis.

Smoking increases the risk of Crohn's disease. Some women find that their disease is exacerbated by taking oral contraceptives, while others find it can help keep their flare ups at bay.

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Campylobacter jejuni enteritis mistaken for ulcerative colitis
From Journal of Family Practice, 3/1/92 by Robert Cooper

Campylobacter jejuni is the most frequent bacterial cause of diarrhea in the United States, but is often not detected by routine stool cultures.[1] With the increased use of endoscopy, it is important to note that campylobacter colitis is easily confused with ulcerative colitis.

Case History

A 20-year-old white college football trainer reported to his family physician with a 2-week history of bloody diarrhea. He stated that he had had a 6.8 kg (15 lb) weight loss (10% of body weight) over the 2 weeks. There was no family history of ulcerative colitis or regional enteritis. A review of systems revealed a 2-week history of diffuse abdominal pain, but no skin rash, fever, or arthritis. Self-treatment with over-the-counter medications had been unsuccessful.

The patient was admitted to the hospital for rehydration and further diagnostic evaluation. A stool specimen was negative for ova and parasites but positive for both white blood cells and red blood cells. Urinalysis revealed an increased urine specific gravity of 1.03 and 2+ ketones. The patient's white blood count was 6.9 x [10.sup.9]/L (6900/cu mm); hemoglobin level was 164 g/L (16.4 g/dL), and the erythrocyte sedimentation rate was 30 mm/h. Manual differential of white blood count revealed 67% segmented, 1% bands, 27% lymphocytes, 2% monocytes, and 3% eosinophils. Stool cultures were ordered for Campylobacter, Yersinia, and Clostridium difficile.

Because of increasing blood loss through the rectum, the patient underwent colonoscopy, and multiple ulcerative regions were noted. No drop in the hematocrit was noted. The diagnosis given on the biopsy report was "ulcerative colitis, active phase." A second opinion was obtained; that pathologist also reported "severe diffuse colitis most consistent with ulcerative colitis."

After the results of the stool culture were reported as "no enteric pathogens," consultation was sought with a gastroenterologist, who reported seeing similar symptoms in cases of Campylobacter jejuni diarrhea. The patient was started on amoxicillin 250 mg by mouth three times daily. On recheck of the laboratory data, it was found that only the results of the routine stool culture and sensitivity tests had been reported, and that Campylobacter jejuni had in fact been cultured even though the routine culture (which tests for Salmonella and Shigella) had been negative.

The patient improved rapidly on the antibiotic regimen. He was discharged with a prescription for an additional 3 days of amoxicillin. One year later the patient had had no more episodes of diarrhea.

After discovering the correct diagnosis, the pathologist at the tertiary center presented slides of the case to his residents in a teaching conference. All of them identified the slides as a classic case of ulcerative colitis.

Discussion

The microscopic appearance of Shigella, Salmonella, Amebiasis, ischemic colitis, Crohn's disease, antibiotoc-associated colitis, and ulcerative colitis can be quite similar. If the pathologist is alerted that Campylobacter is suspected, a Steiner or Dieterle stain could be done. These silver stains are not routinely done on colitis specimens.[2-4]

Laboratories in the United States that routinely check for Campylobacter have found that Campylobacter is the most common bacterial cause of gastroenteritis.[1] Campylobacter is found in up to 17% of all bloody stool specimens submitted for culture.[1] Ulcerative colitis, by contrast, has an incidence of 2 to 7 cases per 100,000 people in the United States.[5] Campylobacter frequently causes bloody diarrhea with numerous polymorphonuclear neutrophils in the stool. Campylobacter may be isolated from the blood of infected patients, and Campylobacter produces a cytotoxin and an enterotoxin that may account for cases in which watery diarrhea occurs. Approximately 97% of patients stop excreting the organism within 4 to 7 weeks, but the other 3% may continue to excrete it for several years. Carriers are far more numerous in tropical countries than in the United States.

Campylobacter jejuni is usually transmitted through contaminated food, milk, or water. Unlike other foodborne causes of gastroenteritis, such as Salmonella and Staphylococcus, Campylobacter does not multiply in food. It is thought to be transmitted sexually in the homosexual population.[6]

A prodromal illness and blood in the stool suggest Campylobacter infection. Usually the prodrome consists of headache, fever and malaise for 1 to 2 days. Following this stage is a period usually lasting from 1 day to 1 week or longer of abdominal pain, watery or grossly bloody diarrhea, and fever to 40 [degrees] C (104 [degrees] F). This disease is usually self-limited over 4 to 5 days, but in 10% to 20% of cases it lasts 2 weeks, and even longer in 5% to 10% of cases.

In the worst cases there can be severe colitis with tenesmus, pseudoappendicitis from mesenteric lymphadenitis, toxic megacolon mimicking acute ulcerative colitis, or bacteremia. It is worth repeating, however, that most cases resolve without antimicrobial therapy.[7]

Diagnosis

With a patient who has complained of bloody diarrhea, prolonged diarrhea with or without blood, having eight or more stools a day, or rapid weight loss, a stool examination should be done. If white blood cells are present, then both a routine stool culture and Campylobacter culture should be done.[8] This sequence of cultures is cost-effective even though a special medium (Campy-BAP, a thiogrycalate base with vancomycin, trimethoprim, cephalothin, polymyxin B, and amphotericin B) and temperature (42 [degrees] C)have to be used for the Campylobacter culture. It is cost-effective because the general stool and Campylobacter cultures are only done when white cells are present in the initial examination. Also, Campylobacter causes more bacterial diarrhea than the Salmonella and Shigella organisms that are detected in the routine stool examination. Therefore, a diagnosis of the patient can be accomplished relatively quickly and economically if the preceding culture is used.[9] The differential diagnosis of Campylobacter diarrhea includes ulcerative colitis and Salmonella, Shigella, Escherichia coli, and Clostridium difficile enteritis.

Treatment

For mild cases of gastroenteritis, treatment is limited to maintaining the patient's electrolyte and fluid levels. Oral electrolyte and glucose solutions such as Gatorade will be helpful. In at least one study, strong antidiarrheal agents such as loperamide tended to prolong the illness.[10,11] They should not be used in patients with blood in the stool or high fever.[12] Bismuth preparations can provide some symptomatic relief and should be tried before stronger agents. One expert recommends two PeptoBismol tablets chewed every one-half hour, with up to eight doses administered initially.[13] In more severe cases, ie, those patients having fever, bloody diarrhea, and more than eight stools per day, or those in which diarrhea persists for more than 1 week or steadily worsens, treatment may be started immediately after stool cultures are obtained.[10]

While awaiting the results of the cultures, ciprofloxacin may be a good choice for treatment of a worsening patient. In a study[14] of 38 cases of bacterial diarrhea including 19 patients with Campylobacter jejuni, 3 with Shigella species, and 16 with Salmonella species, treatment with ciprofloxacin resulted in negative stool cultures in all patients within 48 hours. Relapse occurred in four of the patients with salmonellosis within 3 weeks after the end of treatment. When the results of the cultures are obtained, the most therapeutic and cost-effective treatment may then be decided. Ciprofloxacin, however, is contraindicated in pregnant women and children.[15] Other antibiotics that may be useful once the diagnosis of Campylobacter jejuni is established include erythromycin (the drug of choice in children), doxycycline, furazolidine, and amoxicillin.[11,16-23]

Summary

A patient with serve prolonged diarrhea with stool positive for white blood cells but negative for ova and parasites should have comprehensive stool culture performed that include examination for Campylobacter. Ciprofloxacin 500 mg by mouth twice daily for 5 days is the suggested therapy for Campylobacter jejuni, and if the patient's condition is severe enough, it can be started white the cultures are pending. One must always remember that the microscopic biopsy appearance and clinical presentation of Campylobacter jejuni and ulcerative colitis are quite similar.

Acknowledgments

This paper is dedicated to the memory of Dick Nowell, MD, who served as the consultant gastroenterologist on the first case reported in this paper.

Appreciation is expressed to Jackie Tutor, RN, for her contributions to this manuscript.

References

[1.] Feingold SM, Boron EJ. Diagnostic microbiology. 7th ed. St

Louis: CV Mosby, 1986:461-5. [2.] Blaser MJ, Parsons RB, Wang W-LL. Acute colitis caused by

Campylobacter fetus ss jejuni. Gastroenterology 1980; 78:448. [3.] Chandra L, Barrowman, JA, Kutty KP, et al. Campylobacter infection

mimicking a relapse of ulcerative colitis. J Can Med Assoc

1982; 126:389. [4.] Loss RW, Mangla JC, Pereira M. Campylobacter colitis presenting

as inflammatory bowel disease with segmental colonic ulcerations.

Gastroenterology 1980; 79:138. [5.] Wyngaarden JB. Cecil textbook of medicine. 17th ed. Philadelphia:

WB Saunders, 1985. [6.] Perlman DM. Persistent Campylobacter jejuni infections in patients

infected with human immune deficiency virus (HIV). Ann Intern

Med 1988; 108:540-6. [7.] Breeling JL. Newly recognized bacterial causes of infectious diarrhea.

Infect Disease Pract 1989; 12(4):1-7. [8.] Lopez WC, Ferrante WA. Acute diarrhea. Primary Care Emerg

Decis 1988; 4(3):1. [9.] Alpers DH, Greenbury JL, Sodenon WA. Gastroenteritis treatment

tips. Patient Care 1990; Mar 30:18-31. [10.] Dupont HL. Subacute diarrhea: to treat or wait. Hosp Pract 1989;

Mar 30:111-8. [11.] Bruckstein AD. Diagnosis and therapy of acute and chronic diarrhea.

Postgrad Med 1989; 86:151-9. [12.] Gorbach SL. Travelers' diarrhea. JAWA 1985; 253:2700-4. [13.] Rosenthal M. Rational approach to the pathogens of diarrhea.

Infect Dis News 1990; 3(7):21-2. [14.] Pichler HET, Diridl G, Stickler K, Wolf D. Clinical efficacy of

ciprofloxacin compared with placebo in bacterial diarrhea. Am J

Med 1987; 82(suppl 4A):329-32. [15.] Physicians' Desk Reference. 45th ed. Oradell, NJ: Medical Economics

Co, 1991:1542. [16.] Van Der Auwera P, Scorneaux B. In vitro susceptibility of Campylobacter

jejuni to 27 antimicrobial agents and various combinations

of B-lactams with clavulanic acid or sulbactam. Antimicrob

Agents Chemother 1985; 28:37-40. [17.] Anders BJ, Paisley JW, Lauer BA, et al. Double-blind placebo

controlled trial of erythromycin for treatment of Campylobacter

enteritis. Lancer 1982; 1:131-2. [18.] Pitkanen T. Pettersson T, Ponka A, et al. Effect of erythromycin on

the fecal excretion of Campylobacter fetus subspecies jejuni. J Infect

Dis 1982; 145:128. [19.] Mandel BK, Ellis ME, Dunbar EM, et al. Double-blind placebo-controlled

trial of erythromycin in the treatment of clinical Campylobacter

infection. J Antimicrob Chemother 1984; 13:619-23. [20.] Robins-Browne RM, Mackenjie MKR, Bodasing MN, et al.

Treatment of Campylobacter-associated enteritis with erythromycin.

Am J Dis Child 1983; 137:282-5. [21.] Pai CH, Gillis F, Tuomanen E, et al. Erythromycin in treatment of

Campylobacter enteritis in children. Am J Dis Child 1983; 137:

286-8. [22.] Nolan CM, Johnson KE, Coyle MB, et al. Campylobacter jejuni

enteritis: efficacy of antimicrobial and antimotility drugs. Am J

Gastroenterol 1983; 78:621-6. [23.] Salazar-Lindo E, Sach RB, Chea-Woo E, et al. Early treatment

with erythromycin of Campylobacter jejuni-associated dysentery in

children. J Pediatr 1986; 109:355-60.

COPYRIGHT 1992 Dowden Health Media, Inc.
COPYRIGHT 2004 Gale Group

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