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PubMed1979

Pathology of salmonella colitis.

Salmonella colitis was encountered in eight patients. In seven, the disorder simulated ulcerative colitis both clinically and radiologically. The salmonella infection in the eighth patient was superimposed upon hitherto unrecognized ulcerative colitis. In mild cases the histological appearances of rectal biopsies were nonspecific, consisting of edema of the mucosa with focal inflammatory cell infiltration. More severe cases were characterized by neutrophils infiltrating the walls of degenerating crypts, and in one case there were microthrombi in the mucosa. One patient who was thought to have fulminant ulcerative colitis had a hemicolectomy. The resected specimen exhibited marked hemorrhage and ulceration. There were crypt abscesses in unulcerated areas but there was also extensive necrosis of the mucosa, hemorrhage in the mucosa and submucosa, and microthrombi extending from small vessels in the mucosa into venules in the submucosa similar to the picture seen in acute ischemic colitis. In this case there was intense edema and inflammation in the submucosa as well as in the mucosa.

Abscess↗
PubMed1976

Salmonella typhimurium colitis.

A patient in whom Salmonella typhimurium infection caused a localised colitis is described. Colitis has been demonstrated in experimental animals infected with S. typhimurium and noted at post mortem in patients dying from S. typhimurium infection. However colitis is an infrequently recognised feature of this infection in man, the usual diagnosis being one of gastroenteritis. There have been four other cases reported with radiological evidence of colonic involvement due to salmonella infection. Colitis probably occurs more frequently than is usually recognised in this condition and must be distinguished from ulcerative colitis.

Adult↗
PubMed1979

Campylobacter colitis.

Eleven consecutive patients with diarrhoea from whose stools campylobacter were isolated were investigated by sigmoidoscopy and rectal biopsy. Eight had definite proctitis, and in seven biopsy specimens were abnormal with histological changes ranging from non-specific colitis to gross colitis with goblet-cell depletion and crypt-abscess formation. Nine of the patients passed blood in their stools, and in all but one abdominal pain was a feature of the illness. Severe campylobacter colitis may be clinically, sigmoidoscopically, and histologically difficult to differentiate from ulcerative colitis and is a differential diagnosis in acute colitis.

Adolescent↗
PubMed1979

Light and electron microscopic studies of antibiotic associated colitis in the hamster.

Lincomycin and its analogue, clindamycin, are capable of producing mild to severe colonic mucosal injury in humans (antibiotic associated colitis). Patients with the disorder may have severe diarrhoea, pseudomembranous plaques, confluent pseudomembranes, and/or a frank, diffuse haemorrhagic colitis. The present study was designed to assess the Golden Syrian hamster as an animal model for antibiotic associated colitis and to describe lesions seen in the animal model by light, transmission electron, and scanning electron microscopy. A colitis was produced in Golden Syrian hamsters by oral or parenteral administration of lincomycin, clindamycin, or N-demethyl clindamycin. Animals were killed at intervals and microscopic studies made of sequential morphological changes in the ileum, caecum, and colon. The microscopic lesions in the early stages of the disorder were abnormalities within the brush border, cellular oedema, and hyperaemia. Changes in the intracellular organelles were observed in more severely damaged epithelial cells. Epithelial hyperplasia resulted in the piling up of cells on the mucosal surfaces. In specimens with the most severe damage, complete loss of epithelium from the mucosal surface was observed. Pseudomembranous plaques were occasionally seen. Comparison of the clinical, gross, and histological features of the animal disease with the human disorder suggest that, although minor differences are present, the hamster model is suitable for experimental studies of antibiotic associated colitis.

Animals↗
PubMed1975

Bacterial studies of Clindamycin-associated colitis. A preliminary report.

The cause of pseudomembraneous colitis is not known but has been attributed to an alteration in the microbial flora of the colon. To test this hypothesis, a blind, prospective study was undertaken in which fecal samples were cultured quantitatively for aerobic and anaerobic organisms. The patients from which these samples were taken were all receiving clindamycin and had diarrhea secondary to the use of the drug. We were able to show definite differences in the colonic microflora which correlated with the presence of pseudomembranes on biopsy. Those patients who had diarrhea and pseudomembranous colitis showed a striking decrease, both quantitatively and qualitatively, in the number of anaerobes present. Those patients who had diarrhea but no pseudomembranes had large numbers of anaerobes which qualitatively approximated normal fecal cultures but quantitatively were fewer in number. A third group of patients, which had resolving pseudomembranous colitis, and were no longer symptomatic, had large numbers of anaerobic organisms which approximated those found in normal fecal cultures. There were no differences among the three groups with regard to facultative anaerobic microflora. Thus, the presence of pseudomembranous colitis correlated directly with a striking quantitative and qualitative decrease in the anaerobic microflora of the colon. The symptom of diarrhea alone appeared to have no meaning with regard to changes in the bacterial flora. Resolution of pseudomembranous colitis was associated with a return of the anaerobic microflora.

Bacteroides↗
PubMed1975

Growth retardation in children with ulcerative colitis: the effect of medical and surgical therapy.

The growth of 37 children with ulcerative colitis have been analyzed. While conventional growth charts showed only percentile changes in height, height data plotted on Tanner et al.'s growth charts showed increases and decreases in growth velocity. Growth retardation is a prominent complication of ulcerative colitis with onset on bowel symptoms. Both ulcerative colitis and "high-dose" steroid therapy (greater than 12 mg/sq m/day of cortisol) can hinder growth but in some instances there is a growth spurt after high-dose steroid therapy. "Low-dose" steroid therapy does not retard growth. Colectomy is more effective than high-dose steroid therapy in reversing the growth retardation caused by ulcerative colitis and is of greatest value if not delayed too long. Growth following subtotal colectomy with ileorectal anastomosis (Aylett procedure) is not likely to be as much as that after subtotal colectomy with ileostomy. Growth retardation is infrequently the only indication for surgical intervention but ileostomy and colectomy are appropriate for this complication of ulcertive colitis in itself when not improved by adequate medical treatment.

Adolescent↗
PubMed1978

Protective effect of metronidazole in experimental ulcerative colitis.

Administration of carrageenan to guinea pigs produces colonic lesions which are similar to those noted in idiopathic ulcerative colitis of human beings. This model was used to determine fecal flora changes and response to antimicrobial probes during the evolution of carrageenan-induced colitis. The results of fecal flora analysis showed that mean coliform concentrations increased from 10(2.7) to 10(7.4) per g during the initial stages of colonic ulceration. Pretreatment of carrageenan recipients with antimicrobials directed against coliforms reduced the concentrations of these organisms, but failed to attenuate the disease process. On the other hand, pretreatment with metronidazole, an antimicrobial primarily active against anaerobic bacteria, prevented carrageenan-induced colitis in a majority of animals. Delayed treatment with metronidazole until after colitis was established showed no salutory benefits. These results suggest that anaerobic bacteria play a role in the initial events of carrageenan-induced colitis in the guinea pig model.

Animals↗
PubMed1978

[Pathology of ulcerative colitis (author's transl)].

The macroscopic and histological appearance, and the local immune response in ulcerative colitis are discussed. The main criteria for the differentiation between ulcerative colitis and Crohn's disease of the large bowel are reviewed. The risk to develope carcinoma in the large bowel is greater in patients with total ulcerative colitis than in the general population. Precancerous changes in rectal and colonoscopical biopsies are a useful parameter in detecting early cancer in colitis. A description of the morphology of precancerous changes in ulcerative colitis is given.

Biopsy↗
PubMed1979

Prevention of clindamycin-induced colitis in hamsters by Clostridium sordellii antitoxin.

Toxins produced by Clostridium difficile have been implicated in the etiology of antibiotic-induced colitis. Clostridium difficile antitoxin is not available, but recent studies have shown that toxins present in the feces of patients with this disease are neutralized by Clostridium sordellii antitoxin. We found that C. sordellii antitoxin neutralized toxins produced in broth cultures of either C. sordellii or C. difficile and that passive immunization with C. sordellii antitoxin before challenge with clindamycin prevented colitis in hamsters. Significantly fewer antitoxin-treated animals than unimmunized controls developed diarrhea and died with hemorrhagic colitis. Administration of 300 U of antitoxin parenterally either on the day of challenge with clindamycin or 24 hr later provided significant protection (25% mortality vs. 100% mortality in controls, P less than 0.01). None of eight animals given antitoxin (300 U) both on the day of challenge and 24 hr later died. Filtrates prepared from cecal contents of dead or killed hamsters were tested for toxicity by intraperitoneal injection into hamsters and by addition to monolayers of monkey kidney cells. Fecal filtrates from antitoxin-protected animals were not toxic in these assays, but filtrates from control animals were uniformly toxic. Passive immunization against clostridial toxins was protective against clindamycin-associated colitis in this model. This finding further substantiates the importance of these toxins in the pathogenesis of antibiotic-induced colitis.

Animals↗
PubMedDate not supplied

Antibiotic-associated colitis: effects of antibiotics on Clostridium difficile and the disease in hamsters.

Fifteen isolates of Clostridium difficile from hamsters and human patients were inhibited or killed by low concentrations of metronidazole, vancomycin, penicillin, and ampicillin; the isolates were often reesistant to tetracycline, cephalosporins, trimethoprim-sulfamethoxazole, clindamycin, erythromycin, and aminoglycosides. Antibiotics to which C. difficile was susceptible were able to prevent or postpone the colitis caused by clindamycin in hamsters. Colitis could be produced by treatment of hamsters with any one of these antibiotics. Production of colitis not only involved selection of resistant variants, but in some instances seemed to result from the acquisition of organisms after treatment, their persistence despite treatment, or from subinhibitory cecal concentrations of antibiotic (explainable by either pharmacologic factors or enzymatic inactivation). As in humans, no organisms other than C. difficile have been implicated conclusively as etiologic agents of colitis in hamsters. Our results suggest it may be wise to use isolation precautions for patients with colitis caused by C. difficile.

Animals↗
PubMed1978

[Pseudomembranous colitis caused by antibiotics].

A case of antibiotic-induced pseudomembranous colitis is presented. Following resection of a carcinoma of the colon, an 81-year old man was treated with clindamycin for 9 days and with epicillin for another 9 days. One week after discontinuation of antibiotics the patient developed progressively severe diarrhea. Death from central pulmonary embolism ensued 10 days after the onset of diarrhea. Autopsy revealed severe pseudomembranous colitis of the entire large intestine. Pseudomembranous colitis is often observed as a complication after the administration of different antibiotics. The Anglo-American literature contains several recent reports of clindamycin-induced pseudomembranous colitis. The etiopathology of this drug-induced disease is still unclear. A possible interpretation is an antibiotic-induced change in the intestinal flora. Recent observations suggest that toxin-producing clostridia are responsible for the pseudomembranous colitis.

Adenocarcinoma↗
PubMed1978

The rectal biopsy appearances in Salmonella colitis.

Rectal biopsies were examined from 22 patients with Salmonella infection of food-poisoning type and from seven patients with inflammatory bowel disease and coincidental Salmonella infection. In the former group the changes observed were mucosal oedema with acute inflammation of varying severity but with preservation of the crypt architecture. Crypt abscesses were present in a few cases but were usually localized in the crypt and mucus depletion only occurred with severe inflammation. These features are not specific and are similar to those seen in other types of infective colitis such as Shigella dysentery, gonococcal proctitis and amoebic colitis. In the majority of cases of infective colitis the appearances are usually sufficiently distinctive, however, to distinguish them from those seen in ulcerative colitis and Crohn's disease. The changes in the biopsies from the seven patients with coincidental Salmonella infection were in general those of the underlying idiopathic inflammatory bowel disease.

Adolescent↗
PubMed1975

The in-vitro action of lymphocytes on autologous colon epithelial cells in ulcerative colitis.

The action in culture of peripheral blood lymphocytes on autologous large-intestinal epithelial cells was studied in 13 patients with severe mucosal ulcerative colitis. Two different methods were used to measure lymphocyte activity. These showed that autologous-lymphocyte-induced release of isotopic label and detachment in monolayer culture of large-intestinal epithelial cells was increased in acute ulcerative colitis when compared with findings in the same studies in six normal subjects. Subsequently in four of the six patients who responded to cortisone it was shown that lymphocyte activity against epithelial cells returned to the normal range. Further control studies showed little lymphocyte activity against autologous skin and ileum, suggesting that autologous-lymphocyte-induced damage of large-intestinal epithelial cells is a tissue-specific reaction in patients with acute ulcerative colitis. The absence of reactivity in other colonic inflammatory diseases also suggested that such increased in vitro lymphocyte activity is disease-specific for ulcerative colitis.

Adolescent↗
PubMed1978

Overlap in the spectrum of non-specific inflammatory bowel disease--'colitis indeterminate'.

It is stated that 10-20% of cases of non-specific inflammatory bowel disease cannot be classified. Thirty such cases, designated colitis indeterminate at the time of colectomy, were identified from the pathology files of St. Mark's Hospital. The Histopathological features of the surgical specimens and any available biopsy specimens were studied. In nearly all the cases urgent surgery had been required and the features of incipient or established fulminating disease were present. The pathology of these cases of Crohn's disease and ulcerative colitis overlapped, and differentiating features were scant or unreliable. Accepted criteria of Crohn's disease--namely, fissuring ulceration, transmural inflammation, and a maintained goblet-cell population--were found in cases subsequently proved to be ulcerative colitis. Disease activity greatly affected the evaluation of morphological features. Many of the difficulties were resolved when biopsy material obtained during a quiescent phase was examined. The specimens gave a dynamic perspective of the disease process, often more valuable than the static, non-specific picture of acute disease seen in the surgical specimens. Case of colitis indeterminate form a small distinctive group in the spectrum of inflammatory bowel disease which is characterised by a common pattern of pathology that presents a diagnostic dilemma.

Acute Disease↗
PubMed1976

Colonic lymphoma complicating ulcerative colitis.

Colonic lymphoma is a rare complication of ulcerative colitis. Two cases are described in patients who had had ulcerative colitis for 12 and 22 years respectively. Both patients presented with a recent change in their symptoms, which had become increasingly severe and which had not remitted with customary treatment for ulcerative colitis. Physical and haematological examinations revealed no evidence of generalized lymphoma, though barium enema studies indicated the sites of the lymphomatous lesions superimposed on chronic ulcerative colitis which were confirmed at operation and biopsy.

Colitis, Ulcerative↗
PubMed1977

Antibiotic-associated colitis.

Among 26,294 hospitalized patients monitored by the Boston Collaborative Drug Surveillance Program (BCDSP), 8,948 (34%) received at least one antibiotic, and none were diagnosed as having drug-induced colitis to in-hospital antibiotic exposure. Seven patients who had taken antibiotics as outpatients, however, were admitted with antibiotic-associated colitis. Six of these patients had taken lincomycin prior to the onset of symptoms; one had taken ampicillin. Six of the patients were hospitalized at a New Zealand hospital and one at a hospital in Canada. The five patients with lincomycin-associated colitis at the New Zealand hospital were admitted over an 11-month period. Severe colitis due to antibiotics has been a rare event in the BCDSP experience, especially in the United States.

Adult↗
PubMed1975

[Investigations on the ultrastructural pathology of the ulcerative colitis (author's transl)].

The ultrastructural pathology of ulcerative colitis was investigated on a group of 37 colitis patients. Among the epithelial changes, the alterations of the microvilli and of the glycocalyx of the surface epithelium are quite evident. These alterations may possibly be understood as a morphological substrate of a partly impaired "mucosa block" of the surface epithelium (IgA- and "secretory piece" deficiency). Hypothetically, this partly impaired "mucosa block" is considered to be an essential pathogenetic moment of ulcerative colitis. The inflammatory infiltrate of the stratum proprium mucosae is characterized in particular by numerous lymphocytes, plasma cells and macrophages. The close topographical interrelation of these cells observed here seems to indicate a functional cooperation in the auto-immunological process, as it is discussed here in connection with ulcerative colitis.

Adult↗
PubMed1978

Serial carcinoembryonic antigen (CEA) blood levels in patients with ulcerative colitis.

Fifty-seven patients with ulcerative colitis were folloued 1-49 months (mean, 18 months) with serial CEA determinations during periods of remission, mild relapses, and severe relapses. Elevated CEA titers correlated with activity and possibly extent of disease: 12% of patients with proctitis, 47% of patients with left-sided colitis, and 60% of patients with transverse or universal colitis had elevated CEA titers during a flare. Moreover, 24% of patients with mild flares and 86% of patients with severe flares had elevated CEA titers. Ninety-two percent of patients with extensive disease and severe flares had elevated CEA titers. Elevated CEA titers were correlated with histologic findings in three patients. Inflammation of mucosa was demonstrated by colonoscopy and confirmed by biopsy in one patient with persistently elevated CEA titers during clinical remission. In two other patients with active disease whose CEA titers fell prior to colectomy, marked denudation of colonic mucosa was noted. In this study, a transiently elevated CEA titer indicated either clinically active ulcerative colitis or active inflammation of colonic mucosa.

Carcinoembryonic Antigen↗