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Pseudomembranous colitis (PMC) is an infectious colitis usually occurring as a complication of antibiotic use. The computed tomographic (CT) appearances of 26 patients with PMC were reviewed. Twenty-three patients demonstrated an abnormal bowel wall, with an average wall thickness of 14.7 mm (range, 3-32 mm); in three patients, bowel wall thickness was normal. Contrast material trapped between thickened folds corresponded to the broad transverse bands described on plain radiographs. Pancolonic involvement was seen in 13 cases, while seven patients had right-sided involvement only; three patients had bowel wall thickening limited to the rectosigmoid only. Although the CT appearance of PMC is not highly specific, the diagnosis may be suggested in the proper clinical setting.

A variety of inflammatory diseases of the colon, which can be differentiated from inflammatory bowel disease (IBD) and infectious colitis by their clinical, endoscopic and histological characteristics, are reported as non-IBD and non-infectious colitis. These diseases include microscopic colitis, ischemic colitis, segmental colitis associated with diverticula, radiation colitis, diversion colitis, eosinophilic colitis and Behcet's colitis. The etiopathogenesis of most of these diseases remains obscure and the epidemiological data are rather limited. These conditions are often troublesome for the patient and are associated with diagnostic difficulties for the physician. In many cases the treatment is empirical and there is a need for future research using randomized controlled trials.

1) -Abstract- Ulcerative colitis (UC) is a chronic inflammatory disorder of the gastrointestinal tract that affects the large bowel. Its etiology remains controversial. However, an infectious or immunologic origin is considered the primary cause. The onset of UC is typically slow and insidious, but some patients may present acutely with symptoms mimicking infectious colitis. We report a case of ulcerative colitis mimicking acute hemorrhagic colitis at initial presentation. A 60-year-old man was referred to Yeungnam University Hospital for bloody diarrhea and abdominal pain. Sigmoidoscopy revealed mildly edematous mucosa in the rectum and hyperemic mucosa with petechiae in the sigmoid colon. The patient was treated with antibiotics for several days, and his symptoms improved. However, after one month, his bloody diarrhea relapsed. Follow-up sigmoidoscopy revealed mucosal friability in the rectum and sigmoid colon. He was diagnosed with ulcerative colitis, and his symptoms were improved with mesalazine and a steroid enema.

In reviewing the contribution from Shetler et al. [4], several issues emerged that beg clarification. I agree that there are increasing numbers of this infectious colitis that may be life threatening, especially in debilitated, hospitalized patients with significant comorbid illness [1]. Of the eight men (ages 63–79) reported by Shetler et al., only three (38%) were discharged from the hospital and five died (mortality rate, 62%), although two of the five patients who died actually responded to treatment and did not die of septic colitis. The authors emphasize decompression in the title of their article, but in my experience the threat of overwhelming sepsis leading to multiple system organ failure overshadows the risk of perforation from megacolon as may be seen in other disorders, such as colonic pseudoobstruction or Ogilvie’s syndrome. Of the three deaths due to fulminant pseudomembranous colitis, none were caused by perforation but rather overwhelming sepsis as evidenced by the reported acidosis, fever, refractory hypotension, and progressive organ failure (renal, respiratory, and cardiac) culminating in cardiovascular collapse. This study describes an ingenious method of deliv

Cyclooxygenase-2 has shown increased expression on crypt epithelium, inflammatory cells of the lamina propria and myenteric neural cells of active inflammatory bowel disease. In tuberculosis colitis, colonoscopic findings are multiple discrete ulcers on terminal ileum, ic valve and cecum with normal surrounding mucosa which are similar with Crohn's colitis. Pathologically the two disease show similar chronic inflammation and granuloma because typical acid fast bacilli and caseation necrosis are not usually detected by biopsy. We evaluated Cox-2 expression on mucosal biopsy and surgical specimen of tuberculous colitis comparing with Crohn's colitis and nonspecific infectious colitis using immunohistochemistry. This study included 10 patients with tuberculous colitis which are confirmed by antituberculosis treatment, and 10 patients with active Crohn's colitis and 10 patients with acute infectious colitis. We find high Cox-2 expression on both crypt epithelium and laminar propria lymphocyte (LPL) in all of tuberculous colitis (10 of 10). There are low and weak expression on epithelium (two of 10) and LPL (nine of 10) of Crohn's colitis and epithelium (one of 10) and LPL (seven of 10) of infectious colitis. Cox-2 expression on crypt epithelium in patients with tuberculous colitis is significantly higher than Crohn's colits and infectious colitis (P

A unique endoscopic appearance of a single linear ulcer has been noted at colonoscopy in a group of patients with acute abdominal symptoms, often in the clinical setting of an ischemic event. Twelve patients (8F/4M, mean 75.2 yr) with endoscopic evidence of only a single ulcerated band running along the longitudinal axis of the colon (colon single-stripe sign, CSSS) were further studied. The CSSS was >8 cm in length and isolated to a segment of the left colon. To better understand the etiology of this lesion, the clinical characteristics and course of CSSS were compared with 26 cases of ischemic colitis with large circumferential ulcers (15F/11M, mean 63.7 yr) and 58 consecutive patients with other forms of non-ischemic colitis including IBD (25 cases), infectious colitis (13), radiation colitis (4), amyloid (1), nonspecific colitis (15)(36F/22M, mean 48.1 yr). RESULTS: Both CSSS and ischemic colitis groups were older than the non-ischemic colitis group. Unequivocal evidence of a preceding ischemic event was noted with comparable frequency (p=0.2) in the CSSS and ischemic colitis groups, significantly different from the non-ischemic colitis group (p

The colonic biopsy specimens of 22 patients with colitis and positive stool cultures for Campylobacter jejuni were studied in order to obtain histological and immunohistochemical criteria to differentiate Campylobacter colitis from chronic inflammatory bowel disease. In addition we tried to identify Campylobacter inclusions by means of immunohistochemistry and electron microscopy as evidence for invasion of the colonic mucosa. The results show that the majority of patients with Campylobacter colitis have the histological picture of acute infectious colitis with increased numbers of IgA and IgM containing plasma cells in the colonic mucosa in contrast with patients with active chronic inflammatory bowel disease who show increases of IgA and IgG (ulcerative colitis) or IgA-, IgM and IgG containing plasma cells (M Crohn) in their colonic biopsies. The results of immunohistochemical stainings with Campylobacter antiserum show invasion of Campylobacter in the colonic mucosa. These findings were confirmed ultrastructurally.

The expression of plasminogen activators was analysed in mucosal homogenates from inflammatory bowel disease patients to determine whether the urokinase-type (u-PA) is implicated in the pathogenesis of mucosal tissue injury. Homogenates of mucosal biopsy tissue from ulcerative colitis, Crohn's disease, infectious colitis and normal control patients were subjected to polyacrylamide gel electrophoresis. The types of plasminogen activator present were detected by zones of lysis in a fibrin-agarose gel overlay. All the tissues studied displayed tissue plasminogen activator activity (t-PA). In ulcerative colitis, 18 of the 19 diseased colon biopsies, but none of six biopsies from uninvolved areas of the same colon, showed u-PA activity. Similar results were found in 12 Crohn's disease patients. Biopsies from the infectious colitis group and from radiation colitis patients also showed both u-PA and t-PA activity. The age, sex, duration of disease, and presence and type of treatment did not affect u-PA expression in the inflamed mucosa. The results suggest that u-PA may be implicated in the mediation of tissue injury in the inflamed intestinal mucosa.

The histopathology of rectosigmoid biopsies from 20 patients with bloody diarrhea resulting from verotoxin-producing Escherichia coli infection is reported. The biopsies displayed a range of appearances, from normal to mild, nonspecific inflammation to acute infectious-type colitis. Surface-adherent or invasive bacteria were not identified. The morphologic features of infectious colitis and the absence of bacteria suggest that verotoxin may be responsible for the pathologic changes.

Parameters in the differential diagnosis of enterocolitis have been poorly evident for many years. Development and profitable employment of endoscopic instruments were the first step towards advancing the diagnostic facilities in inflammatory bowel disease. The microbiologic examination of mucosal biopsies creates a new diagnostic dimension, and it distinctly seems to increase the diagnostic sensitivity for pathogens. Within fifteen months 152 patients admitted to the gastroenterologic unit with acute, or symptoms of exacerbated, bowel disease were examined for the aetiologic agents. Compared with former reports, idiopathic inflammatory bowel disease (IIBD) such as Crohn's disease (32.2%) and ulcerative colitis (18.4%) were decreased. Infectious colitis (22.3%), mostly Campylobacter or Yersinia infections, was, sometimes exclusively, diagnosed by bioptic microbiology, non-classifiable forms of colitis (21.7%), and rare forms (5.4%) were diagnosed more often. It proved to be important that IIBD was frequently superinfected by Campylobacter, Yersinia and Chlamydia, and the differential diagnosis was complicated, since these microorganisms can mimic IIBD. The results suggest that coloileoscopy combined with bioptic microbiologic investigation additional to faecal samples should include a search for Campylobacter and Yersinia. It appears indispensable that the final diagnosis "Crohn's disease" or "ulcerative colitis" should be confirmed by sequential coloileoscopy and microbiologic examination.

Histopathology can play an important role in diagnosing infictious colitis for several reasons. First, colonic mucosal biopsy can often reliably differentiate acute self limited colitis (ASLC). or infectious type colitis, from idiopathic inflammatory bowel disease (IBD). In ASLC, crypt architecture is normal and the inflammatory infiltrate in the lamina propria predominantly acute, ie, polymorphonuclear cells. In IBD, in contrast, crypt architecture is often abnormal nd the inflammatory infiltrate in the lamina propria in both acute and chronic, ie, polymorphonuclear cells, plasma cells ,and lymphocyte are present in increased numbers. Second, biopsy may give a clue to the specific infection. Biopsy may reveal the presence of specific parasites such asEntamoeba histolytica, cryptosporidia or schistosomiasis. Viral inclusions are seen when cytomegalovirus or herpes simplex type II virus infect the colon. Granulomas usually indicate Crohn's disease but can he seen with infections due toChlamydia trachomatis,Treponema pallidumandMycobacterium tuberculosis. Both chlamydial and syphilitic proctitis are rare and usually seen in homosexually active men. Finally, pseudomembranes, when present, suggest pseudomembranous colitis due to an overgrowth of toxigenicClostridium difficile. In summary, mucosal biopsy is helpful in differentiating ASLC from IBD in most cases. Sometimes, it provides a clue to the specific infection.

Summary Four hundred forty-five rectal suction biopsies from 212 patients were examined in an effort to assess the clinical usefulness of this technique. A method was evolved which provided good specimens. These specimens were then embedded and cut in a uniform fashion to permit microscopic study of properly oriented, serial sections. Histologic categories of normal, equivocal, and abnormal were recognized. Common sources of artifacts were also recognized (1) trauma; (2) too small a specimen; (3) lymphoid nodules; and (4) proximity to the anus. Patients were grouped into clinical categories for analysis:(1) normal; (2) probably normal; (3) edema; (4) colonic polyp; (5) celiac sprue ; (6) infectious colitis; (7) regional enteritis; (8) ulcerative colitis; (9) unclassified diarrhea; and (10) miscellaneous. Some abnormal specimens were obtained in all of the clinical groups except the normal and probably normal. Abnormal findings including crypt abscess were most frequent and most severe in idiopathic and infectious colitis although no specific histologic pattern was invariably associated with this single disease entity. The biopsies were evaluated without knowledge of the clinical facts. A good diagnostic correlation was obtained between careful sigmoidoscopy and biopsy obtained on the same day. Despite the nonspecificity of the abnormalities seen, biopsy was of considerable clinical value as an adjunct to sigmoidoscopy in that objective evidence of early organic disease was often obtained by biopsy when the clinical picture pointed to no more than a functional disturbance.

The enormous interest currently given to colitis in general and their treatment in particular prompts me to share the methods that I have been using for many years and with great success in the treatment of colitis of infectious origin, which include colitis caused by an infection of a very diverse nature: or entering the intestine from the outside , such as amoeba dysenteriae Councilman et Lafleur s. entamoeba hystolytica Schaudinn, bac. dysenteriae Schiga-Kruse s. bacterium dysenteriae Migula, bac. Flexner'a, bac. His-Roussel'a, bac. Strong'a, pseudo-dysentery bacilli, or developing due to increased virulence of the regulars of the intestine, for example, b. coli, b. proteus, streptococci, etc., or, finally, colitis, as a complication in other infectious diseases, for example, with typhoid fever, measles, flu, etc., and all these forms of colitis are so similar to each other that it is impossible to distinguish them from each other neither by clinical signs, nor by the course: there may be mild and severe cases, acute and chronic, regardless of their origin; one and the same symptomatology is reduced to local and general phenomena; in the latter case, as a result of the general intoxication of the body with the waste products of the intestinal flora absorbed from the intestine (feverish state, coated tongue, headaches, general fatigue, darkening of consciousness, convulsions, decline in heart activity, etc.); as for the symptoms of local origin, they boil down to colicky abdominal pain, increased urge to lower, tenesmus, secretion of blood and mucus, as an expression of intoxication of the mucous membrane of the colon and rectum, caused by the same intestinal flora. All these symptoms in their entirety and essence form the basis of the course and direction of the doctor's thought at the patient's bedside. We have to think, as G.I.Ivashentsev quite reasonably states1), about the destruction and elimination of the infectious principle, the neutralization and elimination of toxins, the prevention and treatment of severe lesions of the colon mucosa. All these conditions are met in the best way by our method of treatment. In the current state of our knowledge, the specific treatment of colitis recedes into the background.

The appearances of the colon on barium enema examination in 7 patients with infectious colitis due to Salmonella and Shigella are described.The roentgenologic alterations of the upper gastrointestinal tract and small bowel were studied in 2 of the 7 patients.Diffuse involvement of the colon was seen in 2 patients and segmental disease with variable rectal and colonic involvement was present in the remaining 5.In general, the features were those of ulcerations, spasm and edema.The changes were found to be reversible in all patients who responded to therapy. These latter features of an acute colitis which may revert to normal should differentiate infectious colitis from both Crohn's colitis and ulcerative colitis.

This prospective evaluation of patients presenting with mucoid bloody diarrhea and suspected idiopathic inflammatory bowel disease demonstrated a 38% incidence of infectious colitides. The infectious agents detected were Campylobacter, Salmonella, Shigella, Amoeba, and Clostridium difficile. An increased awareness and the utilization of selective culture media should allow the clinician to definitively diagnose patients who present with signs and symptoms suggestive of idiopathic inflammatory bowel disease.

Eighty four colonic biopsy specimens were obtained from patients with ulcerative colitis, Crohn's disease, radiation colitis, infectious colitis, and from normal controls. Paired specimens were examined by histological and immunohistochemical methods using monoclonal antibodies to the beta chain of HLA-DR antigen. The expression of HLA-DR antigen in mucosal epithelial cells was strongly related to whether the specimens were actively inflamed: epithelial cells from 34 of 37 inflamed specimens (nu three of 42 non-inflamed specimens) were HLA-DR positive (p less than 0.0001). Epithelial cells were uniformly HLA-DR negative in specimens from normal control patients despite the presence of HLA-DR positive lymphoid cells and macrophages in the lamina propria. Epithelial cells in specimens from patients with ulcerative colitis, Crohn's disease, and radiation colitis were HLA-DR positive in 30 of 33 inflamed biopsy specimens and in only three of 25 non-inflamed specimens (p less than 0.0001). Epithelial cells were HLA-DR positive in nine of 10 biopsy specimens from patients with acute infectious colitis (p less than 0.01).

Toxic megacolon or toxic dilatation of the colon is an ominous complication of inflammatory bowel disease (IBD). It is characterized by acute dilatation of the colon to greater than six cm in diameter and is associated with signs of systemic toxicity. Classically, toxic megacolon is associated with the fulminant phase of ulcerative colitis, but it has also been described in other disease states and is a recognized complication of granulomatous or Crohn’s colitis as well. It has been described in patients with pseudomembranous colitis secondary to antibiotic usage, ischemic colitis, and infectious colitis secondary to shigellosis or amebiasis.

Colitis encompasses a spectrum of disorders, each with its own natural history and therapy. In the elderly, the relative prevalence of these entities is markedly different than in younger patients, with infectious colitis the most common type, followed by antibiotic-associated disease and ischemic colitis. The last is rarely recurrent and half of the episodes resolve spontaneously.

Amebic colitis needs to be considered in the differential diagnosis of infectious colitis or inflammatory bowel disease (IBD). Misdiagnosing amebic colitis as idiopathic inflammatory disease may be fatal. Although stool studies remain the initial approach to diagnosis, the incidence of false-negatives associated with this method is high. We report two cases of amebic colitis presenting as inflammatory bowel disease in which the diagnosis of amebic colitis was made by serology. Neither patient had any risk factors for acquiring amebiasis. Paired serology for amebic infections (2-4 weeks apart) should be performed in patients being evaluated for infectious colitis and inflammatory bowel disease.

An acute febrile illness with dysentery and colitis developed in a 26-year-old man following a wilderness outing. Campylobacter fetus ssp. jejuni was subsequently grown on blood cultures drawn during the acute illness and 9 days later when the patient was asymptomatic. Proctosigmoidoscopic and histopathologic evidence of acute colitis was present on admission and resolved on follow-up examination. Campylobacter fetus spp. jejuni infection should be considered in the etiology of acute infectious colitis.

A condition known as diversion colitis frequently develops in segments of the colorectum after surgical diversion of the fecal stream; it persists indefinitely unless the excluded segment is reanastomosed. The disease is characterized by bleeding from inflamed colonic mucosa that mimics the bleeding of idiopathic inflammatory bowel disease, and it may culminate in stricture formation. We hypothesized that this condition is caused by the absence of luminal short-chain fatty acids, the preferred metabolic substrates of colonic epithelium. We studied four patients with diversion colitis, none of whom had evidence of Crohn's, idiopathic ulcerative, or infectious colitis. The excluded segment of the rectosigmoid contained negligible concentrations of short-chain fatty acids. When D-glucose was instilled, it did not undergo appreciable anaerobic fermentation. Instillation of a solution containing short-chain fatty acids twice daily resulted in the disappearance of symptoms and the inflammatory changes observed at endoscopy, over a period of four to six weeks. Remission has been maintained for up to 14 months (in one patient) by instillation daily to twice weekly. Administering enemas containing isotonic saline, or omitting treatment for periods of two to four weeks during the regimen, by contrast, did not produce any improvement or rapid relapse of the colitis. Histologic observation revealed a distinctive type of mucosal inflammation that resolved more slowly and less completely than the gross appearance of the inflamed mucosa. From these preliminary studies we infer that diversion colitis may represent an inflammatory state resulting from a nutritional deficiency in the lumen of the colonic epithelium, which is effectively treated by local application of short-chain fatty acids, the missing nutrients.

In colonic biopsies of 33 patients with acute colitis caused by campylobacter, salmonella, or shigella immunoglobulin containing cells were determined quantitatively using an indirect immunoperoxidase technique and morphometry with a graphic tablet. The findings were compared with those of 10 patients without histological abnormalities, 10 patients with Crohn's disease of the colon, and 10 patients with ulcerative colitis. Biopsies of patients with acute infectious colitis had increased numbers of IgA containing cells and to a lesser extent IgM containing cells but not IgG containing cells compared with controls. Compared with the patients with active chronic idiopathic inflammatory bowel disease the patients with acute colitis showed significantly lower relative and absolute numbers of IgG containing cells. We therefore conclude that quantitative assessment of immunoglobulin containing cells in colonic biopsies may be useful in the differential diagnosis of acute infectious colitis and chronic idiopathic inflammatory bowel disease.

In 40 distal ileal and 40 colonic biopsies of arthritic patients mostly without gastrointestinal symptoms, but with histological evidence of acute or chronic inflammation of the gut, the number of immunoglobulin (Ig) containing plasma cells was studied morphometrically using a peroxidase antiperoxidase technique. Compared with controls, the ileal mucosal biopsies showed an increase of IgA and IgG in acute ileitis. In chronic ileitis there was an increase of IgA, IgG, and IgM similar to Crohn's disease. In colonic biopsies there was a significant increase of all immunoglobulin classes in acute inflammation. In chronic inflamed mucosa there was also an increase of all three Ig classes. The Ig distribution, however, was significantly different in acute and chronic colitis. These findings give immunohistochemical evidence of the existence of two different types of inflammation related to reactive arthritis or the peripheral joint involvement of ankylosing spondylitis. The Ig pattern in acute colitis is similar to that found in infectious colitis, suggesting an enterobacterial origin of the arthritis in this group of patients although bacteriological and serological investigations were negative. In the chronic type of arthritis related ileocolitis, the pattern of Ig containing cells is similar to that found in Crohn's disease but different from infectious and ulcerative colitis, which makes the hypothesis that a great number of these arthritis patients suffer from asymptomatic or subclinical Crohn's disease acceptable.

Introduction Encephalopathy is a rare disease caused by adverse effects of antibiotic drugs such as metronidazole. The incidence of metronidazole-induced encephalopathy is unknown, although several previous studies have addressed metronidazole neurotoxicity. Here, we report the case of a patient with reversible cerebellar dysfunction on magnetic resonance imaging, induced by prolonged administration of metronidazole for the treatment of infectious colitis. Case presentation A 71-year-old Asian man, admitted to our hospital with hematochezia, underwent Hartmann's operation for the treatment of colorectal cancer three years ago. He was diagnosed with an infectious colitis by colonoscopy. After taking metronidazole, he showed drowsiness and slow response to verbal commands. Brain magnetic resonance imaging showed obvious bilateral symmetric hyperintensities within his dentate nucleus, tectal region of the cerebellum, and splenium of corpus callosum in T2-weighted images and fluid attenuated inversion recovery images. Our patient's clinical presentation and magnetic resonance images were thought to be most consistent with metronidazole toxicity. Therefore, we discontinued metronidazole, and his cerebellar syndrome resolved. Follow-up magnetic resonance imaging examinations showed complete resolution of previously noted signal changes. Conclusion Metronidazole may produce neurologic side effects such as cerebellar syndrome, and encephalopathy in rare cases. We show that metronidazole-induced encephalopathy can be reversed after cessation of the drug. Consequently, careful consideration should be given to patients presenting with complaints of neurologic disorder after the initiation of metronidazole therapy.

We have employed a single phase antibody radioimmunoassay to determine rectal tissue and secretion immunoglobulin (Ig) levels in children with documented infectious colitis. All children had positive stool culture and/or rectal swab for pathogen, abnormal proctosigmoidoscopy and pathologic diagnosis of acute colitis. Tissue was placed in rectal organ culture for 24 hours and explants were homogenized (H) and assayed for IgA, IgG and IgM. Secretions (S) were collected over center well of organ culture plate and assayed for Ig's. Results were expressed as μg Ig per mg tissue protein. Results were compared with a control population of children with Functional Abdominal Pain who had normal proctosigmoidoscopy and pathogen-negative stool cultures. There appears to be a marked symmetrical increase in rectal tissue Ig's whether comparing total Ig (p

A FREQUENTLY encountered diagnostic problem in older persons is acute abdominal pain accompanied by bloody diarrhea, invoking the differential diagnosis of diverticulitis, inflammatory bowel disease, infectious colitis, carcinoma of the colon, and ischemic colitis. 1,2 The roentgenographic manifestations of ischemic colitis, namely, "thumbprinting," bowel-wall edema, ulcerations, intramural dissection of barium, and stricture, often resemble those of these other disease processes, and recognition may be difficult. 3,4 Acute vascular insufficiency of the colon is a disease complex that presents as a spectrum ranging in severity from gangrenous infarction causing peritonitis and shock to a trivial episode of abdominal pain and diarrhea that a patient may recall only in retrospect. 5,6 Where in this continuum an individual patient may fall depends on the duration and extent of the ischemia, the efficiency of collateral circulation, and the extent of bacterial invasion. 7,8 Gangrenous Colitis The catastrophic expression of colonic ischemia, gangrenous colitis, is

Background Inflammatory bowel diseases are associated with increased expression of zinc-dependent Matrix Metalloproteinase 9 (MMP-9). A stark dysregulation of intestinal mucosal homeostasis has been observed in patients with chronic inflammatory bowel diseases. We therefore sought to determine the contribution of MMP-9 to the pathogenesis of Citrobacter rodentium-induced colitis and its effects on gut microbiome homeostasis. Results Wild-type and MMP-9−/− mice aged 5–6 weeks were challenged with C. rodentium by orogastric gavage and sacrificed either 10 or 30 days post-infection. Disease severity was assessed by histological analysis of colonic epithelial hyperplasia and by using an in vivo intestinal permeability assay. Changes in the inflammatory responses were measured by using qPCR, and the composition of the fecal microbiome evaluated with both qPCR and terminal restriction fragment length polymorphism. Activation and localization of MMP-9 to the apical surface of the colonic epithelium in response to C. rodentium infection was demonstrated by both zymography and immunocytochemistry. The pro-inflammatory response to infection, including colonic epithelial cell hyperplasia and barrier dysfunction, was similar, irrespective of genotype. Nonmetric multidimensional scaling of terminal restriction fragments revealed a different fecal microbiome composition and C. rodentium colonization pattern between genotypes, with MMP-9−/− having elevated levels of protective segmented filamentous bacteria and interleukin-17, and lower levels of C. rodentium. MMP-9−/− but not wild-type mice were also protected from reductions in fecal microbial diversity in response to the bacterial enteric infection. Conclusions These results demonstrate that MMP-9 expression in the colon causes alterations in the fecal microbiome and has an impact on the pathogenesis of bacterial-induced colitis in mice.