Infectious Colitis – StatPearls – NCBI Bookshelf

Continuing Education Activity

The management of infectious colitis is complex, and new approaches have been introduced. The basic and clinical aspects of infectious colitis must be clearly defined to achieve satisfactory outcomes. This activity reviews infectious colitis, and focusses on the etiology, epidemiology, pathophysiology, evaluation, management, and complications of infectious colitis, and highlights the role of the interprofessional team in improving healthcare outcomes.

Objectives:

• Identify the etiology and along with accompanying risk factors for infectious colitis.

• Describe the pathophysiology in infectious colitis.

• Summarize the evaluation process infectious colitis.

• Review the management options available for infectious colitis.

Access free multiple choice questions on this topic.

Introduction

Colonic infection by bacteria, viruses, or parasites results in an inflammatory-type of diarrhea and accounts for the majority of cases presenting with acute diarrhea. These patients present with purulent, bloody, and mucoid loose bowel motions, fever, tenesmus, and abdominal pain. Common bacteria causing bacterial colitis include Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis. Common causes of viral colitis include Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus. Parasitic infestation, such as Entamoeba histolytica, a protozoan parasite, is capable of invading the colonic mucosa and causing colitis. Sexually transmitted infection affecting the rectum merit consideration during assessment. These diseases can occur in patients with HIV infection and men who have sex with men and may include Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex, and Treponema pallidum.

The patients present with rectal symptoms that mimic inflammatory bowel disease, including rectal pain, tenesmus, bloody mucoid discharge, and urgency. Detailed medical history and identification of specific associated risks are essential in establishing the diagnosis. Stool microscopy and culture and endoscopy are crucial to the diagnosis. However, stool culture helps in the diagnosis of less than 50% of patients presenting with bacterial colitis, and endoscopic examinations usually reveal non-specific pathological changes. Therefore, an approach is needed to evaluate and diagnose the cause of colitis and exclude non-infectious causes. This activity discusses current strategies to diagnose and manage infectious colitis and how to make a high index of suspicion based on clinical presentation and use investigation methods to reach a final diagnosis. This activity discusses the etiology, epidemiology, pathophysiology, clinical presentation, evaluation, differential diagnosis, complications, and management of patients with infectious colitis.  

Etiology

Infectious colitis may result from infection with:

1. Bacterial infections: including Campylobacter jejuni, Salmonella, Shigella, Escherichia coli (including these subgroups – enterotoxigenic E. coli, enteropathogenic E. coli, enterohemorrhagic E. coli, enteroinvasive E. coli, enteroaggregative E. coli), Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis.

2. Viral infection: Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus (CMV).

3. Parasitic infection such as Entamoeba histolytica (causes amoebic colitis)

4. Sexually transmitted infections: Particularly infections affecting the rectum in patients with HIV infection and men who have sex with men may include the following infections: Neisseria gonorrhoeae, Chlamydia trachomatis (causes lymphogranuloma venereum), Herpes simplex 1 and 2, and Treponema pallidum (causes syphilis).

Enterotoxigenic E. coli is the leading cause of traveler’s diarrhea. Enteroaggregative E. coli can cause traveler’s diarrhea, but it is not the leading cause. Enterohemorrhagic E. coli has two main serotypes E. coli O157: H7 and non-O157: H7; the natural reservoirs of both serotypes are cows. Therefore, the infection is related to the consumption of inadequately cooked beef, or contaminated milk or vegetables. They are responsible for outbreaks in developed countries.[1]

Two of these subgroups cause non-bloody diarrhea: enterotoxigenic E. coli and enteroaggregative E. coli; both produce enterotoxins that induce chloride and water secretion and inhibit their absorption. However, enterohemorrhagic E. coli (both strains E coli O157: H7 and non-O157: H7) causes bloody diarrhea and produce Shiga-like toxins, resulting in a clinical picture similar to Shigella
dysenteriae infection.[2]

Both enteropathogenic E. coli and enteroinvasive E. coli do not produce toxins. Enteropathogenic E. coli is responsible for outbreaks, particularly in children less than two years of age, while enteroinvasive E. coli causes acute self-limited colitis and is responsible for outbreaks mainly in developing countries. However, the outbreaks in Nottingham, the UK, in 2004, highlight the need for its consideration as a potential pathogen in foodborne outbreaks in Europe.[3]  

Children (in daycare centers), elderly (in nursing homes), and immunocompromised individuals are susceptible to these infections. The fecal-oral route, animal host, and ingestion of contaminated food and water are the usual modes of infection.

Food and water contaminations with pathogenic bacteria may cause large outbreaks of diseases.

Epidemiology

Bacterial colitis accounts for up to 47% of cases of acute diarrhea.[4]
Campylobacter jejuni is the number one bacterial cause of diarrheal illness worldwide with an estimated prevalence of 25 to 30 per 100000 population. For Salmonella infection, an estimated 1.2 million annual cases of non-typhoidal salmonellosis occurred in the United States.

Shigellosis incidence worldwide reported to be approximately 165 million cases, but mortality has decreased in the last three decades because of improvement in laboratory diagnosis and treatment. In the United States, estimates are approximately 500000 cases per year, with 38 to 45 deaths.[5]

Yersinia enterocolitica colitis commonly presents in young children in the winter. In the United States, estimate are one case per 100000 individuals each year.

Clostridium difficile infection in hospitalized adults in the United States increased from 4.5 cases per 1000 discharge in 2001 to 8.2 cases in 2010 and a mortality rate of 7%.[6] Another study from the United Stated on Clostridium infection estimated 500000 cases in 2011 with 83000 recurrence and 29300 deaths.

Mycobacterium tuberculosis is the third most common site of extra-pulmonary tuberculosis, accounting for 12.8% of all cases under this category.[7] The recurrence of tuberculosis in developing countries parallels the AIDS epidemic distribution closely.[8] Other factors for increasing rates of tuberculosis in many developed countries are related to the migrant population, deterioration in social conditions, cutbacks in public health surveillance services, and increased prevalence of immune-suppressed individuals (AIDS, those receiving biological agents in diseases such as rheumatoid arthritis, and inflammatory bowel disease).[9]

Amebiasis ranks as the second leading cause of death due to protozoan infection after malaria, Chagas disease, and leishmaniasis.[10]

The prevalence of CMV infection in percent colitis is in the range of 21% to 34%.[11] CMV reactivation in patients with severe ulcerative colitis has a reported prevalence of 4.5% to 16.6% and as high as 25% in patients requiring colectomy for severe colitis.

Infectious proctitis among HIV-positive and HIV-negative men varied and in a recent study was as follows: chlamydia (23% versus 22%, respectively), gonorrhoea (13% versus 11%), HSV-1 (14% versus 6%), and HSV-2 (22% versus 12%), lymphogranuloma venereum (8% versus 0.7%), more than one infection (18% versus 9%). Approximately thirty-two percent of HSV proctitis had external anal ulcerations.[12]

Pathophysiology

Infection with Campylobacter jejuni is a result of orally ingested contaminated food or water. Several factors influence infections, including the dose of bacteria ingested, the virulence of organisms, and the immunity of the host. The median incubation period is from 2 to 4 days. C. jejuni multiplies in the bile and then invade the epithelial layers and travel to the lamina propria producing a diffuse, bloody, edematous enteritis.

Pseudomembranous colitis is caused by toxin-producing Clostridium difficile. The disease develops as a result of altered normal microflora (usually by antibiotic therapy such as cephalosporin and beta-lactam antibiotics) that enables overgrowth and colonization of the intestine by Clostridium difficile and production of its toxins.[13]

Enterotoxigenic E. coli produces heat-labile (HL) and heat-stable (ST) toxins. The HL toxins activate adenyl cyclase in enterocytes resulting in increased cAMP and stimulation of chloride secretion and inhibition of absorption. The ST toxins bind to guanylate cyclase resulting in increased cGMP and effects on cellular transporters similar to those caused by LT toxins resulting in secretory non-inflammatory diarrhea (this explains the limited histopathological changes in this infection).[14]

Enteropathogenic E. coli can produce proteins for “attaching” and “effacing” (A/E) lesions, which enable the bacteria to get tightly attached to the enterocytes apical membranes and causing effacement or loss of the microvilli. As stated earlier, enteropathogenic E. coli does not produce toxins, and their underlying mechanisms for causing diarrhea is by attaching and effacing lesions.[15]

Enterohemorrhagic E. coli; both of its serotypes E. coli O157: H7 and non-O157: H7 produce Shiga-like toxins similar to Shigella dysenteriae infection. However, E. coli O157: H7 strains are more likely to cause outbreaks compared to non-O157: H7 serotypes. They produce bloody diarrhea and are responsible for the development of hemolytic-uremic syndrome and ischemic colitis.[16]

Enteroinvasive coli do not produce toxins; they invade enterocytes and cause self-limited colitis. Exact details of their pathogenetic mechanisms are still not fully understood.

Enteroaggregative E. coli produces enterotoxins related to Shigella enterotoxins and ST toxins of enterotoxigenic E. coli. They attach themselves to enterocytes via adherence fimbriae.

Immunity to Mycobacterium tuberculosis undergoes mediation via T-cells resulting in macrophage stimulation to kill the bacteria. Reactivation of infection or re-exposure to the bacillus in a sensitized individual, as it is the case in most Mycobacterium tuberculosis colitis cases resulting in rapid defense reactions and increased tissue necrosis accompanied by loss of T-cell immunity (tuberculin test in these patients becomes negative although used to be previously positive, which is consistent with fading T-cell protection).[17]

Primary CMV infection in immunocompetent individuals is usually asymptomatic. However, in patients whose immune response is compromised, they develop symptoms in different body organs, including CMV colitis.

Research concerning genetics and molecular sciences of Entamoeba histolytica have brought new understanding about mechanisms by which the parasite impose invasive abilities and pathological lesions in the colon and extracolonic organs. Host factors predisposing to infection are also under research.[17]

Histopathology

No significant differences appear in histological biopsies taken from the rectum of patients with different bacterial infections. However, the absence of crypt architecture distortion or basal plasmacytosis helps differentiate acute infectious colitis from chronic inflammation caused by inflammatory bowel disease.

Infection with Escherichia coli O157: H7 may show changes similar to those of ischemic colitis (small atrophic crypts, hyalinized lamina propria, and fibrin thrombi).

Yersinia enterocolitica shows inflammatory changes, ulcerations in the cecum and terminal ileum areas, hyperplasia of Peyer patches, microabscesses, and granulomas. (This condition requires differentiation from Crohn disease and Mycobacterium tuberculosis involving the terminal ileum/caecum area).

Colonic histopathological changes are limited in enterotoxigenic E. coli, enteroinvasive E. coli, and enteroaggregative E. coli infections.

In Mycobacterium tuberculosis, characteristic granulomas with central caseation are present; tubercle bacilli are identifiable with acid-fast stains.[18]

The diagnosis of CMV colitis requires histological examination of biopsy tissues, taken from the ulcer edge or base. Patients with punched-out ulcers are associated with an increase in inclusion bodies on histology [Yang H et al. 2017]. Colonic mucosal biopsies stained with H & E may reveal the typical inclusion associated with CMV colitis, “owl eye appearance” inclusion bodies, which are highly specific for CMV. However, H & E staining has low sensitivity compared to immunohistochemistry, which is considered the gold standard for diagnosing CMV colitis.[19]

The histological features of biopsies taken from the rectum are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests, including serology and PCR, are essential in making such differentiation.

History and Physical

Detailed medical history and identification of exposure risks are helpful in the diagnosis. It is essential to mention here that individuals with sickle cell anemia, hemolytic anemia, immunosuppression (corticosteroids, chemotherapy, and AIDS), and extremity of age are at a higher risk of Salmonella infection.  Patients with bacterial colitis present with non-specific symptoms, including diarrhea, fever, tenesmus, and abdominal pain. Patients with Yersinia enterocolitica infection may present with a syndrome indistinguishable from acute appendicitis (mesenteric adenitis, mild fever, and ileocecal tenderness).

The incidence of Clostridium difficile is higher in patients with inflammatory bowel disease, particularly ulcerative colitis. Any antibiotic can trigger the disease, but the most common antibiotics responsible are cephalosporins, clindamycin, carbapenems, trimethoprim, sulfonamides, fluoroquinolone, and penicillin combinations.[13]

Patients with Mycobacterial tuberculosis may present with abdominal pain, blood per rectum, fever, sweating, tiredness, and pallor. They may give a past medical history of the treatment of pulmonary tuberculosis. They may have abdominal tenderness in the right iliac fossa (the ileocecal area is the most commonly involved site in intestinal tuberculosis).[18]

Viral colitis (Norovirus, Rotavirus, and Adenovirus) are common in infants and young children. Affected patients present with nausea, vomiting, watery diarrhea, and abdominal pain. CMV infection is frequently symptomatic in immune-competent patients. Again, symptoms are usually non-specific, including diarrhea, abdominal pain, fever, malaise, rectal bleeding, and weight loss. However, hematochezia and diarrhea are the most frequent symptoms. It is difficult to distinguish between ulcerative colitis from CMV colitis based on clinical presentation.[14]

Amoebic colitis usually presents with diarrhea, mucoid discharge, hematochezia, tenesmus, and abdominal bloating. Contaminated water supplies and poor sanitation are often the cases for traveling overseas to endemic areas and increased risk of fecal-oral transmission of amebas.

Patients with colitis-associated with sexually transmitted infection present with anorectal pain, with a purulent, mucoid or bloody discharge, tenesmus, or urgency. The sexual history is vital in evaluating these patients. 

Evaluation

Diagnosis of colitis centers on clinical findings, laboratory tests, endoscopy, and biopsy. Endoscopy and biopsy should not be the primary investigations and may be necessary after a critical evaluation of the patient’s condition and the results from the initial examination.

Because infection is a common etiology of colitis and can produce clinical presentations indistinguishable from inflammatory bowel disease, microbiological studies and cultures for bacterial and parasitic infestations should be the initial investigations. Laboratory tests including complete blood count, ESR, CRP, arterial blood gases, activated partial thromboplastin time, serum albumin, total protein, blood urea, creatinine, and electrolytes should be ordered. Polymerase chain reaction-based molecular methods (PCR-based multiplex GI pathogens) can help in the rapid identification of nvestigationsSalmonella, Shigella, and Yersinia from primary stool samples. Abdominal and pelvis CT scan, colonoscopy, tissue biopsies, and fecal cultures (multiple specimens) and antimicrobial susceptibility testing should help differentiate infectious from non-infectious causes of colitis and guiding treatment.[15]

Recently multidetector CT scans of the abdomen were used to differentiate between inflammatory bowel disease and acute colitis related to bacterial infection. The five signs described to diagnose bacterial colitis are (1) continuous distribution, (2) empty colon, (3) absence of fat stranding, (4) absence of a “comb’ sign, and (5) absence of enlarged lymph nodes.[16]

The diagnosis of active Mycobacterium tuberculosis colitis focuses on clinical presentation, clinical examination, and laboratory investigations. A complete blood count may reveal low hemoglobin, leukocytosis, and moderately elevated ESR. Chest X-ray may reveal fibrotic changes, cavitation, or old scar of pulmonary tuberculosis; an abdominal roentgenogram may reveal prominent large bowel. Abdominal and pelvis CT scans may show diffuse thickening of the colonic wall, especially of the terminal ileum and the cecum. A colonoscopy usually shows diffuse ulceration throughout the colon, from the rectum to cecum. Histopathological biopsies taken from the cecum show caseating granuloma and chronic inflammatory cells. Mantoux skin test (tuberculin test) is usually requested. This test does not measure immunity to tuberculosis but the degree of hypersensitivity to tuberculin. The results must be interpreted carefully with consideration to the patient’s medical risk factors. Usually, the Mantoux test becomes negative in these patients after being previously positive, indicating the fading of resistance to the organism.[17] PCR testing and cultures of intestinal fluid for bacterial species and acid-fast bacillus are requested.

Diagnosis of CMV colitis uses clinical findings, laboratory tests, and endoscopic findings. Endoscopy and tissue CMV-specific immunohistochemistry (IHC) and or PCR CMV DNA quantification are needed to confirm the diagnosis [20]. 

In amoebic colitis, rectosigmoid involvement may present on colonoscopy; however, the cecum is the most commonly involved site, followed by the ascending colon (showing colonic inflammation, erythema, oedematous mucosa, erosions, white or yellow exudates, and ulcerations). The presence of amoebic trophozoites on histopathological examination or intestinal fluid cultures is important in the diagnosis. Serum E. histolytica antibody examination and antibody titer greater than 1:128 is considered positive.[17][10]

For patients with suspected sexually transmitted infections of the rectum, histological features of biopsies taken are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests are usually helpful; these include:

• Gonorrhea: Microscopic examination of smears from the lesions showing Gram-negative diplococci. Culture and sensitivity tests of smears taken from lesions.

• Lymphogranuloma venereum: Genotyping of Chlamydia trachomatis- DNA PCR.

• Genital/rectal herpes: Swabs from rectal vesicles or ulcers to detect DNA by PCR.

• Syphilis: Dark-field microscopy, PCR, direct fluorescent antibody test, treponemal antigen-based enzyme immunoassays (EIAs) for IgG and IgM antibodies, Treponema pallidum hemagglutination assay (TPHA), Treponema pallidum particle agglutination assay (TPPA), and fluorescent treponemal antibody absorption (FTA-ABS) test.[20]

Treatment / Management

Not all infectious colitis requires antibiotic therapy; patients with mild to moderate C. jejuni or Salmonella infections do not need antibiotic treatment because the infection is self-limited. Treatment with quinolinic acid antibiotics is only for patients with dysentery and high fever suggestive of bacteremia. Also, patients with AIDS, malignancy, transplantation, prosthetic implants, valvular heart disease, or extreme age will require antibiotic therapy. For mild to moderate C. difficile infection, metronidazole is the preferred treatment. In severe cases of C. difficile infection, oral vancomycin is the recommended approach. In complicated cases, oral vancomycin with intravenous metronidazole is the recommendation.[18]

In patients, particularly children, with enterohemorrhagic E. coli (E. coli O157: 7H and non-O157: H7), antibiotics are not recommendations for treating infection because killing the bacteria can lead to increased release of Shigella toxins and enhance the risk of the hemolytic uremic syndrome.[2]

Because of rising multidrug resistance to antituberculous treatment, cases with active Mycobacterium tuberculosis colitis receive therapy with rifampin, isoniazid, pyrazinamide, and ethambutol for 9 to 12 months. The reader should review the recent guidelines by the World Health Organisation on treating developing resistance in tuberculosis.[19]  

The majority of patients with CMV colitis who are immunocompetent may need no treatment with antiviral medications. However, antiviral therapy in immunocompetent patients with CMV colitis could be limited to males over the age of 55 who suffer from severe disease and have co-morbidities affecting the immune system such as diabetes mellitus or chronic renal failure; consider an assessment of the colon viral load. The drug of choice is oral or intravenous ganciclovir.[19]

Treatment of E. histolytica is recommended even in asymptomatic individuals. Noninvasive colitis may be treated with paromomycin to eliminate intraluminal cysts. Metronidazole is the antimicrobial of choice for invasive amoebiasis. Medications with longer half-lives (such as tinidazole and ornidazole) allow for shorter treatment periods and are better tolerated. After completing a 10-day course of a nitroimidazole, the patient should be placed on paromomycin to eradicate the luminal parasites. Fulminant amoebic colitis requires the addition of broad-spectrum antibiotics to the treatment due to the risk of bacterial translocation.[21]

Because of emerging resistance in gonorrhea, current treatment as per current guidelines comprises intramuscular ceftriaxone 500 mg together with an oral dose of azithromycin 1 g. Alternative protocols could be cefixime 400 mg stat or ciprofloxacin 500 mg orally stat.

The treatment of lymphogranuloma venereum uses doxycycline orally twice daily for three weeks, or erythromycin 500 mg orally four times daily for three weeks.[22]

Genital/rectal herpes simplex is treated with acyclovir 400 mg three times daily or valaciclovir 500 mg twice daily for five days. Analgesia and saline bathing could soothe the pain. Intravenous therapy is an option if the patient tolerates oral treatment poorly. Consider prolonging treatment if new lesions develop. For recurrent genital/rectal herpes, lesions are usually mild, may need no specific treatment. Symptomatic treatment could help. Challenging cases such as those with recurrence at short intervals may require referral for specialized advice. The partner should also have an examination and treatment if the lesion is active.

Syphilis treatment is with penicillin (the drug of choice). A single dose of 2.4 mega units of intramuscular benzathine benzylpenicillin is the recommendation for early syphilis or three doses at weekly intervals with late syphilis. Doxycycline could be an alternative treatment for individuals sensitive to penicillin. Follow up patients to ensure clearance from infection and notification are required.[23]

Differential Diagnosis

• Inflammatory bowel disease

• Colorectal cancer

• Diverticulitis

• Ischemic colitis

• Irritable bowel disease

• Drug-induced colitis

• Radiation-associated colitis

• Colitis complicating immune deficiency disorders

• Graft-versus-host disease

• Acute appendicitis/ileocecal mass: The differential diagnosis may include:

Prognosis

Most infectious colitis cases last approximately seven days, with severe cases lingering for several weeks. If left untreated, prolonged disease may be confused for ulcerative colitis.[24]

Complications

Complications include[25][26][27][23]: 

• Intestinal perforation

• Toxic megacolon (Clostridium difficile-associated colitis, Salmonella, Shigella, Campylobacter jejuni, Cytomegalovirus, Rotavirus), and fulminant form of amebiasis

• Pseudo-membrane formation (Clostridium difficile)

• Hemorrhagic colitis (enteroinvasive E. coli, enterohemorrhagic E. coli)

• Hemolytic-uremic syndrome (enterohemorrhagic E coli, Campylobacter jejuni, Shigella)

• Post-infectious irritable bowel syndrome, dyspepsia

• Guillain-Barre syndrome (Campylobacter jejuni colitis [serotype HS:19], Cytomegalovirus colitis)

• Encephalitis, seizure (Shigella)

• Reactive arthritis (Shigella, Campylobacter jejuni, Yersinia enterocolitica colitis)

• Pancreatitis, cholecystitis, meningitis, purulent arthritis (Campylobacter jejuni)

• Septic shock and death (Shigella, Clostridium difficile)

• Elevated serum pancreatic enzymes without clinical pancreatitis (Salmonella)

• Renal failure, shock (Clostridium difficile)

• Hypoglycemia, hyponatremia (Shigella)

• Erythema nodosum (Yersinia enterocolitica)

• Patients with CMV colitis complicating inflammatory bowel disease may develop severe hemorrhage, megacolon, fulminant colitis, or colon perforation; these complications contribute to the high risk of mortality

Deterrence and Patient Education

Patients need to receive counsel regarding the importance of antibiotic adherence, as well as any signs of relapse or worsening condition.

Pearls and Other Issues

In managing patients presenting with colitis, computed tomography scans, colonoscopy, and biopsies could help differentiate between infectious and noninfectious colitis. However, these investigations are of little help in deciding the infectious agent causing colitis. Microbiological studies, including microscopy, cultures, and sensitivity, and PCR DNA tests are of high value in defining the etiology of an infectious cause. Treatment of infectious colitis should be individualized depending on the patient’s age, causative agent, risk factors, presence of comorbidities, and current guidelines of management of infectious colitis. Antibiotics treatment of children with E. coli O157: H7 infection increases the risk of hemolytic uremic syndrome and should be avoided.  

Enhancing Healthcare Team Outcomes

Infectious colitis is complex and requires an interprofessional team for the diagnosis, management, and early detection of complications. The team comprises a gastroenterologist, infectious disease consultant, pathologist, microbiologist, pharmacist, clinical pharmacologist, and general practitioner, which covers the range of expertise needed for the management of infectious colitis and handling any complications. All members of the interprofessional healthcare team, including clinicians (MDs, DOs, NPs, PAs), specialists, specialty-trained nursing staff, and pharmacists, need to communicate and collaborate across disciplinary lines in their areas of expertise to keep the entire team informed and current on the status of the case and changes required. [Level 5]

The nursing staff should monitor the follow-up of the patient. If signs and symptoms fail to resolve and/or signs or symptoms of dehydration develop, the nursing staff should arrange a return visit or possibly recommend emergency department evaluation.

Careful assessment of the patient condition and involvement of the healthcare team in evaluation and decision making is necessary for better outcomes. The nurse assigned to patient education should focus on teaching patients to wash hands, eating only well-cooked foods, and drinking bottled water, particularly during traveling, which are the essential preventable measures that patients need to know. 

Figure

Radiograph of an infant with necrotizing enterocolitis. Contributed by RadsWiki.net (CC By-S.A. 3.0 https://creativecommons.org/licenses/by-sa/3.0/deed.en)

Figure

Gross Pathology of neonatal necrotizing enterocolitis, Autopsy, infant, abdominal distention, necrosis, hemorrhage, peritonitis due to perforation. Contributed by The Centers for Disease Control and Prevention (CDC)

References

1.

Uhlich GA, Sinclair JR, Warren NG, Chmielecki WA, Fratamico P. Characterization of Shiga toxin-producing Escherichia coli isolates associated with two multistate food-borne outbreaks that occurred in 2006. Appl Environ Microbiol. 2008 Feb;74(4):1268-72. [PMC free article: PMC2258581] [PubMed: 18083883]

2.

Tarr PI, Gordon CA, Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 2005 Mar 19-25;365(9464):1073-86. [PubMed: 15781103]

3.

Newitt S, MacGregor V, Robbins V, Bayliss L, Chattaway MA, Dallman T, Ready D, Aird H, Puleston R, Hawker J. Two Linked Enteroinvasive Escherichia coli Outbreaks, Nottingham, UK, June 2014. Emerg Infect Dis. 2016 Jul;22(7):1178-84. [PMC free article: PMC4918187] [PubMed: 27314432]

4.

Jewkes J, Larson HE, Price AB, Sanderson PJ, Davies HA. Aetiology of acute diarrhoea in adults. Gut. 1981 May;22(5):388-92. [PMC free article: PMC1419238] [PubMed: 7250751]

5.

Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, Griffin PM. Foodborne illness acquired in the United States–major pathogens. Emerg Infect Dis. 2011 Jan;17(1):7-15. [PMC free article: PMC3375761] [PubMed: 21192848]

6.

Reveles KR, Lee GC, Boyd NK, Frei CR. The rise in Clostridium difficile infection incidence among hospitalized adults in the United States: 2001-2010. Am J Infect Control. 2014 Oct;42(10):1028-32. [PubMed: 25278388]

7.

Cherian JJ, Lobo I, Sukhlecha A, Chawan U, Kshirsagar NA, Nair BL, Sawardekar L. Treatment outcome of extrapulmonary tuberculosis under Revised National Tuberculosis Control Programme. Indian J Tuberc. 2017 Apr;64(2):104-108. [PubMed: 28410692]

8.

Han JK, Kim SH, Choi BI, Yeon KM, Han MC. Tuberculous colitis. Findings at double-contrast barium enema examination. Dis Colon Rectum. 1996 Nov;39(11):1204-9. [PubMed: 8918425]

9.

Karagiannis S, Papaioannou D, Goulas S, Psilopoulos D, Mavrogiannis C. Intestinal tuberculosis in a patient on infliximab treatment. Gastrointest Endosc. 2008 Jun;67(7):1178-9; discussion 1179. [PubMed: 18329027]

10.

Stanley SL. Amoebiasis. Lancet. 2003 Mar 22;361(9362):1025-34. [PubMed: 12660071]

11.

Wada Y, Matsui T, Matake H, Sakurai T, Yamamoto J, Kikuchi Y, Yorioka M, Tsuda S, Yao T, Yao S, Haraoka S, Iwashita A. Intractable ulcerative colitis caused by cytomegalovirus infection: a prospective study on prevalence, diagnosis, and treatment. Dis Colon Rectum. 2003 Oct;46(10 Suppl):S59-65. [PubMed: 14530660]

12.

Bissessor M, Fairley CK, Read T, Denham I, Bradshaw C, Chen M. The etiology of infectious proctitis in men who have sex with men differs according to HIV status. Sex Transm Dis. 2013 Oct;40(10):768-70. [PubMed: 24275725]

13.

Slimings C, Riley TV. Antibiotics and hospital-acquired Clostridium difficile infection: update of systematic review and meta-analysis. J Antimicrob Chemother. 2014 Apr;69(4):881-91. [PubMed: 24324224]

14.

Levin A, Yaari S, Stoff R, Caplan O, Wolf DG, Israeli E. Diagnosis of Cytomegalovirus Infection during Exacerbation of Ulcerative Colitis. Digestion. 2017;96(3):142-148. [PubMed: 28848127]

15.

Jessurun J. The Differential Diagnosis of Acute Colitis: Clues to a Specific Diagnosis. Surg Pathol Clin. 2017 Dec;10(4):863-885. [PubMed: 29103537]

16.

Plastaras L, Vuitton L, Badet N, Koch S, Di Martino V, Delabrousse E. Acute colitis: differential diagnosis using multidetector CT. Clin Radiol. 2015 Mar;70(3):262-9. [PubMed: 25522900]

17.

Stauffer W, Ravdin JI. Entamoeba histolytica: an update. Curr Opin Infect Dis. 2003 Oct;16(5):479-85. [PubMed: 14502002]

18.

Di X, Bai N, Zhang X, Liu B, Ni W, Wang J, Wang K, Liang B, Liu Y, Wang R. A meta-analysis of metronidazole and vancomycin for the treatment of Clostridium difficile infection, stratified by disease severity. Braz J Infect Dis. 2015 Jul-Aug;19(4):339-49. [PubMed: 26001980]

19.

Falzon D, Schünemann HJ, Harausz E, González-Angulo L, Lienhardt C, Jaramillo E, Weyer K. World Health Organization treatment guidelines for drug-resistant tuberculosis, 2016 update. Eur Respir J. 2017 Mar;49(3) [PMC free article: PMC5399349] [PubMed: 28331043]

20.

Hook EW. Syphilis. Lancet. 2017 Apr 15;389(10078):1550-1557. [PubMed: 27993382]

21.

Haque R, Huston CD, Hughes M, Houpt E, Petri WA. Amebiasis. N Engl J Med. 2003 Apr 17;348(16):1565-73. [PubMed: 12700377]

22.

Stoner BP, Cohen SE. Lymphogranuloma Venereum 2015: Clinical Presentation, Diagnosis, and Treatment. Clin Infect Dis. 2015 Dec 15;61 Suppl 8:S865-73. [PubMed: 26602624]

23.

Dean R, Gill D, Buchan D. Salmonella colitis as an unusual cause of elevated serum lipase. Am J Emerg Med. 2017 May;35(5):800.e5-800.e6. [PubMed: 27865572]

24.

Papaconstantinou HT, Thomas JS. Bacterial colitis. Clin Colon Rectal Surg. 2007 Feb;20(1):18-27. [PMC free article: PMC2780149] [PubMed: 20011357]

25.

Autenrieth DM, Baumgart DC. Toxic megacolon. Inflamm Bowel Dis. 2012 Mar;18(3):584-91. [PubMed: 22009735]

26.

Horiki N, Furukawa K, Kitade T, Sakuno T, Katsurahara M, Harada T, Tano S, Yamada R, Hamada Y, Inoue H, Tanaka K, Gabazza EC, Ishii N, Fukuda K, Omata F, Fujita Y, Tachibana H, Takei Y. Endoscopic findings and lesion distribution in amebic colitis. J Infect Chemother. 2015 Jun;21(6):444-8. [PubMed: 25787830]

27.

Törnblom H, Holmvall P, Svenungsson B, Lindberg G. Gastrointestinal symptoms after infectious diarrhea: a five-year follow-up in a Swedish cohort of adults. Clin Gastroenterol Hepatol. 2007 Apr;5(4):461-4. [PubMed: 17445752]

Infectious Colitis – StatPearls – NCBI Bookshelf

Continuing Education Activity

The management of infectious colitis is complex, and new approaches have been introduced. The basic and clinical aspects of infectious colitis must be clearly defined to achieve satisfactory outcomes. This activity reviews infectious colitis, and focusses on the etiology, epidemiology, pathophysiology, evaluation, management, and complications of infectious colitis, and highlights the role of the interprofessional team in improving healthcare outcomes.

Objectives:

• Identify the etiology and along with accompanying risk factors for infectious colitis.

• Describe the pathophysiology in infectious colitis.

• Summarize the evaluation process infectious colitis.

• Review the management options available for infectious colitis.

Access free multiple choice questions on this topic.

Introduction

Colonic infection by bacteria, viruses, or parasites results in an inflammatory-type of diarrhea and accounts for the majority of cases presenting with acute diarrhea. These patients present with purulent, bloody, and mucoid loose bowel motions, fever, tenesmus, and abdominal pain. Common bacteria causing bacterial colitis include Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis. Common causes of viral colitis include Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus. Parasitic infestation, such as Entamoeba histolytica, a protozoan parasite, is capable of invading the colonic mucosa and causing colitis. Sexually transmitted infection affecting the rectum merit consideration during assessment. These diseases can occur in patients with HIV infection and men who have sex with men and may include Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex, and Treponema pallidum.

The patients present with rectal symptoms that mimic inflammatory bowel disease, including rectal pain, tenesmus, bloody mucoid discharge, and urgency. Detailed medical history and identification of specific associated risks are essential in establishing the diagnosis. Stool microscopy and culture and endoscopy are crucial to the diagnosis. However, stool culture helps in the diagnosis of less than 50% of patients presenting with bacterial colitis, and endoscopic examinations usually reveal non-specific pathological changes. Therefore, an approach is needed to evaluate and diagnose the cause of colitis and exclude non-infectious causes. This activity discusses current strategies to diagnose and manage infectious colitis and how to make a high index of suspicion based on clinical presentation and use investigation methods to reach a final diagnosis. This activity discusses the etiology, epidemiology, pathophysiology, clinical presentation, evaluation, differential diagnosis, complications, and management of patients with infectious colitis.  

Etiology

Infectious colitis may result from infection with:

1. Bacterial infections: including Campylobacter jejuni, Salmonella, Shigella, Escherichia coli (including these subgroups – enterotoxigenic E. coli, enteropathogenic E. coli, enterohemorrhagic E. coli, enteroinvasive E. coli, enteroaggregative E. coli), Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis.

2. Viral infection: Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus (CMV).

3. Parasitic infection such as Entamoeba histolytica (causes amoebic colitis)

4. Sexually transmitted infections: Particularly infections affecting the rectum in patients with HIV infection and men who have sex with men may include the following infections: Neisseria gonorrhoeae, Chlamydia trachomatis (causes lymphogranuloma venereum), Herpes simplex 1 and 2, and Treponema pallidum (causes syphilis).

Enterotoxigenic E. coli is the leading cause of traveler’s diarrhea. Enteroaggregative E. coli can cause traveler’s diarrhea, but it is not the leading cause. Enterohemorrhagic E. coli has two main serotypes E. coli O157: H7 and non-O157: H7; the natural reservoirs of both serotypes are cows. Therefore, the infection is related to the consumption of inadequately cooked beef, or contaminated milk or vegetables. They are responsible for outbreaks in developed countries.[1]

Two of these subgroups cause non-bloody diarrhea: enterotoxigenic E. coli and enteroaggregative E. coli; both produce enterotoxins that induce chloride and water secretion and inhibit their absorption. However, enterohemorrhagic E. coli (both strains E coli O157: H7 and non-O157: H7) causes bloody diarrhea and produce Shiga-like toxins, resulting in a clinical picture similar to Shigella
dysenteriae infection.[2]

Both enteropathogenic E. coli and enteroinvasive E. coli do not produce toxins. Enteropathogenic E. coli is responsible for outbreaks, particularly in children less than two years of age, while enteroinvasive E. coli causes acute self-limited colitis and is responsible for outbreaks mainly in developing countries. However, the outbreaks in Nottingham, the UK, in 2004, highlight the need for its consideration as a potential pathogen in foodborne outbreaks in Europe.[3]  

Children (in daycare centers), elderly (in nursing homes), and immunocompromised individuals are susceptible to these infections. The fecal-oral route, animal host, and ingestion of contaminated food and water are the usual modes of infection.

Food and water contaminations with pathogenic bacteria may cause large outbreaks of diseases.

Epidemiology

Bacterial colitis accounts for up to 47% of cases of acute diarrhea.[4]
Campylobacter jejuni is the number one bacterial cause of diarrheal illness worldwide with an estimated prevalence of 25 to 30 per 100000 population. For Salmonella infection, an estimated 1.2 million annual cases of non-typhoidal salmonellosis occurred in the United States.

Shigellosis incidence worldwide reported to be approximately 165 million cases, but mortality has decreased in the last three decades because of improvement in laboratory diagnosis and treatment. In the United States, estimates are approximately 500000 cases per year, with 38 to 45 deaths.[5]

Yersinia enterocolitica colitis commonly presents in young children in the winter. In the United States, estimate are one case per 100000 individuals each year.

Clostridium difficile infection in hospitalized adults in the United States increased from 4.5 cases per 1000 discharge in 2001 to 8.2 cases in 2010 and a mortality rate of 7%.[6] Another study from the United Stated on Clostridium infection estimated 500000 cases in 2011 with 83000 recurrence and 29300 deaths.

Mycobacterium tuberculosis is the third most common site of extra-pulmonary tuberculosis, accounting for 12.8% of all cases under this category.[7] The recurrence of tuberculosis in developing countries parallels the AIDS epidemic distribution closely.[8] Other factors for increasing rates of tuberculosis in many developed countries are related to the migrant population, deterioration in social conditions, cutbacks in public health surveillance services, and increased prevalence of immune-suppressed individuals (AIDS, those receiving biological agents in diseases such as rheumatoid arthritis, and inflammatory bowel disease).[9]

Amebiasis ranks as the second leading cause of death due to protozoan infection after malaria, Chagas disease, and leishmaniasis.[10]

The prevalence of CMV infection in percent colitis is in the range of 21% to 34%.[11] CMV reactivation in patients with severe ulcerative colitis has a reported prevalence of 4.5% to 16.6% and as high as 25% in patients requiring colectomy for severe colitis.

Infectious proctitis among HIV-positive and HIV-negative men varied and in a recent study was as follows: chlamydia (23% versus 22%, respectively), gonorrhoea (13% versus 11%), HSV-1 (14% versus 6%), and HSV-2 (22% versus 12%), lymphogranuloma venereum (8% versus 0.7%), more than one infection (18% versus 9%). Approximately thirty-two percent of HSV proctitis had external anal ulcerations.[12]

Pathophysiology

Infection with Campylobacter jejuni is a result of orally ingested contaminated food or water. Several factors influence infections, including the dose of bacteria ingested, the virulence of organisms, and the immunity of the host. The median incubation period is from 2 to 4 days. C. jejuni multiplies in the bile and then invade the epithelial layers and travel to the lamina propria producing a diffuse, bloody, edematous enteritis.

Pseudomembranous colitis is caused by toxin-producing Clostridium difficile. The disease develops as a result of altered normal microflora (usually by antibiotic therapy such as cephalosporin and beta-lactam antibiotics) that enables overgrowth and colonization of the intestine by Clostridium difficile and production of its toxins.[13]

Enterotoxigenic E. coli produces heat-labile (HL) and heat-stable (ST) toxins. The HL toxins activate adenyl cyclase in enterocytes resulting in increased cAMP and stimulation of chloride secretion and inhibition of absorption. The ST toxins bind to guanylate cyclase resulting in increased cGMP and effects on cellular transporters similar to those caused by LT toxins resulting in secretory non-inflammatory diarrhea (this explains the limited histopathological changes in this infection).[14]

Enteropathogenic E. coli can produce proteins for “attaching” and “effacing” (A/E) lesions, which enable the bacteria to get tightly attached to the enterocytes apical membranes and causing effacement or loss of the microvilli. As stated earlier, enteropathogenic E. coli does not produce toxins, and their underlying mechanisms for causing diarrhea is by attaching and effacing lesions.[15]

Enterohemorrhagic E. coli; both of its serotypes E. coli O157: H7 and non-O157: H7 produce Shiga-like toxins similar to Shigella dysenteriae infection. However, E. coli O157: H7 strains are more likely to cause outbreaks compared to non-O157: H7 serotypes. They produce bloody diarrhea and are responsible for the development of hemolytic-uremic syndrome and ischemic colitis.[16]

Enteroinvasive coli do not produce toxins; they invade enterocytes and cause self-limited colitis. Exact details of their pathogenetic mechanisms are still not fully understood.

Enteroaggregative E. coli produces enterotoxins related to Shigella enterotoxins and ST toxins of enterotoxigenic E. coli. They attach themselves to enterocytes via adherence fimbriae.

Immunity to Mycobacterium tuberculosis undergoes mediation via T-cells resulting in macrophage stimulation to kill the bacteria. Reactivation of infection or re-exposure to the bacillus in a sensitized individual, as it is the case in most Mycobacterium tuberculosis colitis cases resulting in rapid defense reactions and increased tissue necrosis accompanied by loss of T-cell immunity (tuberculin test in these patients becomes negative although used to be previously positive, which is consistent with fading T-cell protection).[17]

Primary CMV infection in immunocompetent individuals is usually asymptomatic. However, in patients whose immune response is compromised, they develop symptoms in different body organs, including CMV colitis.

Research concerning genetics and molecular sciences of Entamoeba histolytica have brought new understanding about mechanisms by which the parasite impose invasive abilities and pathological lesions in the colon and extracolonic organs. Host factors predisposing to infection are also under research.[17]

Histopathology

No significant differences appear in histological biopsies taken from the rectum of patients with different bacterial infections. However, the absence of crypt architecture distortion or basal plasmacytosis helps differentiate acute infectious colitis from chronic inflammation caused by inflammatory bowel disease.

Infection with Escherichia coli O157: H7 may show changes similar to those of ischemic colitis (small atrophic crypts, hyalinized lamina propria, and fibrin thrombi).

Yersinia enterocolitica shows inflammatory changes, ulcerations in the cecum and terminal ileum areas, hyperplasia of Peyer patches, microabscesses, and granulomas. (This condition requires differentiation from Crohn disease and Mycobacterium tuberculosis involving the terminal ileum/caecum area).

Colonic histopathological changes are limited in enterotoxigenic E. coli, enteroinvasive E. coli, and enteroaggregative E. coli infections.

In Mycobacterium tuberculosis, characteristic granulomas with central caseation are present; tubercle bacilli are identifiable with acid-fast stains.[18]

The diagnosis of CMV colitis requires histological examination of biopsy tissues, taken from the ulcer edge or base. Patients with punched-out ulcers are associated with an increase in inclusion bodies on histology [Yang H et al. 2017]. Colonic mucosal biopsies stained with H & E may reveal the typical inclusion associated with CMV colitis, “owl eye appearance” inclusion bodies, which are highly specific for CMV. However, H & E staining has low sensitivity compared to immunohistochemistry, which is considered the gold standard for diagnosing CMV colitis.[19]

The histological features of biopsies taken from the rectum are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests, including serology and PCR, are essential in making such differentiation.

History and Physical

Detailed medical history and identification of exposure risks are helpful in the diagnosis. It is essential to mention here that individuals with sickle cell anemia, hemolytic anemia, immunosuppression (corticosteroids, chemotherapy, and AIDS), and extremity of age are at a higher risk of Salmonella infection.  Patients with bacterial colitis present with non-specific symptoms, including diarrhea, fever, tenesmus, and abdominal pain. Patients with Yersinia enterocolitica infection may present with a syndrome indistinguishable from acute appendicitis (mesenteric adenitis, mild fever, and ileocecal tenderness).

The incidence of Clostridium difficile is higher in patients with inflammatory bowel disease, particularly ulcerative colitis. Any antibiotic can trigger the disease, but the most common antibiotics responsible are cephalosporins, clindamycin, carbapenems, trimethoprim, sulfonamides, fluoroquinolone, and penicillin combinations.[13]

Patients with Mycobacterial tuberculosis may present with abdominal pain, blood per rectum, fever, sweating, tiredness, and pallor. They may give a past medical history of the treatment of pulmonary tuberculosis. They may have abdominal tenderness in the right iliac fossa (the ileocecal area is the most commonly involved site in intestinal tuberculosis).[18]

Viral colitis (Norovirus, Rotavirus, and Adenovirus) are common in infants and young children. Affected patients present with nausea, vomiting, watery diarrhea, and abdominal pain. CMV infection is frequently symptomatic in immune-competent patients. Again, symptoms are usually non-specific, including diarrhea, abdominal pain, fever, malaise, rectal bleeding, and weight loss. However, hematochezia and diarrhea are the most frequent symptoms. It is difficult to distinguish between ulcerative colitis from CMV colitis based on clinical presentation.[14]

Amoebic colitis usually presents with diarrhea, mucoid discharge, hematochezia, tenesmus, and abdominal bloating. Contaminated water supplies and poor sanitation are often the cases for traveling overseas to endemic areas and increased risk of fecal-oral transmission of amebas.

Patients with colitis-associated with sexually transmitted infection present with anorectal pain, with a purulent, mucoid or bloody discharge, tenesmus, or urgency. The sexual history is vital in evaluating these patients. 

Evaluation

Diagnosis of colitis centers on clinical findings, laboratory tests, endoscopy, and biopsy. Endoscopy and biopsy should not be the primary investigations and may be necessary after a critical evaluation of the patient’s condition and the results from the initial examination.

Because infection is a common etiology of colitis and can produce clinical presentations indistinguishable from inflammatory bowel disease, microbiological studies and cultures for bacterial and parasitic infestations should be the initial investigations. Laboratory tests including complete blood count, ESR, CRP, arterial blood gases, activated partial thromboplastin time, serum albumin, total protein, blood urea, creatinine, and electrolytes should be ordered. Polymerase chain reaction-based molecular methods (PCR-based multiplex GI pathogens) can help in the rapid identification of nvestigationsSalmonella, Shigella, and Yersinia from primary stool samples. Abdominal and pelvis CT scan, colonoscopy, tissue biopsies, and fecal cultures (multiple specimens) and antimicrobial susceptibility testing should help differentiate infectious from non-infectious causes of colitis and guiding treatment.[15]

Recently multidetector CT scans of the abdomen were used to differentiate between inflammatory bowel disease and acute colitis related to bacterial infection. The five signs described to diagnose bacterial colitis are (1) continuous distribution, (2) empty colon, (3) absence of fat stranding, (4) absence of a “comb’ sign, and (5) absence of enlarged lymph nodes.[16]

The diagnosis of active Mycobacterium tuberculosis colitis focuses on clinical presentation, clinical examination, and laboratory investigations. A complete blood count may reveal low hemoglobin, leukocytosis, and moderately elevated ESR. Chest X-ray may reveal fibrotic changes, cavitation, or old scar of pulmonary tuberculosis; an abdominal roentgenogram may reveal prominent large bowel. Abdominal and pelvis CT scans may show diffuse thickening of the colonic wall, especially of the terminal ileum and the cecum. A colonoscopy usually shows diffuse ulceration throughout the colon, from the rectum to cecum. Histopathological biopsies taken from the cecum show caseating granuloma and chronic inflammatory cells. Mantoux skin test (tuberculin test) is usually requested. This test does not measure immunity to tuberculosis but the degree of hypersensitivity to tuberculin. The results must be interpreted carefully with consideration to the patient’s medical risk factors. Usually, the Mantoux test becomes negative in these patients after being previously positive, indicating the fading of resistance to the organism.[17] PCR testing and cultures of intestinal fluid for bacterial species and acid-fast bacillus are requested.

Diagnosis of CMV colitis uses clinical findings, laboratory tests, and endoscopic findings. Endoscopy and tissue CMV-specific immunohistochemistry (IHC) and or PCR CMV DNA quantification are needed to confirm the diagnosis [20]. 

In amoebic colitis, rectosigmoid involvement may present on colonoscopy; however, the cecum is the most commonly involved site, followed by the ascending colon (showing colonic inflammation, erythema, oedematous mucosa, erosions, white or yellow exudates, and ulcerations). The presence of amoebic trophozoites on histopathological examination or intestinal fluid cultures is important in the diagnosis. Serum E. histolytica antibody examination and antibody titer greater than 1:128 is considered positive.[17][10]

For patients with suspected sexually transmitted infections of the rectum, histological features of biopsies taken are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests are usually helpful; these include:

• Gonorrhea: Microscopic examination of smears from the lesions showing Gram-negative diplococci. Culture and sensitivity tests of smears taken from lesions.

• Lymphogranuloma venereum: Genotyping of Chlamydia trachomatis- DNA PCR.

• Genital/rectal herpes: Swabs from rectal vesicles or ulcers to detect DNA by PCR.

• Syphilis: Dark-field microscopy, PCR, direct fluorescent antibody test, treponemal antigen-based enzyme immunoassays (EIAs) for IgG and IgM antibodies, Treponema pallidum hemagglutination assay (TPHA), Treponema pallidum particle agglutination assay (TPPA), and fluorescent treponemal antibody absorption (FTA-ABS) test.[20]

Treatment / Management

Not all infectious colitis requires antibiotic therapy; patients with mild to moderate C. jejuni or Salmonella infections do not need antibiotic treatment because the infection is self-limited. Treatment with quinolinic acid antibiotics is only for patients with dysentery and high fever suggestive of bacteremia. Also, patients with AIDS, malignancy, transplantation, prosthetic implants, valvular heart disease, or extreme age will require antibiotic therapy. For mild to moderate C. difficile infection, metronidazole is the preferred treatment. In severe cases of C. difficile infection, oral vancomycin is the recommended approach. In complicated cases, oral vancomycin with intravenous metronidazole is the recommendation.[18]

In patients, particularly children, with enterohemorrhagic E. coli (E. coli O157: 7H and non-O157: H7), antibiotics are not recommendations for treating infection because killing the bacteria can lead to increased release of Shigella toxins and enhance the risk of the hemolytic uremic syndrome.[2]

Because of rising multidrug resistance to antituberculous treatment, cases with active Mycobacterium tuberculosis colitis receive therapy with rifampin, isoniazid, pyrazinamide, and ethambutol for 9 to 12 months. The reader should review the recent guidelines by the World Health Organisation on treating developing resistance in tuberculosis.[19]  

The majority of patients with CMV colitis who are immunocompetent may need no treatment with antiviral medications. However, antiviral therapy in immunocompetent patients with CMV colitis could be limited to males over the age of 55 who suffer from severe disease and have co-morbidities affecting the immune system such as diabetes mellitus or chronic renal failure; consider an assessment of the colon viral load. The drug of choice is oral or intravenous ganciclovir.[19]

Treatment of E. histolytica is recommended even in asymptomatic individuals. Noninvasive colitis may be treated with paromomycin to eliminate intraluminal cysts. Metronidazole is the antimicrobial of choice for invasive amoebiasis. Medications with longer half-lives (such as tinidazole and ornidazole) allow for shorter treatment periods and are better tolerated. After completing a 10-day course of a nitroimidazole, the patient should be placed on paromomycin to eradicate the luminal parasites. Fulminant amoebic colitis requires the addition of broad-spectrum antibiotics to the treatment due to the risk of bacterial translocation.[21]

Because of emerging resistance in gonorrhea, current treatment as per current guidelines comprises intramuscular ceftriaxone 500 mg together with an oral dose of azithromycin 1 g. Alternative protocols could be cefixime 400 mg stat or ciprofloxacin 500 mg orally stat.

The treatment of lymphogranuloma venereum uses doxycycline orally twice daily for three weeks, or erythromycin 500 mg orally four times daily for three weeks.[22]

Genital/rectal herpes simplex is treated with acyclovir 400 mg three times daily or valaciclovir 500 mg twice daily for five days. Analgesia and saline bathing could soothe the pain. Intravenous therapy is an option if the patient tolerates oral treatment poorly. Consider prolonging treatment if new lesions develop. For recurrent genital/rectal herpes, lesions are usually mild, may need no specific treatment. Symptomatic treatment could help. Challenging cases such as those with recurrence at short intervals may require referral for specialized advice. The partner should also have an examination and treatment if the lesion is active.

Syphilis treatment is with penicillin (the drug of choice). A single dose of 2.4 mega units of intramuscular benzathine benzylpenicillin is the recommendation for early syphilis or three doses at weekly intervals with late syphilis. Doxycycline could be an alternative treatment for individuals sensitive to penicillin. Follow up patients to ensure clearance from infection and notification are required.[23]

Differential Diagnosis

• Inflammatory bowel disease

• Colorectal cancer

• Diverticulitis

• Ischemic colitis

• Irritable bowel disease

• Drug-induced colitis

• Radiation-associated colitis

• Colitis complicating immune deficiency disorders

• Graft-versus-host disease

• Acute appendicitis/ileocecal mass: The differential diagnosis may include:

Prognosis

Most infectious colitis cases last approximately seven days, with severe cases lingering for several weeks. If left untreated, prolonged disease may be confused for ulcerative colitis.[24]

Complications

Complications include[25][26][27][23]: 

• Intestinal perforation

• Toxic megacolon (Clostridium difficile-associated colitis, Salmonella, Shigella, Campylobacter jejuni, Cytomegalovirus, Rotavirus), and fulminant form of amebiasis

• Pseudo-membrane formation (Clostridium difficile)

• Hemorrhagic colitis (enteroinvasive E. coli, enterohemorrhagic E. coli)

• Hemolytic-uremic syndrome (enterohemorrhagic E coli, Campylobacter jejuni, Shigella)

• Post-infectious irritable bowel syndrome, dyspepsia

• Guillain-Barre syndrome (Campylobacter jejuni colitis [serotype HS:19], Cytomegalovirus colitis)

• Encephalitis, seizure (Shigella)

• Reactive arthritis (Shigella, Campylobacter jejuni, Yersinia enterocolitica colitis)

• Pancreatitis, cholecystitis, meningitis, purulent arthritis (Campylobacter jejuni)

• Septic shock and death (Shigella, Clostridium difficile)

• Elevated serum pancreatic enzymes without clinical pancreatitis (Salmonella)

• Renal failure, shock (Clostridium difficile)

• Hypoglycemia, hyponatremia (Shigella)

• Erythema nodosum (Yersinia enterocolitica)

• Patients with CMV colitis complicating inflammatory bowel disease may develop severe hemorrhage, megacolon, fulminant colitis, or colon perforation; these complications contribute to the high risk of mortality

Deterrence and Patient Education

Patients need to receive counsel regarding the importance of antibiotic adherence, as well as any signs of relapse or worsening condition.

Pearls and Other Issues

In managing patients presenting with colitis, computed tomography scans, colonoscopy, and biopsies could help differentiate between infectious and noninfectious colitis. However, these investigations are of little help in deciding the infectious agent causing colitis. Microbiological studies, including microscopy, cultures, and sensitivity, and PCR DNA tests are of high value in defining the etiology of an infectious cause. Treatment of infectious colitis should be individualized depending on the patient’s age, causative agent, risk factors, presence of comorbidities, and current guidelines of management of infectious colitis. Antibiotics treatment of children with E. coli O157: H7 infection increases the risk of hemolytic uremic syndrome and should be avoided.  

Enhancing Healthcare Team Outcomes

Infectious colitis is complex and requires an interprofessional team for the diagnosis, management, and early detection of complications. The team comprises a gastroenterologist, infectious disease consultant, pathologist, microbiologist, pharmacist, clinical pharmacologist, and general practitioner, which covers the range of expertise needed for the management of infectious colitis and handling any complications. All members of the interprofessional healthcare team, including clinicians (MDs, DOs, NPs, PAs), specialists, specialty-trained nursing staff, and pharmacists, need to communicate and collaborate across disciplinary lines in their areas of expertise to keep the entire team informed and current on the status of the case and changes required. [Level 5]

The nursing staff should monitor the follow-up of the patient. If signs and symptoms fail to resolve and/or signs or symptoms of dehydration develop, the nursing staff should arrange a return visit or possibly recommend emergency department evaluation.

Careful assessment of the patient condition and involvement of the healthcare team in evaluation and decision making is necessary for better outcomes. The nurse assigned to patient education should focus on teaching patients to wash hands, eating only well-cooked foods, and drinking bottled water, particularly during traveling, which are the essential preventable measures that patients need to know. 

Figure

Radiograph of an infant with necrotizing enterocolitis. Contributed by RadsWiki.net (CC By-S.A. 3.0 https://creativecommons.org/licenses/by-sa/3.0/deed.en)

Figure

Gross Pathology of neonatal necrotizing enterocolitis, Autopsy, infant, abdominal distention, necrosis, hemorrhage, peritonitis due to perforation. Contributed by The Centers for Disease Control and Prevention (CDC)

References

1.

Uhlich GA, Sinclair JR, Warren NG, Chmielecki WA, Fratamico P. Characterization of Shiga toxin-producing Escherichia coli isolates associated with two multistate food-borne outbreaks that occurred in 2006. Appl Environ Microbiol. 2008 Feb;74(4):1268-72. [PMC free article: PMC2258581] [PubMed: 18083883]

2.

Tarr PI, Gordon CA, Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 2005 Mar 19-25;365(9464):1073-86. [PubMed: 15781103]

3.

Newitt S, MacGregor V, Robbins V, Bayliss L, Chattaway MA, Dallman T, Ready D, Aird H, Puleston R, Hawker J. Two Linked Enteroinvasive Escherichia coli Outbreaks, Nottingham, UK, June 2014. Emerg Infect Dis. 2016 Jul;22(7):1178-84. [PMC free article: PMC4918187] [PubMed: 27314432]

4.

Jewkes J, Larson HE, Price AB, Sanderson PJ, Davies HA. Aetiology of acute diarrhoea in adults. Gut. 1981 May;22(5):388-92. [PMC free article: PMC1419238] [PubMed: 7250751]

5.

Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, Griffin PM. Foodborne illness acquired in the United States–major pathogens. Emerg Infect Dis. 2011 Jan;17(1):7-15. [PMC free article: PMC3375761] [PubMed: 21192848]

6.

Reveles KR, Lee GC, Boyd NK, Frei CR. The rise in Clostridium difficile infection incidence among hospitalized adults in the United States: 2001-2010. Am J Infect Control. 2014 Oct;42(10):1028-32. [PubMed: 25278388]

7.

Cherian JJ, Lobo I, Sukhlecha A, Chawan U, Kshirsagar NA, Nair BL, Sawardekar L. Treatment outcome of extrapulmonary tuberculosis under Revised National Tuberculosis Control Programme. Indian J Tuberc. 2017 Apr;64(2):104-108. [PubMed: 28410692]

8.

Han JK, Kim SH, Choi BI, Yeon KM, Han MC. Tuberculous colitis. Findings at double-contrast barium enema examination. Dis Colon Rectum. 1996 Nov;39(11):1204-9. [PubMed: 8918425]

9.

Karagiannis S, Papaioannou D, Goulas S, Psilopoulos D, Mavrogiannis C. Intestinal tuberculosis in a patient on infliximab treatment. Gastrointest Endosc. 2008 Jun;67(7):1178-9; discussion 1179. [PubMed: 18329027]

10.

Stanley SL. Amoebiasis. Lancet. 2003 Mar 22;361(9362):1025-34. [PubMed: 12660071]

11.

Wada Y, Matsui T, Matake H, Sakurai T, Yamamoto J, Kikuchi Y, Yorioka M, Tsuda S, Yao T, Yao S, Haraoka S, Iwashita A. Intractable ulcerative colitis caused by cytomegalovirus infection: a prospective study on prevalence, diagnosis, and treatment. Dis Colon Rectum. 2003 Oct;46(10 Suppl):S59-65. [PubMed: 14530660]

12.

Bissessor M, Fairley CK, Read T, Denham I, Bradshaw C, Chen M. The etiology of infectious proctitis in men who have sex with men differs according to HIV status. Sex Transm Dis. 2013 Oct;40(10):768-70. [PubMed: 24275725]

13.

Slimings C, Riley TV. Antibiotics and hospital-acquired Clostridium difficile infection: update of systematic review and meta-analysis. J Antimicrob Chemother. 2014 Apr;69(4):881-91. [PubMed: 24324224]

14.

Levin A, Yaari S, Stoff R, Caplan O, Wolf DG, Israeli E. Diagnosis of Cytomegalovirus Infection during Exacerbation of Ulcerative Colitis. Digestion. 2017;96(3):142-148. [PubMed: 28848127]

15.

Jessurun J. The Differential Diagnosis of Acute Colitis: Clues to a Specific Diagnosis. Surg Pathol Clin. 2017 Dec;10(4):863-885. [PubMed: 29103537]

16.

Plastaras L, Vuitton L, Badet N, Koch S, Di Martino V, Delabrousse E. Acute colitis: differential diagnosis using multidetector CT. Clin Radiol. 2015 Mar;70(3):262-9. [PubMed: 25522900]

17.

Stauffer W, Ravdin JI. Entamoeba histolytica: an update. Curr Opin Infect Dis. 2003 Oct;16(5):479-85. [PubMed: 14502002]

18.

Di X, Bai N, Zhang X, Liu B, Ni W, Wang J, Wang K, Liang B, Liu Y, Wang R. A meta-analysis of metronidazole and vancomycin for the treatment of Clostridium difficile infection, stratified by disease severity. Braz J Infect Dis. 2015 Jul-Aug;19(4):339-49. [PubMed: 26001980]

19.

Falzon D, Schünemann HJ, Harausz E, González-Angulo L, Lienhardt C, Jaramillo E, Weyer K. World Health Organization treatment guidelines for drug-resistant tuberculosis, 2016 update. Eur Respir J. 2017 Mar;49(3) [PMC free article: PMC5399349] [PubMed: 28331043]

20.

Hook EW. Syphilis. Lancet. 2017 Apr 15;389(10078):1550-1557. [PubMed: 27993382]

21.

Haque R, Huston CD, Hughes M, Houpt E, Petri WA. Amebiasis. N Engl J Med. 2003 Apr 17;348(16):1565-73. [PubMed: 12700377]

22.

Stoner BP, Cohen SE. Lymphogranuloma Venereum 2015: Clinical Presentation, Diagnosis, and Treatment. Clin Infect Dis. 2015 Dec 15;61 Suppl 8:S865-73. [PubMed: 26602624]

23.

Dean R, Gill D, Buchan D. Salmonella colitis as an unusual cause of elevated serum lipase. Am J Emerg Med. 2017 May;35(5):800.e5-800.e6. [PubMed: 27865572]

24.

Papaconstantinou HT, Thomas JS. Bacterial colitis. Clin Colon Rectal Surg. 2007 Feb;20(1):18-27. [PMC free article: PMC2780149] [PubMed: 20011357]

25.

Autenrieth DM, Baumgart DC. Toxic megacolon. Inflamm Bowel Dis. 2012 Mar;18(3):584-91. [PubMed: 22009735]

26.

Horiki N, Furukawa K, Kitade T, Sakuno T, Katsurahara M, Harada T, Tano S, Yamada R, Hamada Y, Inoue H, Tanaka K, Gabazza EC, Ishii N, Fukuda K, Omata F, Fujita Y, Tachibana H, Takei Y. Endoscopic findings and lesion distribution in amebic colitis. J Infect Chemother. 2015 Jun;21(6):444-8. [PubMed: 25787830]

27.

Törnblom H, Holmvall P, Svenungsson B, Lindberg G. Gastrointestinal symptoms after infectious diarrhea: a five-year follow-up in a Swedish cohort of adults. Clin Gastroenterol Hepatol. 2007 Apr;5(4):461-4. [PubMed: 17445752]

Infectious Colitis – StatPearls – NCBI Bookshelf

Continuing Education Activity

The management of infectious colitis is complex, and new approaches have been introduced. The basic and clinical aspects of infectious colitis must be clearly defined to achieve satisfactory outcomes. This activity reviews infectious colitis, and focusses on the etiology, epidemiology, pathophysiology, evaluation, management, and complications of infectious colitis, and highlights the role of the interprofessional team in improving healthcare outcomes.

Objectives:

• Identify the etiology and along with accompanying risk factors for infectious colitis.

• Describe the pathophysiology in infectious colitis.

• Summarize the evaluation process infectious colitis.

• Review the management options available for infectious colitis.

Access free multiple choice questions on this topic.

Introduction

Colonic infection by bacteria, viruses, or parasites results in an inflammatory-type of diarrhea and accounts for the majority of cases presenting with acute diarrhea. These patients present with purulent, bloody, and mucoid loose bowel motions, fever, tenesmus, and abdominal pain. Common bacteria causing bacterial colitis include Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis. Common causes of viral colitis include Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus. Parasitic infestation, such as Entamoeba histolytica, a protozoan parasite, is capable of invading the colonic mucosa and causing colitis. Sexually transmitted infection affecting the rectum merit consideration during assessment. These diseases can occur in patients with HIV infection and men who have sex with men and may include Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex, and Treponema pallidum.

The patients present with rectal symptoms that mimic inflammatory bowel disease, including rectal pain, tenesmus, bloody mucoid discharge, and urgency. Detailed medical history and identification of specific associated risks are essential in establishing the diagnosis. Stool microscopy and culture and endoscopy are crucial to the diagnosis. However, stool culture helps in the diagnosis of less than 50% of patients presenting with bacterial colitis, and endoscopic examinations usually reveal non-specific pathological changes. Therefore, an approach is needed to evaluate and diagnose the cause of colitis and exclude non-infectious causes. This activity discusses current strategies to diagnose and manage infectious colitis and how to make a high index of suspicion based on clinical presentation and use investigation methods to reach a final diagnosis. This activity discusses the etiology, epidemiology, pathophysiology, clinical presentation, evaluation, differential diagnosis, complications, and management of patients with infectious colitis.  

Etiology

Infectious colitis may result from infection with:

1. Bacterial infections: including Campylobacter jejuni, Salmonella, Shigella, Escherichia coli (including these subgroups – enterotoxigenic E. coli, enteropathogenic E. coli, enterohemorrhagic E. coli, enteroinvasive E. coli, enteroaggregative E. coli), Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis.

2. Viral infection: Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus (CMV).

3. Parasitic infection such as Entamoeba histolytica (causes amoebic colitis)

4. Sexually transmitted infections: Particularly infections affecting the rectum in patients with HIV infection and men who have sex with men may include the following infections: Neisseria gonorrhoeae, Chlamydia trachomatis (causes lymphogranuloma venereum), Herpes simplex 1 and 2, and Treponema pallidum (causes syphilis).

Enterotoxigenic E. coli is the leading cause of traveler’s diarrhea. Enteroaggregative E. coli can cause traveler’s diarrhea, but it is not the leading cause. Enterohemorrhagic E. coli has two main serotypes E. coli O157: H7 and non-O157: H7; the natural reservoirs of both serotypes are cows. Therefore, the infection is related to the consumption of inadequately cooked beef, or contaminated milk or vegetables. They are responsible for outbreaks in developed countries.[1]

Two of these subgroups cause non-bloody diarrhea: enterotoxigenic E. coli and enteroaggregative E. coli; both produce enterotoxins that induce chloride and water secretion and inhibit their absorption. However, enterohemorrhagic E. coli (both strains E coli O157: H7 and non-O157: H7) causes bloody diarrhea and produce Shiga-like toxins, resulting in a clinical picture similar to Shigella
dysenteriae infection.[2]

Both enteropathogenic E. coli and enteroinvasive E. coli do not produce toxins. Enteropathogenic E. coli is responsible for outbreaks, particularly in children less than two years of age, while enteroinvasive E. coli causes acute self-limited colitis and is responsible for outbreaks mainly in developing countries. However, the outbreaks in Nottingham, the UK, in 2004, highlight the need for its consideration as a potential pathogen in foodborne outbreaks in Europe.[3]  

Children (in daycare centers), elderly (in nursing homes), and immunocompromised individuals are susceptible to these infections. The fecal-oral route, animal host, and ingestion of contaminated food and water are the usual modes of infection.

Food and water contaminations with pathogenic bacteria may cause large outbreaks of diseases.

Epidemiology

Bacterial colitis accounts for up to 47% of cases of acute diarrhea.[4]
Campylobacter jejuni is the number one bacterial cause of diarrheal illness worldwide with an estimated prevalence of 25 to 30 per 100000 population. For Salmonella infection, an estimated 1.2 million annual cases of non-typhoidal salmonellosis occurred in the United States.

Shigellosis incidence worldwide reported to be approximately 165 million cases, but mortality has decreased in the last three decades because of improvement in laboratory diagnosis and treatment. In the United States, estimates are approximately 500000 cases per year, with 38 to 45 deaths.[5]

Yersinia enterocolitica colitis commonly presents in young children in the winter. In the United States, estimate are one case per 100000 individuals each year.

Clostridium difficile infection in hospitalized adults in the United States increased from 4.5 cases per 1000 discharge in 2001 to 8.2 cases in 2010 and a mortality rate of 7%.[6] Another study from the United Stated on Clostridium infection estimated 500000 cases in 2011 with 83000 recurrence and 29300 deaths.

Mycobacterium tuberculosis is the third most common site of extra-pulmonary tuberculosis, accounting for 12.8% of all cases under this category.[7] The recurrence of tuberculosis in developing countries parallels the AIDS epidemic distribution closely.[8] Other factors for increasing rates of tuberculosis in many developed countries are related to the migrant population, deterioration in social conditions, cutbacks in public health surveillance services, and increased prevalence of immune-suppressed individuals (AIDS, those receiving biological agents in diseases such as rheumatoid arthritis, and inflammatory bowel disease).[9]

Amebiasis ranks as the second leading cause of death due to protozoan infection after malaria, Chagas disease, and leishmaniasis.[10]

The prevalence of CMV infection in percent colitis is in the range of 21% to 34%.[11] CMV reactivation in patients with severe ulcerative colitis has a reported prevalence of 4.5% to 16.6% and as high as 25% in patients requiring colectomy for severe colitis.

Infectious proctitis among HIV-positive and HIV-negative men varied and in a recent study was as follows: chlamydia (23% versus 22%, respectively), gonorrhoea (13% versus 11%), HSV-1 (14% versus 6%), and HSV-2 (22% versus 12%), lymphogranuloma venereum (8% versus 0.7%), more than one infection (18% versus 9%). Approximately thirty-two percent of HSV proctitis had external anal ulcerations.[12]

Pathophysiology

Infection with Campylobacter jejuni is a result of orally ingested contaminated food or water. Several factors influence infections, including the dose of bacteria ingested, the virulence of organisms, and the immunity of the host. The median incubation period is from 2 to 4 days. C. jejuni multiplies in the bile and then invade the epithelial layers and travel to the lamina propria producing a diffuse, bloody, edematous enteritis.

Pseudomembranous colitis is caused by toxin-producing Clostridium difficile. The disease develops as a result of altered normal microflora (usually by antibiotic therapy such as cephalosporin and beta-lactam antibiotics) that enables overgrowth and colonization of the intestine by Clostridium difficile and production of its toxins.[13]

Enterotoxigenic E. coli produces heat-labile (HL) and heat-stable (ST) toxins. The HL toxins activate adenyl cyclase in enterocytes resulting in increased cAMP and stimulation of chloride secretion and inhibition of absorption. The ST toxins bind to guanylate cyclase resulting in increased cGMP and effects on cellular transporters similar to those caused by LT toxins resulting in secretory non-inflammatory diarrhea (this explains the limited histopathological changes in this infection).[14]

Enteropathogenic E. coli can produce proteins for “attaching” and “effacing” (A/E) lesions, which enable the bacteria to get tightly attached to the enterocytes apical membranes and causing effacement or loss of the microvilli. As stated earlier, enteropathogenic E. coli does not produce toxins, and their underlying mechanisms for causing diarrhea is by attaching and effacing lesions.[15]

Enterohemorrhagic E. coli; both of its serotypes E. coli O157: H7 and non-O157: H7 produce Shiga-like toxins similar to Shigella dysenteriae infection. However, E. coli O157: H7 strains are more likely to cause outbreaks compared to non-O157: H7 serotypes. They produce bloody diarrhea and are responsible for the development of hemolytic-uremic syndrome and ischemic colitis.[16]

Enteroinvasive coli do not produce toxins; they invade enterocytes and cause self-limited colitis. Exact details of their pathogenetic mechanisms are still not fully understood.

Enteroaggregative E. coli produces enterotoxins related to Shigella enterotoxins and ST toxins of enterotoxigenic E. coli. They attach themselves to enterocytes via adherence fimbriae.

Immunity to Mycobacterium tuberculosis undergoes mediation via T-cells resulting in macrophage stimulation to kill the bacteria. Reactivation of infection or re-exposure to the bacillus in a sensitized individual, as it is the case in most Mycobacterium tuberculosis colitis cases resulting in rapid defense reactions and increased tissue necrosis accompanied by loss of T-cell immunity (tuberculin test in these patients becomes negative although used to be previously positive, which is consistent with fading T-cell protection).[17]

Primary CMV infection in immunocompetent individuals is usually asymptomatic. However, in patients whose immune response is compromised, they develop symptoms in different body organs, including CMV colitis.

Research concerning genetics and molecular sciences of Entamoeba histolytica have brought new understanding about mechanisms by which the parasite impose invasive abilities and pathological lesions in the colon and extracolonic organs. Host factors predisposing to infection are also under research.[17]

Histopathology

No significant differences appear in histological biopsies taken from the rectum of patients with different bacterial infections. However, the absence of crypt architecture distortion or basal plasmacytosis helps differentiate acute infectious colitis from chronic inflammation caused by inflammatory bowel disease.

Infection with Escherichia coli O157: H7 may show changes similar to those of ischemic colitis (small atrophic crypts, hyalinized lamina propria, and fibrin thrombi).

Yersinia enterocolitica shows inflammatory changes, ulcerations in the cecum and terminal ileum areas, hyperplasia of Peyer patches, microabscesses, and granulomas. (This condition requires differentiation from Crohn disease and Mycobacterium tuberculosis involving the terminal ileum/caecum area).

Colonic histopathological changes are limited in enterotoxigenic E. coli, enteroinvasive E. coli, and enteroaggregative E. coli infections.

In Mycobacterium tuberculosis, characteristic granulomas with central caseation are present; tubercle bacilli are identifiable with acid-fast stains.[18]

The diagnosis of CMV colitis requires histological examination of biopsy tissues, taken from the ulcer edge or base. Patients with punched-out ulcers are associated with an increase in inclusion bodies on histology [Yang H et al. 2017]. Colonic mucosal biopsies stained with H & E may reveal the typical inclusion associated with CMV colitis, “owl eye appearance” inclusion bodies, which are highly specific for CMV. However, H & E staining has low sensitivity compared to immunohistochemistry, which is considered the gold standard for diagnosing CMV colitis.[19]

The histological features of biopsies taken from the rectum are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests, including serology and PCR, are essential in making such differentiation.

History and Physical

Detailed medical history and identification of exposure risks are helpful in the diagnosis. It is essential to mention here that individuals with sickle cell anemia, hemolytic anemia, immunosuppression (corticosteroids, chemotherapy, and AIDS), and extremity of age are at a higher risk of Salmonella infection.  Patients with bacterial colitis present with non-specific symptoms, including diarrhea, fever, tenesmus, and abdominal pain. Patients with Yersinia enterocolitica infection may present with a syndrome indistinguishable from acute appendicitis (mesenteric adenitis, mild fever, and ileocecal tenderness).

The incidence of Clostridium difficile is higher in patients with inflammatory bowel disease, particularly ulcerative colitis. Any antibiotic can trigger the disease, but the most common antibiotics responsible are cephalosporins, clindamycin, carbapenems, trimethoprim, sulfonamides, fluoroquinolone, and penicillin combinations.[13]

Patients with Mycobacterial tuberculosis may present with abdominal pain, blood per rectum, fever, sweating, tiredness, and pallor. They may give a past medical history of the treatment of pulmonary tuberculosis. They may have abdominal tenderness in the right iliac fossa (the ileocecal area is the most commonly involved site in intestinal tuberculosis).[18]

Viral colitis (Norovirus, Rotavirus, and Adenovirus) are common in infants and young children. Affected patients present with nausea, vomiting, watery diarrhea, and abdominal pain. CMV infection is frequently symptomatic in immune-competent patients. Again, symptoms are usually non-specific, including diarrhea, abdominal pain, fever, malaise, rectal bleeding, and weight loss. However, hematochezia and diarrhea are the most frequent symptoms. It is difficult to distinguish between ulcerative colitis from CMV colitis based on clinical presentation.[14]

Amoebic colitis usually presents with diarrhea, mucoid discharge, hematochezia, tenesmus, and abdominal bloating. Contaminated water supplies and poor sanitation are often the cases for traveling overseas to endemic areas and increased risk of fecal-oral transmission of amebas.

Patients with colitis-associated with sexually transmitted infection present with anorectal pain, with a purulent, mucoid or bloody discharge, tenesmus, or urgency. The sexual history is vital in evaluating these patients. 

Evaluation

Diagnosis of colitis centers on clinical findings, laboratory tests, endoscopy, and biopsy. Endoscopy and biopsy should not be the primary investigations and may be necessary after a critical evaluation of the patient’s condition and the results from the initial examination.

Because infection is a common etiology of colitis and can produce clinical presentations indistinguishable from inflammatory bowel disease, microbiological studies and cultures for bacterial and parasitic infestations should be the initial investigations. Laboratory tests including complete blood count, ESR, CRP, arterial blood gases, activated partial thromboplastin time, serum albumin, total protein, blood urea, creatinine, and electrolytes should be ordered. Polymerase chain reaction-based molecular methods (PCR-based multiplex GI pathogens) can help in the rapid identification of nvestigationsSalmonella, Shigella, and Yersinia from primary stool samples. Abdominal and pelvis CT scan, colonoscopy, tissue biopsies, and fecal cultures (multiple specimens) and antimicrobial susceptibility testing should help differentiate infectious from non-infectious causes of colitis and guiding treatment.[15]

Recently multidetector CT scans of the abdomen were used to differentiate between inflammatory bowel disease and acute colitis related to bacterial infection. The five signs described to diagnose bacterial colitis are (1) continuous distribution, (2) empty colon, (3) absence of fat stranding, (4) absence of a “comb’ sign, and (5) absence of enlarged lymph nodes.[16]

The diagnosis of active Mycobacterium tuberculosis colitis focuses on clinical presentation, clinical examination, and laboratory investigations. A complete blood count may reveal low hemoglobin, leukocytosis, and moderately elevated ESR. Chest X-ray may reveal fibrotic changes, cavitation, or old scar of pulmonary tuberculosis; an abdominal roentgenogram may reveal prominent large bowel. Abdominal and pelvis CT scans may show diffuse thickening of the colonic wall, especially of the terminal ileum and the cecum. A colonoscopy usually shows diffuse ulceration throughout the colon, from the rectum to cecum. Histopathological biopsies taken from the cecum show caseating granuloma and chronic inflammatory cells. Mantoux skin test (tuberculin test) is usually requested. This test does not measure immunity to tuberculosis but the degree of hypersensitivity to tuberculin. The results must be interpreted carefully with consideration to the patient’s medical risk factors. Usually, the Mantoux test becomes negative in these patients after being previously positive, indicating the fading of resistance to the organism.[17] PCR testing and cultures of intestinal fluid for bacterial species and acid-fast bacillus are requested.

Diagnosis of CMV colitis uses clinical findings, laboratory tests, and endoscopic findings. Endoscopy and tissue CMV-specific immunohistochemistry (IHC) and or PCR CMV DNA quantification are needed to confirm the diagnosis [20]. 

In amoebic colitis, rectosigmoid involvement may present on colonoscopy; however, the cecum is the most commonly involved site, followed by the ascending colon (showing colonic inflammation, erythema, oedematous mucosa, erosions, white or yellow exudates, and ulcerations). The presence of amoebic trophozoites on histopathological examination or intestinal fluid cultures is important in the diagnosis. Serum E. histolytica antibody examination and antibody titer greater than 1:128 is considered positive.[17][10]

For patients with suspected sexually transmitted infections of the rectum, histological features of biopsies taken are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests are usually helpful; these include:

• Gonorrhea: Microscopic examination of smears from the lesions showing Gram-negative diplococci. Culture and sensitivity tests of smears taken from lesions.

• Lymphogranuloma venereum: Genotyping of Chlamydia trachomatis- DNA PCR.

• Genital/rectal herpes: Swabs from rectal vesicles or ulcers to detect DNA by PCR.

• Syphilis: Dark-field microscopy, PCR, direct fluorescent antibody test, treponemal antigen-based enzyme immunoassays (EIAs) for IgG and IgM antibodies, Treponema pallidum hemagglutination assay (TPHA), Treponema pallidum particle agglutination assay (TPPA), and fluorescent treponemal antibody absorption (FTA-ABS) test.[20]

Treatment / Management

Not all infectious colitis requires antibiotic therapy; patients with mild to moderate C. jejuni or Salmonella infections do not need antibiotic treatment because the infection is self-limited. Treatment with quinolinic acid antibiotics is only for patients with dysentery and high fever suggestive of bacteremia. Also, patients with AIDS, malignancy, transplantation, prosthetic implants, valvular heart disease, or extreme age will require antibiotic therapy. For mild to moderate C. difficile infection, metronidazole is the preferred treatment. In severe cases of C. difficile infection, oral vancomycin is the recommended approach. In complicated cases, oral vancomycin with intravenous metronidazole is the recommendation.[18]

In patients, particularly children, with enterohemorrhagic E. coli (E. coli O157: 7H and non-O157: H7), antibiotics are not recommendations for treating infection because killing the bacteria can lead to increased release of Shigella toxins and enhance the risk of the hemolytic uremic syndrome.[2]

Because of rising multidrug resistance to antituberculous treatment, cases with active Mycobacterium tuberculosis colitis receive therapy with rifampin, isoniazid, pyrazinamide, and ethambutol for 9 to 12 months. The reader should review the recent guidelines by the World Health Organisation on treating developing resistance in tuberculosis.[19]  

The majority of patients with CMV colitis who are immunocompetent may need no treatment with antiviral medications. However, antiviral therapy in immunocompetent patients with CMV colitis could be limited to males over the age of 55 who suffer from severe disease and have co-morbidities affecting the immune system such as diabetes mellitus or chronic renal failure; consider an assessment of the colon viral load. The drug of choice is oral or intravenous ganciclovir.[19]

Treatment of E. histolytica is recommended even in asymptomatic individuals. Noninvasive colitis may be treated with paromomycin to eliminate intraluminal cysts. Metronidazole is the antimicrobial of choice for invasive amoebiasis. Medications with longer half-lives (such as tinidazole and ornidazole) allow for shorter treatment periods and are better tolerated. After completing a 10-day course of a nitroimidazole, the patient should be placed on paromomycin to eradicate the luminal parasites. Fulminant amoebic colitis requires the addition of broad-spectrum antibiotics to the treatment due to the risk of bacterial translocation.[21]

Because of emerging resistance in gonorrhea, current treatment as per current guidelines comprises intramuscular ceftriaxone 500 mg together with an oral dose of azithromycin 1 g. Alternative protocols could be cefixime 400 mg stat or ciprofloxacin 500 mg orally stat.

The treatment of lymphogranuloma venereum uses doxycycline orally twice daily for three weeks, or erythromycin 500 mg orally four times daily for three weeks.[22]

Genital/rectal herpes simplex is treated with acyclovir 400 mg three times daily or valaciclovir 500 mg twice daily for five days. Analgesia and saline bathing could soothe the pain. Intravenous therapy is an option if the patient tolerates oral treatment poorly. Consider prolonging treatment if new lesions develop. For recurrent genital/rectal herpes, lesions are usually mild, may need no specific treatment. Symptomatic treatment could help. Challenging cases such as those with recurrence at short intervals may require referral for specialized advice. The partner should also have an examination and treatment if the lesion is active.

Syphilis treatment is with penicillin (the drug of choice). A single dose of 2.4 mega units of intramuscular benzathine benzylpenicillin is the recommendation for early syphilis or three doses at weekly intervals with late syphilis. Doxycycline could be an alternative treatment for individuals sensitive to penicillin. Follow up patients to ensure clearance from infection and notification are required.[23]

Differential Diagnosis

• Inflammatory bowel disease

• Colorectal cancer

• Diverticulitis

• Ischemic colitis

• Irritable bowel disease

• Drug-induced colitis

• Radiation-associated colitis

• Colitis complicating immune deficiency disorders

• Graft-versus-host disease

• Acute appendicitis/ileocecal mass: The differential diagnosis may include:

Prognosis

Most infectious colitis cases last approximately seven days, with severe cases lingering for several weeks. If left untreated, prolonged disease may be confused for ulcerative colitis.[24]

Complications

Complications include[25][26][27][23]: 

• Intestinal perforation

• Toxic megacolon (Clostridium difficile-associated colitis, Salmonella, Shigella, Campylobacter jejuni, Cytomegalovirus, Rotavirus), and fulminant form of amebiasis

• Pseudo-membrane formation (Clostridium difficile)

• Hemorrhagic colitis (enteroinvasive E. coli, enterohemorrhagic E. coli)

• Hemolytic-uremic syndrome (enterohemorrhagic E coli, Campylobacter jejuni, Shigella)

• Post-infectious irritable bowel syndrome, dyspepsia

• Guillain-Barre syndrome (Campylobacter jejuni colitis [serotype HS:19], Cytomegalovirus colitis)

• Encephalitis, seizure (Shigella)

• Reactive arthritis (Shigella, Campylobacter jejuni, Yersinia enterocolitica colitis)

• Pancreatitis, cholecystitis, meningitis, purulent arthritis (Campylobacter jejuni)

• Septic shock and death (Shigella, Clostridium difficile)

• Elevated serum pancreatic enzymes without clinical pancreatitis (Salmonella)

• Renal failure, shock (Clostridium difficile)

• Hypoglycemia, hyponatremia (Shigella)

• Erythema nodosum (Yersinia enterocolitica)

• Patients with CMV colitis complicating inflammatory bowel disease may develop severe hemorrhage, megacolon, fulminant colitis, or colon perforation; these complications contribute to the high risk of mortality

Deterrence and Patient Education

Patients need to receive counsel regarding the importance of antibiotic adherence, as well as any signs of relapse or worsening condition.

Pearls and Other Issues

In managing patients presenting with colitis, computed tomography scans, colonoscopy, and biopsies could help differentiate between infectious and noninfectious colitis. However, these investigations are of little help in deciding the infectious agent causing colitis. Microbiological studies, including microscopy, cultures, and sensitivity, and PCR DNA tests are of high value in defining the etiology of an infectious cause. Treatment of infectious colitis should be individualized depending on the patient’s age, causative agent, risk factors, presence of comorbidities, and current guidelines of management of infectious colitis. Antibiotics treatment of children with E. coli O157: H7 infection increases the risk of hemolytic uremic syndrome and should be avoided.  

Enhancing Healthcare Team Outcomes

Infectious colitis is complex and requires an interprofessional team for the diagnosis, management, and early detection of complications. The team comprises a gastroenterologist, infectious disease consultant, pathologist, microbiologist, pharmacist, clinical pharmacologist, and general practitioner, which covers the range of expertise needed for the management of infectious colitis and handling any complications. All members of the interprofessional healthcare team, including clinicians (MDs, DOs, NPs, PAs), specialists, specialty-trained nursing staff, and pharmacists, need to communicate and collaborate across disciplinary lines in their areas of expertise to keep the entire team informed and current on the status of the case and changes required. [Level 5]

The nursing staff should monitor the follow-up of the patient. If signs and symptoms fail to resolve and/or signs or symptoms of dehydration develop, the nursing staff should arrange a return visit or possibly recommend emergency department evaluation.

Careful assessment of the patient condition and involvement of the healthcare team in evaluation and decision making is necessary for better outcomes. The nurse assigned to patient education should focus on teaching patients to wash hands, eating only well-cooked foods, and drinking bottled water, particularly during traveling, which are the essential preventable measures that patients need to know. 

Figure

Radiograph of an infant with necrotizing enterocolitis. Contributed by RadsWiki.net (CC By-S.A. 3.0 https://creativecommons.org/licenses/by-sa/3.0/deed.en)

Figure

Gross Pathology of neonatal necrotizing enterocolitis, Autopsy, infant, abdominal distention, necrosis, hemorrhage, peritonitis due to perforation. Contributed by The Centers for Disease Control and Prevention (CDC)

References

1.

Uhlich GA, Sinclair JR, Warren NG, Chmielecki WA, Fratamico P. Characterization of Shiga toxin-producing Escherichia coli isolates associated with two multistate food-borne outbreaks that occurred in 2006. Appl Environ Microbiol. 2008 Feb;74(4):1268-72. [PMC free article: PMC2258581] [PubMed: 18083883]

2.

Tarr PI, Gordon CA, Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 2005 Mar 19-25;365(9464):1073-86. [PubMed: 15781103]

3.

Newitt S, MacGregor V, Robbins V, Bayliss L, Chattaway MA, Dallman T, Ready D, Aird H, Puleston R, Hawker J. Two Linked Enteroinvasive Escherichia coli Outbreaks, Nottingham, UK, June 2014. Emerg Infect Dis. 2016 Jul;22(7):1178-84. [PMC free article: PMC4918187] [PubMed: 27314432]

4.

Jewkes J, Larson HE, Price AB, Sanderson PJ, Davies HA. Aetiology of acute diarrhoea in adults. Gut. 1981 May;22(5):388-92. [PMC free article: PMC1419238] [PubMed: 7250751]

5.

Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, Griffin PM. Foodborne illness acquired in the United States–major pathogens. Emerg Infect Dis. 2011 Jan;17(1):7-15. [PMC free article: PMC3375761] [PubMed: 21192848]

6.

Reveles KR, Lee GC, Boyd NK, Frei CR. The rise in Clostridium difficile infection incidence among hospitalized adults in the United States: 2001-2010. Am J Infect Control. 2014 Oct;42(10):1028-32. [PubMed: 25278388]

7.

Cherian JJ, Lobo I, Sukhlecha A, Chawan U, Kshirsagar NA, Nair BL, Sawardekar L. Treatment outcome of extrapulmonary tuberculosis under Revised National Tuberculosis Control Programme. Indian J Tuberc. 2017 Apr;64(2):104-108. [PubMed: 28410692]

8.

Han JK, Kim SH, Choi BI, Yeon KM, Han MC. Tuberculous colitis. Findings at double-contrast barium enema examination. Dis Colon Rectum. 1996 Nov;39(11):1204-9. [PubMed: 8918425]

9.

Karagiannis S, Papaioannou D, Goulas S, Psilopoulos D, Mavrogiannis C. Intestinal tuberculosis in a patient on infliximab treatment. Gastrointest Endosc. 2008 Jun;67(7):1178-9; discussion 1179. [PubMed: 18329027]

10.

Stanley SL. Amoebiasis. Lancet. 2003 Mar 22;361(9362):1025-34. [PubMed: 12660071]

11.

Wada Y, Matsui T, Matake H, Sakurai T, Yamamoto J, Kikuchi Y, Yorioka M, Tsuda S, Yao T, Yao S, Haraoka S, Iwashita A. Intractable ulcerative colitis caused by cytomegalovirus infection: a prospective study on prevalence, diagnosis, and treatment. Dis Colon Rectum. 2003 Oct;46(10 Suppl):S59-65. [PubMed: 14530660]

12.

Bissessor M, Fairley CK, Read T, Denham I, Bradshaw C, Chen M. The etiology of infectious proctitis in men who have sex with men differs according to HIV status. Sex Transm Dis. 2013 Oct;40(10):768-70. [PubMed: 24275725]

13.

Slimings C, Riley TV. Antibiotics and hospital-acquired Clostridium difficile infection: update of systematic review and meta-analysis. J Antimicrob Chemother. 2014 Apr;69(4):881-91. [PubMed: 24324224]

14.

Levin A, Yaari S, Stoff R, Caplan O, Wolf DG, Israeli E. Diagnosis of Cytomegalovirus Infection during Exacerbation of Ulcerative Colitis. Digestion. 2017;96(3):142-148. [PubMed: 28848127]

15.

Jessurun J. The Differential Diagnosis of Acute Colitis: Clues to a Specific Diagnosis. Surg Pathol Clin. 2017 Dec;10(4):863-885. [PubMed: 29103537]

16.

Plastaras L, Vuitton L, Badet N, Koch S, Di Martino V, Delabrousse E. Acute colitis: differential diagnosis using multidetector CT. Clin Radiol. 2015 Mar;70(3):262-9. [PubMed: 25522900]

17.

Stauffer W, Ravdin JI. Entamoeba histolytica: an update. Curr Opin Infect Dis. 2003 Oct;16(5):479-85. [PubMed: 14502002]

18.

Di X, Bai N, Zhang X, Liu B, Ni W, Wang J, Wang K, Liang B, Liu Y, Wang R. A meta-analysis of metronidazole and vancomycin for the treatment of Clostridium difficile infection, stratified by disease severity. Braz J Infect Dis. 2015 Jul-Aug;19(4):339-49. [PubMed: 26001980]

19.

Falzon D, Schünemann HJ, Harausz E, González-Angulo L, Lienhardt C, Jaramillo E, Weyer K. World Health Organization treatment guidelines for drug-resistant tuberculosis, 2016 update. Eur Respir J. 2017 Mar;49(3) [PMC free article: PMC5399349] [PubMed: 28331043]

20.

Hook EW. Syphilis. Lancet. 2017 Apr 15;389(10078):1550-1557. [PubMed: 27993382]

21.

Haque R, Huston CD, Hughes M, Houpt E, Petri WA. Amebiasis. N Engl J Med. 2003 Apr 17;348(16):1565-73. [PubMed: 12700377]

22.

Stoner BP, Cohen SE. Lymphogranuloma Venereum 2015: Clinical Presentation, Diagnosis, and Treatment. Clin Infect Dis. 2015 Dec 15;61 Suppl 8:S865-73. [PubMed: 26602624]

23.

Dean R, Gill D, Buchan D. Salmonella colitis as an unusual cause of elevated serum lipase. Am J Emerg Med. 2017 May;35(5):800.e5-800.e6. [PubMed: 27865572]

24.

Papaconstantinou HT, Thomas JS. Bacterial colitis. Clin Colon Rectal Surg. 2007 Feb;20(1):18-27. [PMC free article: PMC2780149] [PubMed: 20011357]

25.

Autenrieth DM, Baumgart DC. Toxic megacolon. Inflamm Bowel Dis. 2012 Mar;18(3):584-91. [PubMed: 22009735]

26.

Horiki N, Furukawa K, Kitade T, Sakuno T, Katsurahara M, Harada T, Tano S, Yamada R, Hamada Y, Inoue H, Tanaka K, Gabazza EC, Ishii N, Fukuda K, Omata F, Fujita Y, Tachibana H, Takei Y. Endoscopic findings and lesion distribution in amebic colitis. J Infect Chemother. 2015 Jun;21(6):444-8. [PubMed: 25787830]

27.

Törnblom H, Holmvall P, Svenungsson B, Lindberg G. Gastrointestinal symptoms after infectious diarrhea: a five-year follow-up in a Swedish cohort of adults. Clin Gastroenterol Hepatol. 2007 Apr;5(4):461-4. [PubMed: 17445752]

Infectious Colitis – StatPearls – NCBI Bookshelf

Continuing Education Activity

The management of infectious colitis is complex, and new approaches have been introduced. The basic and clinical aspects of infectious colitis must be clearly defined to achieve satisfactory outcomes. This activity reviews infectious colitis, and focusses on the etiology, epidemiology, pathophysiology, evaluation, management, and complications of infectious colitis, and highlights the role of the interprofessional team in improving healthcare outcomes.

Objectives:

• Identify the etiology and along with accompanying risk factors for infectious colitis.

• Describe the pathophysiology in infectious colitis.

• Summarize the evaluation process infectious colitis.

• Review the management options available for infectious colitis.

Access free multiple choice questions on this topic.

Introduction

Colonic infection by bacteria, viruses, or parasites results in an inflammatory-type of diarrhea and accounts for the majority of cases presenting with acute diarrhea. These patients present with purulent, bloody, and mucoid loose bowel motions, fever, tenesmus, and abdominal pain. Common bacteria causing bacterial colitis include Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis. Common causes of viral colitis include Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus. Parasitic infestation, such as Entamoeba histolytica, a protozoan parasite, is capable of invading the colonic mucosa and causing colitis. Sexually transmitted infection affecting the rectum merit consideration during assessment. These diseases can occur in patients with HIV infection and men who have sex with men and may include Neisseria gonorrhoeae, Chlamydia trachomatis, Herpes simplex, and Treponema pallidum.

The patients present with rectal symptoms that mimic inflammatory bowel disease, including rectal pain, tenesmus, bloody mucoid discharge, and urgency. Detailed medical history and identification of specific associated risks are essential in establishing the diagnosis. Stool microscopy and culture and endoscopy are crucial to the diagnosis. However, stool culture helps in the diagnosis of less than 50% of patients presenting with bacterial colitis, and endoscopic examinations usually reveal non-specific pathological changes. Therefore, an approach is needed to evaluate and diagnose the cause of colitis and exclude non-infectious causes. This activity discusses current strategies to diagnose and manage infectious colitis and how to make a high index of suspicion based on clinical presentation and use investigation methods to reach a final diagnosis. This activity discusses the etiology, epidemiology, pathophysiology, clinical presentation, evaluation, differential diagnosis, complications, and management of patients with infectious colitis.  

Etiology

Infectious colitis may result from infection with:

1. Bacterial infections: including Campylobacter jejuni, Salmonella, Shigella, Escherichia coli (including these subgroups – enterotoxigenic E. coli, enteropathogenic E. coli, enterohemorrhagic E. coli, enteroinvasive E. coli, enteroaggregative E. coli), Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis.

2. Viral infection: Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus (CMV).

3. Parasitic infection such as Entamoeba histolytica (causes amoebic colitis)

4. Sexually transmitted infections: Particularly infections affecting the rectum in patients with HIV infection and men who have sex with men may include the following infections: Neisseria gonorrhoeae, Chlamydia trachomatis (causes lymphogranuloma venereum), Herpes simplex 1 and 2, and Treponema pallidum (causes syphilis).

Enterotoxigenic E. coli is the leading cause of traveler’s diarrhea. Enteroaggregative E. coli can cause traveler’s diarrhea, but it is not the leading cause. Enterohemorrhagic E. coli has two main serotypes E. coli O157: H7 and non-O157: H7; the natural reservoirs of both serotypes are cows. Therefore, the infection is related to the consumption of inadequately cooked beef, or contaminated milk or vegetables. They are responsible for outbreaks in developed countries.[1]

Two of these subgroups cause non-bloody diarrhea: enterotoxigenic E. coli and enteroaggregative E. coli; both produce enterotoxins that induce chloride and water secretion and inhibit their absorption. However, enterohemorrhagic E. coli (both strains E coli O157: H7 and non-O157: H7) causes bloody diarrhea and produce Shiga-like toxins, resulting in a clinical picture similar to Shigella
dysenteriae infection.[2]

Both enteropathogenic E. coli and enteroinvasive E. coli do not produce toxins. Enteropathogenic E. coli is responsible for outbreaks, particularly in children less than two years of age, while enteroinvasive E. coli causes acute self-limited colitis and is responsible for outbreaks mainly in developing countries. However, the outbreaks in Nottingham, the UK, in 2004, highlight the need for its consideration as a potential pathogen in foodborne outbreaks in Europe.[3]  

Children (in daycare centers), elderly (in nursing homes), and immunocompromised individuals are susceptible to these infections. The fecal-oral route, animal host, and ingestion of contaminated food and water are the usual modes of infection.

Food and water contaminations with pathogenic bacteria may cause large outbreaks of diseases.

Epidemiology

Bacterial colitis accounts for up to 47% of cases of acute diarrhea.[4]
Campylobacter jejuni is the number one bacterial cause of diarrheal illness worldwide with an estimated prevalence of 25 to 30 per 100000 population. For Salmonella infection, an estimated 1.2 million annual cases of non-typhoidal salmonellosis occurred in the United States.

Shigellosis incidence worldwide reported to be approximately 165 million cases, but mortality has decreased in the last three decades because of improvement in laboratory diagnosis and treatment. In the United States, estimates are approximately 500000 cases per year, with 38 to 45 deaths.[5]

Yersinia enterocolitica colitis commonly presents in young children in the winter. In the United States, estimate are one case per 100000 individuals each year.

Clostridium difficile infection in hospitalized adults in the United States increased from 4.5 cases per 1000 discharge in 2001 to 8.2 cases in 2010 and a mortality rate of 7%.[6] Another study from the United Stated on Clostridium infection estimated 500000 cases in 2011 with 83000 recurrence and 29300 deaths.

Mycobacterium tuberculosis is the third most common site of extra-pulmonary tuberculosis, accounting for 12.8% of all cases under this category.[7] The recurrence of tuberculosis in developing countries parallels the AIDS epidemic distribution closely.[8] Other factors for increasing rates of tuberculosis in many developed countries are related to the migrant population, deterioration in social conditions, cutbacks in public health surveillance services, and increased prevalence of immune-suppressed individuals (AIDS, those receiving biological agents in diseases such as rheumatoid arthritis, and inflammatory bowel disease).[9]

Amebiasis ranks as the second leading cause of death due to protozoan infection after malaria, Chagas disease, and leishmaniasis.[10]

The prevalence of CMV infection in percent colitis is in the range of 21% to 34%.[11] CMV reactivation in patients with severe ulcerative colitis has a reported prevalence of 4.5% to 16.6% and as high as 25% in patients requiring colectomy for severe colitis.

Infectious proctitis among HIV-positive and HIV-negative men varied and in a recent study was as follows: chlamydia (23% versus 22%, respectively), gonorrhoea (13% versus 11%), HSV-1 (14% versus 6%), and HSV-2 (22% versus 12%), lymphogranuloma venereum (8% versus 0.7%), more than one infection (18% versus 9%). Approximately thirty-two percent of HSV proctitis had external anal ulcerations.[12]

Pathophysiology

Infection with Campylobacter jejuni is a result of orally ingested contaminated food or water. Several factors influence infections, including the dose of bacteria ingested, the virulence of organisms, and the immunity of the host. The median incubation period is from 2 to 4 days. C. jejuni multiplies in the bile and then invade the epithelial layers and travel to the lamina propria producing a diffuse, bloody, edematous enteritis.

Pseudomembranous colitis is caused by toxin-producing Clostridium difficile. The disease develops as a result of altered normal microflora (usually by antibiotic therapy such as cephalosporin and beta-lactam antibiotics) that enables overgrowth and colonization of the intestine by Clostridium difficile and production of its toxins.[13]

Enterotoxigenic E. coli produces heat-labile (HL) and heat-stable (ST) toxins. The HL toxins activate adenyl cyclase in enterocytes resulting in increased cAMP and stimulation of chloride secretion and inhibition of absorption. The ST toxins bind to guanylate cyclase resulting in increased cGMP and effects on cellular transporters similar to those caused by LT toxins resulting in secretory non-inflammatory diarrhea (this explains the limited histopathological changes in this infection).[14]

Enteropathogenic E. coli can produce proteins for “attaching” and “effacing” (A/E) lesions, which enable the bacteria to get tightly attached to the enterocytes apical membranes and causing effacement or loss of the microvilli. As stated earlier, enteropathogenic E. coli does not produce toxins, and their underlying mechanisms for causing diarrhea is by attaching and effacing lesions.[15]

Enterohemorrhagic E. coli; both of its serotypes E. coli O157: H7 and non-O157: H7 produce Shiga-like toxins similar to Shigella dysenteriae infection. However, E. coli O157: H7 strains are more likely to cause outbreaks compared to non-O157: H7 serotypes. They produce bloody diarrhea and are responsible for the development of hemolytic-uremic syndrome and ischemic colitis.[16]

Enteroinvasive coli do not produce toxins; they invade enterocytes and cause self-limited colitis. Exact details of their pathogenetic mechanisms are still not fully understood.

Enteroaggregative E. coli produces enterotoxins related to Shigella enterotoxins and ST toxins of enterotoxigenic E. coli. They attach themselves to enterocytes via adherence fimbriae.

Immunity to Mycobacterium tuberculosis undergoes mediation via T-cells resulting in macrophage stimulation to kill the bacteria. Reactivation of infection or re-exposure to the bacillus in a sensitized individual, as it is the case in most Mycobacterium tuberculosis colitis cases resulting in rapid defense reactions and increased tissue necrosis accompanied by loss of T-cell immunity (tuberculin test in these patients becomes negative although used to be previously positive, which is consistent with fading T-cell protection).[17]

Primary CMV infection in immunocompetent individuals is usually asymptomatic. However, in patients whose immune response is compromised, they develop symptoms in different body organs, including CMV colitis.

Research concerning genetics and molecular sciences of Entamoeba histolytica have brought new understanding about mechanisms by which the parasite impose invasive abilities and pathological lesions in the colon and extracolonic organs. Host factors predisposing to infection are also under research.[17]

Histopathology

No significant differences appear in histological biopsies taken from the rectum of patients with different bacterial infections. However, the absence of crypt architecture distortion or basal plasmacytosis helps differentiate acute infectious colitis from chronic inflammation caused by inflammatory bowel disease.

Infection with Escherichia coli O157: H7 may show changes similar to those of ischemic colitis (small atrophic crypts, hyalinized lamina propria, and fibrin thrombi).

Yersinia enterocolitica shows inflammatory changes, ulcerations in the cecum and terminal ileum areas, hyperplasia of Peyer patches, microabscesses, and granulomas. (This condition requires differentiation from Crohn disease and Mycobacterium tuberculosis involving the terminal ileum/caecum area).

Colonic histopathological changes are limited in enterotoxigenic E. coli, enteroinvasive E. coli, and enteroaggregative E. coli infections.

In Mycobacterium tuberculosis, characteristic granulomas with central caseation are present; tubercle bacilli are identifiable with acid-fast stains.[18]

The diagnosis of CMV colitis requires histological examination of biopsy tissues, taken from the ulcer edge or base. Patients with punched-out ulcers are associated with an increase in inclusion bodies on histology [Yang H et al. 2017]. Colonic mucosal biopsies stained with H & E may reveal the typical inclusion associated with CMV colitis, “owl eye appearance” inclusion bodies, which are highly specific for CMV. However, H & E staining has low sensitivity compared to immunohistochemistry, which is considered the gold standard for diagnosing CMV colitis.[19]

The histological features of biopsies taken from the rectum are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests, including serology and PCR, are essential in making such differentiation.

History and Physical

Detailed medical history and identification of exposure risks are helpful in the diagnosis. It is essential to mention here that individuals with sickle cell anemia, hemolytic anemia, immunosuppression (corticosteroids, chemotherapy, and AIDS), and extremity of age are at a higher risk of Salmonella infection.  Patients with bacterial colitis present with non-specific symptoms, including diarrhea, fever, tenesmus, and abdominal pain. Patients with Yersinia enterocolitica infection may present with a syndrome indistinguishable from acute appendicitis (mesenteric adenitis, mild fever, and ileocecal tenderness).

The incidence of Clostridium difficile is higher in patients with inflammatory bowel disease, particularly ulcerative colitis. Any antibiotic can trigger the disease, but the most common antibiotics responsible are cephalosporins, clindamycin, carbapenems, trimethoprim, sulfonamides, fluoroquinolone, and penicillin combinations.[13]

Patients with Mycobacterial tuberculosis may present with abdominal pain, blood per rectum, fever, sweating, tiredness, and pallor. They may give a past medical history of the treatment of pulmonary tuberculosis. They may have abdominal tenderness in the right iliac fossa (the ileocecal area is the most commonly involved site in intestinal tuberculosis).[18]

Viral colitis (Norovirus, Rotavirus, and Adenovirus) are common in infants and young children. Affected patients present with nausea, vomiting, watery diarrhea, and abdominal pain. CMV infection is frequently symptomatic in immune-competent patients. Again, symptoms are usually non-specific, including diarrhea, abdominal pain, fever, malaise, rectal bleeding, and weight loss. However, hematochezia and diarrhea are the most frequent symptoms. It is difficult to distinguish between ulcerative colitis from CMV colitis based on clinical presentation.[14]

Amoebic colitis usually presents with diarrhea, mucoid discharge, hematochezia, tenesmus, and abdominal bloating. Contaminated water supplies and poor sanitation are often the cases for traveling overseas to endemic areas and increased risk of fecal-oral transmission of amebas.

Patients with colitis-associated with sexually transmitted infection present with anorectal pain, with a purulent, mucoid or bloody discharge, tenesmus, or urgency. The sexual history is vital in evaluating these patients. 

Evaluation

Diagnosis of colitis centers on clinical findings, laboratory tests, endoscopy, and biopsy. Endoscopy and biopsy should not be the primary investigations and may be necessary after a critical evaluation of the patient’s condition and the results from the initial examination.

Because infection is a common etiology of colitis and can produce clinical presentations indistinguishable from inflammatory bowel disease, microbiological studies and cultures for bacterial and parasitic infestations should be the initial investigations. Laboratory tests including complete blood count, ESR, CRP, arterial blood gases, activated partial thromboplastin time, serum albumin, total protein, blood urea, creatinine, and electrolytes should be ordered. Polymerase chain reaction-based molecular methods (PCR-based multiplex GI pathogens) can help in the rapid identification of nvestigationsSalmonella, Shigella, and Yersinia from primary stool samples. Abdominal and pelvis CT scan, colonoscopy, tissue biopsies, and fecal cultures (multiple specimens) and antimicrobial susceptibility testing should help differentiate infectious from non-infectious causes of colitis and guiding treatment.[15]

Recently multidetector CT scans of the abdomen were used to differentiate between inflammatory bowel disease and acute colitis related to bacterial infection. The five signs described to diagnose bacterial colitis are (1) continuous distribution, (2) empty colon, (3) absence of fat stranding, (4) absence of a “comb’ sign, and (5) absence of enlarged lymph nodes.[16]

The diagnosis of active Mycobacterium tuberculosis colitis focuses on clinical presentation, clinical examination, and laboratory investigations. A complete blood count may reveal low hemoglobin, leukocytosis, and moderately elevated ESR. Chest X-ray may reveal fibrotic changes, cavitation, or old scar of pulmonary tuberculosis; an abdominal roentgenogram may reveal prominent large bowel. Abdominal and pelvis CT scans may show diffuse thickening of the colonic wall, especially of the terminal ileum and the cecum. A colonoscopy usually shows diffuse ulceration throughout the colon, from the rectum to cecum. Histopathological biopsies taken from the cecum show caseating granuloma and chronic inflammatory cells. Mantoux skin test (tuberculin test) is usually requested. This test does not measure immunity to tuberculosis but the degree of hypersensitivity to tuberculin. The results must be interpreted carefully with consideration to the patient’s medical risk factors. Usually, the Mantoux test becomes negative in these patients after being previously positive, indicating the fading of resistance to the organism.[17] PCR testing and cultures of intestinal fluid for bacterial species and acid-fast bacillus are requested.

Diagnosis of CMV colitis uses clinical findings, laboratory tests, and endoscopic findings. Endoscopy and tissue CMV-specific immunohistochemistry (IHC) and or PCR CMV DNA quantification are needed to confirm the diagnosis [20]. 

In amoebic colitis, rectosigmoid involvement may present on colonoscopy; however, the cecum is the most commonly involved site, followed by the ascending colon (showing colonic inflammation, erythema, oedematous mucosa, erosions, white or yellow exudates, and ulcerations). The presence of amoebic trophozoites on histopathological examination or intestinal fluid cultures is important in the diagnosis. Serum E. histolytica antibody examination and antibody titer greater than 1:128 is considered positive.[17][10]

For patients with suspected sexually transmitted infections of the rectum, histological features of biopsies taken are non-specific and cannot differentiate syphilitic proctitis and lymphogranuloma venereum. Laboratory tests are usually helpful; these include:

• Gonorrhea: Microscopic examination of smears from the lesions showing Gram-negative diplococci. Culture and sensitivity tests of smears taken from lesions.

• Lymphogranuloma venereum: Genotyping of Chlamydia trachomatis- DNA PCR.

• Genital/rectal herpes: Swabs from rectal vesicles or ulcers to detect DNA by PCR.

• Syphilis: Dark-field microscopy, PCR, direct fluorescent antibody test, treponemal antigen-based enzyme immunoassays (EIAs) for IgG and IgM antibodies, Treponema pallidum hemagglutination assay (TPHA), Treponema pallidum particle agglutination assay (TPPA), and fluorescent treponemal antibody absorption (FTA-ABS) test.[20]

Treatment / Management

Not all infectious colitis requires antibiotic therapy; patients with mild to moderate C. jejuni or Salmonella infections do not need antibiotic treatment because the infection is self-limited. Treatment with quinolinic acid antibiotics is only for patients with dysentery and high fever suggestive of bacteremia. Also, patients with AIDS, malignancy, transplantation, prosthetic implants, valvular heart disease, or extreme age will require antibiotic therapy. For mild to moderate C. difficile infection, metronidazole is the preferred treatment. In severe cases of C. difficile infection, oral vancomycin is the recommended approach. In complicated cases, oral vancomycin with intravenous metronidazole is the recommendation.[18]

In patients, particularly children, with enterohemorrhagic E. coli (E. coli O157: 7H and non-O157: H7), antibiotics are not recommendations for treating infection because killing the bacteria can lead to increased release of Shigella toxins and enhance the risk of the hemolytic uremic syndrome.[2]

Because of rising multidrug resistance to antituberculous treatment, cases with active Mycobacterium tuberculosis colitis receive therapy with rifampin, isoniazid, pyrazinamide, and ethambutol for 9 to 12 months. The reader should review the recent guidelines by the World Health Organisation on treating developing resistance in tuberculosis.[19]  

The majority of patients with CMV colitis who are immunocompetent may need no treatment with antiviral medications. However, antiviral therapy in immunocompetent patients with CMV colitis could be limited to males over the age of 55 who suffer from severe disease and have co-morbidities affecting the immune system such as diabetes mellitus or chronic renal failure; consider an assessment of the colon viral load. The drug of choice is oral or intravenous ganciclovir.[19]

Treatment of E. histolytica is recommended even in asymptomatic individuals. Noninvasive colitis may be treated with paromomycin to eliminate intraluminal cysts. Metronidazole is the antimicrobial of choice for invasive amoebiasis. Medications with longer half-lives (such as tinidazole and ornidazole) allow for shorter treatment periods and are better tolerated. After completing a 10-day course of a nitroimidazole, the patient should be placed on paromomycin to eradicate the luminal parasites. Fulminant amoebic colitis requires the addition of broad-spectrum antibiotics to the treatment due to the risk of bacterial translocation.[21]

Because of emerging resistance in gonorrhea, current treatment as per current guidelines comprises intramuscular ceftriaxone 500 mg together with an oral dose of azithromycin 1 g. Alternative protocols could be cefixime 400 mg stat or ciprofloxacin 500 mg orally stat.

The treatment of lymphogranuloma venereum uses doxycycline orally twice daily for three weeks, or erythromycin 500 mg orally four times daily for three weeks.[22]

Genital/rectal herpes simplex is treated with acyclovir 400 mg three times daily or valaciclovir 500 mg twice daily for five days. Analgesia and saline bathing could soothe the pain. Intravenous therapy is an option if the patient tolerates oral treatment poorly. Consider prolonging treatment if new lesions develop. For recurrent genital/rectal herpes, lesions are usually mild, may need no specific treatment. Symptomatic treatment could help. Challenging cases such as those with recurrence at short intervals may require referral for specialized advice. The partner should also have an examination and treatment if the lesion is active.

Syphilis treatment is with penicillin (the drug of choice). A single dose of 2.4 mega units of intramuscular benzathine benzylpenicillin is the recommendation for early syphilis or three doses at weekly intervals with late syphilis. Doxycycline could be an alternative treatment for individuals sensitive to penicillin. Follow up patients to ensure clearance from infection and notification are required.[23]

Differential Diagnosis

• Inflammatory bowel disease

• Colorectal cancer

• Diverticulitis

• Ischemic colitis

• Irritable bowel disease

• Drug-induced colitis

• Radiation-associated colitis

• Colitis complicating immune deficiency disorders

• Graft-versus-host disease

• Acute appendicitis/ileocecal mass: The differential diagnosis may include:

Prognosis

Most infectious colitis cases last approximately seven days, with severe cases lingering for several weeks. If left untreated, prolonged disease may be confused for ulcerative colitis.[24]

Complications

Complications include[25][26][27][23]: 

• Intestinal perforation

• Toxic megacolon (Clostridium difficile-associated colitis, Salmonella, Shigella, Campylobacter jejuni, Cytomegalovirus, Rotavirus), and fulminant form of amebiasis

• Pseudo-membrane formation (Clostridium difficile)

• Hemorrhagic colitis (enteroinvasive E. coli, enterohemorrhagic E. coli)

• Hemolytic-uremic syndrome (enterohemorrhagic E coli, Campylobacter jejuni, Shigella)

• Post-infectious irritable bowel syndrome, dyspepsia

• Guillain-Barre syndrome (Campylobacter jejuni colitis [serotype HS:19], Cytomegalovirus colitis)

• Encephalitis, seizure (Shigella)

• Reactive arthritis (Shigella, Campylobacter jejuni, Yersinia enterocolitica colitis)

• Pancreatitis, cholecystitis, meningitis, purulent arthritis (Campylobacter jejuni)

• Septic shock and death (Shigella, Clostridium difficile)

• Elevated serum pancreatic enzymes without clinical pancreatitis (Salmonella)

• Renal failure, shock (Clostridium difficile)

• Hypoglycemia, hyponatremia (Shigella)

• Erythema nodosum (Yersinia enterocolitica)

• Patients with CMV colitis complicating inflammatory bowel disease may develop severe hemorrhage, megacolon, fulminant colitis, or colon perforation; these complications contribute to the high risk of mortality

Deterrence and Patient Education

Patients need to receive counsel regarding the importance of antibiotic adherence, as well as any signs of relapse or worsening condition.

Pearls and Other Issues

In managing patients presenting with colitis, computed tomography scans, colonoscopy, and biopsies could help differentiate between infectious and noninfectious colitis. However, these investigations are of little help in deciding the infectious agent causing colitis. Microbiological studies, including microscopy, cultures, and sensitivity, and PCR DNA tests are of high value in defining the etiology of an infectious cause. Treatment of infectious colitis should be individualized depending on the patient’s age, causative agent, risk factors, presence of comorbidities, and current guidelines of management of infectious colitis. Antibiotics treatment of children with E. coli O157: H7 infection increases the risk of hemolytic uremic syndrome and should be avoided.  

Enhancing Healthcare Team Outcomes

Infectious colitis is complex and requires an interprofessional team for the diagnosis, management, and early detection of complications. The team comprises a gastroenterologist, infectious disease consultant, pathologist, microbiologist, pharmacist, clinical pharmacologist, and general practitioner, which covers the range of expertise needed for the management of infectious colitis and handling any complications. All members of the interprofessional healthcare team, including clinicians (MDs, DOs, NPs, PAs), specialists, specialty-trained nursing staff, and pharmacists, need to communicate and collaborate across disciplinary lines in their areas of expertise to keep the entire team informed and current on the status of the case and changes required. [Level 5]

The nursing staff should monitor the follow-up of the patient. If signs and symptoms fail to resolve and/or signs or symptoms of dehydration develop, the nursing staff should arrange a return visit or possibly recommend emergency department evaluation.

Careful assessment of the patient condition and involvement of the healthcare team in evaluation and decision making is necessary for better outcomes. The nurse assigned to patient education should focus on teaching patients to wash hands, eating only well-cooked foods, and drinking bottled water, particularly during traveling, which are the essential preventable measures that patients need to know. 

Figure

Radiograph of an infant with necrotizing enterocolitis. Contributed by RadsWiki.net (CC By-S.A. 3.0 https://creativecommons.org/licenses/by-sa/3.0/deed.en)

Figure

Gross Pathology of neonatal necrotizing enterocolitis, Autopsy, infant, abdominal distention, necrosis, hemorrhage, peritonitis due to perforation. Contributed by The Centers for Disease Control and Prevention (CDC)

References

1.

Uhlich GA, Sinclair JR, Warren NG, Chmielecki WA, Fratamico P. Characterization of Shiga toxin-producing Escherichia coli isolates associated with two multistate food-borne outbreaks that occurred in 2006. Appl Environ Microbiol. 2008 Feb;74(4):1268-72. [PMC free article: PMC2258581] [PubMed: 18083883]

2.

Tarr PI, Gordon CA, Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 2005 Mar 19-25;365(9464):1073-86. [PubMed: 15781103]

3.

Newitt S, MacGregor V, Robbins V, Bayliss L, Chattaway MA, Dallman T, Ready D, Aird H, Puleston R, Hawker J. Two Linked Enteroinvasive Escherichia coli Outbreaks, Nottingham, UK, June 2014. Emerg Infect Dis. 2016 Jul;22(7):1178-84. [PMC free article: PMC4918187] [PubMed: 27314432]

4.

Jewkes J, Larson HE, Price AB, Sanderson PJ, Davies HA. Aetiology of acute diarrhoea in adults. Gut. 1981 May;22(5):388-92. [PMC free article: PMC1419238] [PubMed: 7250751]

5.

Scallan E, Hoekstra RM, Angulo FJ, Tauxe RV, Widdowson MA, Roy SL, Jones JL, Griffin PM. Foodborne illness acquired in the United States–major pathogens. Emerg Infect Dis. 2011 Jan;17(1):7-15. [PMC free article: PMC3375761] [PubMed: 21192848]

6.

Reveles KR, Lee GC, Boyd NK, Frei CR. The rise in Clostridium difficile infection incidence among hospitalized adults in the United States: 2001-2010. Am J Infect Control. 2014 Oct;42(10):1028-32. [PubMed: 25278388]

7.

Cherian JJ, Lobo I, Sukhlecha A, Chawan U, Kshirsagar NA, Nair BL, Sawardekar L. Treatment outcome of extrapulmonary tuberculosis under Revised National Tuberculosis Control Programme. Indian J Tuberc. 2017 Apr;64(2):104-108. [PubMed: 28410692]

8.

Han JK, Kim SH, Choi BI, Yeon KM, Han MC. Tuberculous colitis. Findings at double-contrast barium enema examination. Dis Colon Rectum. 1996 Nov;39(11):1204-9. [PubMed: 8918425]

9.

Karagiannis S, Papaioannou D, Goulas S, Psilopoulos D, Mavrogiannis C. Intestinal tuberculosis in a patient on infliximab treatment. Gastrointest Endosc. 2008 Jun;67(7):1178-9; discussion 1179. [PubMed: 18329027]

10.

Stanley SL. Amoebiasis. Lancet. 2003 Mar 22;361(9362):1025-34. [PubMed: 12660071]

11.

Wada Y, Matsui T, Matake H, Sakurai T, Yamamoto J, Kikuchi Y, Yorioka M, Tsuda S, Yao T, Yao S, Haraoka S, Iwashita A. Intractable ulcerative colitis caused by cytomegalovirus infection: a prospective study on prevalence, diagnosis, and treatment. Dis Colon Rectum. 2003 Oct;46(10 Suppl):S59-65. [PubMed: 14530660]

12.

Bissessor M, Fairley CK, Read T, Denham I, Bradshaw C, Chen M. The etiology of infectious proctitis in men who have sex with men differs according to HIV status. Sex Transm Dis. 2013 Oct;40(10):768-70. [PubMed: 24275725]

13.

Slimings C, Riley TV. Antibiotics and hospital-acquired Clostridium difficile infection: update of systematic review and meta-analysis. J Antimicrob Chemother. 2014 Apr;69(4):881-91. [PubMed: 24324224]

14.

Levin A, Yaari S, Stoff R, Caplan O, Wolf DG, Israeli E. Diagnosis of Cytomegalovirus Infection during Exacerbation of Ulcerative Colitis. Digestion. 2017;96(3):142-148. [PubMed: 28848127]

15.

Jessurun J. The Differential Diagnosis of Acute Colitis: Clues to a Specific Diagnosis. Surg Pathol Clin. 2017 Dec;10(4):863-885. [PubMed: 29103537]

16.

Plastaras L, Vuitton L, Badet N, Koch S, Di Martino V, Delabrousse E. Acute colitis: differential diagnosis using multidetector CT. Clin Radiol. 2015 Mar;70(3):262-9. [PubMed: 25522900]

17.

Stauffer W, Ravdin JI. Entamoeba histolytica: an update. Curr Opin Infect Dis. 2003 Oct;16(5):479-85. [PubMed: 14502002]

18.

Di X, Bai N, Zhang X, Liu B, Ni W, Wang J, Wang K, Liang B, Liu Y, Wang R. A meta-analysis of metronidazole and vancomycin for the treatment of Clostridium difficile infection, stratified by disease severity. Braz J Infect Dis. 2015 Jul-Aug;19(4):339-49. [PubMed: 26001980]

19.

Falzon D, Schünemann HJ, Harausz E, González-Angulo L, Lienhardt C, Jaramillo E, Weyer K. World Health Organization treatment guidelines for drug-resistant tuberculosis, 2016 update. Eur Respir J. 2017 Mar;49(3) [PMC free article: PMC5399349] [PubMed: 28331043]

20.

Hook EW. Syphilis. Lancet. 2017 Apr 15;389(10078):1550-1557. [PubMed: 27993382]

21.

Haque R, Huston CD, Hughes M, Houpt E, Petri WA. Amebiasis. N Engl J Med. 2003 Apr 17;348(16):1565-73. [PubMed: 12700377]

22.

Stoner BP, Cohen SE. Lymphogranuloma Venereum 2015: Clinical Presentation, Diagnosis, and Treatment. Clin Infect Dis. 2015 Dec 15;61 Suppl 8:S865-73. [PubMed: 26602624]

23.

Dean R, Gill D, Buchan D. Salmonella colitis as an unusual cause of elevated serum lipase. Am J Emerg Med. 2017 May;35(5):800.e5-800.e6. [PubMed: 27865572]

24.

Papaconstantinou HT, Thomas JS. Bacterial colitis. Clin Colon Rectal Surg. 2007 Feb;20(1):18-27. [PMC free article: PMC2780149] [PubMed: 20011357]

25.

Autenrieth DM, Baumgart DC. Toxic megacolon. Inflamm Bowel Dis. 2012 Mar;18(3):584-91. [PubMed: 22009735]

26.

Horiki N, Furukawa K, Kitade T, Sakuno T, Katsurahara M, Harada T, Tano S, Yamada R, Hamada Y, Inoue H, Tanaka K, Gabazza EC, Ishii N, Fukuda K, Omata F, Fujita Y, Tachibana H, Takei Y. Endoscopic findings and lesion distribution in amebic colitis. J Infect Chemother. 2015 Jun;21(6):444-8. [PubMed: 25787830]

27.

Törnblom H, Holmvall P, Svenungsson B, Lindberg G. Gastrointestinal symptoms after infectious diarrhea: a five-year follow-up in a Swedish cohort of adults. Clin Gastroenterol Hepatol. 2007 Apr;5(4):461-4. [PubMed: 17445752]

Colitis Risk, Symptoms and Treatment

Colitis is a chronic digestive disease characterized by inflammation of the inner lining of the colon.  Infection, loss of blood supply in the colon, Inflammatory Bowel Disease (IBD) and invasion of the colon wall with collagen or lymphocytic white blood cells are all possible causes of an inflamed colon.

Different Types of Colitis

There are many different forms of colitis, including:

• Ulcerative colitis
• Crohn’s colitis
• Diversion colitis
• Ischemic colitis
• Infectious colitis
• Fulminant colitis
• Collagenous colitis
• Chemical colitis
• Microscopic colitis
• Lymphocytic colitis
• Atypical colitis

Risk Factors

• Perforation (rupture) of the bowel: Intestinal perforation occurs when chronic inflammation weakens the intestinal wall ultimately creating a hole.  If a hole forms, a large amount of bacteria can spill into the abdomen and cause infection.  
• Fulminant colitis: This includes the damage of the thickness of the intestinal wall. The normal contractions of the intestinal wall stop temporarily. Eventually, the colon loses muscle tone and begins to expand. X-rays of the abdomen can show trapped gas inside the paralyzed sections of the intestine.    
• Toxic megacolon: The colon dilates and loses its ability to contract properly and move intestinal gas along. Resulting abdominal distension can be severe, and patients should seek medical attention immediately. The goal of treatment is to prevent the bowel from rupturing.  
• Increased risk of colorectal cancer: The risk of colorectal cancer increases with the duration and severity of the disease.     

Signs of Possible Colitis

General signs of colitis can include:

• Intense pain
• Tenderness in the abdomen
• Depression
• Rapid weight loss
• Aches and pains in the joints
• Loss of appetite
• Fatigue
• Changes in bowel habits (increased frequency)
• Fever
• Swelling of the colon tissue
• Erythema (redness) of the surface of the colon
• Ulcers on the colon (in ulcerative colitis) which may bleed
• Mucus and/or blood in stool and rectal bleeding
• Diarrhea, which may occur, although some forms of colitis involve constipation so the stool and bowel movements may appear normal.

Other symptoms may include gas, bloating, indigestion, heartburn, gastro esophageal reflux disease, cramps, bowel urgency and many other uncomfortable aches in the gastrointestinal system.

Detection

Common tests for colitis include X-rays of the colon, testing the stool for blood and pus, sigmoidoscopy and colonoscopy. Additional tests include stool cultures and blood tests, including blood chemistry tests. A high erythrocryte sedimentation rate (ESR) – a measure of how long it takes for red blood cells to settle in a blood sample – is typical of acute colitis.

Treatment

The route of treatment depends on what is causing colitis. Many cases require little more than symptomatic care, including clear fluids to rest the bowel and medications to control pain. Patients who have become acutely ill often need intravenous fluids and other intervention.

• Infection: Infections that cause diarrhea and colitis may potentially require antibiotics, depending on the cause. Viral infections require fluids and time. Some bacterial infections, such as Salmonella, do not need antibiotic therapy; the body is able to get rid of the infection on its own. Other bacterial infections, such as Clostridium difficile, require antibiotic treatment.
• Inflammatory Bowel Disease (IBD): Medications are often used to control IBD. Anti-inflammatory medications may be used initially and medications that suppress the immune system can be added if necessary. Surgery may be an option in severe cases, including removal of the colon and small intestine.
• Ischemic colitis: Treatment for ischemic colitis begins with intravenous fluids to rest the bowel and prevent dehydration. If sufficient blood supply is not restored, surgery may be needed to remove parts of the bowel that lost blood supply.
• Diarrhea and abdominal pain: Diarrhea and abdominal pain are the primary symptoms of colitis. Initial treatment at home may include a clear fluid diet for 24 hours, rest, and Tylenol for pain. If symptoms resolve quickly, no further care is needed.

Prevention

Many people have found that one or more of the following foods have triggered their symptoms:

• Alcohol
• Caffeine
• Carbonated beverages
• Dairy products (if lactose intolerant)
• Dried beans, peas, legumes, dried fruits or berries
• Fruits with pulp or seeds
• Foods containing sulfur or sulfate
• Foods high in fiber (including whole-grained products)
• Hot sauces and spicy foods
• Meats
• Nuts and crunchy nut butters
• Popcorn
• Products containing sorbitol (sugar-free gum and candies)
• Raw vegetables
• Refined sugar
• Seeds

Ulcerative colitis – Causes – NHS

The exact cause of ulcerative colitis is unknown, although it’s thought to be the result of a problem with the immune system.

Autoimmune condition

The immune system is the body’s defence against infection. Many experts believe ulcerative colitis is an autoimmune condition (when the immune system mistakenly attacks healthy tissue).

The immune system normally fights off infections by releasing white blood cells into the blood to destroy the cause of the infection.

This results in swelling and redness (inflammation) of body tissue in the infected area.

In ulcerative colitis, a leading theory is that the immune system mistakes “friendly bacteria” in the colon, which aid digestion, as a harmful infection, leading to the colon and rectum becoming inflamed.

Alternatively, some researchers believe a viral or bacterial infection triggers the immune system, but for some reason it does not “turn off” once the infection has passed and continues to cause inflammation.

It’s also been suggested that no infection is involved and the immune system may just malfunction by itself, or that there’s an imbalance between good and bad bacteria within the bowel.

Genetics

It also seems inherited genes are a factor in the development of ulcerative colitis.

Studies have found more than 1 in 4 people with ulcerative colitis has a family history of the condition.

Levels of ulcerative colitis are also a lot higher in certain ethnic groups, further suggesting that genetics are a factor.

Researchers have identified several genes that seem to make people more likely to develop ulcerative colitis.

It’s believed many of these genes play a role in the immune system.

Environmental factors

Where and how you live also seems to affect your chances of developing ulcerative colitis, which suggests environmental factors are important.

For example, the condition is more common in urban areas of northern parts of western Europe and America.

Various environmental factors that may be linked to ulcerative colitis have been studied, including air pollution, medication and certain diets.

Although no factors have so far been identified, countries with improved sanitation seem to have a higher population of people with the condition.

This suggests that reduced exposure to bacteria may be an important factor.

Page last reviewed: 23 January 2019
Next review due: 23 January 2022

Colitis | UCI Health | Orange County, CA

Colitis is an inflammation of the inner lining of the colon that may result in fever, abdominal pain and diarrhea. 

Other symptoms may include bloody bowel movements, chills, dehydration, a constant urge to have a bowel movement and bloating that may be constant or intermittent.

There are many kinds of colitis, including:

• Infectious colitis (caused by a virus, parasite or bacterial food poisoning)
• Inflammatory bowel disorders (ulcerative colitis and Crohn’s disease)
• Ischemic colitis (caused by loss of blood supply)
• Microscopic colitis (invasion of the colon wall by white blood cells)
• Radiation treatment side effects that affect the large bowel

Treatment depends on the type of colitis. Because some may be more severe and potentially life-threatening, it is important to diagnose the type of colitis when a patient complains of persistent pain and diarrhea — with or without a bloody stool.

For more information about the colitis or to schedule a consultation, please call us at 888-717-4463 or complete our online appointment request form ›

Types of colitis

Infectious colitis

Many varieties of bacteria live in the human gastrointestinal tract. When disease-causing bacteria invade the intestinal system, usually through contaminated food, pain and diarrhea may result. The most common bacterial causes of food-borne illnesses are:

Viruses and parasites also can cause infectious colitis. Many of these infections may resolve themselves in a few days, sometimes with the aid of antibiotics. However, antibiotics themselves can upset the natural bacterial balance in the colon.

Rehydration is an important first step in treating all types of colitis. In severe cases, intravenous fluids may be indicated.

Ischemic colitis

As people get older, the arteries that deliver blood to the gastrointestinal tract can narrow and lead to ischemic colitis, either from spasms or blockages. This can be hastened by other conditions, such as dehydration, diabetes, high or low blood pressure, high cholesterol and anemia.

These painful obstructions are the most common vascular disorder of the intestinal tract among the elderly.

Inflammatory bowel disease

Ulcerative colitis typically involves the rectum and the sigmoid colon (the lowermost end of the colon). It may progress over time to the rest of the colon. The cause of ulcerative colitis is believed to be an overactive immune response that attacks the lining of the colon, causing inflammation, abdominal pain and bloody diarrhea.

Crohn’s disease usually occurs in the last part of the small intestines or the first part of the colon, although it can involve any part of the gastrointestinal tract, even the esophagus or stomach. It may be characterized by lesions interspersed with healthy tissue along the intestinal lining. Sometimes, when Crohn’s disease primarily involves the colon, symptoms identical to ulcerative colitis may be present.

UCI Health has the region’s only comprehensive program to treat inflammatory bowel disease (IBD).

Learn more about our IBD program and how we treat patients with ulcerative colitis and Crohn’s disease.

Microscopic colitis

Microscopic colitis is a rare type of inflammation of the colon that can be classified as collagenous or lymphocytic colitis.

Patients have more subtle inflammation of the colon lining than in other forms of colitis, and they typically suffer from diarrhea, but without blood present in the stool.

It is more common in older women and is thought to be an auto-immune disease.

Diagnosis

To diagnose the type of colitis you have, your physician begins by determining the severity of your symptoms and how long you have had
them. It may be important to know if you have traveled somewhere and encountered a viral, parasitic or food-borne infection.

A physical exam can detect high or low blood pressure that could indicate ischemic colitis, as well as possible areas of tenderness, bloating or masses in the abdominal area.

A stool sample may also be tested. If blood is present, your physician may want to screen you for polyps or colon cancer.

Other tests may help determine if you have a low red blood cell count, which could indicate internal bleeding, or a high white blood
cell count, which could indicate that your body is fighting an infection.

Your physician also may order additional tests, including:

This procedure, performed by a trained physician, examines the interior of the colon with fiberoptic or digital camera attached to a thin flexible tube with a light source. The physician looks for signs of inflammation, the presence of polyps or tumors, and may take a tissue biopsy for testing

View a video about colonoscopy ›

• Computerized tomography (CT) scan

A radiologist scans your colon after a liquid containing barium sulfate is introduced into your colon. The CT scan can provide an X-ray image of your colon with the contrast medium.

Treatment

Infectious colitis usually resolves itself in a matter of days.
Treatment generally involves keeping the patient well hydrated.
Sometimes antibiotics or other medications may be prescribed.

Patients with ischemic colitis need to reduce factors that
contribute to artery narrowing by ensuring adequate hydration and controlling high
blood pressure, high cholesterol and diabetes. In rare cases, severe ischemia can lead
to gangrene, which requires surgical intervention.

Patients with inflammatory bowel disease may need to control their
disease with long-term medical treatment. In severe cases, an operation may be
required.

Patients with microscopic colitis may receive
antidiarrheal medications, steroids or immunosuppressant drugs. Only
rarely is an operation indicated.

90,000 Infectious colitis – causes, symptoms, diagnosis and treatment

Infectious colitis is a polyetiological group of inflammatory diseases of the large intestine that arise as a result of the activation of opportunistic intestinal flora or the ingress of pathogenic microorganisms from the external environment. Manifested by diarrhea with mucus, sometimes with blood and an unpleasant odor, abdominal pain, symptoms of general intoxication and dehydration. Diagnosed on the basis of clinical data, feces cultures, general blood test.If necessary, sigmoidoscopy and colonoscopy are performed. Treatment of infectious colitis is conservative, including antibiotic therapy, antiparasitic drugs, detoxification, and the fight against dehydration).

General information

Infectious colitis is an acute (less often – chronic) disease of the large intestine, which is caused by various types of bacteria, protozoa, sometimes parasites and some viruses, accompanied by general intoxication, dehydration; the process often involves other parts of the gastrointestinal tract.It is widespread everywhere: it is believed that there are no people who have not experienced the manifestations of acute infectious colitis at least once in their life. The problem becomes more urgent in the warm season.

The disease is more common in countries with hot climates, in those areas where access to drinking water is difficult, communications are not developed. The most dangerous regions are the countries of Africa, Southeast and Central Asia. Men and women get sick in the same way, a little more often infectious colitis is diagnosed in young children.The treatment is carried out by infectious disease doctors. Patients can be admitted to the proctology department if the disease is mistaken for nonspecific infectious colitis or other diseases of the colon.

Infectious colitis

Causes

The main cause of infectious colitis is all sorts of bacteria. Most often, the disease is caused by shigella (causative agents of dysentery), E. coli, salmonella, clostridia, yersinia, typhoid bacillus, campylobacter, proteus, staphylococcus.Symptoms of infectious colitis are observed with adenovirus, enterovirus infection, sometimes with diseases caused by rotavirus. Also, colitis can be caused by amoeba, lamblia, and some other types of parasites.

Infectious colitis sometimes develops as a complication of tuberculosis or syphilis. In weakened patients with suppressed immunity, the disease can be caused by fungi (candida, actinomycetes). Fungal infectious colitis is one of the markers of AIDS, and it also occurs in cancer patients taking chemotherapy, or in people who have been treated with steroid hormones for a long time.In case of dysbiosis, provoked by antibiotic therapy or chemotherapy, infectious colitis can be caused by opportunistic bacteria, for example, clostridia.

Pathogenesis

With infectious colitis, inflammatory changes occur in the large intestine, motility is impaired, the secretion of fluid by endothelial cells is increased and the reabsorption of water is impaired, the permeability of the intestinal walls for various toxins that cause general intoxication of the body increases.

Classification

Taking into account morphological changes, the following forms of infectious colitis are distinguished: catarrhal, fibrous, catarrhal-hemorrhagic, phlegmonous, phlegmonous-gangrenous and necrotic. The process can progress quite quickly and move from one form to another, or it can stop at one stage of development. In addition, the form depends on the type of pathogen. Catarrhal forms are characteristic of viral diseases, catarrhal-hemorrhagic forms are typical for dysentery.Clostridia often cause necrotizing and phlegmonous-gangrenous infectious colitis.

Symptoms of infectious colitis

Clinical manifestations of the disease largely depend on its cause. Common to all forms are acute or subacute onset, diarrhea with a large amount of mucus, abdominal pain, often spasmodic in nature, fever, deterioration in general well-being, weakness, dry mucous membranes, tongue coated with white bloom. If the small intestine is involved in the process (enterocolitis develops), the amount of feces increases, the processes of fluid loss intensify and the symptoms of dehydration worsen.In the case of damage to the stomach (gastroenterocolitis), the disease may begin with vomiting.

In dysentery, the sigmoid colon is most often affected. The disease is manifested by diarrhea with a small amount of feces, defecation 3-20 times a day or more. In the feces, mucus and blood are detected, in severe cases, during bowel movements, only small mucous clots streaked with blood are released (rectal spitting). Patients complain of sharp abdominal pains, their body temperature rises to high numbers, symptoms of general intoxication are expressed, sometimes to confusion or loss of consciousness.

Amoebiasis has a similar clinic. This type of infectious colitis develops less acutely, the process involves the blind, ascending colon, or the entire large intestine. Feces with a lot of mucus mixed with blood resemble raspberry jelly. Symptoms of intoxication are not very pronounced, the disease can become chronic or recurrent.

Infectious colitis caused by Salmonella is a muddy-colored diarrhea with an unpleasant odor. The feces are liquid, since the small intestine is also affected.Patients have fever, and severe infectious colitis may be complicated by sepsis and septicemia.

Clostridial pseudomembranous colitis occurs with antibiotic therapy, chemotherapy, or severe dysbiosis. Manifested by fever, cramping abdominal pain, profuse diarrhea with a putrid odor. Pseudomembranous infectious colitis often recurs and may be complicated by intestinal necrosis.

Diagnostics

Laboratory tests are of prime importance in the diagnosis of infectious colitis.To clarify the etiology of the disease, virological, parasitological bacteriological studies of feces are carried out. Less often, blood serum is examined to detect antibodies to a particular pathogen. Blood cultures for sterility can be performed if septic complications are suspected. In a general blood test for bacterial infectious colitis, leukocytosis with a shift of the formula to the left, an increase in ESR can be detected. With viral colitis, the level of lymphocytes rises, and with parasitic colitis, mainly eosinophils.

Endoscopic studies are of an auxiliary nature, since the picture of morphological changes is not specific, and this type of diagnosis is carried out in order to differentiate from other diseases of the large intestine. Rectoromanoscopy proctologists or infectious disease specialists perform with bacterial dysentery, pseudomembranous infectious colitis. Abdominal ultrasound is indicated if complications are suspected. Differentiate infectious colitis with Crohn’s disease, diverticulitis, diverticular disease, dysbiosis.It is also very important to distinguish between different types of infectious colitis, since specific therapy depends on the cause.

Treatment of infectious colitis

For specific treatment, antibiotics are primarily used, preferably oral. For dysentery, the drugs of choice are fluoroquinolones or 8-hydroxyquinolones. Salmonellosis or infectious colitis caused by E. coli requires the use of cephalosporins of the third and fourth generations, which act on gram-negative flora.Pseudomembranous colitis responds best to metronidazole. With amebiasis, direct and indirect amoebicides are used (quiniophone, chloroquine), tetracycline antibiotics, metronidazole. For fungal infectious colitis, antifungal drugs are prescribed.

Rehydration is an important area of ​​treatment for infectious colitis. With a slight to moderate degree of fluid loss, the absence of vomiting, oral saline solutions are used. If the patient’s condition is severe, infusion rehydration and detoxification therapy are performed.With infectious colitis, it is recommended to take probiotics and enzyme preparations (pancreatin).

Forecast and prevention

The prognosis for infectious colitis is quite favorable, since today there are effective methods of etiotropic therapy for this disease. The prognosis worsens in severe forms of infectious colitis caused by clostridia, salmonella, fungi, as well as in debilitated patients with cancer, AIDS patients. Children suffer more severely infectious colitis.Hygiene is the main preventive measure. It is necessary to carefully monitor the purity and shelf life of food products, especially those that are consumed without heat treatment, as well as the quality of the water used.

90,000 causes of occurrence, symptoms of the disease, diagnosis and treatment methods

IMPORTANT!

The information in this section cannot be used for self-diagnosis and self-medication.In case of pain or other exacerbation of the disease, only the attending physician should prescribe diagnostic tests. For a diagnosis and correct treatment, you should contact your doctor.

Colitis: causes, symptoms, diagnosis and treatment.

Definition

Colitis is the general name for a group of diseases characterized by acute or chronic inflammation of the mucous membrane of the large intestine.

Causes of colitis

Colitis can develop as a result of infection, insufficient blood supply to the intestine (ischemia), drug damage, it is secondary to immunodeficiency states, it can occur after radiation therapy of the pelvic organs in gynecological, urological and rectal cancer.

Inflammation of the colon mucosa is characteristic of Crohn’s disease (CD) and ulcerative colitis (UC).

Microscopic colitis is also distinguished, in which the data of X-ray and endoscopic studies of the intestine do not show abnormalities, and signs of inflammation are determined using a biopsy.

Intestinal infections can be caused by bacteria (most commonly Campylobacter jejuni ), viruses, protozoa and parasites.Infection with the bacterium Campylobacter jejuni occurs through the ingestion of contaminated food or water. The development of colitis depends on the number of bacteria trapped in the intestine, their virulence (ability to cause disease) and human immunity. The incubation period is 2-4 days. The bacteria multiply in the bile and then pass through the mucous membrane into the intestines, causing severe inflammation.

Other bacterial pathogens are Salmonella, Shigella and Mycobacterium tuberculosis.

The reason for the development of infectious colitis in patients with weakened immunity, in patients with blood diseases, neoplasms, radiation sickness can be opportunistic microorganisms (representatives of the normal intestinal microflora) – staphylococcus, proteus, E. coli.

Anaerobic bacteria Clostridium difficile , producing toxins, cause pseudomembranous colitis. The disease occurs against the background of changes in the normal intestinal microflora, mainly under the influence of antibiotics (cephalosporins, beta-lactam drugs), which inhibit the growth of other microorganisms and ensure the growth of Clostridium difficile .

Among the viruses that can cause colitis, cytomegalovirus is isolated, among the protozoa – dysentery amoeba ( Entamoeba histolytica ). The parasites, the result of whose vital activity is colitis, include pinworms, roundworms, whipworms, among those circulating in the blood – schistosomes.

Ischemic colitis occurs when there is insufficient blood supply to the large intestine, which leads to mucosal inflammation, ulcers, and hemorrhages.

The longer the violation of blood supply, the more severely the intestines are affected.When normal circulation is resumed, reperfusion syndrome can occur, which leads to further severe bowel damage. Patients with ischemic colitis usually suffer from diseases of the cardiovascular system (heart failure, atherosclerosis, atrial fibrillation), may have malignant neoplasms and pathologies of the blood coagulation system leading to thrombosis. In addition, ischemic damage to the intestine is determined during the so-called iatrogenic (associated with the provision of medical care) interventions – operations to eliminate an aneurysm of the abdominal aorta, in preparation for a colonoscopy or during its conduct.
Colitis can be caused by taking non-steroidal anti-inflammatory drugs, aspirin, proton pump inhibitors, beta-blockers, statins, and immunosuppressive drugs.

The development of microscopic colitis is associated with autoimmune diseases such as celiac disease, type 1 diabetes mellitus, psoriasis, thyroid dysfunction. There are two main subtypes of microscopic colitis – collagenous and lymphocytic.

NUC and CD are referred to as so-called inflammatory bowel diseases.The exact reasons for the development of these diseases are unknown, however, it is likely that in UC, damage to the intestinal wall is accompanied by an autoimmune reaction with the production of antibodies to the intestinal own cells. Among the reasons for the development of CD, hereditary, infectious, immunological, etc. are discussed, but none of the theories at the moment is absolutely confirmed.

Classification of the disease

In addition to the etiological (causal) factor, colitis is subdivided depending on the severity of the process (acute and chronic) and the severity.Chronic colitis is classified by the nature of the course of the disease (continuous, recurrent, intermittent) and by phase (exacerbation or remission). Depending on how much the large intestine is affected in chronic colitis, typhlitis (inflammation of the cecum), transverse (inflammation of the transverse colon), sigmoiditis (inflammation of the sigmoid colon), proctitis (inflammation of the rectum), angular colitis (left and right-sided, depending on the affected bend of the transverse colon), and often they can be combined (proctosigmoiditis).With pancolitis, all parts of the large intestine are affected.

Colitis symptoms

Acute colitis is accompanied by severe painful sensations, patients note pain and cramps in the abdomen and in the rectum (tenesmus). Chronic inflammation is characterized by colic and a feeling of heaviness in the abdomen. Patients may experience constipation, watery diarrhea, sometimes with blood and mucus, bubbling in the abdomen, false urge to defecate, fatigue, fever.

In Crohn’s disease, rectal bleeding, abdominal pain, diarrhea, fever, anemia, lesions of the anal and perianal region with the formation of fistulas, ulcers, and anal fissures are present. Often there are extraintestinal manifestations – arthritis, eye lesions, aphthous stomatitis, erythema nodosum – these lesions are noted in a third of patients with CD and are inextricably linked with intestinal inflammation.

In the clinical picture of ulcerative colitis, pain, tenesmus, blood in the stool and diarrhea at night are also noted.As in CD, the development of UC is accompanied by extraintestinal lesions of the skin, mouth, joints, and organs of vision.

Diagnosis of colitis

Diagnosis of colitis is based on clinical and laboratory findings, endoscopy, and biopsy.

First of all, it is necessary to carry out microbiological studies and cultures to exclude an infectious lesion.

ABC Medicine

Colitis is an inflammation of the lining of the colon.Chronic colitis is not only inflammatory, but also stropic and dystrophic changes in the colon, accompanied by secretory and motor disorders. This disease is one of the most common in the world. It is often combined with inflammatory lesions of the stomach and small intestine (enterocolitis).

Reasons

Infectious . As a rule, they are caused by pathogens of various intestinal infections, most often Salmonella and Shigella.Infectious diseases (mycobacterium tuberculosis, etc.), opportunistic and saprophytic flora of the human intestine caused by dysbiosis also provoke the development of colitis.

Alimentary. They arise from gross and prolonged disturbances in diet and diet. Often, against the background of achilic gastritis, pancreatitis and chronic enteritis, concomitant gastritis develops, their cause is systematic irritation of the colon mucosa due to incomplete digestion of food.

Toxic. They arise due to prolonged intoxication with compounds of lead, mercury, arsenic, phosphorus, etc. Toxic colitis of an endogenous nature can occur due to irritation of the intestinal wall with those products that it removes, for example, with uremia, gout.

Medicinal. Their cause, as a rule, is the long-term uncontrolled intake of laxatives containing antroglycoeids (preparations of buckthorn, rhubarb root, senna leaf, joster fruit, etc.)). Antibiotics and some other medications also have a negative effect.

Allergic. Observed with food allergies, as well as intolerance to a number of chemical and medicinal substances, high individual sensitivity of a person to some types of bacterial intestinal flora and decay products of microorganisms.

Symptoms

There are a number of main symptoms accompanying chronic intestinal colitis:

• rumbling in the stomach;
• tenesmus – false urge to defecate, ending with the release of only mucus;
• Aching pain in the abdomen that occurs after eating a large meal;
• constipation, periodically alternating with diarrhea;
• flatulence with constipation, accompanied by a feeling of heaviness, bloating, psychoemotional and physical discomfort in the patient;
• dyspepsia (nausea, belching, bitterness in the mouth).

Common symptoms include sleep disturbance, irritability, weakness and weight loss.

Diagnostics

Coprological examination

There is a large amount of mucus in the feces, microscopic examination allows to identify erythrocytes and leukocytes. Bacteriological examination of feces makes it possible to detect abnormalities in the colon – opportunistic microflora, changes in normal microflora (dysbiosis).

X-ray examination

X-ray examination (irrigography) is necessary to localize the process, record changes in the relief of the mucous membrane, dyskinesia, and distinguish colitis from other diseases.

Sigmoidoscopy and colonoscopy

In the course of these studies, catarrhal (hyperemic intestinal wall, edema, mucous plaque) and atrophic (pallor, thinning) changes in the mucous membrane of the colon are revealed.

Treatment

Diet. Diet is strictly indicated for patients with chronic colitis. During an exacerbation, No. 4a is assigned, it includes steamed meat and fish dishes, steam omelets, stale white bread, low-fat weak fish and meat broths, porridge on water, jelly, soft-boiled eggs, jelly and bird cherry decoctions, blueberries, quince, pears, rose hips, tea.

Drug treatment. If diarrheal syndrome predominates, astringents, adsorbents are prescribed.In cases where chronic colitis is accompanied by dysbiosis, treatment is carried out with antibacterial drugs. Elimination of enhanced gassing is carried out with activated carbon.

To enroll in the ABC-Medicine clinic for the treatment of chronic colitis, call +7 (495) 223-38-83 .

symptoms, diagnosis, treatment of chronic colitis – Department of the State Hospital of the Central Clinical Hospital of the Russian Academy of Sciences

Chronic colitis – a disease localized in the colon.This is an inflammation of the mucous membrane, which is accompanied by characteristic symptoms – diarrhea, pain, constipation, rumbling, excessive gas formation. This is one of the most common diseases of the digestive system, affecting the mucous, submucous and muscle tissues.

Causes and risk factors

Chronic intestinal colitis can be triggered by a number of reasons:

• Improper diet is the most common cause of illness.Monotony, a minimum of vitamins, a lot of proteins and carbohydrates, little fiber – all these are factors that can affect the development of pathology.
• Low mobility, alcohol consumption.
• Diseases of the stomach and the digestive system as a whole – gastritis, pancreatitis, enteritis, cholecystitis, as a result of which food is improperly processed by enzymes.
• Consequences of acute intestinal infections, worms and other parasites.
• Impaired bowel function, including congenital.
• Consequence of taking drugs that affect the intestinal environment.
• Exogenous intoxication with mercury, arsenic, phosphorus salts, lead.
• Endogenous intoxication caused by uremia, hyperthyroidism.
• Liver failure.
• Exposure to radiation, radiation therapy.
• Atherosclerosis – Causes ischemic colitis in older patients.
• In women during pregnancy.
• After

Most of these risk factors are united by impaired digestion of food, as a result of which the multiplication of pathogenic bacteria is accelerated. The process of assimilation of the basic elements from food is disrupted, and dysbiosis begins.

Symptoms of the disease

The emergence and exacerbation of chronic colitis in adults and children is characterized by a number of signs:

• First of all, the manifestation of the disease is pain of a spastic aching nature.Often localization is the left iliac region, stomach. On examination, the doctor determines the enlarged areas of the rectum. The pain becomes more pronounced after eating and goes away after a bowel movement and gas.
• Problems with stools – often with constipation and faeces that are fragmented and covered with mucus or diarrhea. There is also “obstructive diarrhea” – the release of liquid feces after a portion of the normal.
• Pain when urging to empty the bowels.
• Bloating, rumbling, flatulence.

Types of colitis

Colitis classification depending on the main symptom:

According to the etiology of occurrence, the following types are distinguished:

1. Primary:
   • Infectious – cause pathogenic fungi.
   • Toxic – chemical intoxication.
   • Parasitic – caused by parasites.
   • Allergic – a reaction to drugs or food.
   • Radiation.
   • Lymphocytic, collagen and others – etiology is still unknown.
   • Mechanical – a consequence of multiple constipation.
   • Medication – a reaction to taking antibiotics and other medications.
2. Secondary – is a consequence of other diseases, how to treat it depends on the circumstances that provoked the disease.

Ulcerative colitis is most likely due to allergies. It rarely manifests itself and passes with inflammation and the formation of necrotic ulcers.

Diagnostics

Chronic colitis is detected by the following stages of the examination:

• Coprological studies – analysis of feces in order to determine the quality of metabolic processes and the state of the digestive system as a whole.Signs of colitis are usually white blood cells and red blood cells in the test samples, as well as mucus in large quantities.
• Irrigography or X-ray of the intestine to determine the localization of the disease, assess the state of the mucous membrane, determine dyskinesia.
• Sigmoidoscopy and colonoscopy are important studies to help diagnose catarrhal and atrophic changes in the colon.

Treatment of chronic colitis

The chosen treatment depends on the patient’s condition, the exact diagnosis.If it is possible to treat a patient on an outpatient basis, he does not need to be in the hospital. The treatment regimen depends on which doctor is treating and how serious the situation is.

First of all, it is important to follow the diet. The patient receives recommendations on the menu, a list of what not to eat, advice on diet. The basic rule is fractional meals only with permitted foods. In the stage of exacerbation of the disease, work related to business trips and interfering with the observance of the correct daily routine is prohibited.

Compliance with the diet is complemented by medication and pain pills. Usually these are antibacterial agents, vitamins, enzymes, sorbents, decoctions and herbal tinctures. Physical therapy also has a beneficial effect on the healing process. These are electrophoresis, amplipulse, diadynamic currents, acupuncture.

Possible complications

In case of untimely or incorrect treatment, as well as non-compliance with the recommendations, the patient runs the risk of getting:

• Intestinal bleeding.
• Perforation of the ulcer.
• The appearance of adhesions.
• Diverticulosis
• Intestinal obstruction.

Which doctor to contact

When the first warning signs appear, you must make an appointment with a gastroenterologist. Treatment of chronic colitis in the acute stage in a hospital requires an appointment with a proctologist. Better doctors proctologists in Moscow are available in the clinic of the Central Clinical Hospital of the Russian Academy of Sciences. The arsenal of specialists includes our own modern diagnostic laboratory, the latest examination methods and extensive experience in the effective treatment of diseases.See your doctor in time to avoid complications, learn more about the prevention, diagnosis and treatment of chronic colitis.

90,000 Colitis, symptoms, diagnosis and treatment | Alpha

Colitis: types, symptoms, treatment

Colitis is an inflammation of the lining of the large intestine. The disease often develops against the background of infectious diarrhea, chronic constipation. According to statistics, women experience colitis symptoms more often than men.

Causes of the disease

Colitis of the intestine can be provoked by the following factors:

• Long-term use of antibiotics without medical supervision. Antibacterial drugs destroy beneficial microflora that is involved in the digestion process. The imbalance leads to the growth of pathogenic strains that cause inflammation of the colon. Colitis is caused by Shigella, Campylobacter, Salmonella, Escherichia coli, and other pathogens.
• Hereditary predisposition.The risk of developing colitis increases if the patient’s parents have the disease.
• Ischemia. As a result of a violation of the blood supply, the mucous membrane of the intestinal wall begins to change, become inflamed. Over time, the processes lead to the formation of ulcers and erosion.
• Chronic stress. It has not been proven to have a direct impact on colon health. Medical practice suggests that among patients with an inflammatory process in the intestine, the majority experience constant psycho-emotional overload.
• Autoimmune diseases (ulcerative colitis, Crohn’s disease). The human body’s own defense system begins to attack the cells of the intestinal mucosa. The reason for this reaction is not clear, therefore autoimmune forms are always chronic and most difficult to treat.

Classification of the disease

There are several types of colitis:

• By the nature of the course: acute and chronic.
• Due to development: autoimmune, infectious, medicinal, ischemic, toxic, radiation.

Colitis symptoms

The symptoms of the disease differ in different forms. There are several common symptoms of colorectal mucosa inflammation:

• Dehydration, which is manifested by dizziness, dry mouth, weakness.
• Chills, fever.
• Frequent urge to use the toilet.
• Loose stools mixed with blood and mucus.
• Pain in the lower abdomen.
• Bloating, flatulence.

Chronic intestinal colitis occurs with periods of remission and exacerbations. Many patients manage to contain the disease for a long time, smooth out its manifestations. Exacerbations of intestinal colitis most often occur in spring and autumn, as well as when exposed to provoking factors, for example, with a gross violation of the diet.

Diagnosis of the disease

Diagnosis begins with a consultation with a general practitioner or gastroenterologist.The doctor interviews the patient, specifies the duration and intensity of symptoms, the presence of provoking factors such as smoking, long-term medication. You will need information about the lifestyle, about the patient’s diet, about the presence of colitis in close relatives. After the interview, the doctor palpates the patient’s abdomen and performs other necessary manipulations.

To clarify the diagnosis, a comprehensive examination is prescribed:

• Bowel X-ray with barium.The picture shows the inflamed areas of the mucosa.
• CT scan. A more accurate examination method that allows you to determine the type of colitis that the patient is suffering from.
• Colonoscopy. The procedure is performed by a proctologist to visually examine the intestinal mucosa. During the examination, a biopsy is also done to diagnose microscopic colitis.
• Clinical blood test. According to the results, the general condition of the patient is assessed, the presence or absence of internal bleeding is determined.

Treatment of colitis

Diet

During the treatment of colitis, the patient should refuse food that can irritate the intestinal mucosa. Fatty, spicy, fried foods, spices are excluded from the diet. Be sure to drink clean water or other liquid in large quantities. In chronic colitis, the diet should be lifelong.

Drug therapy

Anti-inflammatory drugs are prescribed to relieve symptoms.Medicines are selected individually, as antibiotics themselves can cause colitis. Some pathogens, such as salmonella, do not require antibacterial drugs and are excreted from the body on their own

In the ischemic form of the disease, intravenous drips are indicated to eliminate dehydration. As soon as the body’s water-salt balance returns to normal, the intestinal symptoms of the disease subside.

Surgical treatment

If anti-inflammatory and immunosuppressive medications fail, the surgeon will remove the affected area.The indications for surgical treatment and its scope are determined by the proctologist.

Operations are performed for colitis caused by Crohn’s disease, ischemic and nonspecific ulcerative colitis of the intestine. Treatment is always traumatic, patients need rehabilitation. After recovery, the doctor will prescribe a supportive diet.

Diagnostics and treatment of intestinal colitis in Nizhny Novgorod

Clinic “Alfa-Health Center” invites you to undergo examination in a modern medical center with the latest equipment.We accept both adult patients and children. Reception is conducted by qualified therapists, gastroenterologists, proctologists. We will help you undergo treatment and forget about colitis for a long time.

To make an appointment at a convenient time, call us at the phone number listed on the website.

Medical Center Axon

Colitis is an inflammatory disease of the colon mucosa.

There are acute and chronic types of colitis.

Acute colitis often occurs simultaneously with enteritis (inflammation of the small intestine) and gastritis (inflammation of the stomach).

SYMPTOMS

Symptoms of acute colitis: severe pain, frequent “rumbling” in the stomach, loss of appetite, loose stools with bleeding, high body temperature.

Acute colitis attacks can be caused by viral infections, food poisoning, toxins.

Chronic colitis is a consequence of the development of acute colitis.It proceeds with frequent periods of exacerbation. This disease is associated with changes in the colon and disorders of its functions.

Chronic colitis is characterized by: alternation of diarrhea and constipation, abdominal pain, a feeling of insufficient bowel movement, nausea, frequent belching, a feeling of bitterness in the mouth, a constant feeling of malaise.

REASONS

Due to the occurrence, the following types of disease are distinguished:
– Ulcerative colitis, or ulcerative colitis (UC), is a chronic inflammation of the colon.- Infectious colitis manifests itself as a result of the ingress of harmful substances into the blood. One of the varieties of infectious colitis is hemorrhagic colitis.
– Ischemic colitis is damage to the tissues of the colon, which is associated with a violation of its blood supply. It is accompanied by intestinal obstruction.
– Toxic or drug-induced colitis is manifested by poisoning with toxins or certain drugs.
– Antibiotic-associated colitis – occurs against the background of treatment with antibiotics, the irrational use of which violates the intestinal microflora.- Spastic colitis is a functional bowel disorder caused by prolonged stress and depression, overwork and hormonal imbalance in the body.

DIAGNOSTICS AND TREATMENT

Diagnosis of colitis begins with the patient’s history and the identification of the causes of the disease. The specialist then physically examines the patient and identifies the painful areas of the intestine by touch. If you suspect colitis, it is necessary to collect material for analyzes of feces and blood.

To detect an inflammatory process in the colon, it is necessary to conduct instrumental studies.For the treatment of colitis, drug therapy is used, as well as diet, physiotherapy, psychotherapy (if the disease is caused by mental disorders).

If symptoms of colitis occur, seek immediate medical attention. Only a doctor can tell how to treat colitis after a diagnosis. Any attempt at self-medication can lead to serious complications.

Be healthy!

Chronic colitis – ProMedicine Ufa

Colitis is an inflammation of the lining of the colon.

Chronic colitis –

is inflammatory, dystrophic and stropic changes in the mucous membrane of the colon, which are accompanied by its motor and secretory disorders. Chronic colitis is one of the most common diseases of the digestive system. Often combined with inflammatory lesions of the small intestine (enterocolitis) and stomach.

Causes

Causes of chronic colitis; infectious diseases (primarily dysentery), nutritional defects, exposure to toxic substances (lead, arsenic, mercury), drugs (uncontrolled intake of antibiotics, laxatives), diseases of the gastrointestinal tract (pancreatitis, gastritis).

Colitis of infectious origin can be caused by causative agents of intestinal infections, primarily Shigella and Salmonella, causative agents of other infectious diseases (Mycobacterium tuberculosis, etc.), opportunistic and saprophytic flora of the human intestine (due to dysbiosis). In therapeutic practice, the most common are colitis of non-infectious origin. Alimentary colitis occurs as a result of long-term and gross violations of the diet and a rational diet.Concomitant colitis accompanying achilic gastritis, pancreatitis with exocrine pancreatic insufficiency or chronic enteritis develop as a result of systematic irritation of the colon mucosa by products of insufficient digestion of food, as well as as a result of dysbiosis. Toxic colitis occurs as a result of prolonged exogenous intoxication with compounds of mercury, lead, phosphorus, arsenic, etc. Medicinal colitis is associated with prolonged uncontrolled use of laxatives containing antroglycoeids (preparations of rhubarb root, buckthorn, Joster fruit, senna leaf, etc.), antibiotics and some other drugs. Toxic colitis of endogenous origin occurs as a result of irritation of the intestinal wall by products excreted by it, formed in the body (with uremia, gout).

Colitis of an allergic nature is observed with food allergies, with intolerance to certain medicinal and chemical substances, increased individual sensitivity of the body to certain types of bacterial intestinal flora and decay products of microorganisms. Colitis due to prolonged mechanical irritation of the colon wall occurs with chronic coprostasis, abuse of laxative enemas and rectal suppositories, etc.e. Chronic colitis often has several etiological factors that mutually reinforce the effect.

Symptoms

Chronic colitis is characterized by pain syndrome in the form of aching and dull pains localized in any part of the abdomen, both cramping and diffuse in nature. Stool disturbance, rumbling, flatulence, painful tenesmus or dyspeptic disorders are a number of specific symptoms characteristic only of pathological processes affecting the gastrointestinal tract.A distinctive symptom of chronic colitis, which makes it possible to differentiate it from other pathologies, is an increase in pain immediately after a meal, cleansing enemas, abdominal tension and relief after emptying the intestines, passing accumulated gases or using antispasmodics. Quite often, with this pathology, the process of defecation occurs 6-7 times a day with the release of mucus or streaks of blood. During palpation of the abdominal organs, the pain syndrome is determined along the colon.

Diagnostics

After a visit to the doctor, the patient will be assigned some tests that will allow a more accurate diagnosis:

Stool analysis. It will show whether the intestines are working properly, whether there is an intestinal infection in the body.

A general blood test is necessary to diagnose the general condition of the patient, and will also allow you to see the number of leukocytes, erythrocytes. Their content can indicate the presence of an inflammatory process or its absence, as well as the level of hemoglobin, which also affects overall well-being.

The doctor may order an ultrasound examination of the intestinal cavity. After all analyzes and research, a diagnosis is made and a course of treatment is prescribed.

Treatment

Exacerbation of the disease most often requires inpatient treatment.