The diagnosis of CMV colitis is based on serology, CMV antigen testing and colonscopy with biopsy.

Clinical suspicion should be aroused in the setting of immunocompromised patient but it is much rarer in immunocompetent patient.

Although it is known that CMV colitis is almost always caused by reactivation of latent CMV infection in immunocompromised patients, new infection of CMV or reinfection of different strain of CMV can cause colitis in immunocompetent hosts.

Because asymptomatic CMV viremia and viruria is common and about 1/3 of symptomatic CMV infection is caused by reinfection of different strain of CMV, the diagnosis of CMV colitis needs more direct causality. It is practically achieved by colonoscopy or sigmoidoscopy tissue sampling and pathological evidence of CMV infection under microscope. Positive CMV IgG doesn't necessarily mean that it is reactivation of latent infection because of the possibility of reinfection of different strain.

The initial diagnostic workup for ulcerative colitis includes the following:

- A complete blood count is done to check for anemia; thrombocytosis, a high platelet count, is occasionally seen

- Electrolyte studies and renal function tests are done, as chronic diarrhea may be associated with hypokalemia, hypomagnesemia and pre-renal failure.

- Liver function tests are performed to screen for bile duct involvement: primary sclerosing cholangitis.

- X-ray

- Urinalysis

- Stool culture, to rule out parasites and infectious causes.

- Erythrocyte sedimentation rate can be measured, with an elevated sedimentation rate indicating that an inflammatory process is present.

- C-reactive protein can be measured, with an elevated level being another indication of inflammation.

- Sigmoidoscopy a type of endoscopy which can detect the presence of ulcers in the large intestine after a trial of an enema.

Although ulcerative colitis is a disease of unknown causation, inquiry should be made as to unusual factors believed to trigger the disease.

The simple clinical colitis activity index was created in 1998 and is used to assess the severity of symptoms.

The diagnosis is usually confirmed by biopsies on colonoscopy. Fecal calprotectin is useful as an initial investigation, which may suggest the possibility of IBD, as this test is sensitive but not specific for IBD.

Biopsies of the mucosa are taken to definitively diagnose UC and differentiate it from Crohn's disease, which is managed differently clinically. Microbiological samples are typically taken at the time of endoscopy. The pathology in ulcerative colitis typically involves distortion of crypt architecture, inflammation of crypts (cryptitis), frank crypt abscesses, and hemorrhage or inflammatory cells in the lamina propria. In cases where the clinical picture is unclear, the histomorphologic analysis often plays a pivotal role in determining the diagnosis and thus the management. By contrast, a biopsy analysis may be indeterminate, and thus the clinical progression of the disease must inform its treatment.

The systemic use of corticosteroids in the context of inflammatory bowel disease.

Symptoms suggestive of colitis are worked-up by obtaining the medical history, a physical examination and laboratory tests (CBC, electrolytes, stool culture and sensitivity, stool ova and parasites et cetera). Additional tests may include medical imaging (e.g. abdominal computed tomography, abdominal X-rays) and an examination with a camera inserted into the rectum (sigmoidoscopy, colonoscopy).

An important investigation in the assessment of colitis is biopsy. A very small piece of tissue (usually about 2mm) is removed from the bowel mucosa during endoscopy and examined under the microscope by a histopathologist. It can provide important information regarding the cause of the disease and the extent of bowel damage.

The prognosis for lymphocytic colitis and collagenous colitis is good, and both conditions are considered to be benign. The majority of people afflicted with the conditions recover from their diarrhea, and their histological abnormalities resolve, although relapses commonly occur if maintenance treatment is not continued.

Other diseases may cause an increased excretion of fecal calprotectin, such as infectious diarrhea, untreated coeliac disease, necrotizing enterocolitis, intestinal cystic fibrosis and neoplastic pediatric tumor cells.

Conditions with similar symptoms as Crohn's disease includes intestinal tuberculosis, Behçet's disease, ulcerative colitis, nonsteroidal anti-inflammatory drug enteropathy, irritable bowel syndrome and coeliac disease.

Conditions with similar symptoms as ulcerative colitis includes acute self-limiting colitis, amebic colitis, schistosomiasis, Crohn's disease, colon cancer, irritable bowel syndrome, intestinal tuberculosis and nonsteroidal anti-inflammatory drug enteropathy.

Lymphocytic and collagenous colitis have both been shown in randomized, placebo-controlled trials to respond well to budesonide, a glucocorticoid. Budesonide formulated to be active in the distal colon and rectum is effective for both active disease and in the prevention of relapse. However, relapse occurs frequently after withdrawal of therapy.

Studies of a number of other agents including antidiarrheals, bismuth subsalicylate (Pepto-Bismol), mesalazine/mesalamine (alone or in combination with cholestyramine), systemic corticosteroids, cholestyramine, immunomodulators, and probiotics have shown to be less effective than budesonide for treating both forms of microscopic colitis.

Anti-TNF inhibitors. split ileostomy, diverting ileostomy, and subtotal colectomy are options for management of steroid-dependent or refractory microscopic colitis. Currently, the need to resort to surgery is limited considering the improvement of drug therapy options. However, surgery is still considered for patients with severe, unresponsive microscopic colitis.

Some people may be admitted into the hospital following the colonoscopy depending on results. It is sometimes necessary to get the patient started on a steroid to speed up the healing of the colon. It may also be necessary to get the patient hydrated from the fluid loss and iron replaced from the loss of blood. After a hospital stay, the patient may be put on a daily medication to manage their chronic colitis. The medication can be an anti-inflammatory or an immunosuppressant. There are many different types of medication used and the doctor will prescribe the one they see fit. If the patient doesn't respond, new medications will be tried until there is a good fit.

Moreover, several studies recently have found significant relationship between colitis and dairy allergy (including: cow milk, cow milk UHT and casein), suggesting some patients may benefit from an elimination diet.

Diagnosis may be simple in cases where the patient's signs and symptoms are idiopathic to a specific cause. However this is generally not the case, considering that many pathogens which cause enteritis may exhibit the similar symptoms, especially early in the disease. In particular, "campylobacter, shigella, salmonella" and many other bacteria induce acute self-limited colitis, an inflammation of the lining of the colon which appears similar under the microscope.

A medical history, physical examination and tests such as blood counts, stool cultures, CT scans, MRIs, PCRs, colonoscopies and upper endoscopies may be used in order to perform a differential diagnosis. A biopsy may be required to obtain a sample for histopathology.

There is a recent optical test, but it requires endoscopy (see Diagnosis). There are no specific blood tests for ischemic colitis. The sensitivity of tests among 73 patients were:

- The white blood cell count was more than 15,000/mm3 in 20 patients (27%)

- The serum bicarbonate level was less than 24 mmol/L in 26 patients (36%)

Plain X-rays are often normal or show non-specific findings. In a series of 73 patients, plain abdominal radiography (56%) showing colic distension in 53% or a pneumoperitoneum in 3%.

CT scans are often used in the evaluation of abdominal pain and rectal bleeding, and may suggest the diagnosis of ischemic colitis, pick up complications, or suggest an alternate diagnosis.

Endoscopic evaluation, via colonoscopy or flexible sigmoidoscopy, is the procedure of choice if the diagnosis remains unclear. Ischemic colitis has a distinctive endoscopic appearance; endoscopy can also facilitate alternate diagnoses such as infection or inflammatory bowel disease. Biopsies can be taken via endoscopy to provide more information. Visible light spectroscopy, performed using catheters placed through the 5 mm channel of the endoscope, is diagnostic (see Diagnosis).

There may be signs of septic shock. A physical examination reveals abdominal tenderness and possible loss of bowel sounds. An abdominal radiography shows colonic dilation. White blood cell count is usually elevated. Severe sepsis may present with hypothermia or leukopenia.

A small bowel follow-through may suggest the diagnosis of Crohn's disease and is useful when the disease involves only the small intestine. Because colonoscopy and gastroscopy allow direct visualization of only the terminal ileum and beginning of the duodenum, they cannot be used to evaluate the remainder of the small intestine. As a result, a barium follow-through X-ray, wherein barium sulfate suspension is ingested and fluoroscopic images of the bowel are taken over time, is useful for looking for inflammation and narrowing of the small bowel. Barium enemas, in which barium is inserted into the rectum and fluoroscopy is used to image the bowel, are rarely used in the work-up of Crohn's disease due to the advent of colonoscopy. They remain useful for identifying anatomical abnormalities when strictures of the colon are too small for a colonoscope to pass through, or in the detection of colonic fistulae (in this case contrast should be performed with iodate substances).

CT and MRI scans are useful for evaluating the small bowel with enteroclysis protocols. They are also useful for looking for intra-abdominal complications of Crohn's disease, such as abscesses, small bowel obstructions, or fistulae. Magnetic resonance imaging (MRI) is another option for imaging the small bowel as well as looking for complications, though it is more expensive and less readily available. MRI techniques such as diffusion-weighted imaging and high-resolution imaging are more sensitive in detecting ulceration and inflammation compared to CT.

A colonoscopy is the best test for making the diagnosis of Crohn's disease, as it allows direct visualization of the colon and the terminal ileum, identifying the pattern of disease involvement. On occasion, the colonoscope can travel past the terminal ileum, but it varies from person to person. During the procedure, the gastroenterologist can also perform a biopsy, taking small samples of tissue for laboratory analysis, which may help confirm a diagnosis. As 30% of Crohn's disease involves only the ileum, cannulation of the terminal ileum is required in making the diagnosis. Finding a patchy distribution of disease, with involvement of the colon or ileum, but not the rectum, is suggestive of Crohn's disease, as are other endoscopic stigmata.

The utility of capsule endoscopy for this, however, is still uncertain. A "cobblestone"-like appearance is seen in approximately 40% of cases of Crohn's disease upon colonoscopy, representing areas of ulceration separated by narrow areas of healthy tissue.

The exact incidence of ischemic colitis is difficult to estimate, as many patients with mild ischemia may not seek medical attention. Ischemic colitis is responsible for about 1 in 2000 hospital admissions, and is seen on about 1 in 100 endoscopies. Men and women are affected equally; ischemic colitis is a disease of the elderly, with more than 90% of cases occurring in people over the age of 60.

Symptoms of pouchitis include Increased stool frequency, urgency, incontinence, nocturnal seepage, abdominal cramping, pelvic discomfort, and arthralgia.

Symptom severity does not always correlate with severity of endoscopically- or histologically-evaluated pouch inflammation. Additionally, these symptoms are not necessarily specific for pouchitis, asthey may arise from other inflammatory or functional pouch disorders such as Crohn's disease of the pouch, cuffitis, pouch sinus, or irritable pouch syndrome. The most reliable tool for diagnosis is endoscopy combined with histologic features (derived from tissue biopsies obtained during endoscopy).

Mild cases usually do not require treatment and will go away after a few days in healthy people. In cases where symptoms persist or when it is more severe, specific treatments based on the initial cause may be required.

In cases where diarrhoea is present, replenishing fluids lost is recommended, and in cases with prolonged or severe diarrhoea which persists, intravenous rehydration therapy or antibiotics may be required. A simple oral rehydration therapy (ORS) can be made by dissolving one teaspoon of salt, eight teaspoons of sugar and the juice of an orange into one litre of clean water. Studies have shown the efficacy of antibiotics in reducing the duration of the symptoms of infectious enteritis of bacterial origin, however antibiotic treatments are usually not required due to the self-limiting duration of infectious enteritis.

Treatment for colitis-X usually does not save the horse. The prognosis is average to poor, and mortality is 90% to 100%. However, treatments are available, and one famous horse that survived colitis-X was U.S. Triple Crown winner Seattle Slew, that survived colitis-X in 1978 and went on to race as a four-year-old.

Large amounts of intravenous fluids are needed to counter the severe dehydration, and electrolyte replacement is often necessary. Flunixin meglumine (Banamine) may help block the effects of toxemia. Mortality rate has been theorized to fall to 75% if treatment is prompt and aggressive, including administration of not only fluids and electrolytes, but also blood plasma, anti-inflammatory and analgesic drugs, and antibiotics. Preventing dehydration is extremely important. Nutrition is also important. Either parenteral or normal feeding can be used to support the stressed metabolism of the sick horse. Finally, the use of probiotics is considered beneficial in the restoration of the normal intestinal flora. The probiotics most often used for this purpose contain "Lactobacillus" and "Bifidobacterium".

The objective of treatment is to decompress the bowel and to prevent swallowed air from further distending the bowel. If decompression is not achieved or the patient does not improve within 24 hours, a colectomy (surgical removal of all or part of the colon) is indicated. When surgery is required the recommended procedure is a subtotal colectomy with end ileostomy. Fluid and electrolyte replacement help to prevent dehydration and shock. Use of corticosteroids may be indicated to suppress the inflammatory reaction in the colon if megacolon has resulted from active inflammatory bowel disease. Antibiotics may be given to prevent sepsis.

Specific types of enterocolitis include:

- necrotizing enterocolitis (most common in premature infants)

- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")

Chemical colitis is a type of colitis, an inflammation of the large intestine or colon, caused by the introduction of harsh chemicals to the colon by an enema or other procedure. Chemical colitis can resemble ulcerative colitis, infectious colitis and pseudomembranous colitis endoscopically.

Prior to 1950, hydrogen peroxide enemas were commonly used for certain conditions. This practice will often result in chemical colitis.

Soap enemas may also cause chemical colitis.

Harsh chemicals, such as compounds used to clean colonoscopes, are sometimes accidentally introduced into the colon during colonoscopy or other procedures. This can also lead to chemical colitis.

Chemical colitis may trigger a flare of ulcerative colitis or Crohn's colitis. Symptoms of colitis are assessed using the Simple Clinical Colitis Activity Index.

At necropsy, edema and hemorrhage in the wall of the large colon and cecum are pronounced, and the intestinal contents are fluid and often blood-stained. Macroscopic and microscopic findings include signs of disseminated intravascular coagulation, necrosis of colonic mucosa and presence of large numbers of bacteria in the devitalized parts of the intestine. Typically, the PCV is >65% even shortly after the onset of clinical signs. The leukogram ranges from normal to neutropenia with a degenerative left shift. Metabolic acidosis and electrolyte disorders are also present. There is leucopenia, initially characterized by neutropenia, which might evolve in neutrophilia. Moreover, haemoconcentration is noted with an increase in the packed cell volume; total proteins are initially increased, but changes into a lower than normal value. The most significant laboratory finding in colitis X is the increase of total cortisol concentration in blood plasma. Histopathologically, the mucosa of the large colon is hemorrhagic, necrotic and covered with fibrohemorrhagic exudate, while the submucosa, the muscular tunic and the local lymphonodes are edematous.

In histology, cryptitis refers to inflammation of an intestinal crypt.

Cryptitis is a non-specific histopathologic finding that is seen in several conditions, e.g. inflammatory bowel disease, diverticular disease, radiation colitis, infectious colitis.

Treatment of collagenous colitis is often challenging. Typically, one or more of the following therapeutic agents are used:

- Bismuth agents, including Pepto-Bismol

- 5-aminosalicylic acid

- Budesonide

- Immunosuppressants, including azathioprine

- Corticosteroids

Pilot-scale studies have shown some evidence of possible benefit for both "Boswellia serrata" extract and specific strains of probiotics in the treatment of collagenous colitis, although larger sample sizes are needed to confirm the results.