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Cytomegalovirus colitis, also known as CMV colitis, is an inflammation of the colon
Causes
The infection is spread by saliva, urine, respiratory droplets, sexual contact, and blood transfusions. Most people are exposed to the virus in their lifetime, but it usually produces mild or no symptoms in healthy people.
However, serious CMV infections can occur in people with weakened immune systems. This includes patients receiving chemotherapy for cancer and patients on immune-suppressing medicines following an organ transplant.
In rare instances, more severe CMV infection involving the GI tract has been reported in people with a healthy immune system.
The systemic use of corticosteroids in the context of inflammatory bowel disease.
Sixty percent of mothers of preterm infants are infected with cytomegalovirus (CMV). Infection is asymptomatic in most instances but 9% to 12% of postnatally infected low birth weight, preterm infants have severe, sepsis-like infection. CMV infection duration can be long and result in pneumonitis in association with fibrosis. CMV infection in infants has an unexpected effect on the white blood cells of the immune system causing them to prematurely age. This leads to a reduced immune response similar to that found in the elderly.
Most healthy people working with infants and children face no special risk from CMV infection. However, for women of child-bearing age who previously have not been infected with CMV, there is a potential risk to the developing unborn child (the risk is described above in the Pregnancy section). Contact with children who are in day care, where CMV infection is commonly transmitted among young children (particularly toddlers), may be a source of exposure to CMV. Since CMV is transmitted through contact with infected body fluids, including urine and saliva, child care providers (meaning day care workers, special education teachers, as well as mothers) should be educated about the risks of CMV infection and the precautions they can take. Day care workers appear to be at a greater risk than hospital and other health care providers, and this may be due in part to the increased emphasis on personal hygiene in the health care setting.
Recommendations for individuals providing care for infants and children:
- Employees should be educated concerning CMV, its transmission, and hygienic practices, such as handwashing, which minimize the risk of infection.
- Susceptible nonpregnant women working with infants and children should not routinely be transferred to other work situations.
- Pregnant women working with infants and children should be informed of the risk of acquiring CMV infection and the possible effects on the unborn child.
- Routine laboratory testing for CMV antibody in female workers is not specifically recommended due to its high occurrence, but can be performed to determine their immune status.
Recommendations for pregnant women with regard to CMV infection:
- Throughout the pregnancy, practice good personal hygiene, especially handwashing with soap and water, after contact with diapers or oral secretions (particularly with a child who is in day care). Sharing of food, eating and drinking utensils, and contact with toddlers' saliva should be avoided.
- Women who develop a mononucleosis-like illness during pregnancy should be evaluated for CMV infection and counseled about the possible risks to the unborn child.
- Laboratory testing for antibody to CMV can be performed to determine if a woman has already had CMV infection.
- Recovery of CMV from the cervix or urine of women at or before the time of delivery does not warrant a cesarean section.
- The demonstrated benefits of breast-feeding outweigh the minimal risk of acquiring CMV from the breast-feeding mother.
- There is no need to either screen for CMV or exclude CMV-excreting children from schools or institutions because the virus is frequently found in many healthy children and adults.
Treatment with hyperimmune globulin in mothers with primary CMV infection has been shown to be effective in preventing congenital disease in several studies. One study did not show significant decrease in the risk of congenital cytomegalovirus infection.
Congential rubella is still a risk with higher risk among immigrant women from countries without adequate vaccination programs.
Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis. They include the following:
- Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn's disease. Few studies have investigated such an association; one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.
- Breastfeeding: Some reports of the protection of breastfeeding in the development of inflammatory bowel disease contradict each other. One Italian study showed a potential protective effect.
- One study of isotretinoin found a small increase in the rate of ulcerative colitis.
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.
Specific types of enterocolitis include:
- necrotizing enterocolitis (most common in premature infants)
- pseudomembranous enterocolitis (also called "Pseudomembranous colitis")
Enterocolitis or coloenteritis is an inflammation of the digestive tract, involving enteritis of the small intestine and colitis of the colon. It may be caused by various infections, with bacteria, viruses, fungi, parasites, or other causes. Common clinical manifestations of enterocolitis are frequent diarrheal defecations, with or without nausea, vomiting, abdominal pain, fever, chills, alteration of general condition. General manifestations are given by the dissemination of the infectious agent or its toxins throughout the body, or – most frequently – by significant losses of water and minerals, the consequence of diarrhea and vomiting.
Among the causal agents of acute enterocolitis are:
- bacteria: "Salmonella", "Shigella", "Escherichia coli", "Campylobacter" etc.;
- viruses: enteroviruses, rotaviruses, Norwalk virus, adenoviruses;
- fungi: candidiasis, especially in immunosuppressed patients or who have previously received prolonged antibiotic treatment;
- parasites: "Giardia lamblia" (with high frequency of infestation in the population, but not always with clinical manifestations), "Balantidium coli", "Blastocystis homnis", "Cryptosporidium" (diarrhea in people with immunosuppression), "Entamoeba histolytica" (produces the amebian dysentery, common in tropical areas).
In Germany, 90% of cases of infectious enteritis are caused by four pathogens, Norovirus, Rotavirus, "Campylobacter" and "Salmonella". Other common causes of infectious enteritis include bacteria such as "Shigella" and "E. coli," as well as viruses such as adenovirus, astrovirus and calicivirus. Other less common pathogens include "Bacillus cereus, Clostridium perfringens, Clostridium difficile" and "Staphylococcus aureus".
"Campylobacter jejuni" is one of the most common sources of infectious enteritis, and the most common bacterial pathogen found in 2 year old and smaller children with diarrhoea. It has been linked to consumption of contaminated water and food, most commonly poultry and milk. The disease tends to be less severe in developing countries, due to the constant exposure which people have with the antigen in the environment, leading to early development of antibodies.
Rotavirus is responsible for infecting 140 million people and causing 1 million deaths each year, mostly in children younger than 5 years. This makes it the most common cause of severe childhood diarrhoea and diarrhea-related deaths in the world. It selectively targets mature enterocytes in the small intestine, causing malabsorption, as well as inducing secretion of water. It has also been observed to cause villus ischemia, and increase intestinal motility. The net result of these changes is induced diarrhoea.
Enteritis necroticans is an often fatal illness, caused by β-toxin of "Clostridium perfringens". This causes inflammation and segments of necrosis throughout the gastrointestinal tract. It is most common in developing countries, however has also been documented in post-World War II Germany. Risk factors for enteritis necroticans include decreased trypsin activity, which prevent intestinal degradation of the toxin, and reduced intestinal motility, which increases likelihood of toxin accumulation.
Research has not revealed any difference in overall risk of dying in patients with ulcerative colitis from that of the background population. The cause-of-death distribution may be different from that of the background population. It is thought that the disease primarily affects quality of life, and not lifespan.
Proctocolitis has many possible causes. Common infectious causes of proctocolitis include Chlamydia trachomatis, LGV (Lymphogranuloma venereum), Neisseria gonorrhoeae, HSV, and Helicobacter species. It can also be idiopathic (see colitis), vascular (as in ischemic colitis), or autoimmune (as in inflammatory bowel disease).
Anoscopy can be used to diagnose the majority of cases of proctocolitis.
Crohn's disease – also known as regional enteritis, it can occur along any surface of the gastrointestinal tract. In 40% of cases it is limited to the small intestine.
Coeliac disease – caused by an autoimmune reaction to gluten by genetically predisposed individuals.
Eosinophilic enteropathy – a condition where eosinophils build up in the gastrointestinal tract and blood vessels, leading to polyp formation, necrosis, inflammation and ulcers. It is most commonly seen in patients with a history of atopy, however is overall relatively uncommon.
Incidence and prevalence of microscopic colitis nears those of ulcerative colitis and Crohn’s disease. Recent studies in North America found incidence rates of 7.1 per 100,000 person-years and 12.6 per 100,000 person-years for collagenous colitis for lymphocytic colitis, respectively.
A higher incidence of autoimmune diseases, for example arthritis, Sjögren's syndrome, thyroid disorders, and coeliac disease, has been reported in patients with microscopic colitis. Associations with various drugs have been found, especially proton pump inhibitors, H blockers, selective serotonin reuptake inhibitors (SSRIs), and non-steroidal anti-inflammatory drugs (NSAIDs). Bile acid diarrhea is found in 41% of patients with collagenous colitis and 29% with lymphocytic colitis. Additionally, smoking has been identified as a significant risk factor of microscopic colitis.
No definite cause has been determined. Some reports have implicated long-term usage of NSAIDs, proton pump inhibitors, and selective serotonin reuptake inhibitors, and other drugs. Associations with other autoimmune disorders suggests that overactive immune responses occur.
Herpes simplex virus is commonly found in humans, yet uncommonly results in systemic manifestations. Suppression of HIV with antiretroviral medications, careful monitoring of immunosuppressive medications are important means of prevention. Antiviral prophylaxis such as daily acyclovir in immunocompromised individuals may be considered.
Antivirals such as acyclovir, famciclovir, or valacyclovir may be used. Intravenous acyclovir is reserved for individuals who cannot swallow due to the pain, individuals with other systemic manifestations of herpes or severely immunocompromised individuals.
Colitis is an inflammation of the colon. Colitis may be acute and self-limited or long-term. It broadly fits into the category of digestive diseases.
In a medical context, the label "colitis" (without qualification) is used if:
- The cause of the inflammation in the colon is undetermined; for example, "colitis" may be applied to "Crohn's disease" at a time when the diagnosis is unknown, or
- The context is clear; for example, an individual with ulcerative colitis is talking about their disease with a physician who knows the diagnosis.
Lymphocytic colitis is a subtype of microscopic colitis, a condition characterized by chronic non-bloody watery diarrhea. The colonoscopy is normal but histology of the mucosal biopsy reveals an accumulation of lymphocytes in the colonic epithelium and connective tissue (lamina propria). Collagenous colitis shares this feature but additionally shows a distinctive thickening of the subepithelial collagen table. The peak incidence of lymphocytic colitis is in persons over age 50; the disease affects women and men equally. Lymphocytic colitis was first described in 1989.
Surgery-associated ischemia may contribute inflammation at the anal transitional zone.
Patients whose cuffitis is refractory to mesalamine and/or corticosteroids should be evaluated for other disease in the cuff area, such as fistula or anastomotic leaks. Cuffitis that is refractory to medication can also be a sign of Crohn's disease of the pouch.
Chronic cuffitis can also contribute to the development of anastomotic stricture.
Cuffitis that is refractory, Crohn's-related, or is associated with surgical complications can contribute to pouch failure.
As a result of microbial symbiosis and immunity, alterations in enteral bacteria may contribute to inflammatory gut diseases. IBD-affected individuals have been found to have 30–50 percent reduced biodiversity of commensal bacteria, such as decreases in Firmicutes (namely Lachnospiraceae) and Bacteroidetes. Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD-affected individuals are more likely to have been prescribed antibiotics in the 2–5 year period before their diagnosis than unaffected individuals. The enteral bacteria can be altered by environmental factors, such as concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.
A subtype of infectious colitis is "Clostridium difficile" colitis, which is informally abbreviated as "c diff colitis". It classically forms and is often referred to as pseudomembranous colitis, which is its (nonspecific) histomorphologic description.
Enterohemorrhagic colitis may be caused by Shiga toxin in "Shigella dysenteriae" or "Shigatoxigenic group" of "Escherichia coli" (STEC), which includes serotype and other enterohemorrhagic "E. coli".
Parasitic infections, like those caused by "Entamoeba histolytica", can also cause colitis.