2Seen here is a loop of bowel attached via the mesentery Seen here is a loop of bowel attached via the mesentery. Note the extent of the veins. Arteries run in the same location.Thus, there is an extensive anastomosing arterial blood supply to the bowel, making it more difficult to infarct. Also,the extensive venous drainage is incorporated into the portal venous system heading to the liver
3This is the normal appearance of terminal ileum. In the upper frame, note the ileocecal valve, andseveral darker ovalPeyer's patches are present on the mucosa. In thelower frame, a Peyer's patch, which is aconcentration of submucosallymphoid tissue, is present. Note the folds are notas prominent here as in the jejunumThis is the normal appearance of small intestinalmucosa with long villi that have occasional gobletcells.The villi provide a large area for digestion andabsorption
4MALDIGESTIONE MALASSORBIMENTO BASI FISIOPATOLOGICHEL’intestino presenta un’enorme area superficiale, incrementata, a livello del tenue, dalla presenzadei microvilli (2 x 108/cm2).La motilità intestinale, parietale e degli stessi villi, consente l’intimo contatto tra parete intestinale esostanze nutritizie e ne favorisce la progressione ed il trasporto nei linfatici.Alcuni processi digestivi si completano nella parete.La porzione prossimale dell’intestino tenue, normalmente è sterile peracidità gastricaperistalsi intestinaleproduzione locale di Ig.Assorbimento differenziatoFe, Ca, vitamine liposolubili, grassi tenue prossimaleGlucidi tenue prossimale e medioAminoacidi tenue medio, ma anche altri trattiSali biliari e vitamina B12 soprattutto tenue distaleAcqua intestino crasso
5Maldigestione - Malassorbimento Alterato assorbimento di proteine, carboidrati, grassi, vitamine liposolubili ed altre vitamine,elettroliti, minerali, acqua, per alterazione di una o più delle seguenti funzioni digestive:digestione intraluminaledigestione terminale (parietale)trasporto transepitelialeDiagnosi: in molti casi è necessaria la biopsia della mucosa intestinaleQuadro anatomo-clinicoGenerale: calo ponderale, diminuzione di crescita,mucositi, edemi da ipoproteinemiaApparato gastroenterico: diarrea con feci abbondantigiallastre, grassose; metorismo; dolori addominali esenso di distensioneSistema emopoietico: anemia ipocromica, emorragieSistema muscolo-scheletrico: tetania, osteomalaciaS. endocrino: amenorrea, infertilità, iperparatiroidismoCute: dermatitiSistema nervoso: neuropatie periferiche
6Inquadramento fisiopatologico dei malassorbimenti da difetto dei meccanismi didigestione intraluminali2. da alterazioni primitive dellamucosa intestinale3. da riduzione della superficieassorbente4. da ostruzione linfatica5. da infezioni6. da cause iatrogene o da farmaci7. da meccanismi sconosciuti
7a - Deficit degli enzimi pancreatici Insufficienza del pancreas esocrinoPancreatite cronicaCarcinoma del pancreasFibrosi cisticaResezione pancreaticab - Deficit della concentrazione dei sali biliariMalattie epaticheMalattie parenchimaliColestasi intra- od extraepaticaInterruzione del circolo enteroepatico della bileDa farmaci ad azione precipitante o sequestrantei sali biliari (neomicina, colestiramina)
8Da alterazioni primitive della mucosa intestinale c – Iperproliferazione batterica(deconiugazione sali biliari)Stasi nella sindrome dell’ansa afferenteStenosi e atresieFistoleAnsa ciecaDiverticolite multipla del tenueSindromi da ipomobilità intestinaleDa alterazioni primitive della mucosa intestinaleDeficit di disaccaridasiLe disaccaridasi (lattasi, sucrasi, maltasi) sono localizzate sulla membrana dellecellule intestinali. L’assenza (congenita o acquisita) di tali enzimi provocadiarrea (osmotica) ed iperproduzione di idrogeno (per fermentazione battericadegli zuccheri non assorbiti).Non sono documentabili alterazioni al microscopio.Diagnosi di certezza: istochimica.
9% 2. Da alterazioni primitive della mucosa intestinale A--lipoproteinemiaMalattia autosomica recessiva: difettosa sintesi di apoproteina B impossibilitàal trasporto di trigliceridi a livello della mucosa intestinale; acidi grassi liberi emonogliceridi penetrano nelle cellule con funzione assorbente, ma non sonoriaggregati in chilomicroni accumulo di lipidi sotto forma di vacuoli visibili almicroscopio ottico; inoltre, si ha ipolipemia, con ipochilomicronemia,ipo-pre-lipoproteinemia (VLDV) e ipo-lipoproteinemia (LDL); alterazione deglieritrociti (acantociti) per difetto della struttura lipidica della membrana.%2. Da alterazioni primitive della mucosa intestinaleMalassorbimento di vitamina B12Disfunzione o resezione ilealePerdita di cellule parietali (anemia perniciosa)
10% 2 - Da alterazioni primitive della mucosa intestinale Cistinuria (autosomica recessiva; eccessiva eliminazione urinaria di AA dibasicia livello del tubulo prossimale renale e del digiuno aminoaciduria,malassorbimento)Amiloidosi (soprattutto associata a malattia immunocitica)Enterite eosinofila (a possibile patogenesi allergica)3. Da riduzione della superficie assorbente del tenueEnteropatia da glutine (morbo celiaco):Malattia intestinale cronica caratterizzata da deficit dell’assorbimento intestinale,legata ad intolleranza per la gliadina ed altre proteine associate al frumento.Colpisce quasi esclusivamente la razza bianca.Casi in Europa 1:EziopatogenesiIpersensibilità al glutine, contenuto nel frumento, che contiene una proteina(gliadina) solubile in alcool ed insolubile in acqua, presente nel grano, nell’orzo,nella segale e nell’avena.Probabile meccanismo: suscettibilità genetica alla gliadina e lesione intestinaleimmunomediata
11Il contatto con la gliadina provoca accumulo di linfociti B sensibilizzati verso la gliadina. Sono presenti anche anticorpi anti-gliadina in circolo.Possibile cross-reattività tra la gliadina ed una proteina dell’adenovirus tipo 12 (possibile fattore ambientale in aggiunta a quello genetico).
13The small intestinal mucosa at high magnification shows marked chronic inflammation in celiac sprue. There is sensitivity to gluten, which contains the protein gliaden, found in cereal grains wheat, oats,barley, and rye. Removing foods containing these grains from the diet will cause this gluten-sensitiveenteropathy to subside. The enteropathy shown here has loss of crypts, increased mitotic activity,loss of brush border, and infiltration with lymphocytes and plasma cells (B-cells sensitized to gliaden).
143. Da riduzione della superficie assorbente del tenue Morbo di Crohn ma anche per: interruzione del circolo enteroepatico biliare iperproliferazione batterica diminuita funzione assorbente ipoproteinemia ( funzione pancreatica)Enteriti diffuse associate a linfoma4 Da ostruzione linfaticaLinfomi intestinali primitivima anche perinteressamento mucoso diffusostenosi iperproliferazione battericaMorbo di WhippleTubercolosiLinfangectasie
15Morbo di WhippleMalattia rara (maschi adulti, anni), a carattere sistemico, con manifestazioni intestinali, responsabili di diarrea cronica e malassorbimento, e coinvolgimento di cute, SNC, cuore, vasi, polmoni, reni, sierose, linfonodi, milza e fegato. Altri segni: poliartrite migrante, disturbi neurologici, versamenti pleurici, linfoadenopatie, febbre.Eziologia probabilmente batterica: microrganismi bastoncelliformi nella tonaca propria, extra- ed intracellulari macrofagi. All’interno di questi, glicoproteine PAS-positive, possibile prodotto batterico.Microrganismi isolati: oltre 25 tipi.La malattia risponde alla terapia antibiotica.Diagnosi: biopsia duodenale o digiunale.
16Celiac disease Abnormal small intestinal mucosa. Villli are short and flattened (yellow arrow). This is seen in malabsorptionsyndromesCeliac diseaseis a genetic, immunologically mediatedsmall bowel enteropathy that causes malabsorption.The immune inflammatory response to gluten frequentlycauses damage to many other tissues of the body.The condition is frequently underdiagnosed because ofits protean presentations. New prevalence data indicatethat symptomatic and latent celiac disease is present inone of 300 people of European descent. Age of onsetranges from infancy to old age.Symptomatic presentations include general ill-health, as well as dermatologic, hematologic, musculoskeletal,mucosal, dental, psychologic and neurologic diseases.Celiac disease has a 95 percent genetic predisposition and, thus, it is frequently associated with autoimmuneconditions such as diabetes mellitus type 1 and thyroid disease.Untreated patients have an increased incidence of osteoporosis and intestinal lymphoma. Excellent diagnosticscreening tests are now available, including those that detect antigliadin and antiendomysial antibodies.Therapy with a gluten-free diet is effective, resulting in complete resolution of symptoms and secondarycomplications in almost all patients. Local and national celiac-sprue associations facilitate care of patients withceliac disease and support dietary compliance.Celiac disease is a gluten enteropathy occurring in both children and adults. The condition is characterized by asensitivity to gluten that results in inflammation and atrophy of the mucosa of the small intestine. Clinicalmanifestations include malabsorption with symptoms of diarrhea, steatorrhea, and nutritional and vitamin deficiencies.Secondary immunologic illnesses, such as atopic dermatitis, dermatitis herpetiformis, alopecia and aphthous ulcers,may be the primary presentation
17PRESENTAZIONE CLINICA PATOGENESIThe immune system is abnormally activated by gluten, specifically the gliadin portion of wheat protein, andprolamines (insoluble proteins) in rye, barley and oats. Thus, celiac disease is a genetic, immunologically mediated,small intestine enteropathy in which mucosal villi are destroyed by cellular and humoral-mediated immunologicreactions to gliadin protein. The loss of functioning villi limits the ability of the small intestine to absorb nutrients,thus adversely affecting all systems of the body. The immunologic response to gluten may also occur secondarily inother bodily tissues, an example being dermatitis herpetiformis.Strong association with specific HLA class II genotypes.Approximately 95 percent of patients with celiac disease have a particular type of HLA DQ alpha and beta chainencoded by two genes, HLA-DQA and HLA-DQBIf people genetically predisposed to celiac disease do not ingest gluten, they have no manifest illness.Delaying ingestion of gluten products through breast feeding or dietary habits may change or delay the onset ofdisease.Viral exposures may trigger an immunologic response in persons genetically susceptible to celiac disease;this occurs with adenovirus type 12, which shares a sequence of eight to 12 amino acids with the toxic gliadinfractionPRESENTAZIONE CLINICADuring the first year of life, an infant may manifest celiac disease with intermittent vomiting, diarrhea, growth delayand failure to thrive. The incidence of this early classic presentation in infants has decreased.Children with celiac disease may present with short stature, anemia, hepatitis, epilepsy and otherextragastrointestinal conditions.With age, these presentations become more subtle: the most frequent symptoms being abdominal pain, aphthousstomatitis and atopic dermatitisGiovani adulti: The initial presentation of celiac disease in patients in their 20s and 30s may be dermatitisherpetiformis. This condition usually appears as clear or blood-tinged vesicles symmetrically distributed over theextensor areas of the elbows, knees, buttocks, shoulders and scalp. Intense pruritus and/or burningsensations in the area occur hours before the onset of the vesicle. Dermatitis herpetiformis flares after consumptionof foods containing a high amount of gluten
18Malattie associate: Diabete mellito di tipo I; Adults Malabsorption.The varied signs and symptoms of malabsorption may be caused by celiac disease or many other diseases.Mild malabsorption may be asymptomatic. With its gradual onset, the classic manifestations of flatulence and bulky,greasy and foul-smelling stools may not be recognized by the patient as signs of celiac disease. Malabsorptionshould be suspected in any patient with weight loss and diarrhea, and the signs and symptoms of specific vitamin ornutritional deficiencies. The latter include visual disturbances, neuropathy, anemia, osteopenic bone disease, tetany,hemorrhagic diathesis or infertilityAnemiaAnemia is a frequent presentation of celiac disease. Screening for occult blood in stool is considered primarily ascreening for cancer, but celiac disease should be considered in the differential diagnosisOsteopeniaOsteopenia may be the initial finding in patients with celiac disease. Reduced mineralization occurs in asymptomaticceliac patients, and that early diagnosis and treatment can prevent bone demineralization.SeizuresThere have been numerous reports of children and adults with seizures associated with celiac disease.Calcificazioni cerebrali sono una frequente complicanza. Chronic folic acid deficiency in untreated patients wasconsidered a possible explanationHepatic Disease.Celiac disease has long been recognized as a cause ofchronic hepatic pathologyComputedtomographicscan showingoccipital calcificationin a patientwith celiac diseaseand epilepsy.Malattie associate: Diabete mellito di tipo I;malattie autoimmuni della tiroide
19Normal small intestinal mucosa is seen at the left, and mucosa involved by celiac sprue at the right. There is bluntingand flattening of villi with celiac disease, and in severe cases a loss of villi with flattening of the mucosa as seen here.Celiac sprue has a prevalence of about 1:2000 Caucasians, but is rarely seen in other races. Over 95% of affectedpatients will express the DQw2 histocompatibility antigen, which suggests a genetic basis
20The small intestinal mucosa at high magnification shows marked chronic inflammation in celiac sprue. There issensitivity to gluten, which contains the protein gliaden, found in cereal grains wheat, oats, barley, and rye.Removing foods containing these grains from the diet will cause this gluten-sensitive enteropathy to subside.The enteropathy shown here has loss of crypts, increased mitotic activity, loss of brush border, and infiltrationwith lymphocytes and plasma cells (B-cells sensitized to gliaden).
21Lactose intolerance SINTOMI Short-bowel syndrome is the inability to digest significant amounts of lactose, the major sugar found in milk. Lactose intolerance iscaused by a shortage of the enzyme lactase, which is produced by the cells that line the small intestine. Lactasebreaks down milk sugar into two simpler forms of sugar called glucose and galactose, which are then absorbedinto the bloodstream. Not all people deficient in lactase have the symptoms commonly associated with lactoseintolerance, but those who do are said to have lactose intolerance.People sometimes confuse lactose intolerance with cow’s milk intolerance because the symptoms are often thesame. However, lactose intolerance and cow’s milk intolerance are not related. Being intolerant to cow’s milk is anallergic reaction triggered by the immune system.Lactose intolerance is a problem caused by the digestive systemSINTOMIPeople who do not have enough lactase to digest the amount of lactose they consume may feel very uncomfortablewhen they digest milk products. Common symptoms, which range from mild to severe, include nausea, cramps,bloating, gas, and diarrhea. Symptoms begin about 30 minutes to 2 hours after eating or drinking foods containinglactoseShort-bowel syndromeSBS, short gut syndrome, anenteric malabsorption syndrome, malabsorption, maldigestion, malnutrition, diarrhea,fluid disturbances, electrolyte disturbances, total parenteral nutrition, TPNThe average length of the adult human small intestine has been calculated at approximately 600 cm from studiesperformed on cadavers. According to Lennard-Jones and to Weser (1983), this figure ranges from cm.Any disease, traumatic injury, vascular accident, or other pathology that leaves less than 200 cm of viable smallbowel places the patient at risk for developing short-bowel syndromeThe short-bowel syndrome is a disorder clinically defined by malabsorption, diarrhea, fluid and electrolytedisturbances, and malnutrition. The final common etiologic factor in all causes of short-bowel syndrome is thefunctional or anatomic loss of extensive segments of small intestine so that absorptive capacity is severelycompromised. Although resection of the colon alone typically does not result in short-bowel syndrome, itspresence or loss can be a critical factor in the management of patients who lose significant amounts ofsmall intestine.
22Massive small intestinal resection compromises digestive and absorptive processes. Adequate digestion and absorption cannot take place, and proper nutritional statuscannot be maintained without supportive care.Examples of clinical conditions that can result in the short-bowel syndrome includemesenteric ischemia,trauma,inflammatory bowel disease,cancer,radiation enteritis,congenital short small bowel,midgut volvulus,multiple small bowel atresias,gastroschisis,meconium peritonitis,and necrotizing enterocolitis.Not all patients with loss of significant amounts of small intestine develop theshort-bowel syndrome. Important cofactors that help to determine whether the syndromewill develop or not include the premorbid length of small bowel, the segment of intestinethat is lost, the age of the patient at the time of bowel loss, the remaining length ofsmall bowel and colon, and the presence or absence of the ileocecal valve.
23DISSENTERIA SHIGELLA, ENTAMOEBA HISTOLYTICA Dysentery - bloody diarrhoea - is one of the most dangerous types of diarrhoea. In general. it is more severe andmore likely to result in death than other forms of acute diarrhoea. Other symptoms can include abdominal cramps, fever, or severe pain during defecationLarge scale outbreaks (epidemics) of dysentery are a particular threat to public health. The death rate can be as highas 15 per cent, and health care services are severely stretched during epidemics. Even when correctly treated, about5 per cent of people with dysentery can die during an epidemic. The bacterium responsible for epidemic dysentery is Shigella dysenteriae type 1 (Sd1 ) (1). S. dysenteriae is one offour species of Shigella. The others are Shigella flexneri, Shigella sonnei and Shigella boydii.These species are usually less dangerous than Sd1 and they do not cause large epidemics. Disease caused by Sd1 tends to be more common in infants, and elderly and malnourished people.Mortality is also highest in these groups. Since Sd1 was first identified late last century, extensive epidemics have been reported in Africa, Asia and LatinAmerica. An epidemic of Sd1 in Latin America between 1969 and 1973 was responsible for more than 500,000 casesof dysentery and 20,000 deathsAltre cause di dissenteria:The most severe episodes of endemic dysentery are caused by other species of Shigella - Shigella flexneri,Shigella boydii and Shigella sonnei.Other pathogens causing endemic dysentery in children include: Campylobacter jejuni,invasive strains of Escherichia coli, non-typhoid Salmonella strains and Entamoeba histolytica
24Shigellosisis a bacterial infection affecting the intestinal tract. It is a fairly common disease; cases occurin New York State each year.Most cases are seen in the summer and early fall and occur as single cases or outbreaksIt is recognized more often in young children.Those who may be at greater risk include children in daycare centers, foreign travelers to certain countries,institutionalized people and active homosexualsShigella germs are found in the intestinal tract of infected people, and is spread by eating or drinking food or watercontaminated by an infected person. It can also be spread by direct contact with an infected personSintomi: People exposed to the shigella germ may experience mild or severe diarrhea, often with fever and tracesof blood or mucous in the stool. Some infected people may not show any symptomsThe symptoms may appear one to seven days after exposure but usually within two to three daysDIARREADiarrhea—loose, watery stools occurring more than three times in one day—is a common problem that usually lasts a day or two and goes away on its own without any special treatment.However, prolonged diarrhea can be a sign of other problems.People with diarrhea may pass more than a quart of stool a day.Diarrhea can cause dehydration, which means the body lacks enough fluid to function properly.Dehydration is particularly dangerous in children and the elderly, and it must be treated promptly to avoid serioushealth problems
25like an intestinal disease. Diarrhea may be caused by a temporary problem, like an infection, or a chronic problem,like an intestinal disease.A few of the more common causes of diarrhea are:Bacterial infections. Several types of bacteria, consumed through contaminated food or water, cancause diarrhea.Common culprits include Campylobacter, Salmonella, Shigella, and Escherichia coli. Viral infections. Many viruses cause diarrhea, including rotavirus, Norwalk virus, cytomegalovirus,herpes simplex virus, and viral hepatitis. Food intolerances. Some people are unable to digest some component of food, such as lactose,the sugar found in milk. Parasites. Parasites can enter the body through food or water and settle in the digestive system.Parasites that cause diarrhea include Giardia lamblia, Entamoeba histolytica, and Cryptosporidium. Reaction to medicines, such as antibiotics, blood pressure medications, and antacids containingmagnesium. Intestinal diseases, like inflammatory bowel disease or celiac disease. Functional bowel disorders, such as irritable bowel syndrome, in which the intestines do not worknormally
26Some people develop diarrhea after stomach surgery or removal of the gallbladder. The reason may be a change in how quickly food moves through the digestive systemafter stomach surgery or an increase in bile in the colon that can occur after gallbladdersurgery.ALTRI SINTOMIDiarrhea may be accompanied by cramping abdominal pain, bloating, nausea, or an urgent need to use the bathroom.Depending on the cause, a person may have a fever or bloody stoolsDiarrhea can be either acute (short-term) or chronic (long-term). The acute form, which lasts less than 4 weeks, isusually related to a bacterial, viral, or parasitic infection. Chronic diarrhea lasts more than 4 weeks and is usuallyrelated to functional disorders like irritable bowel syndrome or inflammatory bowel diseases like celiac diseaseChildren can have acute or chronic forms of diarrhea. Causes include bacteria, viruses, parasites, medications,functional disorders, and food sensitivities. Infection with the rotavirus is the most common cause of acute childhooddiarrhea. Rotavirus diarrhea usually resolves in 3 to 9 daysGeneral signs of dehydration include: thirst, less frequent urination, dry skin, fatigue, light-headednessdark colored urineSigns of dehydration in children includedry mouth and tongueno tears when cryingno wet diapers for 3 hours or moresunken abdomen, eyes, or cheekshigh feverlistlessness or irritabilityskin that does not flatten when pinched and released
27Yellow arrow depicts crescent shaped trophozoite, while the red arrow depicts a teardrop shaped trophozoite of giardiaThis is an example of infectious diarrhea due to Giardia lamblia infection of thesmall intestine.The small pear-shaped trophozoites live in the duodenum and becomeinfective cysts that are excreted. They produce a watery diarrhea.A useful test for diagnosis of infectious diarrheas is stool examination forova and parasites
28Cryptosporidiosis -- Small spherical organisms (red arrow) attached to thebrush border of absorptive intestinalepithelial cells.This is another infectious agent that is becomingmore frequent in immunocompromised patients, particularly those with AIDS. The small round blue organisms at thelumenal border are cryptosporidia. Cryptosporidiosis produces a copious watery diarrhea
29Astrovirus; calicivirus; reovirus (rotavirus; “picorna/enterovirus”) VIRUS CAUSA DI DIARREAAstrovirus; calicivirus; reovirus (rotavirus; “picorna/enterovirus”)Reovirus: Respiratory Enteric Orphan viruses, i.e. infect the human respiratory and intestinal tracts, usuallywithout disease symptomsOne well documented source of infection is the consumption of shellfish (polluted by sewage) - and therefore,they also have economic consequences for fishermen and the food industry.Such viruses often cause mini-epidemics in families, hospital wards, etc and are potentially very dangerous toseriously ill hospital patients.More importantly, these viruses contribute to the massive mortality caused by infantile diarrhoea in developingcountries and are responsible for uncounted millions of deaths each year.Cause di diarrea severa/morte
30COLERACholera is an acute intestinal infection caused by ingestion of food or water contaminated with the bacteriumVibrio cholerae. It has a short incubation period, from less than one day to five days, and produces an enterotoxinthat causes a copious, painless, watery diarrhoea that can quickly lead to severe dehydration and death iftreatment is not promptly given. Vomiting also occurs in most patients.Most persons infected with V. cholerae do not become ill, although the bacterium is present in their faeces for7-14 days. When illness does occur, more than 90% of episodes are of mild or moderate severity and are difficultto distinguish clinically from other types of acute diarrhoea. Less than 10% of ill persons develop typical cholerawith signs of moderate or severe dehydration.BACKGROUNDThe vibrio responsible for the seventh pandemic, now in progress, is known as V. cholerae O1, biotype El Tor.The current seventh pandemic began in 1961 when the vibrio first appeared as a cause of epidemic cholera inCelebes (Sulawesi), Indonesia. The disease then spread rapidly to other countries of eastern Asia and reachedBangladesh in 1963, India in 1964, and the USSR, Iran and Iraq inIn 1970 cholera invaded West Africa, which had not experienced the disease for more than 100 years. The diseasequickly spread to a number of countries and eventually became endemic in most of the continent. In 1991 cholerastruck Latin America, where it had also been absent for more than a century. Within the year it spread to 11countries, and subsequently throughout the continent.Until 1992, only V. cholerae serogroup O1 caused epidemic cholera. Some other serogroups could cause sporadiccases of diarrhoea, but not epidemic cholera. Late that year, however, large outbreaks of cholera began in India andBangladesh that were caused by a previously unrecognized serogroup of V. cholerae, designated O139, synonymBengal. Isolation of this vibrio has now been reported from 11 countries in South-East Asia. It is still unclearwhether V. cholerae O139 will extend to other regions, and careful epidemiological monitoring of the situationis being maintained.
31as can conditions in crowded refugee camps. TRASMISSIONECholera is spread by contaminated water and food. Sudden large outbreaks are usually caused by a contaminatedwater supply. Only rarely is cholera transmitted by direct person-to-person contact. In highly endemic areas, it ismainly a disease of young children, although breastfeeding infants are rarely affected.Vibrio cholerae is often found in the aquatic environment and is part of the normal flora of brackish water andestuaries. It is often associated with algal blooms (plankton), which are influenced by the temperature of the water.Human beings are also one of the reservoirs of the pathogenic form of Vibrio choleraeMan-made and natural disasters can intensify the risk of epidemics considerably,as can conditions in crowded refugee camps.Explosive outbreaks with high case-fatality rates are often the result.For example, in the aftermath of the Rwanda crisis in 1994, outbreaks of cholera causedat least cases and deaths within one month in the refugee camps in Goma,the Congo. Although rarely so deadly, outbreaks continue to be of major public healthconcern, causing considerable socioeconomic disruption as well as loss of life.In 2001 alone, WHO and its partners in the Global Outbreak Alert and Response Networkparticipated in the verification of 41 cholera outbreaks in 28 countries
32The small intestinal mucosa demonstrates marked hyperemia as a result of ischemic enteritis. Such ischemia mostoften results from hypotension (shock) from cardiac failure, from marked blood loss, or from loss of blood supply frommechanical obstruction (as with the bowel incarcerated in a hernia or with volvulus or intussusception). If the bloodsupply is not quickly restored, the bowel will infarct
33On closer inspection, early ischemic enteritis involves the tips of the villi. A colonoscopic view of ischemic colitis withminimal overlying exudate is shown below. In general, bowel is hard to infarct from atherosclerotic vascular narrowingor thromboembolization because of the widely anastomosing blood supply. Thus, most cases of bowel ischemia andinfarction result from generalized hypotension and decreased cardiac output
34The mucosal surface of the bowel seen here shows early necrosis with hyperemia extending all the way frommucosa to submucosal and muscular wall vessels. The submucosa and muscularis, however, are still intact
35At higher magnification with more advanced necrosis, the small intestinal mucosa shows hemorrhage with acuteinflammation in this case of ischemic enteritis
36The dark red infarcted small intestine contrasts with the light pink viable bowel. The forceps extend through aninternal hernia in which a loop of bowel and mesentery has been caught. This is one complication of adhesionsfrom previous surgery. The trapped bowel has lost its blood supply.
37This is normal colonic mucosa This is normal colonic mucosa. Note the crypts that are lined by numerous goblet cells. In the submucosa is alymphoid nodule. The gut-associated lymphoid tissue as a unit represents the largest lymphoid organ of the body
38Typical pseudomembranes adherent to the colonic mucosa in antibiotic-associated colitis. The illness occurs after acourse of broad-spectrum antibiotics, which permitovergrowth of the bacteria Clostridium difficile.This is an example of pseudomembranous enterocolitis.The mucosal surface of the colon seen here is hyperemicand is partially covered by a yellow-green exudate. The mucosaitself is not eroded. Broad spectrum antibioticusage (such as clindamycin) and/or immunosuppression allowsovergrowth of bacteria such as Clostridium dificileor S. aureus or fungi such as Candida to cause this appearance.The colonoscopic appearance is seen below
39This is another example of pseudomembranous inflammation, this time in the ileum. A greenish-yellow exudatecovers most of the mucosal surface
40Microscopically, the pseudomembrane is seen to be composed of inflammatory cells, necrotic epithelium,and mucus in which the overgrowth of microorganisms takes place. The underlying mucosa shows congestedvessels, but is still intact
41At higher magnification, the overlying pseudomembrane at the left has numerous inflammatory cells, mainly neutrophils
42Left: Hypervascularity of the rectal mucosa in a 65 year-old man who had previously undergone radiation therapy forcarcinoma of the prostate. Center: Close-up of vascular ectasias of the rectal mucosa following radiation therapy for prostatic carcinoma ina 75 year-old man. Right: Post-irradiation mucosal vascular changes in a 73 year-old woman with rectal bleeding.
4324 year-old with bloodydiarrhea. Sigmoidoscopyrevealed mucosalinflammation witherythema (redness),edema(swelling), granularityand loss of the normalvascular pattern. Stoolculture grew Salmonella.34 year-old man, infected with HIV, who presented with diarrhea. Sigmoidoscopyrevealed mucosal inflammation with focal mucosal hemorrhage, edematous foldsand polypoid lesions. Biopsies demonstrated viral inclusions consistent withcytomegalovirus70 year-old woman with AIDS,whose symptoms includeddiarrhea. At colonoscopy, a large,deep U-shaped ulcer was found inthe cecum (left). A second ulcer was seen in the rectum at retroflexion (center). Biopsies were consistent withcytomegalovirus infection. Extensive ulceration in the poorly prepped colon of a 33 year old man with AIDS (right), whohad presented with colonic pseudo-obstruction. Biopsies demonstrated CMV
4472 year-old woman who presented with abdominal pain, bloody diarrhea and weight loss. She had been taking significantamounts of nonsteroidal antiinflammatory agents (NSAIDs) forarthritis. Colonoscopy revealed segmental mucosal inflammationwith ulceration. Although grossly similar in appearance toischemic colitis, the typical histological features of ischemiccolitis (mucosal necrosis, fibrosis of the lamina propria and cryptatrophy, and overlying fibrinopurulent membrane) were notpresent on biopsy.44 year-old man, a frequent user of cocaine, who presentedwith bloody diarrhea. Colonoscopy revealed a range offindings from areas of congestion (upper right) to sessilepolyps (upper left) to lesions resembling pedunculatedpolyps (lower left). Stool cultures were all negative.Biopsies revealed mucosal congestion and inflammation.The tips of the more polypoid lesions showed severeischemia histologically
45Colonoscopy, Enterobius Vermicularis (pinworms) – Endoscopy reveals an area of mucosal erythema awhite "s" shaped organism with features of e. vermicularisPinworms (Enterobiasis vermicularis) -- Intestinal lumencontaining a cross section of an adult e. vermicularisdemonstrating a central intestine of the worm (yellow arrow)and lateral ala (red arrow).