Campylobacter jejuni isthemostcommonbacterialentericpathogenindevelopedcountriesandalsocausestraveler’sdiarrhea.Mostisolatesarenoninvasive.Salmonella andShigella spp.areinvasiveandassociatedwithexudativebloodydiarrhea(dysentery).Salmonella infectionisacommoncauseoffoodpoisoning.S. typhi cancausesystemicdisease(typhoidfever).
PseudomembranouscolitisisoftentriggeredbyantibiotictherapythatdisruptsthenormalmicrobiotaandallowsC. difficile tocolonizeandgrow.Theorganismproducestoxinsthatdisruptepithelialfunction.Fecalmicrobialtransplantationisbecomingmorecommonasatherapeuticapproachinindividualswithrecurrentdisease.
Rotavirus isthemostcommoncauseofseverechildhooddiarrheaanddiarrhealmortalityworldwide.Thediarrheaissecondarytolossofmatureenterocytes,resultinginmalabsorptionaswellassecretion.
Parasitic andprotozoal infectionsaffectoverhalfoftheworld’spopulationonachronicorrecurrentbasis.
In general, diverticular disease refers to acquired pseudodiverticular outpouchings of the colonic mucosa and sub-mucosa. Such colonic diverticula are rare in individuals younger than 30 years of age, but the prevalence approaches 50% in Western adult populations older than 60 years of age. Diverticula generally are multiple, and the condition is referred to as diverticulosis. This disease is much less common in developing countries, probably because of dietary differences.
Colonic diverticula tend to develop under conditions of elevated intraluminal pressure in the sigmoid colon. This is facilitated by the unique structure of the colonic muscularis propria, where nerves, arterial vasa recta, and their connective tissue sheaths penetrate the inner circular muscle coat to create discontinuities in the muscle wall. In other parts of the intestine, these gaps are reinforced by the external longitudinal layer of the muscularis propria, but in the colon, this muscle layer is discontinuous, being gathered into three bands termed taeniae coli. High luminal pressures may be generated by exaggerated peristaltic contractions, with spasmodic sequestration of bowel segments that may be exacerbated by diets low in fiber, which reduce stool bulk.
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MORPHOLOGYAnatomically,colonicdiverticulaaresmall,flasklikeoutpouchings,usually0.5to1cmindiameter,thatoccurinaregulardistributioninbetweenthetaeniaecoli(
Fig.15.25AandB ).Theyaremostcommoninthesigmoidcolon,butotherregionsofthecolonmaybeaffected.Colonicdiverticulahaveathinwallcomposedofaflattenedoratrophicmucosa,compressedsubmucosa,andattenuatedmuscularispropria—often,thislastcomponentistotallyabsent(
Fig.15.25CandD ).Obstructionofdiverticulawithstasisofcontents,leadstoinflammatorychanges,producingdiverticulitis andperidiverticulitis.Becausethewallofthediverticulumissupportedonlybythemuscularismucosaandathinlayerofsubserosaladiposetissue,inflammation,increasedpressure,andmucosaluclerationwithinanobstructeddiverticulumcanreadilyresultinperforation. Withorwithoutperforation,recurrentdiverticulitismaycausesegmentalcolitis,fibroticthickeninginandaroundthecolonicwall,orstrictureformation.
Most individuals with diverticular disease remain asymptomatic throughout their lives. About 20% of those affected
Fig. 15.26 Distributionoflesionsininflammatoryboweldisease.ThedistinctionbetweenCrohndiseaseandulcerativecolitisisbasedprimarilyonmorphology.