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Bacterial infections of intestine in animals
- 1. Bacterial Infections ofIntestine
- 2. Bacterial survival,persistence, and proliferation are controlled by virulence genes Bacterial virulence can be resolved into five components: attachment colonization or entry into the host evasion of host defense multiplication and/or spread within the host, and damage to the host, by direct virulence attributes, or by stimulation of an immunoinflammatory response transmission to other susceptible animals.
- 3. Escherichia coli E.colihas several virulence factors which promote colonization or adhesion to the mucosa they cause metabolic dysfunction or death of enterocytes they affect the local or systemic vasculature or they promote invasion and septicemia. "Enterotoxigenic" E. coli (ETEC) cause secretory small-bowel diarrhea stimulated by enterotoxins Common cause of neonatal diarrhea in many spp.
- 4. "Enteropathogenic" E.coli (EPEC) In humans may colonize the mucosa of the intestine by a mechanism involving adhesion-effacement Also called as "enteroadherent" E. coli- EAEC, or "attachingeffacing“ E. coli – AEEC Uncommon in animals Some don’t produce toxins but cause villus atrophy Some secrete cytotoxins with local and systemic effects e.g. shiga, verotoxins "Enteroinvasive" E. coli (EIEC) can be internalized by surface enterocytes and subsequently septicemia develop
- 5. Enterotoxigenic colibacillosis Majorforms of diarrhea in neonatal pigs, calves, and lambs, as well as in humans. Mucosal colonization and toxin production are important virulence attributes Toxins can stimulate electrolyte and water secretion from the intestinal cells Colonization and enterotoxin production must occur together for disease to ensue. Associated with minor microscopic inflammation or limited or no architectural changes
- 6. Bacteria adhereto mucosa in small intestine and proliferate Fimbriae, or pili (polymers of protein pilin) are colonization factors Attach to specific glycoconjugate receptors on the surface of enterocytes Age related ETEC produces two classes of plasmid encoded proteins- heat-labile toxin (LT) and heat-stable toxin (ST) Heat-labile toxin cause chloride secretion by enterocytes, sodium, and water following osmotically from the mucosa Effects on the cell are irreversible
- 7. Heat-stable toxin(STa, STb) STa causes an increase in cyclic guanosine monophosphate, which inhibits Na/C1 co-transpor and therefore water absorption by surface enterocytes, while in crypt epithelium it promotes C1- and water secretion. STb (in pigs mostly)may cause secretion by stimulation of prostaglandin E2 and 5- hydroxytryptamine production. Exfoliation and atrophy of villi
- 8. At Necropsy: difficult to differentiate from other causes of diarrhea Characteristic fluid content in the flaccid small and large bowel, usually with clotted milk still in the stomach No other remarkable finding In contrast to the viruses and Isospora, ETEC usually does not cause significant villus atrophy Small clumps of bacteria may be found on surface of enterocytes especially in ileum Some neutrophils in propria
- 9. Enterotoxic colibacillosisin a piglet. Villi are tall and crypts are short, as is expected in a 2-3-day-old animal
- 10. Bacteria on thesurface of enterocytes (arrow)
- 11. Enterotoxic colibacillosis ina calf. Mild neutrophil infiltrate in lamina propria and between base of villi, Atrophy of villi not evident, surface epithelium normal. (Courtesy ofJJ Hadad, CL Gyles.)
- 12. Enteropathogenic colibacillosis causedirect damage to the mucosa a characteristic mechanism of attachment to, and effacement of epithelium More common in humans In animals rabbit, pigs, dogs Initial attachment by fimbriae Attachment causes secretion of bacterial proteins e.g. intimin Translocated intimin receptor, a bacterial protein is transported into the cytoplasm of enterocytes This is then expressed as a receptor for intimin Reorganization of cellular cytoskeleton It results in formation of cupped pedestal-like structures beneath the attached bacteria, and the subsequent loss of microvilli
- 13. Mild tosevere atrophy of villi Attenuation of surface cells, or microerosions, in the large intestine Fusion of villi may occur in small intestine, and goblet-cell numbers are depleted in both large and small bowel. Moderate mucosal congestion, and local infiltration by neutrophils. A distinct subset of EPEC is the Shiga toxin- producing E. coli (STEC), also known as enterohemorrhagic E. coli (EHEC). Inhibition of protein synthesis in target cells and induce apoptosis, some produce hemolysin
- 14. Animals maycarry EHEC serotype O157:H7, a major pathogen in humans, In calves under 4 weeks of age strains of EHEC have been associated with a syndrome of erosive fibrinohemorrhagic enterocolitis and deysentery At necropsy, gross lesions are usually confined to the spiral colon and rectum, Ileum and cecum are occasionally involved with mild fibrinous or fibrinohemorrhagic enteritis/typhlitis In the colon, mild patchy congestion of the mucosa to marked mucosal reddening, with adherent mucus, necrotic debris, and blood colonic contents are fluid and frequently bloodtinged
- 15. Congestion ofthe margins of mucosal folds in the rectum, or overt fibrinohemorrhagic proctitis. Mesenteric lymph nodes are often enlarged Microscopically, in affected small intestine the profile of villi is ragged or markedly scalloped, and they are blunted, moderately atrophic, or fused. Epithelial cells in colon and small bowel are short, rounded up, and in some cases exfoliating singly or in small clumps, causing focal microerosions Coccobacilli Glands in the large bowel may be dilated, lined by flattened epithelium, and filled with sloughed epithelium and leukocytes
- 17. TEM: Colon ofa calf infected with enterohemorrhagic E.coli
- 18. Septicemic cotibacillosis commonlyin calves results from reduced transfer or absorption of maternal colostral immunoglobulin, or from intercurrent disease or debilitation. Aerobactin produced by plasmid colV help in bacterial survival in low iron extracellular envoirnment Endotoxin released by dying bacteria causes the vascular damage and shock mildly congested or blue-red, slightly rubbery lungs, and a firm spleen, evidence of omphalitis Serosal hemorrhage in severe acute cases with hydropericardiaum, congestion of intestine
- 19. Subacute casesmay develop localized infection on serous surfaces,in the joints and meninges. Fibrinous peritonitis, pleuritis, and pericarditis, fibrinopurulent arthritis and meningitis, and hypopyon
- 20. Salmonellosis S. bongoriand S.enterica. six subspecies of S. enterica (enterica, salamae, arizonae, diarizonae, indica, and houtenae) S. enterica enterica common in humans and animals S. enterica Typhimurium (new terminology writing pattern, serotype capitalized not italicized ) S. Typhi (humans), S. Dublin (cattle), and S. Choleraesuis (swine) S. Typhimurium,causes enterocolitis in young animals in most species Asymptomatic Salmonella carriage may be common
- 21. Pathogenesis stages: entry of the bacteria into the host attainment of the primary site of infection, usually the enterocyte attachment to the surface (colonization) invasion of enterocytes. minimal infective oral dose of 107-109 Must overcome the non specific resistance like salivary enzymes, acid pH of the gastric environment. Mucus and lysozymes in the glycocalyx, peristalsis, and constant sloughing of enterocytes
- 22. Invading salmonellain some spp enter the mucosa through M cells in payer’s patches In salmonellosis characterized by enterocolitis organism remains spread mesenteric lymph nodes For bacteremia organism must survive in macrophages and disseminated including motility, pili, or fimbriae, effector proteins Invasion of enterocytes, especially those in the ileum, occurs within 12 hours of oral infection with the help of type 3 protein LPS containing serotypes can more efficiently survive in the pahgolysosomes
- 23. Diarrhea insalmonellosis is not mediated by enterotoxins Effector proteins associated with SPI-1 induce secretory diarrhea by blocking chloride channel closure Proteins encoded in SPI-5 also promote neutrophil recruitment and electrolyte secretion Inflammation induced PG E2 which can cause chloride hypersecretion Cellular death reduces absorptive surface area Thus diarrhea is an outcome of active secretion of electrolyte, malabsorption due to reduced mucosal surface area and enterocyte competence, and inflammatory exudation
- 24. Pseudomembrane formationcan occur Thrombosis of mucosal venules is common in Salmonella enteritis Enteritis in salmonellosis is characterized by fibrinous or fibrinohemorrhagic exudates Some salmonella strain may survive in macrophages by inhibiting NADPH oxidase-mediated oxidative killing These strains may cause septicemia The carrier state is important in the epidemiology of the disease.
- 25. Salmonellosis in horses S. Typhimurium prevalence is increasing, especially that of multidrug- resistant definitive phage type 104 Many horses are Salmonella carriers, and when they are stressed, diarrhea follows. Abortion of pregnant mares has been associated with S. Abortusequi Peracute, acute, chronic, asymptomatic carrier Septicemic form occur in 1-6 week age Diarrhea, often with characteristic green color,blood, casts may be present Febrile , rapid death in 2-3 days
- 26. Acute septicemiccases show small hemorrhages on the serous or mucosal membranes visceral lymph nodes are enlarged, juicy and hemorrhagic Marked pulmonary congestion and edema, and renal cortical pallor and medullary congestion Peracute lesions: intense hyperemia of the gastric mucosa, probably venous infarction, with some edema, hemorrahage In acute cases, there is diffuse and intense fibrinohemorrhagic inflammation of the cecum and colon gray-red pseudomembrane
- 27. In chronicsalmonellosis extensive or patchy fibrinous or ulcerative lesions of the cecum and colon Histologically, acute ileocecocolic lymphadenitis, hemorrhage, necrosis, or diphtheresis intestine, fibrin thromobsis, mononuclear infiltration
- 29. Salmonellosis in cattle S. Typhimurium and S. Dublin In calves, salmonellosis is a febrile disease typified by dejection, dehydration, and usually diarrhea Feces are yellow or gray, may contain blood or mucous foul odour Enlargement of mesenteric lymph nodes and gross enteric lesions moderately severe gastrointestinal inflammation, acute swelling, and hemorrhage of the visceral lymph nodes Enteritis may be catarrhal, but sometimes it is hemorrhagic or more commonly causes exudation of yellow fibrin mucosa overlying the lymphoid tissues may become necrotic and slough
- 30. In fibrinousenteritis,ground glass appearance of mucosa Intestinal lesions are usually most severe in the ileum Microscopic lesions in intestine thin layer of fibrinocellular exudate on the surface of short and blunt villi Extensive necrosis and ulceration of the mucosa, with fibrin and neutrophils exuding from the ulcerated areas into the lumen Mononuclear cells in lamina propria Fibrin thrombi are often evident in proprial capillaries and venuels Centers of lymphoid follicles in the Peyer's patches are completely involuted.
- 31. The liveris often pale with many minute paratyphoid nodules. spleen, macrophage reaction is sometimes diffuse diffuse. "Paratyphoid" granulomas may also be found microscopically in the kidney, lymph nodes, and bone marrow.
- 35. In subacutesalmonellosis of calves, there may be cranial bronchopneumonia, usually with adhesions and abscessation. Purulent exudate is in synovial cavities Salmonellosis in adult cattle may occur in outbreaks Associated with chronic diarrhea and loss of condition Carrier status for years, shed in milk
- 36. Yersiniosis Yersinia enterocoliticaand Y. pseudotuberculosis are gram- negative organisms. Enterocolitis, mesenteric lymphadenitis, and, less commonly, septicemia in sheep, cattle, goats, deer, and pigs organisms invade through the intestinal epithelium or M cells Enormous recruitment of neutrophils and ensuing destruction of cytoarchitecture of payer’s patches and overlying epithelium Mild gross lesions in subacute and chronic cases Abnormally fluid intestinal content, with congestion, edema, roughening, and perhaps small loci of pallor, focal hemorrhages, erosion, or mild ulceration and fibrin effusion. Raised nodules up to 5 mm in diameter, with depressed centers, may be evident in affected large bowel. histologically by masses of gramnegative coccobacilliforming microcolonies, in the lamina propria of villi and around the necks of crypts
- 37. Microabscesses, moderateatrophy of villi and hyperplasia of crypts In fulminant Yersinia infection in all species, there is fibrinous orfibrinohemorrhagic enterocolitis, caseous necrotic debris Caseous mesenteric lymphadenitis, with mature pyogranulomas containing microcolonies of bacteria, surrounded by neutrophils and giant cells
- 39. Enteritis associated withCampylobacter spp. Campylobacter jejuni and C. coli (important in humans) C.jejuni, can cause enteritis in animals Many human infections are acquired by drinking raw milk, or from other animal foodstuff, especially poultry products. C. jejuni has been associated with bloody mucoid diarrhea in dogs May cause Lymphoplasmacytic inflammation centered on ileum and colon "Weaner colitis" is a diarrhea in sheep with high morbidity, southeastern Australia due to unidentified Campylobacter spp
- 40. Enteric clostridial infections Clostridium perfringens, five toxigenic spp C. difficile fibrinous enteritis, especially in horses, neonatal pigs, and dogs C.piliforme (formerly Bacillus pilformis) causes Tyzzer's disease, characterized by enteritis and colitis, usually with multifocal necrotic hepatitis and myocarditis, C. chauvoei causing blackleg-like myositis C. septicum causes clostridial abomasitis (braxy) in sheep, calves C. botulinum causes toxicoinfectious botulism in horses, cattle
- 42. Toxins alpha toxinis a lecithinase that acts on cell membranes, producing hemolysis or necrosis of cells beta toxin is a poreforming toxin that induces a variety of neurologic effects epsilon toxin is a protoxin iota toxin increases capillary permeability. Kappa toxin is a collagenase, and lambda a nonspecific proteinase.
- 43. C. perfringensand C. difficile requires a change in the enteric microenvironment like change in feed, abnormally nutrient-rich digesta, antibiotic therapy altered pancreatic exocrine function or trypsin inhibitors, reduced motility, and primary infections with agents such as Canine parvovirus, or coccidia
- 44. Mechanism of diseaseproduction local necrotizing effects of toxin on the mucosa, causing hemorrhagic, fibrinous, or necrotic enteritis secretory effects of locally acting enterotoxin, causing diarrhea and minor mucosal lesions; or systemic absorption of (entero) toxin, with effects at sites distant from the gut
- 45. Clostridium perfringens typeA Most common of the five types microflora of both soil and intestinal tract major toxin is the alpha toxin, collagenase and hyaluronidase minor toxins enteritis in foals; enterocolitis in horses; necrotizing enterocolitis in neonatal piglets; hemorrhagic enteritis in lambs and neonatal calves; diarrhea, and hemorrhagic enteritis in dogs; as well as necrotic enteritis in chickens. produce gas gangrene in humans and animals Foals: lesions localized to small intestine, the mucosa of which was dark purple. Histologically: marked diffuse necrosis of the mucosa
- 46. white scoursin suckling pigs and diarrhea in feeder pigs necrotizing enterocolitis, villus atrophy, and serositis Hemorrhagic canine gastroenteritis:often found dead lying in a pool of bloody excreta; sometimes hemorrhagic diarrhea is noted prior to death. Autopsy reveals hemorrhagic enteritis and colitis Hemorrhagic bowel syndrome has been described in mainly dairy cattle in the USA. Acute illness, with bloating, gut stasis, and melena. Necrohemorrhagic enteritis with extensive intraluminal hemorrhage
- 50. Clostridium perfringens typeB lamb and calf dysentery,usually in lambs up to 10-14 days Lambs may die without signs, Abdominal pain semifluid dark feces mixed or coated with blood abdomen is often tympanitic The characteristic lesion is extensive hemorrhagic enteritis serous or blood-stained fluid in peritoneal cavity Penetrating ulcers and peritonitis in sever cases wall of the intestine is hemorrhagic, and the areas of necrosis extend deeply into the mucous membrane,
- 51. liver isusually pale and friable, spleen is normal or slightly enlarged and pulpy. kidneys may be enlarged, edematous, pale, and soft from toxic degeneration pericardial sac contains abundant clear gelatinous fluid, the myocardium is pale and soft, and hemorrhagic Similar disease in calves
- 52. Clostridium perfringens typeC Adult sheep and goats, feeder cattle, and in neonatal lambs, calves, foals, and pigs. In adult sheep, C. pefringens type C causes "struck"a disease of pastured animals, mortality rate of 5-15% Sometimes sudden death, sometime abdominal pain, straining At necropsy,: the peritoneal cavity contains up to 3 liters of clear, pale-yellow fluid that clots on exposure to air Becomes stained with hemoglobin if necropsy is delayed small intestine is intensely hyperemic, either in
- 53. primary intestinallesion is superficial mucosal necrosis that advances more deeply, with a peripheral leukocytic reaction, congestion, and hemorrhage disease in feedlot cattle is similar to "struck.“ jejunal and ileal content are bloody with fibrin clots and necrotic debris. Excessive straw-colored pleural and pericardial fluid and petechiation of epicardium and endocardium are
- 54. Clostridium perfringens typeD Enterotoxemia ("pulpy kidney" disease, "overeating" disease) sheep and goats Focal symmetrical encephalomalacia (FSE) of sheep is caused by the epsilon toxin of type D. Toxin binds to receptors on endothelial cells, especially in the brain and renal tubular epithelial cells Mostly course is peracute and the animal is found dead survivers show drooling,rapid breathing, hyperesthesia, straining, opisthotonos, and terminal coma or convulsions. In adult sheep, in which the clinical course may be
- 55. neurological signsmay develop except in goats large amounts of grain or concentrate predisposes Starch helps in bacterial proliferation and toxins production Toxin is absorbed through the mucosa Necropsy: Putrefactive changes occur rapidly. excessive straw-colored pericardial fluid congestion and edema of the lungs hemorrhage beneath the endocaMium of the left ventricle Blotchy hemorrhages beneath the parietal peritoneum are characteristic
- 56. Liver congested,spleen enlarged pulpy Short lengths of the small intestine are distended with gas, and are hyperemic. medullary congestion, hemorrhage, and tubular degeneration but rapid autolysis or delayed necropsy can cause pulpy kidney Hyperglycemia and glucosuria associated with the toxemia, Brain lesions occur in lambs with subacute enterotoxemia focal symmetrical encephalomalacia.
- 57. Pattern of brainlesion 1. basal ganglia, internal capsule, dorsolateral thalamus,and substantia nigra are involved commonly 2. white matter of the frontal gyri, sparing only the communicating U fibers. lesion begins with edema, leaking of plasma and RBC Calves: Splenic swelling is more common in calves than in lambs, and rapid autolysis of the kidney is not a prominent finding,
- 58. Histologically mild degenerationand necrosis of the epithelium of the proximal convoluted tubules with edema, congestion, and interstitial hemorrhage in the renal cortex, and congestion of the medulla (these are autolytic changes but are useful diagnostically); superficial desquamation in the intestine with congestion, and numerous typical bacilli in the contents; congestion and hemorrhage of the spleen with disruption ofreticulum; subepicardial hemorrhage and degeneration in the Purkinje network; and proteinaceous edema fluid in the lungs
- 59. In goats peracute,acute, chronic, and subclinical. mild to severe hyperemia of the mucosa, especially of the distal small intestine, cecum, and spiral colon The affected areas may be covered by a thin layer of fibrin. The intestinal contents are olive-green to red and mucoid. The mesenteric lymph nodes are enlarged and edematous. Hydropericardium, pulmonary edema, and "pulpy" kidneys may be seen, but are inconsistent, and brain lesions are absent.
- 60. In naturalcases, the microscopic lesions in the small intestine vary from a mild pleocellular leukocytic reaction in the lamina propria to a mild fibrinous, or, rarely, hemorrhagic enteritis. the tips of the villi are necrotic, eroded, and covered by fibrinocellular exudates or blood.Villus atrophy may follow.
- 63. Clostridium perfringens typeE cause intestinal disease in calves. Congested abomasum, hemorrhagic enteritis Acute death
- 64. Paratuberculosis (Johne's disease) Mycobacterium avium subsp, paratuberculosis resistance to killing in macrophages marked loss of muscle mass and serous atrophy of fat depots, intermandibular edema, and fluid effusion in the body cavities Plaques of intimal fibrosis and mineralization may be evident in the thoracic aorta The mesenteric nodes, particularly the ileocecat, are always enlarged, pale, and edematous, especially in the medulla. Lymphangitis is common, diffuse thickening of the mucosa, which is folded into transverse rugae, the crests of which may be congested.
- 65. transmural granulomatousenteritis Granulomatous lymphadenitis
Editor's Notes
- #7 Receptors diminish in later age
- #13 Effacement (histology), the shortening, or thinning, of a tissue
- #20 Hypopyon is inflammatory cells in the anterior chamber of eye.
- #29 Satmonel|osis in a foal Salmonella Typhimurium. A. Focal and coatescent ulceration and diphtheresis invotving iteocecat vatve and mucosa. B. Nodutar ulcerative lesions in colon in chronic satmonettosis. C. Superficial necrosis and effusion from colonic mucosa: several thrombosed vessels are in the propria (arrows).