Bacterial infections of intestine in animals

Bacterial Infections of Intestine

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.

Escherichia coli E.coli has 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.

"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

Enterotoxigenic colibacillosis Major forms 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

Bacteria adhere to 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

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

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

Enterotoxic colibacillosis in a piglet. Villi are tall andcrypts are short, as is expected in a 2-3-day-old animal

Bacteria on the surface of enterocytes (arrow)

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Enterotoxic colibacillosis in a calf. Mild neutrophil infiltratein lamina propria and between base of villi, Atrophy of villi not

evident,surface epithelium normal. (Courtesy ofJJ Hadad, CL Gyles.)


Enteropathogenic colibacillosis cause direct 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

Mild to severe 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

Animals may carry 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

Congestion of the 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

TEM: Colon of a calf infected with enterohemorrhagic E.coli

Septicemic cotibacillosis commonly in 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

Subacute cases may develop localized infection on serous surfaces,in the joints and meninges.

Fibrinous peritonitis, pleuritis, and pericarditis, fibrinopurulent arthritis and meningitis, and

hypopyon

Salmonellosis S. bongori and 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

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

Invading salmonella in 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

Diarrhea in salmonellosis 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

Pseudomembrane formation can 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.

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

Acute septicemic cases 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

In chronic salmonellosis 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

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

In fibrinous enteritis,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.

The liver is 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.

In subacute salmonellosis 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

Yersiniosis Yersinia enterocolitica and 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

Microabscesses, moderate atrophy 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

Enteritis associated with Campylobacter 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

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

Toxins alpha toxin is 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.

C. perfringens and 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

Mechanism of disease production 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

Clostridium perfringens type A 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

white scours in 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

Clostridium perfringens type B 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,

liver is usually 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

Clostridium perfringens type C 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 patches or along most of its length with ulceration

primary intestinal lesion 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

Clostridium perfringens type D 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 several days, diarrhea with the passage of dark semifluid feces is common.

neurological signs may 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

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.

Pattern of brain lesion 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,

Histologically mild degeneration and 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

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.

In natural cases, 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.

Clostridium perfringens type E cause intestinal disease in calves. Congested abomasum, hemorrhagic enteritis Acute death

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.

transmural granulomatous enteritis Granulomatous lymphadenitis

Bacterial infections of intestine in animals

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Transcript of Bacterial infections of intestine in animals