Swine GI diseases Flashcards

0
Q

What are the main differentials for hemorrhagic diarrhea in piglets from newborn to 7 days old?

A

Clostridium perfringens type C, colibacillosis

Brachyspira hyodysenteriae usually does not affect nursing piglets, but is the other differential.

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1
Q

Describe the clinical presentation of Clostridium perfringens type C.

A

Disease is generally explosive with 100% mortality if piglets born to nonimmune sows. Death is from severe necrotizing enteritis.
Peracute - death of piglets 12-36 hours old that may or may have developed hemorrhagic diarrhea.
Acute - 2 days of reddish brown diarrhea containing grey, necrotic debris with ensuing death by 3 days of age.
Subacute - persistent non hemorrhagic diarrhea that is yellow initially then changes to clear liquid with flecks of necrotic debris. Piglets remain alert but usually die from dehydration by 5-7 days of age.
Chronic - intermittent or persistent diarrhea for several weeks, with feces yellow-grey and mucoid. Pigs may die after several weeks of clinical signs.

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2
Q

Describe pathogenesis and toxin formation in C. perfringens.

A

C. perfringens type A is a normal inhabitant of swine and produces disease when large numbers if organisms build up in jejunum and ileum. Produces alpha toxin that can cause necrosis of enterocytes, leading to profuse loss of electrolytes and fluids. Type A does not invade the enterocytes.

C. perfringens type C produce a trypsin-sensitive beta toxin responsible for much of the necrotizing lesions. These organisms attach to enterocytes and result in loss of microvilli and damage to terminal capillaries with increased capillary permeability. This is followed by rapid progressive necrosis of remaining villus enterocytes, crypt cells, and mesenchymal structures in lamina propria and muscular is mucosa.

LAM, p 648

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3
Q

Is vaccination effective for Clostridium perfringens?

A

Yes, routine vaccination will prevent disease. Sows can be vaccinated with a toxoid at time of breeding or midgestation, and then again 2 weeks prior to farrowing. Piglets from immune sows will be protected by colostrum.

LAM, p 648

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4
Q

Describe the clinical presentation of TGE.

A

Vomiting, severe diarrhea, high mortality in piglets less than 2 weeks old is most characteristic.
Anorexia, vomiting, and/or diarrhea develops within days in susceptible animals of all ages, particularly in winter.
Differential for yellow to white watery diarrhea in piglets newborn to several weeks old includes TGE, colibacillosis, rotavirus, and coccidiosis.

LAM, p 649

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5
Q

Describe the general clinical signs of Salmonellosis in pigs.

A

Salmonellosis can be subclinical or with multiorgan involvement, including septicemia, pneumonia, meningitis, lymphadenitis, abortion, and enterocolitis.

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6
Q

Describe the etiologic agent for TGE.

A

Coronavirus - Pleomorphic, enveloped, positive-sense, single-stranded RNA virus.
Other Coronaviruses infecting pigs: hemagglutinating encephalomyelitis virus, porcine respiratory coronavirus, porcine epidemic diarrhea virus.
TGEV is antigenically related to FIPV and canine coronavirus, and each can be experimentally infected with the other. Because of this, it has been suggested that cats and dogs may be reservoirs for TGEV.

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7
Q

Describe the gross and histologic changes associated with TGEV.

A

Grossly, stomach distended with milk, with foci of hemorrhages on diaphragmatic side of mucosa. Small intestine is filled with watery material and curds of undigested milk.
Histo - severe villus atrophy in jejunum and ileum; villus:crypt ratio is 1:1 (normal is 7:1); enterocytes are low-cuboidal or flattened.

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8
Q

Describe transmission of TGEV.

A

In herds with enzootic TGEV, older animals will be asymptomatic, but diarrhea will develop in piglets 1-2 weeks old. In enzootic herds, morbidity and mortality will usually be low, making diagnosis more difficult and requiring discrimination between other common causes of neonatal diarrhea such as rotavirus and colibacillosis.
Birds are thought to be a reservoir, and dogs and cats are also suggested as potential reservoir.

LAM, p 649-50

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9
Q

Describe the characteristics of porcine rotavirus.

A

Four (A-D) serogroups of rotavirus affect swine, with A being most common. These are further classified into serotypes based on surface antigens VP4 and VP7.
Rotaviruses are nonenveloped with double-stranded RNA genome.

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10
Q

Describe the clinical presentation of rotavirus in swine.

A

Most severe in naive pigs 1-5 days old. Typically, anorexia, lethargy, some vomiting, and profuse watery, white-yellow diarrhea with flocculent material. Death from dehydration is 50-100% in piglets. Those that recover return to normal 3-5 days after diarrhea onset.
Disease is less severe if 1 week old or older. Usually subclinical after 21-28 days of age.
Disease is usually mild and self-limiting if other enteric pathogens are absent. If rotavirus is found in clinically ill post-weaning pigs, a mixed infection etiology should be suspected.
Differential for yellow-white watery diarrhea in piglets newborn to several weeks old include rotavirus, colibacillosis, TGEV, coccidiosis, and nematodiasis.

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11
Q

Describe the pathology and pathogenesis associated with rotavirus infection in pigs.

A

Gross lesions confined to small bowel. Wall of distal half of SI is typically thin and dilated with watery material. Cecum and colon are similarly dilated with watery material. Mesenteric lymph nodes are small and tan. Gross lesions in pigs over 21 days old are variable or absent.
Histologic ally, degeneration and loss of enterocytes on tips of villi, increased thickness of lamina propria due to infiltration of neutrophils and mononuclear cells, reduction in villus height from duodenum to ileocecal juncture.
Rotavirus replicates in cytoplasm of enterocytes and M cells overlying Peyer’s patches, and lining epithelium of colon and cecum. Diarrhea is result of destruction of enterocytes on villi tips. Osmotic diarrhea ensues.

LAM, p 650

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12
Q

Describe prevention strategies for rotavirus in pigs.

A

Rotavirus is enzootic in most herds, so exclusion is difficult. Minimize viral challenge with good sanitation, and boosting passive immunity through exposure of replacement gilts to feces from the herd prior to first parturition.
MLV and inactivated virus vaccines are available. Immunity is serotype specific and duration is unknown.

LAM, p 651

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13
Q

Describe Balantidium coli in swine.

A

Ciliated protozoan that colonizes cecum and anterior colon usually as commensal. Zoonotic.

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14
Q

Describe clinical presentation of B. coli in swine.

A

Usually subclinical, but may present as acute typhlitis or colitis. B. coli invades necrotic tissue. Can cause ulcerative enterocolitis, which can be fatal. Weight loss, anorexia, weakness, lethargy, watery diarrhea, tenesmus, rectal prolapse.
Not considered a primary pathogen. Often secondary to Oesophagostomum, Trichuris suis, and some types of infectious agents.

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15
Q

Describe coccidiosis in swine.

A

Eimeria spp. - non pathogenic in swine
Cryptosporidium parvum - typically subclinical in swine 6-12 weeks old; clinical disease involves nonhemorrhagic diarrhea
Isospora suis - clinical neonatal coccidiosis, affects nursing piglets 1-2 weeks old

16
Q

Describe clinical presentation of Isospora suis.

A

In nursing piglets 1-2 weeks old. Yellow-grey diarrhea pasty-watery. Piglets usually continue to nurse.
Differential includes I. suis, colibacillosis, Clostridium perfringens, TGEV, Strongyloides ransomi.

LAM, p 651

17
Q

What is the general pathogenic mechanism of Enteropathogenic E. coli (EPEC)?

A

EPEC, also referred to as attaching and effacing E. coli (AEEC), attaches to enteric epithelium using fimbrial adhesins, efface the micro villi and invade the epithelium cells.

LAM, p 647

18
Q

Why are some pigs inherently resistant to colibacillosis?

A

They lack receptors on their epithelial cell brush borders to which fimbriae bind.

LAM, p 647

19
Q

Describe the gross lesions associated with colibacillosis.

A

In the edema disease syndrome, there is marked edema of mesenteric lymph nodes, mesentery, stomach wall, large intestine, subcutaneous lymph nodes, eyelids, subcutaneous tissues, lungs, liver and gallbladder. The mucosa of the SI and stomach may contain extensive hemorrhages.

20
Q

Describe the pathogenesis of ETEC.

A

Mucopolysaccharide capsule -antiphagocytic and not very antigenic
K1 polysaccharide - enhances bacterial resistance to complement-mediated killing by inhibiting alternative pathway to complement activation
O chain polysaccharide - very long; in cell wall; binds membrane attack complex resulting from complement activation distant from the cell membrane so that it cannot lose the cell
Specialized fimbriae, K88(F4), K99(F5), F6, and F41 - permit adherence and colonization of the enterocytes
Heat labile toxins - elevate levels of adenylate cyclase leading to efflux of Na and Cl ions and water out of the cell
SLT-IIe - heat-labile, Shiga-like toxin; binds to and damages vascular endothelium, resulting in edema, hemorrhage, and thrombosis
Sta and Stb - heat labile toxins; cause elevated levels of prostaglandins in enterocytes, which may enhance diarrhea

LAM, p 647

21
Q

What is the control strategy for pigs that are infected with Salmonella?

A

Pigs proven to have Salmonella should be culled due to zoonotic potential.

22
Q

How long will pigs shed when infected with Salmonella?

A

Infected swine may shed Salmonella for 5 months or more.

23
Q

What are your differentials for watery, yellow diarrhea in weaned pigs?

A

Salmonellosis, colibacillosis, TGE, coccidiosis, and nematodiasis.

24
Q

Describe the clinical signs associated with S. typhimurium.

A

S. typhimurium typically causes enterocolitis.

Enterocolitis begins with watery, yellow diarrhea associated with fever, anorexia, and dehydration that lasts for several days to weeks, sometimes with intermittent relapses. Diarrhea with blood or mucus is NOT a prominent feature.

25
Q

Describe the clinical signs associated with S. typhisuis.

A

S. typhisuis associated with localized epizootics with chronic wasting, caseous lymphadenitis, diarrhea, and pneumonia.

26
Q

Describe the clinical signs associated with S. cholerasuis (var. kunzendorf).

A

Salmonella cholerasuis (var. kunzendorf) most frequently causes septicemia and/or pneumonia.

27
Q

Which Salmonella spp most frequently causes septicemia and/or pneumonia?

A

Salmonella cholerasuis (var. kunzendorf)

28
Q

Which Salmonella spp is associated with localized epizootics with chronic wasting, caseous lymphadenitis, diarrhea, and pneumonia?

A

S. typhisuis

29
Q

Which Salmonella spp typically causes enterocolitis?

A

S. typhimurium