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7th LAM 2 Meleah > Lecture 7/8: Neonatal D+ and Post-weaning condition: Grower and Finisher Pigs > Flashcards

Lecture 7/8: Neonatal D+ and Post-weaning condition: Grower and Finisher Pigs Flashcards

1
Q

What bacteria cause swine dysentery and spirochaetal colitis?

A

SD- Brachyspira hyodysenteriae

SC- Brachyspira pilosicoli

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2
Q

What causes severe infectious disease characterized by mucohemorragic D+ and marked inflammation limited to the large intestine (Cecum or colon)?

A

SD

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3
Q

Which results in milder colitis in younger piglets?

A

SC

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4
Q

Which occurs more frequently during growing finishing periods

A

SD

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5
Q

Swine dysentery also affects this animal?

A

infects and persists in rodents

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6
Q

What lead to the decrease in prevalence of SD?

A

bc of successful eradication and effective manure removal techniques

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7
Q

Where do we see an increased incidence of spirochaetal colitis and SD?

A

during the summer and in organic antibiotic free farms

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8
Q

Describe the epidemiological transmission of spirochaetal colitis and SD?

A

transmission through ingestion of infected fecal material. Can persist in lagoon water and moist feces for 2 months and soil for 18 days. Mice can shed agent for 180 days and dogs for 13 days. Mice, carrier sows, purchased stock can transmit also birds, flies, and fomites

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9
Q

Describe the D+ seen with SD and SC?

A

Mucoid D+ (usually gray to yellow) and thats what first appears…..then it becomes mucohemorrhagic with excess mucus and fresh blood apparent

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10
Q

What other signs are present with SD and SC besides D+?

A

TAIL TWITCHING or a humped gaunt appearance dehydration signs (sunken eyes, marked weakness, hollow flanks, and weight loss)

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11
Q

Tell me about the morbidity and mortality with untreated herds with SD or SC?

A

Untreated herds high mortality and morbidity can approach 50%

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12
Q

How do we dx SD or SC?

A

CS
gross PM lesions
Culture from fecal swabs or colonic scrapings of acute unmedicated cases

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13
Q

How do we prevent SD or SC?

A

replacement pigs from SD free herds after 30-60 quarantine

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14
Q

How do we eliminate SD or SC?

A

Elimination of SD:

  1. )early weaning to a clean site
  2. )extensive medication (tiamulin, carbadox, lincomycin) after culling debilitated animals
  3. ) depopulation with thorough cleaning and disinfection during dry and warm months
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15
Q

Is there an vaccine for SD or SC

A

there is but not that effective!

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16
Q

What 2 strains of salmonella are host adapted for swine?

A

S. cholerasuis

S. typhimurium

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17
Q

Salmonellosis results in ____ and _____ nand sometimes there is tissue localization of infection at various sites

A

septicemia and enterocolitis

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18
Q

INFECTIONS IN _______swine may serve as a source of salmonella infection to humans via contamination of pork products

A

asymptomatic

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19
Q

How common is salmonella and what age bracket of pigs does it mostly occur in?

A

Disease is less common but occurs mostly in weaned or growing pigs

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20
Q

Describe the epidemiological spread of Salmonella in pigs?

A

Asymptomatic swine may harbor inapparent infections that persist in their tonsils, intestine, lymph nodes, or gall bladder. They may shed the agent in feces

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21
Q

Describe the transmission of salmonella in swine

A

Transmission is through fecal oral route, contaminated feed and water and aerosols. Rodents and wild birds are believed to be important disseminators(spreaders) of salmonella

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22
Q

When do we often see salmonella in pigs?

A

during or following stressful events, prolonged transport, drought, overcrowding, change of rations, parturition, prolonged treatment with drugs or antibiotics, or another disease in the herd

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23
Q

Septicemic salmonellosis from S. ________: can cause acute onset of an outbreak and acute death in thrifty pigs, low morbidity but high mortality in ill pigs. What other CS do you see?

A

S. cholerasuis

often see inappetance, depression, huddling, weakness, temperatures up to 107 and red to purple

24
Q

What do you see from Septicemic salmonellosis from S. cholerasuis on the extremities?

A

discoloration of skin of the extremeties (cyanosis)

25
Q

S. typhimurium causes what kind of salmonellosis? State the CS

A

Enterocolitic Salmonellosis

Initially moderate anorexia and D+ that may be watery to yellow and intermittent, progression to mucus, fibrin, and blood in the feces. Surviving animals become emaciated or gain weight slowly

26
Q

How do we ID

A

Enterocolitic Salmonellosis and Septicemic salmonellosis from history CS and PM lesions

Culture and identification from multiple organ samples, liver, spleen, mesenteric lymph nodes, colon

27
Q

How do control Enterocolitic Salmonellosis and Septicemic salmonellosis?

A 
dry housing
proper animal density
good ventilation
high standard of sanitation
purchase of animals from free herds
quarantine 
all in all out
exclusion of rodents, birds, pets, and wildlife
HACCP in slaughter houses
28
Q

How do we treat Enterocolitic Salmonellosis and Septicemic salmonellosis

A 
Carbadox
Gentamycin
Neomycin
Tiamulin
Ceftiofur
Parenteral treatment in septicemic form
29
Q

_______ can be acute resulting in rapid death, chronic or subclinical depending of the causal strain?

A

Salmonellosis

30
Q

Lawsonia intracellularis causes what syndrome in pigs and what classification of bacteria is that?

A

Porcine Proliferative Enteritis (Ileitis, intestinal adenomatosis) obligate intracellular organism

31
Q

Describe Porcine Proliferative Enteritis (PPE and what type of disease it is?

A

PPE is an enteric disease characterized by hyperplasia of crypt enterocytes with inflammation and sometimes ulceration or hemorrhage

32
Q

What age group is Porcine Proliferative Enteritis common in?

A

Common in young adults; and chronic or necrotic form usually during the grower phase

33
Q

Describe the epidemiology with PPE?

A

Incubation, recovery, and carrier phase of L. intracellularis infection is quite long in some pigs, carrier swine transmit to other pigs in feces

Carrier dams have been demonstrated to infect their litters as early as 6 days of age

outbreaks are associated with stress

34
Q

Describe the common CS with Porcine Proliferative Enteritis?

A

Infection often results in subclinical disease

In acute cases D+ with brownish to black unclotted blood, pallor, weakness , and rapid death are common

35
Q

Subacute to chronic cases of Porcine Proliferative Enteritis occur more frequently in what stage and what CS do you often see?

A

grower stages; sporadic D+ and wasting with variation in growth rate

36
Q

What disease is Porcine Proliferative Enteritis often confused with?

A

hemorragic bowel syndrome because of sudden death with blood in intestinal tract

37
Q

How do we control and prevent Porcine Proliferative Enteritis?

Is there good screening tests?

A

Elimination is difficult

no good screening tests

prevention is by minimizing stressors such as transportation sorting or commingling

vaccination of grower pigs

38
Q

How do we Treat Porcine Proliferative Enteritis?

A 
tylosin
tetracyclines
lincomycin
tiamulin
carbadox
39
Q

What syndrome usually is seen in 6-20 week old pigs in the USA?

A

Actinobacillas Pleuropnemonia

40
Q

Actinobacillas Pleuropnemonia organism secretes these 4 things

A

4 exotoxins: Apxl; Apxll; ApxIII and ApxIV

41
Q

What is the Actinobacillas Pleuropnemonia eidemiology transmission?

A

Most transmission is by direct contact of APP via nasal secretions but transmission may be via aerosol at least for short distances.

Overstocking, inadequate ventilation, coinfection with other respiratory pathogens, or unsual stress may facilitate transmission

42
Q

Swine that survive Actinobacillas Pleuropnemonia often remain ______

A

carriers

43
Q

How do we dx Actinobacillas Pleuropnemonia?

A

Isolation and ID of APP is confirmatory through PCR of toxins, Serology using ELISA or compliment fixation

44
Q

How do we control Actinobacillas Pleuropnemonia?

A 
Closed herd
replacements from farms free of APP
all in all out
avoid overstocking
proper ventilation
vaccination of piglets 5-7 weeks and sows
45
Q

How do we treat Actinobacillas Pleuropnemonia

A

parenteral, in water or feed: using tiamulin, tulathromycin, chlortetracycline, ceftiofur, tilmicosin, florfenicol, enrofloxacin, and procaine penicillin G

46
Q

What CS do we often see with Actinobacillas Pleuropnemonia, whats commin in acute outbreaks

A

In acute outbreaks: sudden deaths are COMMON

Early signs include sudden onset of prostration, high temps, apathy, anorexia, stiffness, and perhaps V+ and D+. A shallow non productive cough is occasionally present. Cyanosis high mortality in fattening pigs, abortions in sows, chronic cough, slow growth

47
Q

What organism causes Progressive Atrophic Rhinitis?

A

caused by toxigenic strains of Bordetella bronchiseptica and Pasturella multocida (primarily type D)

48
Q

What CS in the early stages characterizes Progressive Atrophic Rhinitis

A

Early stages you will see snuffling, sneezing, snorting, and perhaps nosebleed which may progress to atrophy and distortion of the turbinates, nasal and facial bones of some affected pigs

49
Q

Why is Progressive Atrophic Rhinitis in the US becoming rare?

A

due to early weaning, age segregation, and vaccination

50
Q

Which Progressive Atrophic Rhinitis strain causes atrophy of turbinates leading to top mild lesions?

A

Toxigenic bordetella

51
Q

Which Progressive Atrophic Rhinitis strain can be isolated from tonsils of animal with out with out disease and what does it produce and cause and predispose to?

A

Toxigenic pasteurella; it produces a potent dermonecrotizing toxin that causes marked turbinate atrophy which could be a lifetime,

Bordetella colonization predisposes to pasteurella colonization

52
Q

Describe the epidemiological spread of Progressive Atrophic Rhinitis?

A
  • DUST (endotoxin, mold, peptidoglycans)
  • ammonia predisposing factors
  • disease introd. by inapparent carriers from other farms or carrier sows
  • infected pglets can transmit
  • rhinitis caused by other infectious agent can predispose
  • overstocking
  • substandard housing or sanitation
  • continuous use of facilities
  • failure to use all in all our production methods
53
Q

What clinical signs do we often see with Progressive Atrophic Rhinitis?

A

Sneezing, snorting, and a serous or mucopurulent nasal discharge (early signs)

54
Q

Progressive Atrophic Rhinitis obstructs the flow of _____ through the infraorbital ducts and tears flow from the ____ _____ of the eyes causing “dirty” hair below canthus, nose ____, growth ______, secondary bronchitis/penumonia, lateral or dorsal deviation of the snout resulting in shortening of the snout or wrinking of the skin over the snout.

A

medial canthus; bleed; retardation

55
Q

How do we control Progressive Atrophic Rhinitis?

A 
improvement of husbandry
management and housing
including ventilation
vaccination of sows or pigs
antimicrobial to sows or piglets around farrowing or weaning (not very effective)

7th LAM 2 Meleah (20 decks)

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