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

Question 1

What bacteria cause swine dysentery and spirochaetal colitis?

Answer 1

SD- Brachyspira hyodysenteriae

SC- Brachyspira pilosicoli

Question 2

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

Answer 2

SD

Question 3

Which results in milder colitis in younger piglets?

Answer 3

SC

Question 4

Which occurs more frequently during growing finishing periods

Answer 4

SD

Question 5

Swine dysentery also affects this animal?

Answer 5

infects and persists in rodents

Question 6

What lead to the decrease in prevalence of SD?

Answer 6

bc of successful eradication and effective manure removal techniques

Question 7

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

Answer 7

during the summer and in organic antibiotic free farms

Question 8

Describe the epidemiological transmission of spirochaetal colitis and SD?

Answer 8

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

Question 9

Describe the D+ seen with SD and SC?

Answer 9

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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

Untreated herds high mortality and morbidity can approach 50%

Question 12

How do we dx SD or SC?

Answer 12

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

Question 13

How do we prevent SD or SC?

Answer 13

replacement pigs from SD free herds after 30-60 quarantine

Question 14

How do we eliminate SD or SC?

Answer 14

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

Question 15

Is there an vaccine for SD or SC

Answer 15

there is but not that effective!

Question 16

What 2 strains of salmonella are host adapted for swine?

Answer 16

S. cholerasuis

S. typhimurium

Question 17

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

Answer 17

septicemia and enterocolitis

Question 18

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

Answer 18

asymptomatic

Question 19

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

Answer 19

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

Question 20

Describe the epidemiological spread of Salmonella in pigs?

Answer 20

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

Question 21

Describe the transmission of salmonella in swine

Answer 21

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

Question 22

When do we often see salmonella in pigs?

Answer 22

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

Question 23

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?

Answer 23

S. cholerasuis

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

Question 24

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

Answer 24

discoloration of skin of the extremeties (cyanosis)

Question 25

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

Answer 25

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

Question 26

How do we ID

Answer 26

Enterocolitic Salmonellosis and Septicemic salmonellosis from history CS and PM lesions Culture and identification from multiple organ samples, liver, spleen, mesenteric lymph nodes, colon

Question 27

How do control Enterocolitic Salmonellosis and Septicemic salmonellosis?

Answer 27

``` 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 ```

Question 28

How do we treat Enterocolitic Salmonellosis and Septicemic salmonellosis

Answer 28

``` Carbadox Gentamycin Neomycin Tiamulin Ceftiofur Parenteral treatment in septicemic form ```

Question 29

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

Answer 29

Salmonellosis

Question 30

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

Answer 30

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

Question 31

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

Answer 31

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

Question 32

What age group is Porcine Proliferative Enteritis common in?

Answer 32

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

Question 33

Describe the epidemiology with PPE?

Answer 33

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

Question 34

Describe the common CS with Porcine Proliferative Enteritis?

Answer 34

Infection often results in subclinical disease In acute cases D+ with brownish to black unclotted blood, pallor, weakness , and rapid death are common

Question 35

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

Answer 35

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

Question 36

What disease is Porcine Proliferative Enteritis often confused with?

Answer 36

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

Question 37

How do we control and prevent Porcine Proliferative Enteritis? Is there good screening tests?

Answer 37

Elimination is difficult no good screening tests prevention is by minimizing stressors such as transportation sorting or commingling vaccination of grower pigs

Question 38

How do we Treat Porcine Proliferative Enteritis?

Answer 38

``` tylosin tetracyclines lincomycin tiamulin carbadox ```

Question 39

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

Answer 39

Actinobacillas Pleuropnemonia

Question 40

Actinobacillas Pleuropnemonia organism secretes these 4 things

Answer 40

4 exotoxins: Apxl; Apxll; ApxIII and ApxIV

Question 41

What is the Actinobacillas Pleuropnemonia eidemiology transmission?

Answer 41

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

Question 42

Swine that survive Actinobacillas Pleuropnemonia often remain ______

Answer 42

carriers

Question 43

How do we dx Actinobacillas Pleuropnemonia?

Answer 43

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

Question 44

How do we control Actinobacillas Pleuropnemonia?

Answer 44

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

Question 45

How do we treat Actinobacillas Pleuropnemonia

Answer 45

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

Question 46

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

Answer 46

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

Question 47

What organism causes Progressive Atrophic Rhinitis?

Answer 47

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

Question 48

What CS in the early stages characterizes Progressive Atrophic Rhinitis

Answer 48

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

Question 49

Why is Progressive Atrophic Rhinitis in the US becoming rare?

Answer 49

due to early weaning, age segregation, and vaccination

Question 50

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

Answer 50

Toxigenic bordetella

Question 51

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?

Answer 51

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

Question 52

Describe the epidemiological spread of Progressive Atrophic Rhinitis?

Answer 52

- 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

Question 53

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

Answer 53

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

Question 54

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.

Answer 54

medial canthus; bleed; retardation

Question 55

How do we control Progressive Atrophic Rhinitis?

Answer 55

``` 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) ```