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LA Infectious Disease > Unit 3 - Swine Respiratory > Flashcards

Unit 3 - Swine Respiratory Flashcards

1
Q

What is the etiologic agent of enzootic pneumonia?

A

Mycoplasma hyopnuemoniae

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2
Q

M. hypopneumoniae causes a chronic pneumonia characterized by what?

A

A persistent, nonproductive cough, loss of condition, and growth retardation

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3
Q

T/F: M. hyopneumonia is the etiologic agent of Enzootic pneumonia, but many bacterial and viral agents usually contribute to the production of disease and vice-versa.

A

True

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4
Q

What contributes to enzootic disease?

A

Poor environment with excessive pit gases and heavy microbial air loads along with secondary/primary invaders

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5
Q

It is estimated that ___-____% of sows in enzootic pneumoniaherds are chronic carriers.

A

10-20%

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6
Q

How is enzootic pneumonia transmitted?

A

Primarily by droplet and contact

Airborne infection is also suspected

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7
Q

When is clinical disease associated with enzootic pneumonia seen mainly? How long do they persist?

A

After 12 weeks of age and persists 6 weeks or longer

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8
Q

What clinical signs are associated with enzootic pneumonia?

A

Dry, nonproductive cough
Unthrifty appearance
Fever (if secondary invaders are involved)
Normal appetite

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9
Q

T/F: There is generally low morbidity associated with enzootic pneumonia, but high mortality.

A

false - high morbidity, low to moderate mortality

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10
Q

T/F: In well-managed herds, enzootic pneumonia is easily distinguished.

A

False - it often goes clinically silent

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11
Q

What gross lesions are associated with enzootic pneumonia?

A

Purple to tan areas of consolidation in the cranioventral portions of the lungs - atelectic and smaller than surrounding lung
Catarrhal exudate in bronchi and bronchioles
Swollen and edematous bronchial lymph nodes

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12
Q

What microscopic lesions are associated with enzootic pneumonia?

A

Lymphocytes around the airways and blood vessels

Extensve destruction of tracheal cilia

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13
Q

How is enzootic pneumonia diagnosed?

A

Clinical signs, lesions, FA test, and culture (not routine)

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14
Q

How is enzootic pneumonia preventeD?

A

Vaccination, management, and elimination protocols

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15
Q

What is the vaccination protocol for enzootic pneumonia?

A

Vaccination of growing pigs at weaning or 3 weeks later

Routine immunization of replacement gilts

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16
Q

What management practices are ideal for prevention of enzootic pneumonia?

A

All-in all-out
Improve air quality
Reduce crowding

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17
Q

What antibiotics can be given for treatment of enzootic pneumonia?

A

Need to give early
Tetracycline
Enrofloxacin - approved for swine respiratory disease

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18
Q

What are the possible elimination protocols for enzootic pneumonia?

A

Depop-repop
Herd closure and medication
Whole herd medication without closure
Change of flow in a parity segregated flow

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19
Q

What are the pros and cons of depop-repop for enzootic pneumonia?

A

Pros - can eliminate more than one disease at the same time, can improve genetics in the sow herd
Cons - complete loss of production for a period of time unless an off-site replacement female operation is available

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20
Q

What is the protocol for herd closure and medication for enzootic pneumonia?

A

Expose all replacements
Close the herd for 240 days
Immunize the whole herd every 90 days
Medicate - eg. lincomycin in water for gilts and Draxxin at birth and 14 days for piglets

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21
Q

T/F: Whole herd medication without closure to eliminate enzootic pneumonia is faster but has a lower success rate.

A

True

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22
Q

What is the protocol for whole herd medication without closure of herd for enzootic pneumonia elimination?

A

Treat all sows and gilts on site
Repeat at 14 days
Wean all piglets off-site
Bring in negative replacement gilts

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23
Q

What is the protocol for change of flow in a parity segregated flow for enzootic pneumonia elimination?

A

Have older immune sows at a separate site (parity segregated)
Add negative replacements to older sow site
Flow the system backwards until 240 days have passed
Return flow to normal after 240 days have passed

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24
Q

What do influenza virus bind to?

A

sialic a cids on cells of the upper and lower respiratory tract

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25
Q

Humans have sialic acids that bind to ___, ___, and _____ influenza viruses.

A

H1, H2, H3

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26
Q

T/F: Pigs have receptors for both human and avian influenza viruses and they can serve as a recombination ‘vessel’ for mixing of viral genetic elements.

A

True

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27
Q

T/F: There has been considerable antigenic drift in the swine influenza viruses.

A

True

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28
Q

How is swine influenza transmitted?

A

airborne transmission

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29
Q

What strain of swine influenza do we see more commonly now? In the past?

A

Now - H1N1`

Past - H3N2

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30
Q

What age group does swine influenza target?

A

All of dem - it can infect swine of all ages

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31
Q

What clinical signs are associated with swine influenza?

A

Sudden onset of anorexia, depression, muscular pain, fever, dyspnea with ‘thumpy or jerky’ respiration, cough, conjunctival discharge
Reluctance to move and will not eat

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32
Q

Morbidity due to swine influenza is (low/high) and mortality is (low/high).

A

high, low

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33
Q

How long does it take for uncomplicated recovery from swine influenza to occur?

A

7-10 days

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34
Q

What does infection of pregnant sows with swine influenza result in?

A

Higher neonatal mortality, smaller litters, and slower growth rates

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35
Q

An increased incidence of ______ ______ in pigs >120 lb has been linked to influenza, PRRSV, and other respiratory disease outbreaks.

A

gastric ulcers

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36
Q

What lesions does swine influenza cause?

A

Necrotizing bronchiolitis and bronchitis

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37
Q

How is swine influenza diagnosed?

A

Clinical signs

IHC on lung tissue

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38
Q

What population is more likely to be vaccinated against swine influenza?

A

Weaners and nursery pigs

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39
Q

Vaccine for swine influenza is available commercially for both _____ and _____ virus, but most vaccine used today in commercial herds is ____.

A

H1N1 and H3N2

Autogenous

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40
Q

When are replacement gilts vaccinated against swine influenza? Sows? Boars

A

Replacement gilts - 6 and 4 weeks pre-farrowing
Sows - once at about 3 or 4 weeks
Same schedule as sows

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41
Q

T/F: Influenza vaccines that do not stimulate antibody that blocks virus binding to host tissues may lead to enhanced viral binding

A

True

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42
Q

What management practices can be used to control swine influenza?

A

Good sanitation
Prevent mixing of livestock
All-in all-out by site

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43
Q

What is the etiologic agent of pasteurellosis?

A

P. multocida

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44
Q

What is the most common P. multocida type and serotype reported from pneumonic lesions?

A

Type A serotype 3

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45
Q

P. multocida is frequently found in where in normal swine?

A

In the upper respiratory tract

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46
Q

What lesions are associated with pateurellosis?

A

Purulent bronchopneumonia superimposed on the lesions of the primary disease agent

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47
Q

How is pasteurellosis diagnosed?

A

Bacteriologic culture

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48
Q

How sis pasteurellosis prevented?

A

Control other diseases

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49
Q

What primary diseases are associated with pasteurellosis?

A

Mycoplasma diseases, atrophic rhinitis, infleunza, inclusion body rhinitis, ascarid larval migration, and lung worms

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50
Q

How is pasteurellosis treated?

A

Early treatment with abx - Ceftiofur, tulathromycin, tiamulin, tetracycline, or tilmicosin in feed

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51
Q

Why shouldn’t tilmicosin be given parenterally in swine?

A

There is a very low margin of safety - kills pigs

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52
Q

Actinobacillus pleuropneumonia (APP) causes acute pleuropneumonia in pigs characterized by what?

A

Fever, respiratory distress, and a high rate of mortality in some outbreaks

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53
Q

Where does APP reside in chronic carrier pigs? How is it spread?

A

Resides in the tonsils

Spread by droplet and contact

54
Q

T/F: In a susceptible herd, APP causes overt disease without the influence of stress factors.

A

False - The organism may spread subclinically until stress factors occur which cause expression of overt disease

55
Q

What are the different forms of disease caused by APP?

A

Peracute, acute, and chronic

56
Q

What clinical signs are associated with peracute APP infection?

A 
Fever - 104-106 
Apathetic
Anorexic
\+/- Vomiting
Severe dyspnea with a blood-stained frothy discharge from nose and mouth
Moist suppressed cough
Cyanosis of the skin and mucous membranes
Acute death
57
Q

What clinical signs are associated with acute APP?

A

They either die or develop chronic disease

58
Q

What clinical signs are associated with chronic APP infection?

A

Chronic cough
Reduced appetite
Retarded growth rate

59
Q

T/F: Arthritis, abortion, septicemia, and CNS are occationally reported with APP infection.

A

True

60
Q

What lesions does APP cause (general)?

A

Diffuse fibrinous pleuropneumonia - edema, hemorrhage, and neutrophilic exudate with foci of coagulative necrosis
Raised lesions with an irregular surface and are dark, red, firm, and swollen
Pleuritis
+/- pericarditis

61
Q

What lesions are associated with chronic APP?

A

In addition to the fibrinous pleuropneumonia, pulmonary abscesses and adhesions develop

62
Q

What class of toxins are produced by APP?

A

RTX toxins - There are 4 that it produces by the big one is the ApX toxin

63
Q

What does the ApX toxin produced by APP cause?

A

Lysis of the netrophils resulting in release of their lysosomal enzymes onto pulmonary tissues giving rise to acute disease

64
Q

What differentials should be considered with APP infection?

A

A. suis, S. suis, P. multocida, S. cholerasuis

65
Q

How is APP infection diagnosed?

A

Clinical signs, lesions, bacterial culture, serologic tests

66
Q

How is APP infection treated?

A

Antimicrobials: Penicillin at high rates, sulfonamides, tetracycline in feed, LA 200, tiamulin in water, or exceed

67
Q

How is APP infection controlled?

A

All-in all-out production, SEW or MEW, minimize stress, improve ventilation
Cull seropositive adult carriers
Depop-repop
Vaccination (not commonly done)

68
Q

Most outbreaks of Actinobacillus suis occur in what populations?

A

Naive swine and particularly in recently weaned pigs or grow-finish pigs derived from SEW systems

69
Q

Where is A. suis found in healthy pigs?

A

The nasal cavity

Occasionally repro tract in sows

70
Q

How does invasion of A. suis likely occur? How does it spread?

A

Invade - Through the tonsil

Spread - blood

71
Q

What clinical signs are associated with A. suis infection?

A 
Sudden death
Septicemia
Fever
Dyspnea
Vascular congestion or cyanotic extremities
Arthritis
Enteritis
Occasional necrosis of the feet and tail have been reported
Occasional CNS signs
Possible abortion
72
Q

What clinical signs are associated with A. suis infections in older pigs?

A

Acute dyspnea
Depression
Anorexia
Rare occasions - skin lesions resembling erysipelas

73
Q

Mortality in young pigs with A. suis infections can be as high as ____%.

A

50%

74
Q

What lesions are associated with A. suis infection?

A

Hemorrhages in many organs - especially lungs in older piglets and growers
Serous or serofibrinous exudates in the abdominal and thoracic cavities
Polyarthritis

75
Q

How is A. suis diagnosed?

A

History, signs, and lesions are suggestive

Confirmed by culture

76
Q

Why is serologic diagnosis of A. suis unreliable?

A

There is cross-reaction with APP

77
Q

How is A. suis infection prevented?

A

Autogenous bacterins - some protection from APP bacterins too

78
Q

How is A. suis infection treated?

A

Abx - prmpt

79
Q

What is the etiologic agent of Glasser’s disease?

A

Glaeserella parasuis

80
Q

What is Glasser’s disease?

A

Septicemia and acute polyserositis, arthritis, and meningitis in young swine

81
Q

Where is G. parasuis carried?

A

In the upper respiratory tracts

82
Q

How is G. parasuis transmitted? To who is it transmitted?

A

Contact and droplet to young pigs by 2-5 weeks of age and spreads laterally through a group of pigs

83
Q

What are important factors in the onset of Glasser’s disease?

A

Stresses associated with transport, mixing, fighting, weaning, and diet changes

84
Q

What type of infections can markedly increase the severity of clinical Glasser’s disease?

A

Viral infections

85
Q

How long is the typical incubation period for Glasser’s disease?

A

12-72 hours

86
Q

What clinical signs are associated with Glasser’s disease?

A 
Sudden onset of fever
\+/- abdominal distention or tenderness
\+/- labored breathing
\+/- coughing
\+/- lameness
\+/- orchitis
\+/- CNS signs
87
Q

What lesions are associated with Glasser’s disease?

A

Peritonitis, pleuritis, pericarditis, meningitis, arthritis, and orchitis
Hemorrhages may be found in the liver, spleen, and kidneys

88
Q

How is Glasser’s disease diagnosed?

A

Based on lesions and culture

89
Q

How is Glasser’s disease treateD?

A

abx - penicillin, ampicillin, tetracyclines, sulfathiaole, or potentiated sulfonamides

90
Q

What are the rule outs for Glasser’s disease?

A

Streptococcal infection
Erysipelas
M. hyorrhinis polyserositis and arthritis

91
Q

How is Glasser’s disease prevented?

A

Minimize stress, vaccinate, exposure via fence contact

92
Q

What does S. dysgalactiae subsp. equisimilis cause?

A

Arthritis, septicemia, and meningitis in young piglets

Occasional infections such as valvular endocarditis in grower/finishers

93
Q

What does S. porcinus cause?

A

It is a rare cause of septicemia and abscesses

94
Q

Environmental streptococci infections are most common in what age group?

A

Piglets 1-3 weeks of age

95
Q

How are Streptococcal diseases prevented/controleld?

A 
Sanitation
Disinfect equipment for clipping needle teeth
Ensure adequate colostrum
Reduced abrasiveness of flooring
Navel dipping
Vaccination in problem herds
96
Q

S. suis is a common cause of what disease processes?

A

Septicemia, meningitis, arthritis, and bronchopneumonia

97
Q

What are the three clinical forms of S. suis infection?

A

Neonatal septic emia
Suppurative meningitis
Bronchopneumonia

98
Q

S. suis neonatal septicemia is seen in what population of pigs? What happens?

A

Young pigs with absence of colostal immunity

Pigs die within 24 hours

99
Q

S. suis suppurative meningitis is seen in what population of pigs?

A

Pigs 10 days to 4 months

100
Q

S. suis bronchopneumonia is seen in what population of pigs?

A

In all ages - more common in pigs 6-12 weeks of age and more severe in young pigs

101
Q

What lesions, additional to the three clinical forms, can S, suis cause?

A

Endocarditis, arthritis, vaginitis, and abortions in sows - incidence of these is low

102
Q

How is S. suis transmitted?

A

From sow to piglet as they are passed through the birth canal
Between herds by carrier pigs, +/- flies, +/- fomites

103
Q

T/F: S. suis is not durable and does not last long in the environment.

A

False - it survives long periods in feces, dust, and dead carcasses

104
Q

How is S. suis infection diagnosed?

A 
History
CS and lesions
Culture
Lancefield typing (group D)
Serotyping - may change over time on a farm
105
Q

What DDx should be considered with S. suis?

A

Pseudorabies
Glasser’s disease
S. equisimilis

106
Q

How is S. suis infection prevented and controlled?

A

Good management - minimize stress from overcrowding, poor ventilation, and mixing and moving of pigs
Treat clinically affected pigs

107
Q

Commercial bacterins for S. suis are aailable for what types?

A

Types 1, 1.5, and 2

108
Q

T/F: Immunization for S. suis is not very effective.

A

True

109
Q

What causes progressive atrophic rhinitis?

A

P. multocida toxigenic capsular type D or A and/or Bordatella bronchiseptica

110
Q

Progressive atrophic rhinitis is a chronic disease of swine characterized by what?

A

Rhinitis, atrophy or the nasal turbinates. deviation of the nasal septum, malformation of the facial bones, and growth retardation

111
Q

What plays major contributing roles in the development of progressive atrophic rhinitis?

A

Poor air quality and noxious gases, certain other
bacterial agents such as Glaesserella parasuis, Pseudomonas aeruginosa and
Fusobacterium necrophorum, and probably some viral agents

112
Q

How does transmission occur in cases of progressive atrophic rhinits?

A

lateral transmission - contact and airborne droplets

113
Q

What clinical signs are associated with early or mild progressive atrophic rhinitis?

A

Sneezing and snuffling during quiet periods
Serous nasal discharge,
excessive lacrimation and a roughened hair coat.

114
Q

What clinical signs are associated with chronic atrophic rhinitis?

A

Shortening and deviation
of the snout, folding/wrinkling of skin over snout, malapposition of teeth, epistaxis,
sneezing, pneumonia, and decreased growth rate

115
Q

What does the P. multocida toxin produced in cases of atrophic rhinitis do?

A 
Activates mature bone cells to release cytokines that enhance bone resorption and impair bone formation
Hepatotoxicity
Shortening of long bones
Decreased growth rate
Epistaxis
116
Q

How is atrophic rhinitis diagnosed?

A

Slaughter checks/lesions
Clinical signs
Culture

117
Q

How is atrophic rhinitis controlled?

A 
Purchase negative breeding stock
Monitor for disease presence in herd
Improve management and environment - all in all-out, proper ventilation
Eradication
Immunization
Biosecurity
118
Q

How is atrophic rhinitis eradicated?

A

MEW - abx to the sow combined with pre-farrowing immunization
MEW - abd to piglets at weaning, wean at 8-14 days of age
Nasal swabs - culture for toxogenic P. multocida and cull positives

119
Q

If used, what is the vaccination protocol with P. multocida toxoid?

A

2 doses prior to farrowing

Pigs one dose at 7 days and one at 14-28 days of age

120
Q

When do atrophic rhinitis vaccines yield the best results?

A

When the disease is more severe and current control methods have supplanted immunization programs

121
Q

How is atrophic rhinitis treated?

A

Abx - early

It is better to prevent it

122
Q

What biosecurity measures are recommended for atrophic rhinitis control?

A

Prevention of exposure to infected swine, cats, dogs, rodents, vehicles, and personel from infected units, and complete confinement

123
Q

What does B. bronchiseptica alone cause in neonates?

A

Lower respiratory infections

124
Q

What is the etiologic agent of inclusion body rhinitis?

A

Cytomegalvirus

125
Q

How is cytomegalovirus transmitted?

A

By contact or aerosol from nasal secretions of

carriers, which probably include sows

126
Q

What population of pigs typically get inclusion body rhinits?

A

Piglets 1-4 weeks of age

127
Q

What clinical signs are associated with inclusion body rhinitis?

A

Moderate fever, anorexia, weakness, plugging of the nasal passages with mouth breathing
+/- coughing and poling

128
Q

What may infection of naive pregnant sows and gilts with cytomegalovirus cause?

A

Birth of dead, mummified, stillborn or weak piglets

129
Q

What lesions are almost pathognomonic to inclusion body rhinitis?

A

Highly inflamed and hemorrhagic nasal mucosa

130
Q

How is inclusion body rhinitis diagnosed?

A

Gross lesions, PCR, histopath

131
Q

T/F: There is no treatment, no vaccine, and control measures are not needed for inclusion body rhinitis.

A

True

LA Infectious Disease (33 decks)

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