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
Humans have sialic acids that bind to ___, ___, and _____ influenza viruses.
H1, H2, H3
26
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.
True
27
T/F: There has been considerable antigenic drift in the swine influenza viruses.
True
28
How is swine influenza transmitted?
airborne transmission
29
What strain of swine influenza do we see more commonly now? In the past?
Now - H1N1` | Past - H3N2
30
What age group does swine influenza target?
All of dem - it can infect swine of all ages
31
What clinical signs are associated with swine influenza?
Sudden onset of anorexia, depression, muscular pain, fever, dyspnea with 'thumpy or jerky' respiration, cough, conjunctival discharge Reluctance to move and will not eat
32
Morbidity due to swine influenza is (low/high) and mortality is (low/high).
high, low
33
How long does it take for uncomplicated recovery from swine influenza to occur?
7-10 days
34
What does infection of pregnant sows with swine influenza result in?
Higher neonatal mortality, smaller litters, and slower growth rates
35
An increased incidence of ______ ______ in pigs >120 lb has been linked to influenza, PRRSV, and other respiratory disease outbreaks.
gastric ulcers
36
What lesions does swine influenza cause?
Necrotizing bronchiolitis and bronchitis
37
How is swine influenza diagnosed?
Clinical signs | IHC on lung tissue
38
What population is more likely to be vaccinated against swine influenza?
Weaners and nursery pigs
39
Vaccine for swine influenza is available commercially for both _____ and _____ virus, but most vaccine used today in commercial herds is ____.
H1N1 and H3N2 | Autogenous
40
When are replacement gilts vaccinated against swine influenza? Sows? Boars
Replacement gilts - 6 and 4 weeks pre-farrowing Sows - once at about 3 or 4 weeks Same schedule as sows
41
T/F: Influenza vaccines that do not stimulate antibody that blocks virus binding to host tissues may lead to enhanced viral binding
True
42
What management practices can be used to control swine influenza?
Good sanitation Prevent mixing of livestock All-in all-out by site
43
What is the etiologic agent of pasteurellosis?
P. multocida
44
What is the most common P. multocida type and serotype reported from pneumonic lesions?
Type A serotype 3
45
P. multocida is frequently found in where in normal swine?
In the upper respiratory tract
46
What lesions are associated with pateurellosis?
Purulent bronchopneumonia superimposed on the lesions of the primary disease agent
47
How is pasteurellosis diagnosed?
Bacteriologic culture
48
How sis pasteurellosis prevented?
Control other diseases
49
What primary diseases are associated with pasteurellosis?
Mycoplasma diseases, atrophic rhinitis, infleunza, inclusion body rhinitis, ascarid larval migration, and lung worms
50
How is pasteurellosis treated?
Early treatment with abx - Ceftiofur, tulathromycin, tiamulin, tetracycline, or tilmicosin in feed
51
Why shouldn't tilmicosin be given parenterally in swine?
There is a very low margin of safety - kills pigs
52
Actinobacillus pleuropneumonia (APP) causes acute pleuropneumonia in pigs characterized by what?
Fever, respiratory distress, and a high rate of mortality in some outbreaks
53
Where does APP reside in chronic carrier pigs? How is it spread?
Resides in the tonsils | Spread by droplet and contact
54
T/F: In a susceptible herd, APP causes overt disease without the influence of stress factors.
False - The organism may spread subclinically until stress factors occur which cause expression of overt disease
55
What are the different forms of disease caused by APP?
Peracute, acute, and chronic
56
What clinical signs are associated with peracute APP infection?
``` 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
What clinical signs are associated with acute APP?
They either die or develop chronic disease
58
What clinical signs are associated with chronic APP infection?
Chronic cough Reduced appetite Retarded growth rate
59
T/F: Arthritis, abortion, septicemia, and CNS are occationally reported with APP infection.
True
60
What lesions does APP cause (general)?
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
What lesions are associated with chronic APP?
In addition to the fibrinous pleuropneumonia, pulmonary abscesses and adhesions develop
62
What class of toxins are produced by APP?
RTX toxins - There are 4 that it produces by the big one is the ApX toxin
63
What does the ApX toxin produced by APP cause?
Lysis of the netrophils resulting in release of their lysosomal enzymes onto pulmonary tissues giving rise to acute disease
64
What differentials should be considered with APP infection?
A. suis, S. suis, P. multocida, S. cholerasuis
65
How is APP infection diagnosed?
Clinical signs, lesions, bacterial culture, serologic tests
66
How is APP infection treated?
Antimicrobials: Penicillin at high rates, sulfonamides, tetracycline in feed, LA 200, tiamulin in water, or exceed
67
How is APP infection controlled?
All-in all-out production, SEW or MEW, minimize stress, improve ventilation Cull seropositive adult carriers Depop-repop Vaccination (not commonly done)
68
Most outbreaks of Actinobacillus suis occur in what populations?
Naive swine and particularly in recently weaned pigs or grow-finish pigs derived from SEW systems
69
Where is A. suis found in healthy pigs?
The nasal cavity | Occasionally repro tract in sows
70
How does invasion of A. suis likely occur? How does it spread?
Invade - Through the tonsil | Spread - blood
71
What clinical signs are associated with A. suis infection?
``` 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
What clinical signs are associated with A. suis infections in older pigs?
Acute dyspnea Depression Anorexia Rare occasions - skin lesions resembling erysipelas
73
Mortality in young pigs with A. suis infections can be as high as ____%.
50%
74
What lesions are associated with A. suis infection?
Hemorrhages in many organs - especially lungs in older piglets and growers Serous or serofibrinous exudates in the abdominal and thoracic cavities Polyarthritis
75
How is A. suis diagnosed?
History, signs, and lesions are suggestive | Confirmed by culture
76
Why is serologic diagnosis of A. suis unreliable?
There is cross-reaction with APP
77
How is A. suis infection prevented?
Autogenous bacterins - some protection from APP bacterins too
78
How is A. suis infection treated?
Abx - prmpt
79
What is the etiologic agent of Glasser's disease?
Glaeserella parasuis
80
What is Glasser's disease?
Septicemia and acute polyserositis, arthritis, and meningitis in young swine
81
Where is G. parasuis carried?
In the upper respiratory tracts
82
How is G. parasuis transmitted? To who is it transmitted?
Contact and droplet to young pigs by 2-5 weeks of age and spreads laterally through a group of pigs
83
What are important factors in the onset of Glasser's disease?
Stresses associated with transport, mixing, fighting, weaning, and diet changes
84
What type of infections can markedly increase the severity of clinical Glasser's disease?
Viral infections
85
How long is the typical incubation period for Glasser's disease?
12-72 hours
86
What clinical signs are associated with Glasser's disease?
``` Sudden onset of fever +/- abdominal distention or tenderness +/- labored breathing +/- coughing +/- lameness +/- orchitis +/- CNS signs ```
87
What lesions are associated with Glasser's disease?
Peritonitis, pleuritis, pericarditis, meningitis, arthritis, and orchitis Hemorrhages may be found in the liver, spleen, and kidneys
88
How is Glasser's disease diagnosed?
Based on lesions and culture
89
How is Glasser's disease treateD?
abx - penicillin, ampicillin, tetracyclines, sulfathiaole, or potentiated sulfonamides
90
What are the rule outs for Glasser's disease?
Streptococcal infection Erysipelas M. hyorrhinis polyserositis and arthritis
91
How is Glasser's disease prevented?
Minimize stress, vaccinate, exposure via fence contact
92
What does S. dysgalactiae subsp. equisimilis cause?
Arthritis, septicemia, and meningitis in young piglets | Occasional infections such as valvular endocarditis in grower/finishers
93
What does S. porcinus cause?
It is a rare cause of septicemia and abscesses
94
Environmental streptococci infections are most common in what age group?
Piglets 1-3 weeks of age
95
How are Streptococcal diseases prevented/controleld?
``` Sanitation Disinfect equipment for clipping needle teeth Ensure adequate colostrum Reduced abrasiveness of flooring Navel dipping Vaccination in problem herds ```
96
S. suis is a common cause of what disease processes?
Septicemia, meningitis, arthritis, and bronchopneumonia
97
What are the three clinical forms of S. suis infection?
Neonatal septic emia Suppurative meningitis Bronchopneumonia
98
S. suis neonatal septicemia is seen in what population of pigs? What happens?
Young pigs with absence of colostal immunity | Pigs die within 24 hours
99
S. suis suppurative meningitis is seen in what population of pigs?
Pigs 10 days to 4 months
100
S. suis bronchopneumonia is seen in what population of pigs?
In all ages - more common in pigs 6-12 weeks of age and more severe in young pigs
101
What lesions, additional to the three clinical forms, can S, suis cause?
Endocarditis, arthritis, vaginitis, and abortions in sows - incidence of these is low
102
How is S. suis transmitted?
From sow to piglet as they are passed through the birth canal Between herds by carrier pigs, +/- flies, +/- fomites
103
T/F: S. suis is not durable and does not last long in the environment.
False - it survives long periods in feces, dust, and dead carcasses
104
How is S. suis infection diagnosed?
``` History CS and lesions Culture Lancefield typing (group D) Serotyping - may change over time on a farm ```
105
What DDx should be considered with S. suis?
Pseudorabies Glasser's disease S. equisimilis
106
How is S. suis infection prevented and controlled?
Good management - minimize stress from overcrowding, poor ventilation, and mixing and moving of pigs Treat clinically affected pigs
107
Commercial bacterins for S. suis are aailable for what types?
Types 1, 1.5, and 2
108
T/F: Immunization for S. suis is not very effective.
True
109
What causes progressive atrophic rhinitis?
P. multocida toxigenic capsular type D or A and/or Bordatella bronchiseptica
110
Progressive atrophic rhinitis is a chronic disease of swine characterized by what?
Rhinitis, atrophy or the nasal turbinates. deviation of the nasal septum, malformation of the facial bones, and growth retardation
111
What plays major contributing roles in the development of progressive atrophic rhinitis?
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
How does transmission occur in cases of progressive atrophic rhinits?
lateral transmission - contact and airborne droplets
113
What clinical signs are associated with early or mild progressive atrophic rhinitis?
Sneezing and snuffling during quiet periods Serous nasal discharge, excessive lacrimation and a roughened hair coat.
114
What clinical signs are associated with chronic atrophic rhinitis?
Shortening and deviation of the snout, folding/wrinkling of skin over snout, malapposition of teeth, epistaxis, sneezing, pneumonia, and decreased growth rate
115
What does the P. multocida toxin produced in cases of atrophic rhinitis do?
``` 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
How is atrophic rhinitis diagnosed?
Slaughter checks/lesions Clinical signs Culture
117
How is atrophic rhinitis controlled?
``` Purchase negative breeding stock Monitor for disease presence in herd Improve management and environment - all in all-out, proper ventilation Eradication Immunization Biosecurity ```
118
How is atrophic rhinitis eradicated?
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
If used, what is the vaccination protocol with P. multocida toxoid?
2 doses prior to farrowing | Pigs one dose at 7 days and one at 14-28 days of age
120
When do atrophic rhinitis vaccines yield the best results?
When the disease is more severe and current control methods have supplanted immunization programs
121
How is atrophic rhinitis treated?
Abx - early | It is better to prevent it
122
What biosecurity measures are recommended for atrophic rhinitis control?
Prevention of exposure to infected swine, cats, dogs, rodents, vehicles, and personel from infected units, and complete confinement
123
What does B. bronchiseptica alone cause in neonates?
Lower respiratory infections
124
What is the etiologic agent of inclusion body rhinitis?
Cytomegalvirus
125
How is cytomegalovirus transmitted?
By contact or aerosol from nasal secretions of | carriers, which probably include sows
126
What population of pigs typically get inclusion body rhinits?
Piglets 1-4 weeks of age
127
What clinical signs are associated with inclusion body rhinitis?
Moderate fever, anorexia, weakness, plugging of the nasal passages with mouth breathing +/- coughing and poling
128
What may infection of naive pregnant sows and gilts with cytomegalovirus cause?
Birth of dead, mummified, stillborn or weak piglets
129
What lesions are almost pathognomonic to inclusion body rhinitis?
Highly inflamed and hemorrhagic nasal mucosa
130
How is inclusion body rhinitis diagnosed?
Gross lesions, PCR, histopath
131
T/F: There is no treatment, no vaccine, and control measures are not needed for inclusion body rhinitis.
True