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Infectious diseases I & II > Inf. diseases II - Swine diseases (resp.) > Flashcards

Inf. diseases II - Swine diseases (resp.) Flashcards

1
Q

PRCV

A

PORCINE RESPIRATORY CORONAVIROSIS

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2
Q

PORCINE RESPIRATORY CORONAVIROSIS (PRC) is very contagious disease of

A

weaner pigs that is characterized by coughing, sneezing and mild respiratory infection.

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3
Q

PORCINE RESPIRATORY CORONAVIROSIS (PRC) is very contagious disease of weaner pigs that is characterized by

A

coughing, sneezing and mild respiratory infection.

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4
Q

Describe the causative agent of PRCV

A

porcine respiratory corona virus

RNA

G.Alphacoronavirus
F.Coronaviridae

Variant of TGEV so infection with PRCV makes pigs immune to TGEV.

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5
Q

Serotypes of of PRCV

A

Many serotypes with different virulence.

Most of the serotypes do not cause illness.

Only the most virulent serotype causes mild respiratory disease.

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6
Q

PRCV survival in environment

A

Virus can survive in the environment for long time

Enzootic in swine herds worldwide.
Infection is subclinical in many infected herds.

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7
Q

Target demographic of PRCV

A

Infects piglets of all ages.

Clinical illness in 1-6 month-old pigs.

Infection occurs mostly right after weaning.

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8
Q

Morbidity of PRCV

A

low

Enzootic in swine herds worldwide

Infection is subclinical in many infected herds

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9
Q

Transmission of PRCV

A

Excretion: respiratory, feces
Excretion up to 2 weeks after infection.
Mostly respiratory excretion.

Airborne respiratory transmission
Direct contact

Route: respiratory

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10
Q

Clinical signs of PRCV

A

Mild fever
Dyspnea, polypnea, anorexia – variable degrees.

Co-infection with other respiratory pathogens. If mono-infection, the suckling piglets may have a cough for a short period – may go unnoticed.

Adult mostly subclinical with no clinical signs.

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11
Q

Post mortem signs of PRCV. (2)

A

Bronchointerstitial pneumonia (5-60%).

(Cranial and middle lung lobe have thick consistence, dark red to purple color.)

If secondary bacterial infections – lesions are more severe.

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12
Q

Material for diagnosis of PRCV. (2)

A

nasal swabs
lungs

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13
Q

Lab analyses for diagnosis of PRCV. (3)

A

RT-PCR and highly specific competitive ELISA are the only diagnostic measures that can differentiate PRCV and TGEV!

Virus isolation

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14
Q

Prevention & control of PRCV. (3)

A

Not a big problem for general herd health – no prevention measures in place.

No vaccines.

NB! Infection with PRCV make the pigs immune to TGEV!

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15
Q

Alt. name for mycoplasmal pneumonia

A

Enzootic pneumonia

However, note, some sources try to differentiate these two into 2 separate diseases.

Some say Mycoplasmal pneumonia describes only the effects of the mycoplasma and when there is secondary infection involved as well, it would be called enzootic pneumonia.

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16
Q

mycoplasmal pneumonia or Enzootic pneumonia is a chronic respiratory disease of pigs, caused by

A

Mycoplasma hyopneumoniae, characterized by sporadic disease of coughing and decrease in growth rate.

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17
Q

mycoplasmal pneumonia or Enzootic pneumonia is a chronic respiratory disease of pigs, caused by Mycoplasma hyopneumoniae, characterized by

A

sporadic disease of coughing and decrease in growth rate.

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18
Q

Causative agent of MP

A

MP = Mycoplasma pneumonia
Mycoplasma hyopneumoniae, gram neg. bacterium.

Primary agent – “opens the door” for other agents. Secondary agent: Pasteurella multocida.

Can also be other, e.g. Haemophilus parasuis, Actinobacillus pleuropneumoniae

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19
Q

Where is MP found?

A

mycoplasmal pneumonia found worldwide

also in estonia

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20
Q

When does MP typically occur?

A

Seasonal – higher occurrence rate from November to March

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21
Q

Morbidity of MP

A

Morbidity decreases with increasing age

Finishing pigs and adults may recover completely

Herd morbidity <93%

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22
Q

Transmission of MP

A

Excretion: respiratory
Coughing and sneezing: spread is 5-6m
Spread to neighboring farms with aerosols within 3,2 km radius

Aerogenic
Direct contact
Route: respiratory

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23
Q

IP of MP

A

IP: 10-16 days
Mostly chronic, rarely acute outbreaks

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24
Q

Clinical signs of acute MP

A

Mostly chronic, rarely acute outbreaks.

Signs of acute:
Acute respiratory distress, acute pneumonia
Dehydration
Fever

Morbidity <100%
High mortality in all age groups

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25
Q

Clinical signs of chronic MP

A

In endemic herds Young piglets are usually infected at 3-10 weeks of age, clinical signs seen in suckling piglets.

Dry cough (7-8 coughs in one episode)
Worsens while moving (e.g. during feeding)

Difficulties to breath
Uneven growth rate, loss of appetite

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26
Q

Post mortem signs of MP. (4)

A

Lung lesions, Catarrhal pneumonia
Bronchial LNs – enlarged, edematous

With secondary infections:
Pleuritis and pericarditis
Hepatization and congestion with a suppurative bronchopneumonia

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27
Q

the most common respiratory infection in pigs:

A

Enzootic pneumonia (aka mycoplasmal pneumonia) with or without secondary bacterial invasion, is the most common respiratory infection in pigs!

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28
Q

Material for diagnosis of MP. (3)

A

Blood
Colostrum
Lung tissue

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29
Q

Lab analyses for diagnosis of MP. (2)

A

Serology (ELISA) – antibodies from sera and colostrum.

Detecting organism – lung tissue culture, immunofluorescence, PCR, antigen-ELISA.

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30
Q

Tx for MP

A

Long course AB for secondary infections.

31
Q

Prevention & control of MP. (3)

A

Improve husbandry (decrease stress)
Cull infected
Vaccination (only decreases severity)

32
Q

APP

A

Actinobacillus pleuropneumonia(e)

33
Q

Actinobacillus pleuropneumonia is a contagious disease of pigs, caused by?
And characterized by?

A

Actinobacillus pleuropneumoniae, characterized by pneumonia and sudden and rapid deaths.

34
Q

Describe the causative agent of APP.

A

grem neg. non-motile coccobacillus bacteria, Actinobacillus pleuropneumoniae.

In older literature: Haemophilus pleuropneumoniae.

High virulence.

35
Q

Biotypes and their serotypes of APP. (2)

A

Biotype 1 – has 13 serotypes
Biotype 2 – has 2 serotypes

Different countries have different serotypes.
In one herd there can be more than one serotype at the same time!

36
Q

APP survival in environment

A

Does not survive in the environment for long.

Drying an sun light deactivate
Contagious only for few days

37
Q

Where and when in the world can APP be found?

A

Worldwide distribution,
<70% of herds are seropositive.

More common during winter and spring.

38
Q

On primary introduction to herd, APP infects who most commonly?

A

2-4 moth-old growing pigs

In endemic herds: weaners and new animals

39
Q

Morbidity of APP

A

<50%

40
Q

Mortality of APP

A

1-10%

Dependent on the virulence of the serotype

41
Q

Where does APP localize in the body?

A

Agent localizes in tonsils and lungs of clinically healthy – infection can occur after stressful event.

42
Q

Transmission of APP.

A

Excretion: nasal & pulmonary discharge

Direct contact
Aerosols – to other farms close by

Route: respiratory

43
Q

IP of APP

A

4-24h

44
Q

Forms of APP (3)

A

peracute, acute and chronic

45
Q

Clinical signs of peracute APP (2)

A

Fever 41-42°C
Death in just few hours

46
Q

Clinical signs of acute APP (6)

A

Severe respiratory distress
High fever

Labored respirations with exaggerated abdominal component
Cyanosis

Frequent blood-stained frothy discharge from nose and mouth
Death in 1-2 days

47
Q

Clinical signs of chronic APP (4)

A

Common sequel to acute case
Initially febrile and anorexic
Respiratory distress is less severe
Persistent cough may develop

48
Q

Post mortem signs of APP

A

First lesions form in the middle of the lung lobe

Pleuritis
Hemorrhagic and fibrinous pleuropneumonia

Sequestration in chronic form

49
Q

Material for diagnosis of APP (3)

A

Swab from nasal cavity
Lung tissue, tonsils

50
Q

Lab analyses for diagnosis of APP (4)

A

Bacteriology
Serotyping
PCR
Serology (ELISA)

51
Q

Tx for APP (2)

A

ABs and vaccination NB! Vaccines are serotype specific!

Ab Tx often disappointing – has to be treated in early stages of the disease to be effective.
(Penicillin, ampicillin, cefalosporins)

Recovered sows and gilts should be culled from herd since they stay seropositive and therefore can be source of infection to other (especially piglets).

52
Q

NPAR =
PAR =

A

NPAR = Nonprogressive atrophic rhinitis
PAR = Progressive atrophic rhinitis

53
Q

Causative agents of
NPAR =
PAR =

A

NPAR = Bordetella bronchiseptica
PAR = Pasteurella multocida

54
Q

Bordetella bronchiseptica causes what type of rhinitis?

A

NPAR = Nonprogressive atrophic rhinitis

55
Q

Pasteurella multocida causes what type of rhinitis?

A

PAR = Progressive atrophic rhinitis

56
Q

Which is more severe NPAR or PAR?

A

progressive

57
Q

ATROPHIC RHINITIS is an infectious disease of swine characterized by

A

stunted development or deformation of the nasal turbinate and septum.

58
Q

NONPROGRESSIVE ATROPIC RHINITIS (NPAR) is a chronic infectious disease of pigs, caused by Bordetella bronchiseptica, characterized by

A

usually transient turbinate atrophy.

59
Q

PROGRESSIVE ATROPHIC RHINITIS (PAR) is a chronic infectious disease of pigs, caused by Pasteurella multocida, characterized by

A

shortening or distortion of the snout, sneezing, nasal discharge and epistaxis.

60
Q

Describe the causative agent of NPAR (3)

A

Agent: toxigenic Bordetella bronchiseptica

Produces heat-labile toxin

Gram–, small, motile, aerobic cocci

61
Q

Describe the causative agent of PAR

A

toxigenic gram neg. non-motile
type D and A

62
Q

Target demo for NPAR and PAR

A

NPAR: Potential pathogen for other mammals (cats, dogs, rats). But strains causing turbinate atrophy are isolated only from pigs.

PAR: Organism colonizes the tonsils of clinically normal pigs.

In both, Pigs are infected at early age, is a disease of young growing pigs.

63
Q

Morbidity of NPAR

A

Morbidity 25-50%

Is higher for PAR

64
Q

Main diffs between NPAR and PAR other than causative agent. (4)

A

NPAR is mild while PAR is severe.
NPAR is transient and can heal, PAR is nonreversible.

B. bronchiseptica produces heat-labile toxin while P. multocida produces thermolabile and dermonectoric atrophic rhinitis toxin.

NPAR is Apparent 2-4 weeks after infection while PAR is apparent in just a few days

65
Q

Where does B. bronchiseptica live?

A

B. bronchiseptica colonizes the ciliated mucosa of the resp.tract

66
Q

Transmission of AR

A

Excretion: nasal discharge
Infection reservoir: infected sows infect piglets.

Direct contact
Droplets
Fomites

Route: respiratory, oral

67
Q

IP for AR

A

IP: 5-15 days

NPAR 2-4 weeks
PAR few days

68
Q

Clinical signs of atrophic rhinitis (6)

A

Sneezing (piglets 3-9 weeks of age)
Nasal discharge
Epistaxis

Deformity of face with nasal bones (twisted snout)

Visible most commonly in pigs 8-10 weeks old within 3-4 weeks after infection

Growth rate may be decreased

69
Q

Post mortem signs of AR (3)

A

Atrophy of the nasal mucosa

Decalcification and atrophy of the turbinate and ethmoid bones. In severe cases they have disappeared completely.

70
Q

Grading AR

A

Post mortem examination of cross-section of snout: Section at the level of the second premolar tooth.

Grading the severity of lesions:
Grade 0 – no deviation or absolute normality, with nasal septum straight and turbinates symmetrical and filling nasal cavities.

Grade 1 – Slight irregularity, asymmetry, or distortion of the nasal structures without atrophy.

Grade 2 – Marked distortion of nasal structure but without marked atrophy.

Grade 3 – Definite atrophy of the turbinates with or without distortion.

Grade 4 – More severe atrophy with severe atrophy of one or more turbinates.

Grade 5 – Very severe atrophy in which all turbinates have virtually disappeared.

71
Q

Material for diagnosis of AR

A

nasal swabs

72
Q

Lab analyses for diagnosis of AR. (2)

A

Isolating the organism (bacteriology)

Histology – formalin-fixed cross-section of snout at level of second premolar

73
Q

Tx of AR (2)

A

Early on: ABs (tylosin, oxytetracycline, trimetoprim-sulfadoxine)

Later: no Tx – favor culling

74
Q

Prevention & control of AR. (2)

A

Good husbandry & Vaccination

Culling of chronically infected animals

Infectious diseases I & II (33 decks)

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