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

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

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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
Clinical signs of chronic MP
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
26
Post mortem signs of MP. (4)
Lung lesions, Catarrhal pneumonia Bronchial LNs – enlarged, edematous With secondary infections: Pleuritis and pericarditis Hepatization and congestion with a suppurative bronchopneumonia
27
the most common respiratory infection in pigs:
Enzootic pneumonia (aka mycoplasmal pneumonia) with or without secondary bacterial invasion, is the most common respiratory infection in pigs!
28
Material for diagnosis of MP. (3)
Blood Colostrum Lung tissue
29
Lab analyses for diagnosis of MP. (2)
Serology (ELISA) – antibodies from sera and colostrum. Detecting organism – lung tissue culture, immunofluorescence, PCR, antigen-ELISA.
30
Tx for MP
Long course AB for secondary infections.
31
Prevention & control of MP. (3)
Improve husbandry (decrease stress) Cull infected Vaccination (only decreases severity)
32
APP
Actinobacillus pleuropneumonia(e)
33
Actinobacillus pleuropneumonia is a contagious disease of pigs, caused by? And characterized by?
Actinobacillus pleuropneumoniae, characterized by pneumonia and sudden and rapid deaths.
34
Describe the causative agent of APP.
grem neg. non-motile coccobacillus bacteria, Actinobacillus pleuropneumoniae. In older literature: Haemophilus pleuropneumoniae. High virulence.
35
Biotypes and their serotypes of APP. (2)
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
APP survival in environment
Does not survive in the environment for long. Drying an sun light deactivate Contagious only for few days
37
Where and when in the world can APP be found?
Worldwide distribution, <70% of herds are seropositive. More common during winter and spring.
38
On primary introduction to herd, APP infects who most commonly?
2-4 moth-old growing pigs In endemic herds: weaners and new animals
39
Morbidity of APP
<50%
40
Mortality of APP
1-10% Dependent on the virulence of the serotype
41
Where does APP localize in the body?
Agent localizes in tonsils and lungs of clinically healthy – infection can occur after stressful event.
42
Transmission of APP.
Excretion: nasal & pulmonary discharge Direct contact Aerosols – to other farms close by Route: respiratory
43
IP of APP
4-24h
44
Forms of APP (3)
peracute, acute and chronic
45
Clinical signs of peracute APP (2)
Fever 41-42°C Death in just few hours
46
Clinical signs of acute APP (6)
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
Clinical signs of chronic APP (4)
Common sequel to acute case Initially febrile and anorexic Respiratory distress is less severe Persistent cough may develop
48
Post mortem signs of APP
First lesions form in the middle of the lung lobe Pleuritis Hemorrhagic and fibrinous pleuropneumonia Sequestration in chronic form
49
Material for diagnosis of APP (3)
Swab from nasal cavity Lung tissue, tonsils
50
Lab analyses for diagnosis of APP (4)
Bacteriology Serotyping PCR Serology (ELISA)
51
Tx for APP (2)
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
NPAR = PAR =
NPAR = Nonprogressive atrophic rhinitis PAR = Progressive atrophic rhinitis
53
Causative agents of NPAR = PAR =
NPAR = Bordetella bronchiseptica PAR = Pasteurella multocida
54
Bordetella bronchiseptica causes what type of rhinitis?
NPAR = Nonprogressive atrophic rhinitis
55
Pasteurella multocida causes what type of rhinitis?
PAR = Progressive atrophic rhinitis
56
Which is more severe NPAR or PAR?
progressive
57
ATROPHIC RHINITIS is an infectious disease of swine characterized by
stunted development or deformation of the nasal turbinate and septum.
58
NONPROGRESSIVE ATROPIC RHINITIS (NPAR) is a chronic infectious disease of pigs, caused by Bordetella bronchiseptica, characterized by
usually transient turbinate atrophy.
59
PROGRESSIVE ATROPHIC RHINITIS (PAR) is a chronic infectious disease of pigs, caused by Pasteurella multocida, characterized by
shortening or distortion of the snout, sneezing, nasal discharge and epistaxis.
60
Describe the causative agent of NPAR (3)
Agent: toxigenic Bordetella bronchiseptica Produces heat-labile toxin Gram–, small, motile, aerobic cocci
61
Describe the causative agent of PAR
toxigenic gram neg. non-motile type D and A
62
Target demo for NPAR and PAR
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
Morbidity of NPAR
Morbidity 25-50% Is higher for PAR
64
Main diffs between NPAR and PAR other than causative agent. (4)
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
Where does B. bronchiseptica live?
B. bronchiseptica colonizes the ciliated mucosa of the resp.tract
66
Transmission of AR
Excretion: nasal discharge Infection reservoir: infected sows infect piglets. Direct contact Droplets Fomites Route: respiratory, oral
67
IP for AR
IP: 5-15 days NPAR 2-4 weeks PAR few days
68
Clinical signs of atrophic rhinitis (6)
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
Post mortem signs of AR (3)
Atrophy of the nasal mucosa Decalcification and atrophy of the turbinate and ethmoid bones. In severe cases they have disappeared completely.
70
Grading AR
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
Material for diagnosis of AR
nasal swabs
72
Lab analyses for diagnosis of AR. (2)
Isolating the organism (bacteriology) Histology – formalin-fixed cross-section of snout at level of second premolar
73
Tx of AR (2)
Early on: ABs (tylosin, oxytetracycline, trimetoprim-sulfadoxine) Later: no Tx – favor culling
74
Prevention & control of AR. (2)
Good husbandry & Vaccination Culling of chronically infected animals

Infectious diseases I & II (33 decks)

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