(said in class) you can guess the distribution of lesions based on if it's caused by bact or virus... explain
in bact usually in cr ventral lung lobes-- bc its the first bronchi to branch off- and the R side branches before L so R cr vent lung lobe. But virus spread is almost always hematologic- so more diffuse ((can get diffuse pattern if bacteremia but then see oher sigs of bacteremia too)
3 main ways PRRS is transmitted?
(1) Pig-to-pig via aerosol or semen (2) Fomites (trucks, boxes, boots, etc…, PRRSV survives longest in the cold) NEEDLES! (3) Biting Insects
2 etiological agents!! (1) Bordetella bronchiseptica causes a non-progressive form of AR. It is a Aerobic, Gram-negative rod. It Colonizes the nasal passages of swine. (2) Progressive (severe) AR is caused by toxigenic Pasteurella multocida. (Isolated from tonsils & nasal swabs.)... When both organisms are present, AR is especially symptomatic
why does pasturella cause the severe AR?
Produces a potent dermonecrotizing toxin --> Turbinate atrophy as well as bony alterations in nasal & facial bones
who might have a genetic predisposition to AR?
what kinda environment can make AR even worse?
Caustic air environments exacerbate the symptoms
what management practice can you do that will help with AR?
Segregated Early Weaning (SEW) may help eliminate the bugs.
clinical signs of AR can appear in pigs as young as..
1 wk old (commonly appears shortly after weaning)
what are the early signs/how do the CSs of AR progress
early signs: Sneezing & snorting with a serous or mucopurulent nasal discharge. You will start to see Dirty or discolored hair and skin around the eyes. Eventual progress to Severe turbinate atrophy, bloody & crooked noses, followed by increased incidence of respiratory tract lesions & infections
Control measures fall into three major categories:...
(1) Improvement of husbandry, management, & housing. (2) Vaccination program for the breeding stock, pigs, or both. (3) Administration of antibiotics to sows & piglets around the time of farrowing/weaning (questionable efficacy)
(1) Chronic persistent, nonproductive cough. (Severity increases with excessive dust, irritating gases, or concurrent infections) (2) Stunted growth & Decreased feed efficiency in the face of near-normal appetites.
what is morbidity/mortality like?
High morbidity & Low mortality.
where are lesions from mycoplasma pneumonia located?
Cranioventral, (bc bacteria!!) well demarcated, pneumonic lesions
what do lung lesions look like from MP? Acute vs chronic? what do they lung lesions tell you?
(1) CHRONIC: Atelectatic & dark gray. (2) ACUTE: tend to be reddish brown or light gray with edema, mucus, & inflammatory cells in the airways....Mucopurulent exudate can be squeezed from airways... (3) imPORTANT TO NOTE: Neither gross nor microscopic lesions are pathognomonic for M. hyopneumoniae.
Dx of MP (said we don't need to know)
(1) ID of the agent in post mortem lung samples by: FA, IHC or PCR techniques (2) Serologic tests including CF & ELISA may be useful on a herd basis (Many pigs without active disease have antibodies to M. hyopneumoniae or other cross-reacting mycoplasmas)
what can you do to try to control MP?
SEW (segregated early wearning) or MEW (medicated early weaning) will help control but not eliminate infxn
ACTINOBACILLUS PLEUROPNEUMONIAE(APP) + Actinobacillus suis
is APP acute or chronic?
Severe, highly contagious. Sudden onset, short clinical course, high morbidity, & high mortality
what is morbidity and mortality like for APP?
high morbidity, & high mortality.....superfast instakill
how do actinobacillus pleuropneumoniae and actinobacillus suis compare?
Suis can cause similar disease & lesions but is not as contagious as APP.
how is APP transmitted?
Aerosol transmission by close contact and short distance.
where do pigs shed APP from?
Many pigs harbor organism in upper airways
what kinda bact is APP?
Hemolytic, Gram-negative, capsulated, coccobacillary rod. It is highly host-specific with 2 Biotypes & 15 serotypes
how labile is APP?
The organism does not persist for any significant time in the environment.
what is one of the reasons APP is such a huge asshole? (what makes it so virulent?)
CREATES LOTS OF TOXINS! (1) The APP organism secretes 4 exotoxins together called RTX toxins which are Cytotoxic &/or hemolytic (2) Produces abundant endotoxin
what are the EXOtoxins APP produces collectively called?
what is Satellitism?
It means if you want to grow a particular type of pathogen on agar, you will need a DIFF pathogen grown on the same agar (a "nurse" colony) to allow the one you are interested in to grow. APP needs a satellite colony
what are clinical signs like for APP?
Acute outbreaks --> Sudden deaths!!! You will see Sudden onset of prostration, high temperatures, apathy, anorexia, stiffness. A shallow, nonproductive cough is occasionally present (in class he said usually productive), it will progress to Dyspnea with open mouth breathing, +/- foamy, bloody discharge from the mouth & nose. ALSO There is early peripheral cyanosis of extremities. also ABORTIONS can occur in acutely affected females
how would you describe the lesions of APP?
Necro-hemorrhagic areas of lung consolidation with fibrinous pleuritis.Lungs are dark red to black, firm, & develop areas of infarction. Bloody froth often fills larger airways.
what might the thoracic cavity look like with APP cases?
The thoracic cavity often contains blood-tinged fluid.
what will CHRONIC cases of APP look like?
Large, sequestered or encapsulated nodules of necrosis in the lungs. May incompletely resolve as abscesses. Can also see fibrinous adhesions
how would you describe the lungs affected by APP? how would you know if it was chronic?
dark red, heavy, solid lungs. fibrinous pleuritis in chronic cases
dx (said he wouldnt ask dx tests) of APP?
(1) A culture technique using immunomagnetic separation has been described for isolating the organism from mixed bacterial populations (2) PCR for the RTX toxin genes (3) CF, ELISA, & hemolysin neutralization serology tests also are useful for diagnosis of APP on a herd basis
is there vx for app?
what is the most important management thing with controlling APP?
Acute outbreaks of APP demand what measures? What about chronic cases?
immediate parenteral antimicrobial treatment combined with antibiotics in feed or water for a few weeks (Tiamulin, Tulathromycin, Chlortetracycline, Ceftiofur, Tilmicosin, Florfenicol, Enrofloxacin & PPG ). Chronic cases usually are unresponsive to treatment
how does actinobacillus suis behave? what is a CS of this he pointed out?
Behaves like APP but less severe and shorter duration. Generalized septicemia like H. parasuis 7 Erysipelas
what kinda toxin does A. Suis produce?
Produces Type I hemolysin
is there a vx for A. Suis?
no, only a vx for APP ( Autogenous vaccines used in refractory cases)
if you culture A. Suis, what do you do to tx?
Antibiotics ASAP!!!!!!!!!! (injectable, water, feed...) Correct diagnosis is critical
what is onset of SIV like? What is the most identifiable CS?
Rapidly spreading viral disease with a short course of 5-7 days, it will have Sudden onset of fever, oculonasal discharge, prostration, & weakness (like any other flu) and Paroxysmal coughing. (deep barking cough)
what is morbidity/mortality of SIV like?
Low mortality in uncomplicated outbreaks. Nearly all of the herds in the Midwest have antibodies. other part in notes said: Morbidity is high & mortality is low.
what is the etiological agent of SIV?
In the U.S. SIV is caused by type A influenza viruses (family Orthomyxoviridae).
what is the classic subtype of swine flu? what are some other subtypes?
H1N1 is the classic swine subtype. (H3N2 & H1N2 are other subtypes)
how labile is SIV?
Swine influenza virus does not survive more than two weeks outside the host & is inactivated by many disinfectants.
CSs of swine flu? Age most commonly seen?
Most common in pigs > 12 woa.. Sudden onset of marked respiratory illness. Signs include: Prostration, Weakness, Fevers (104° to 106° F), Paroxysmal coughing, Anorexia, & Conjunctivitis, Occulonasal discharge. Herd is largely recovered in 1 – 2 weeks.
what can inc the mortality/severity of swine flu?
Concurrent infections with other respiratory diseases can increase mortality & increase recovery time
what do lung lesions of SIV look like? other resp related lesions?
Lobular distribution (so more diffuse) of congestion, firmness, atelectasis, emphysema, & pneumonia. Lesions often appear as distinct & scattered lobules. Airways may contain blood-tinged exude, and there might be Moderate Regional lympadenopathy
(dx- dont need to know) Detection of antigen or virus is most successful when? how?
most successful from acutely affected (febrile) pigs. FA on fresh lung sections, IHC on formalin-fixed lung, VI from nasal swabs or lung tissue., PCR of nasal swabs or lungs, ELISA on nasal swabs, Paired serum samples (note that Several subtypes of SIV can be present in a group of pigs)
he said for tx, all you might need is....
might just need some NSAIDs in the water (make sure theyre eating tho, or ulcers)
would you use abx with SIV?
helps with 2* bact infxn
are there SIV vx?
who do you give SIV vx to?
Vaccination prior to farrowing provides colossal antibodies Vaccination of breeding herd protects offspring until 12-16 weeks of age (Maternal antibody inference is a problem.)
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