Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
36 Cards in this Set
- Front
- Back
|
what is the aetiology behind post-weaning multi systemic wasting syndrome? |
Porcine circovirus type 2 |
|
|
Is PMWS in Nz and if so what are the consequences? |
yes, discovered in NI in 2003 and south island in 2005. Initially in north island it did not spread, but caused devastating losses on farm of up to 60% mortality. On entry t SI it spread like a propagating epidemic. |
|
|
What was discovered about PCV2 after discovery of PMWS? |
That PCV2 is actually everywhere and is associated with other pig diseases such as PRDC, Reprofailure PDNS these are called porcine circovirus associated diseases |
|
|
Describe the pathogenesis imuunosuppression of PMWS |
Two major genotypes and many other minor ones, PCV2a used to dominate, now PCV2b. Pig only virus, transmission in semen and direct contact. The virus replicated in macrophages and T lymphocytes so you get huge amounts of virus in the lymphoid tissues, kidney, lungs and liver, Both stimulates and swamps the immune system resulting in immune depletion and effective immunosuppression. |
|
|
What are the clinical signs of PMWS? |
Loss of T and B lymphocytes, infiltration of macrophages and giant cells into organs (liver and kidney) Highly susceptible to secondary infection range of gross pathology 80% have interstitial pneumonia also ulcers, polyserositis, enteritis washing, enlarged lymph nodes, PDNS, dyspnoea, diarrhoea, jaundice, fever, death Almost complete failure of antibiotics |
|
|
How do you diagnose PMWS? |
Clinical signs Interstitial pneumonia Histology of lung, liver, LN, tonsils, kidneys, small intestine, spleen response to vaccination |
|
|
Name the vaccines available for PMWS and requirements |
Circoflex and reslure- single doses to be given 2-4 weeks prior to infection |
|
|
Describe the pathogenesis of PDNS |
PCV2 associated, involves antigen-antibody complexes precipitation out in kidney (causing glomerulonephritis) and causing vasculitis especially in the skin. Results in fever, lethargy ,skin lesions, swollen back legs, enlarged pale kidneys |
|
|
Describe swine dysentery |
Caused by brachyspira hyodysenteriae- a gram negative anaerobe Causes diarrhoea, has mild form of disease in NZ Maintained on farm by clinically normal carriers |
|
|
What special requirements are needed to test for brachyspira hypdysenteria? |
As it can only survive O2 for short periods of time and is a slow grower, it can be quickly outgrown by other anaerobes so need selective inhibitory media |
|
|
Describe the pathogenesis of swine dysentery |
They survive passing through the stomach but effect the large intestine only Replicate to millions per square cm to stimulate and outpouring of mucous Damage epithelium and get into the submucosa Inflammation and oedema of the colon, fibrinous exudate Bleeding from epithelium Create malabsorptive diarrhoea in colon- not toxigenic |
|
|
How can you diagnose swine dysentery? |
By histology of the colon- shows lots of spirochetes attached to colonic mucosa |
|
|
How do you treat swine dysentery? |
Cabadox for weaner, monensin for finishers/growers |
|
|
How can you eradicate swine dysentrery? |
simultaneously medicate the whole herd with a dose adequate to eradicate the carrier state followed by at least two months of a lower dose to prevent reinfection Start rodent control measures at the same time Do in summer when the environmental survival time is shorter |
|
|
What is spirochaetal colitis? |
A milder form of SD caused by brachyspira pilisicoli, carried by ducks so harder to keep out long term |
|
|
How can salmonella present in pigs? |
Generalised septicaemia/pneumonia (dyspnoea, cough depression, cyanosis, fever, death) and enteritis (watery diarrhoea, may have blood) Disease is rare , infection is not - outbreaks occur associated with stress. |
|
|
What do endotoxins cause in salmonella infection? |
inflammation, damage to blood vessels, necrosis of mucosa |
|
|
What PM lesions would you see with salmonella infection? |
petechia in kidneys, enlarged haemorrhage mesenteric lymph nodes, acute interstitial pneumonia, SI inflammation, necrotic colitis |
|
|
How would you treat salmonellosis? |
For acute septicaemia- inject antibiotics For enteric it can usually be controlled by in water or in feed medication |
|
|
What is the main cause of respiratory disease in NZ? |
Bacterial - primary and secondary pathogens interact to cause porcine respiratory disease complex |
|
|
Name the two primary pathogens causing respiratory disease in pigs |
Mycoplasma hyppneumonia: not severe itself but predisposes to enzootic pneumonia and superinfection with Pasteuralla multocida and Bordatella bronchispetica Actinobacillus pleuropneumonia: gram negative encapsulated rod which produces haemolytic and cytotoxic toxins - get acute fibrinohaemorrhagic pneumonia to chronic and necrotising pneumonia with pleurisy |
|
|
Describe enzootic pneumonia in pigs |
Mycoplasma hyopneumonia predisposes by binding cilia, stopping them from working and destroying the mucocilary apparatus preventing ability to clear pathogens When dust and bugs are not cleared by the body, enzootic pneumonia occurs |
|
|
What does enzootic pneumonia look like grossly |
cranioventral lobes consolidated, acute lesions are red and purple, chronic lesions more grey, shrunken and impressed. Dx based on clinical signs and lung lesions |
|
|
What are the clinical signs of enzootic pneumonia? |
dry, non productive cough, poor growth, increased incidence of other disease |
|
|
What sort of disease does actinobacillus pleuropneumonia cause? |
acute fibrinohaemorhhagiv pneumonia and chronic necrosising pneumonia Off feed, soughing ,poor growth, abnormal breathing, pleurisy death Dx on clinical signs and dark red infarcts/pleurisy Treat ASAP with antibiotics at 5 times the label dose! |
|
|
What does pasteurella present as and what disease is it associated with ? |
Causes a puffing pig with a bad moist cough _ is an important risk factor for EP- if you control EP, you will control pasteurella Lung tends to be eve more firm and meaty than just with EP and will have suppurative material on cut surface. |
|
|
Describe the aetiology of erysipelothrix |
A gram positive, non spore forming rod that can grow aerobically and anaerobically Can be found in anything contaminated by infected animals, 50% of pigs carry in their tonsils |
|
|
How does erysipelothrix disease occur? |
When bug invades tonsils or enters wound from contaminated environment Bacteria and septicaemia in 24 hours Vascular damage causes fever and skin infarcts Bug gone from blood 3-5 days later and blood culture is only possible for a short period during bacteraemia it may localise in the joints or heart valves |
|
|
What does chronic erysipelothrix cause? |
arthritis due to invasion of the joints- too late to treat |
|
|
How should you treat erysipolthrix? |
Very responsive to one dose of penicillin but giver 3 days to minimise chronic effects. |
|
|
How can you easily control sarcoptes on a piggery? |
Treat sows with dectomax or ivermectin when they go to the farrowing room |
|
|
Describe the Epidemiology of PRRS |
not in NZ but in around 80% of herds in the states Virus is shed in faeces, urine and saliva for 100 days, shed in semen for 90 days and persists in the tonsils for 160 days regardless Transmission mainly pig to pig, very small infective dose required |
|
|
What are the clinical signs of PRRS? |
Late abortions in third trimester off food, lethargic, fever, dyspnoea, cyanosis, blotches, nervous signs, vomiting, some pigs die, some sows abort Then lots of aboritons , mummies, weak piglets, stillborns Seoncdary infections - PRDC |
|
|
Describe the pathology of PRRS |
Virus enters and replicates in macrophages, peaks in viraemia after 1-2 weeks, highest concentration in lungs and lymph nodes, induces inflammation, kills cells due to bystander apoptosis, causes interstitial pneumonia, non collapsing lungs, grossly enlarged lymph nodes |
|
|
How do you diagnose PRRS? |
Clinical signs , non collapsable lungs and enlarged LNs, definitive diagnosis by lab |
|
|
What is the treatment for PRRS? |
Almost no response to treatment Poor response to vaccine once pigs exposed |
