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36 Cards in this Set

  • Front
  • Back

(SA) What 2 major diseases are caused by Porcine Circovirus II?

1- Post-Weaning Multisystemic Wasting Syndrom (PMWS)


2- Porcine Dermatitis & Nephropathy Syndrome (PDNS)

(LA) Make a diagnostic pathway for Post-weaning Multisystemic Wasting Syndrome (PMWS)?

History


- Sudden outbreaks of disease with up to 60% mortality


Clinical signs


- Lethargy, weight loss, enlarged LNs, Dyspnoea, Diarrhoea, jaundive, fever and death


- You also see immunosuppression - so secondary infections very common


Gross pathology


- 80% show non colapsable lungs (interstitial pneumonia)


- Ulcers are common


- Polyserositis


- Enteritis


Further diagnostic tests


- histology (lungs, liver, lymph nodes, kidney, small intestine, spleen or tonsils)

(SA) Whats the difference between PMWS & PDNS?

Both are caused by porcine circovirus type II. Post-weaning multisystemic disease is a generic wasting disease that occurs sporadically and in outbreaks. The virus replicates in macrophages and T lymphocytes so is immunosuppressive. Porcine dermatitis & nephropathy syndrome involves a hypersensitivity component. Lots of circulating virus is bound by antigen, these complexes can then be filtered out by kidneys (causing glomerulonephritis) or stuck in capillaries of the skin (causing vasculitis and dermatitis). Both these diseases can occur concurrently in the same animal.

(SA) Briefly explain the general pathogenesis and list the various manifestations of Vitamin E deficiency

Vitamin E is an antioxidant and therefore its depletion leads to excessive oxidative damage caused by free radicals.


Can cause


- Mulberry heart disease (sudden death)


- Muscular dystrophy


- Hepatosis Dietetica (death of hepatocytes)


- Gastric Ulcers

(SA) List some differentials for gastrointestinal disease in pigs

• Swine dysentery


• Spirochaetal colitis


• Dietary colitis


• Salmonellosis


• Proliferative enteropathy


• Haemorrhagic bowel syndrome


• Gastric ulceration


• Rectal stricture


• Worms

(SA) Describe the prevalence and transmission of Swine Dysentery (SD)

- Not all herds are infected with it


- It's thought that NZ has a milder form of the disease


- Faecal-oral transmission from clinically infected or carrier pigs


- Can be transmitted by other animals including dogs, rodents, & flies


- Resistant organism and can survive in effluent ponds, work equipment and gumboots etc

(LA) Design a treatment and eradication program for a piggery suffering from an outbreak of Swine Dysentery

Treatment


In-feed, In-water antibiotics


- Weaners = Carbadox(Mecadox-plus)- 50g/T (1k/T)


- Growers/finishers = Monensin, off-label is first choice – 0.5-1 kg/T


Prevention


- Minimise stressors e.g. decrease stocking rate


Eradication


- Depopulate


- Eliminate carriers. This is done by high done antibiotics to eliminate the carrier state. You don't know which ones are carriers so have to medicate whole herd


- Control rodents, dogs, flies


- Improve hygiene



(MC) What are some differentials for Swine Dysentery? (select all that apply)


A- Spirochaetal Colitis


B- PRRS


C- Trichuris Suis


D- Salmonella


E- PMWS

A, C, D

(SA) List some differences between Swine Dysentery and Spirochaetal Colitis

- Ducks are carriers of spirochaetal colitis, not SD


- Spirochaetal colitis is like a milder form of swine dysentery


- Spirochaetal colitis tends to affect pigs earlier than SD

(SA) Describe the 3 presentations of Salmonellosis in pigs

1- Septicaemia: more common in young pigs. Clinical signs include dyspnoea, depression, cough, ear tip necrosis, cyanosis, fever and death


2- Acute enteric form: Produces yellow, watery diarrhoea +/- blood.


3- Chronic enteric form: Produces emaciated pigs with persistent diarrhoea. May progress to rectal strictures.

(LA) You encounter a piggery with a suspected Salmonellosis outbreak. How would you diagnose it? How would you treat it? What preventative measures could you put in place?

Diagnosis


Always suspect Salmonellosis in scouring pigs. Especially if there's cyanosis and necrotic material in faeces. Do a post-mortem and you will see some of the following: acute interstitial pneumonia, enlarged haemorrhagic mesenteric LNs, Enlarged nodular liver, enteritis, GIT ulcers and petechial haemorrhages on kidneys (in septicaemic form). Culture faecal samples (enteric form) or lungs/liver/spleen (septicaemic form) to confirm Salmonellosis.


Treatment


Acute septicaemic ones must be injected with antibiotics


Enteric ones can have in-feed antibiotics


Prevention


Minimise stress, good hygiene, keep pens clean. Adopt an 'all-in, all-out' management system - bit extreme really.

(MC) What clinical signs can Brucella Suis cause? (check all that apply)


A- Orchitis/epididymitis


B- Pneumonia


C- Infertility


D- Diarrhoea


E- Abortion


F- Urinary Tract Infection

A, C, E

(SA) What is the pathogenesis of African Swine Fever?

o Large DNA virus, stable in environmento Replicates in monocytes and macrophages of LNso Viraemia occurs at ~4 day post-infectionfollowed by replication at secondary sites (LNs. Spleen, bone marrow, lungs,liver, kidneys where it replicates in monocytes and macrophages and endothelialcells)o This results in phagocytosis of infectedendothelial cells → this increases vascular permeability → haemorrhageo Also causes lymphopenia, thrombocytopaenia andDICo Alveolar oedema is what will kill them.

(SA) What clinical signs would you see with African Swine Fever?

o Pregnant sows will aborto Fever (>40°C)


o Haemorrhages in skin, may bleed from nose and intestine (Melaena)


o Enlarged lymph nodes


o Dyspnoea, nasal froth, vomiting


o Lots of sick, dying pigs + sudden deaths - up to 100% mortality

(SA) Describe the epidemiology of PRRS (Porcine Reproductive & Respiratory Syndrome)

The disease arose in the 80's. There are two major lineages of the virus, one arising from Europe, the other in the USA. It's exotic to NZ but apparently we are bound to get it (-_-). It has been eradicated from Sweden, South Africa and Chile. 80% of herds in the USA are affected. The small ssRNA virus spreads rapidly and is very genetically diverse with new mutants arising all the time. The virus doesn't survive well in the environment but is can survive in frozen pig products. It is pH sensitive.


The virus is shed in faeces, urine and saliva after 100 days but it is shed in semen after only 90 days. It is transmitted mainly via pig-pig contact but can also be transmitted via semen (AI), pig meat, parenteral exposure (processing equipment, shared needles, bites, scratches), on fomites, insect vectors, in the air (risk depends on proximity etc).

(LA) Describe how PRRS might become established in NZ and how we might go about controlling it

Getting to NZ


Pig meat containing the virus must enter the country. Then the infected pig meat must be fed to a pig (virus must still be viable, this is most likely to occur in backyard piggeries where the owners feed the pigs food scrape - naughty). Once PRRS has established in that herd. It can easily spread to other herds via vets, selling of infected pigmeat (and that getting feed to some more pigs), or in the air to close by pigs.


Eradication and Control


No treatment. Total depopulation or Partial depopulation (requires immune sows).


Close herd for 200 days (no live animal inputs).


Test and removal


Initiate staunch biosecurity e.g. serological testing, sentinel pigs, air filtration

(LA) How would you diagnose a case of PRRS in NZ?

History


Backyard piggery feeding food scrapes. Doesnt vaccinate them and their reproductive performance is not very good. In a naive herd (so every herd in NZ), the whole herd will be affected.


Clinical Signs


Severity of signs will depend on strain. Largely reproductive and respiratory signs.


- Over the first 2-3 weeks post-infection


Anorexic, lethargic, fever, dyspnoea, cyanosis, blotchy skin, nervous signs, vomiting, deaths and some sows abort


- Over the next 3-4 months


Lots more sows abort, mummies, stillbirths, weak piglets born, high pre-weaning mortality and mortality remains high in grower herd


- After 4 months


Clinical signs start to decrease


Pathology


- Highest concentration of lungs and lymph nodes (virus isolation maybe a good idea)


- Interstitial pneumonia (non-collapsible lungs) and enlarged LNs


Diagnostic test


- First you call MAF and they will handle it yo


- But lab does PCR, ELISA, IHC, virus isolation etc

(MC) Which of the following statements about PRRS immunity is FALSE?


A- Sterilising immunity can be achieved after 200 days


B- Immunity is largely strain specific


C- Immunity is slow to develop


D- Complete immunity is never achieved, can only decrease duration and severity of disease


E- Modified live vaccines are the only kind of vaccine to provide meaningful immunity

D

(SA) What age groups of commercial pigs are affected most by Suid Herpesvirus 1 and what clinical signs can affected pigs show?

• Clinical signs vary with pig age and immunity• Very high (100%) mortality in suckers and weaners, high (~50%) mortality in growers, up to 10% mortalities in older pigs• Fever, loss of appetite, nervous signs, sneezing, coughing, laboured breathing• Effect on sows depends on stage of gestation o Abortions, mummies, SB, non-viable piglets

Which of the following statements about Foot & Mouth Disease is true?


A- Pigs feed food scrapes are no more at risk than pigs that aren't


B- Pigs are considered reservoir hosts


C- Can be transmitted via pig milk


D- It's not very contagious


E- It causes pruritus

C

(SA) List the clinical signs of a pig affected by foot and mouth disease

o Lamenesso Depressiono Fevero Abortionso Dribblingo Chompingo Vesicles/blisters and erosions on hoof walls

(SA) List other potential differentials for foot and mouth

o Vesicular Stomatitis (VD)o Swine Vesicular disease (SVD)o Vesicular Exanthema (VE) o Seneca Valley Virus (SV)o Parsnips

(SA) Name 1 coronavirus that affects pigs

• SARS – affects pigs, cows, horses, cats, dogs and humans

• Pig specific viruses


o Porcine Respiratory Coronavirus (PRCV)o Porcine Epidemic Diarrhoea Virus (PEDV)o Transmissible gastroenteritis virus (TGEV)o Haemagglutinating encephalomyelitis virus (HEV)o Toroviruses

(MC) What is TGE?


A- Transmissible Granulomatous Encephalopathy


B- Traditional Granulomatous Enteritis


C- Transmissible Gastroenteritis


D- Triglyceride Excess


E- Total Gay Expert

C

(SA) How can you eradicate TGE?

Maximise exposure and close herd - allows time for immunity to develop (it takes 3 months for good immunity to develop)

(SA) How might you maximise exposure to Porcine Epidemic Diarrhoea Virus to build up immunity?

o Feed blended intestines of affected stock to all sowso Monitor sows for diarrhoea, redoes any that don’t scouro Can shorten outbreak to 8 weeks rather than 4 months

T/F -Porcine Epidemic Diarrhoea Virus and Transmissible Gastoenteritis cause indistinguishable disease (well the lab can distinguish it)

True

(SA) Describe the pathogenesis of Japanese Encephalitis

o Virus replicates in skin and local LN before disseminatingo It can reach the CNS within 3 days of infectiono Can cross placenta and invade foetuso Leads to abortions, SMEDI, weak piglets is infections occurs before day 70 of pregnancy

(SA) Describe the Pathogenesis of Classical Swine Fever

 Within 6 days of infection, it is throughout the pig Replicates in macrophages and monocytes and vascular endothelial cells Immunosuppressive with depletion of lymphocytes – delay in immune response Inflammation of endothelial cells and thrombocytopaenia LNs swollen and haemorrhagic

(SA) Why is Sarcoptic Mange a problem for pigs?

Negative effect on pig production: increased FCR, decreased growth rates and increased post-weaning mortality - lost moneys


Welfare issue - irritation



(LA) Describe a diagnostic pathway for diagnosing Sarcoptic Mange in pigs



You mostly see sarcoptic mange in backyard piggeries.


You'll see skin lesions due to irritation in affected animals (reddened skin and crusts - see thickened skin in chronic cases), lesions evident in ear.


Diagnose with treatment trial as its easy to treat, or skin scrape from behind ear



(SA) Describe a treatment plan for Sarcoptic Mange

• Treat sows pre-farrowingo This will ensure the piglets don’t get infectedo Mange-free piglets can be weanedo Weaned piglets stay mange-free if they have no direct contact with other infected weaners (or infected growers)o Transfer mange-free pigs to grower-finishero Weekly batches of grower-finisher pigs remain mange-free provided no direct contact with other infected grower-finisher pigs• Treat witho Dectomax (35d WHP) – injection One shot should cure pigs (treat every pig to eradicate from farm) Assuming all pigs were treated correctly But should inject pigs twice, just in case some were missed/underdosedo Ivomec (28d WHP) – injectiono In feed compounded Ivermectin for 7+ days (0.1mg/kg)

(SA) How does ringworm present in pigs?

You see a big greasy patch on the skin as opposed to a 'ring'. It's non-pruritic. More than one pig is usually affected. Does not always spontaneously resolve in adult pigs.

(MC) What is the main differential of Ringworm in pigs?


A- PDNS


B- Pityriasis Rosea


C- Sarcoptic mange


D- Fleas


E- Suid Herpesvirus 1

B

(SC) What are some clinical signs of fleas?

o Can see fleas on sowso Lots of bites over uddero Sows will sleep away from straw (bad forpiglets)o Sows spend a lot of time in wallows

(MC) What is the major species of lice that affects pigs in NZ?


A- Linognathus Suis


B- Trichodectes Suis


C- Haematopinus Suis


D- Bovicola Bovis


E- Linognathus Vituli

C