Sheep Resp Disease - Adults

Question 1

What type of organisms causes Maedi Visna?

Answer 1

Lentivirus - non-oncogenic slow RNA retrovirus

Question 2

How does Maedi Visna initially present? What does it go on to do to the immune system?

Answer 2

• Initial Oro-nasal infection –> slow replicating lymphoid hyperplasia. Mainly affecting monocytes, macrophages & dendritic cells are main target cells.
• MV latent in genome of the monocytes (Trojan horses) so evade host immune system.

Question 3

What are the 3 possible manifestiations of maedia visna?

Answer 3

Up to 3 manifestations of the same condition:

• 1st: Maedi – dyspnoea & heavy lungs 4-5y post infection
• 2nd: Visna – progressive nervous signs 2-3y post infection – dragging back legs (top right pic)
• 3rd: Indurative lymphocytic mastitis

Question 4

How is maedi visna spread?

Answer 4

• SPREAD- Close contact - respiratory spread in aerosol
• Also spread in milk or colostrum of infected ewe, so their lambs are effected
• Some transfer possible via placenta & semen – small importance compared to respiratory and milk spread

Question 5

How can you control maedi visna?

Answer 5

• Easier to prevent infection than to eradicate it, difficult to eradicate as have to test large numbers of sheep and some sheep incubate it that don’t show up on the test
• Buy in MV accredited replacements or isolate & test
• Prevent contact with neighbouring flocks
• Eradication easier if at low level (test & cull)

Question 6

If you have a high level of infection, how can you control maedi visna?

Answer 6

Cull flock & restock with accredited sheep – possibly most cost effective. But accredited sheep are largely pedigrees, so if you want commercial ewes – wont find these accredited mule producers.

2. Try and reduce losses through management:

• keep flock young
• split into older & younger sheep for management as far as possible, so younger sheep are at less risk
• cull thin/suspect cases, or offspring of suspect sheep – reduces spread
• Run a less intensive system to reduce spread

Question 7

Is there a diagnostic test for maedi visna?

What is the problem with it?

Answer 7

• Aim to increase awareness of the disease, using screening tests
• Blood sample 12 thinner/suspect cases/older sheep – probably 12 culls anyway.
• Package price £35 & VAT – expensive and long term commitment to try and get rid of MV in the flock
• NB Make sure you know what you will do if you find it!

Question 8

Is there a vaccine available for Maedi Visna?

Answer 8

Prospect of vaccination is unlikely, this virus evades immune system of flock.

Question 9

What kind of organism causes Ovine Pulmonary Adenocarcinoma?

Answer 9

Jaagsiekte sheep retrovirus (JSRV) - a beta retrovirus

Question 10

How does the disease with Ovine Pulmonary Adenocarcinoma initially present and how does it progress?

Answer 10

•Oronasal infection

–> neoplastic proliferation of Clara cells & type II pneumocytes (within lungs)

–> adenocarcinoma with ++white foaming fluid.

Question 11

What is the incubation for Ovine Pulmonary Adenocarcinoma?

What ages is it seen in most?

Answer 11

Long incubation – seen mainly above 2 years old [possible 2 m - 11 y!]

Question 12

What breed have a predominance of Ovine Pulmonary Adenocarcinoma?

Answer 12

Predominance in Scottish black face, mules and greyface. Low numbers in some breeds such as Suffolk’s – is there genetic effect? Likely there is s genetic predisposition. But also worse in some parts of the country

Question 13

Can you test for Ovine Pulmonary Adenocarcinoma?

Answer 13

• No immune response so no serology possible
• PCR test possible in respiratory system & peripheral blood lymphocytes – But this test has a low sensitivity as virus levels fluctuate & for this reason this test is not commercially available
• Effectively no test in the live animal!! So cannot say what is prevalence of OPA in a flock. One of the best ways is to open them up

Question 14

What is the problem with testing for Ovine Pulmonary Adenocarcinoma?

Answer 14

• Effectively no test in the live animal!! So cannot say what is prevalence of OPA in a flock. One of the best ways is to open them up
• Monitoring very 4 months for 2 years showed presence of virus in individuals very variable – often +ve & then –ve 4 months later. No animals consistently positive and none consistently negative.
• None were consistently +ve & some consistently –ve.
• Only 1 in 20 infected animals actually developed disease.

Question 15

What is the control for Ovine Pulmonary Adenocarcinoma?

Answer 15

• 1. Identify & cull infected & offspring – very difficult without a test.
• 2. Manage in single age groups – keep young separate from adults
• 3. Reduce close contact – try not to house, reduce stocking density, try not to trough feeding as secretions are full with virus. Need good hygiene!
• 4. Snatch lambing & rear artificially – successful in German case study (Voigt)

Question 16

What is Caseous Lymphadenitis caused by?

Answer 16

Cause by Corynebacterium pseudotuberculosis

(bacterium with lipid coat)

Question 17

How long does caseous lymphadenitis survive for?

What is its incubation period?

Answer 17

• Survives for a long time: 8mths in soil, 24h in dip. Difficult to get rid of once in!
• Incubation = 42 days-4mths

Question 18

How does caseous lymphadenitis spread and progress? I.e. what causes the disease?

Answer 18

• Infected wound → Bacteria spreads to draining lymph node → inflammation → micro abscesses → coalescence of abscesses → green pus (bacteria, cellular debris, eosinophils) → caseation of puss → walling off → further multiplication → release of exotoxin → typically caseous abscess with ‘onion ring’ appearance of the abscess
• Exotoxin, Phospholipase D, damages cell membranes & is essential in pathogenesis

Question 19

Can caseous lymphadenitis be sorted with antibiotics?

Answer 19

No

Question 20

How is caseous lymphadenitis spread?

Answer 20

Respiratory spread

Spread at close contact – at Gathering, Clipping, Dipping, Showering – any where they are close togethers

Question 21

What increases the risk of a sheep getting caseous lymphadenitis?

Answer 21

• Longer time spent gathered post-clip/dip/shower
• Showering sheep instead of other treatments
• Gathering into dusty yards under cover
• Older ewes have a higher prevalence than younger ewes
• Ram have higher prevalence than ewes (?management)
• Risk is very low pre-weaning transfer is low, so not so important to snatch lambs at birth
• Submandibular and parotid LNs is where you often see it, large areas of swelling
• The longer time they spend gathered, increased risk of getting it

Question 22

Where is caseous lymphadenitis common in rams?

Answer 22

• CLA common in inguinal & scrotal lymph nodes of rams at breeding soundness exam as they are checked for fertility, but predominantly seen in the LNs around the head and neck
• BUT semen quality was normal & no organism excreted in semen
• 18% of UK terminal sire flocks estimated to be infected 12 yrs ago

Question 23

What is the diagnosis of caseous lymphadenitis?

Answer 23

• Culture of organism – though don’t lance abscesses & encourage spread – reveals organism and cause contamination locally! If already have burst abscess, then swab that and send for culture, but don’t lance an abscess!
• ELISA – detects antibodies to the surface antigen Phospholipidase D (PLD) (Sensitivity 87% & Specificity 98%). From blood sample. Pretty poor sensitivity, so means 13% will be a false negative. But high specificity, if you get a positive, means its likely to definitely be positive!

Question 24

What is vacciantion like for caseous lymphadenitis?

Answer 24

Glanvac (6-in-1; Zoetis) – Australian vaccine - we dont really like it here!! A last resort to use this vaccine accordingto lady on the podcast!

• Can only use in UK under Special Import License (VMD)
• Made up of formalin-killed bacteria & toxoid – not the greatest vaccine, fairly crude
• Flock protection varies from 25%-90% - very variable!
• Needs 2 doses of vaccine a month apart & annual booster
• Maternal Derived Immunity affects lamb immune response up to ~10 weeks old
• Affects any eradication program using serology as not DIVA

Question 25

What kind of vaccine is available for caseous lymphadenitis?

Answer 25

Autogenous vaccine – possible under an Emergency License issued by the VMD. Expensive with varied results.

MOREDUN VACCINE (DIVA) – enriched GM bacterium using IP (up-regulates protein) Needs commercialisation & completion of regulatory requirements → 4+ yrs?

Certainly a DIVA vaccine would be very useful!

• Meanwhile – continue to advise flocks to keep CLA out & restrict spread to minimise impact
• Elimination is possible - Scottish hill flock of 1000 ewes -10% sero+ve in 2007→0.4% sero+ve in 2009 – & no clinical cases still in 2011.
• BUT whole flock blood testing at 3 monthly intervals! This is really not practical in a large sheep flock and very expensive!
• A last resort to start using the Australian vaccine

Question 26

What kind of disease is caused by laryngeal chondritis?

What signs do you see?

Answer 26

• Acute obstructive upper respiratory condition – esp 18-24mth old Texels, Beltex & Southdowns – generally sheep with thick necks!
• Severe dyspnoea with laryngeal stridor as they are breathing - often fatal. Resp distress

Question 27

Is laryngeal chondritis more common in ewes or rams?

What kind of lesions do you see?

Answer 27

• More common in rams than ewes.
• Affected animals stand with mouth open and struggle to breathe.
• Chronic suppurative lesions (generally assoc. with A pyogenes) within arytenoid cartilages. Also E coli & F necrophorum Can also show up

Question 28

What is the aetiology of laryngeal chondritis?

Answer 28

•Unclear aetiology – probably associated with short thick necks & high concentrate feeding for sales. Probably genetic disposition worth bearing in mind.

Question 29

What is the treatment for laryngeal chondritis?

Answer 29

• Consider 20mg Dexamethasone as one off treatment on presentation & a weeks course of antibiotics (suggest amox/clav off licence)
• Emergency tracheostomy often necessary under local infiltration anaesthesia – though this will not be simple as stress will exacerbate condition! Need to get animal on back and makes the situation worse due to the stress. Consider giving iv Dexamethasone 4-6 hours before attempting procedure.
• If you do attempt this surgery, replace tube twice daily initially & then on a daily basis. If obstruction remains after three weeks then surgery to remove necrotic tissue is necessary though prospects poor.
• NB recurrence will probably occur despite treatment in up to 50% of cases – so bear this in mind.
• Treated as individual case. Dusty feeds make it worse.