UNIVERSITY OF SURREY

FARM ANIMAL PATHOLOGY AND DISEASE SURVEILLANCE SERVICE

WINTER 2018/19 NEWSLETTER Welcome to the latest newsletter from the Veterinary Pathology Centre (VPC) at the

University of Surrey.

You will find below, a link to the recently published UKSF’s update on the approach to animal

health surveillance, a few reminders, information on related forthcoming events being held at

the vet school and details of the interesting cases that we have seen over the last few

months.

The UKSFs approach to animal health surveillance: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/771423/uksf-animal-surveillance-approach.pdf Quick, but important, reminders:

Abortion season – Each year sheep abortions comprise a large proportion of sheep

investigations. The most common causes of abortion are enzootic abortion, toxoplasma and

campylobacter. In December, the Small Ruminant Species expert Group published an article in

the Veterinary Record as an update on sheep abortions

https://veterinaryrecord.bmj.com/content/183/17/528. This included guidance on sample

selection for investigation of the cause of abortion.

If wishing to submit sheep abortion material, the cost of the ‘free’ carcase collection needs to

be considered during the triage discussion with the PVS. APHA, in the first instance,

encourage the PVS to sample foetuses of a sheep abortion on the farm. The triage discussions

should include known previous history of abortion on the holding, has there been a previous

diagnosis made on the farm and have appropriate preventive measures been taken.

The sample selection guide may be helpful to assist the PVS in achieving a diagnosis of the

common causes of abortion. However if a diagnosis has not been achieved through PVS

sampling and abortions continue or if ewes are sick then it is reasonable to offer free carcase

collection for further investigation as this would be of surveillance value.

The importance of fresh submissions:

We have a 48 hour window in place to help ensure the quality of the post-mortem

examination, thereby giving you and your clients the greatest value for money. If severely

autolysed (48+ hours), gross lesions are often difficult to identify and further testing (e.g.

histology and bacteriology) may give inconclusive results at best. Please encourage your

clients to keep the carcass cool, away from scavengers AND CALL TO SUBMIT AS SOON AS

POSSIBLE.

Ear tag numbers save time:

Please have the ear tag number(s) ready as they will be needed by the pathology centre

receptionist when calling, as it is important to correctly identify the carcass on arrival.

Batch submissions:

We offer a reduced rate for batch submissions (where multiple casualties occur as part of the

same disease event) - please see our website for more details.

APHA collection service link:

To check if you are in an area where free collection is available, follow this link:

http://apha.defra.gov.uk/postcode/pme.asp

For more information, please visit: http://www.surreyvetpathology.com/pathology-

services/surveillance-services and look at the Surveillance Post-mortem examination prices.

Please do not hesitate to contact us if you would like to provide feedback or have any questions

about using our service. It is important that the responsible veterinary surgeon calls us to

discuss a case before submission, to ensure that it is eligible for a surveillance post-mortem

examination. Eligible cases are heavily subsidised by the APHA and do not incur additional

fees for routine diagnostic tests.

We look forward to working with you all.

EVENTS:

20th Nov 2019: National Sheep Association Conference

Details to follow.

Dr Pernille Jorgensen, CandVetMed MRCVS.

Surveillance Lead

Farm Animal Pathology and Disease Surveillance Officer

INTERESTING CASES:

Cattle:

Copper poisoning

Figure 1a+b: Multiple necrotic/haemorrhagic foci on surface of liver and in the parenchyma.

An eight-month-old castrated Simmental cross presented with sudden death, bloody exudate from the

nose, and was subsequently submitted for post-mortem examination. The animal was housed indoors

with 15 other calves, which were bought onto the farm at two weeks of age. The group was fed with

grass/maize silage and hard feed until three weeks prior, when they were switched to maize silage.

The calf was in good condition. Gross findings at post-mortem examination consisted of widespread

subcutaneous haemorrhage and oedema of the, neck, shoulder and thoracic areas, in addition to the

presence of multiple necrotic / haemorrhagic foci on the liver surface and in the parenchyma, which

felt fibrotic on palpation (Figure 1a+b). The mucosa of the pharynx and trachea was congested and

oedematous, and a bloat line was evident in the oesophagus.

Histopathological examination of the liver confirmed severe massive hepatic necrosis, a condition

which can be a result of acute hepatotoxicity or a hypoxic injury. Fresh kidney and liver tissue was

submitted for copper analysis, and a high kidney copper concentration of 6710 μmol/kg DM was

confirmed and found to be consistent with a diagnosis of clinical copper toxicity (ref. interval 141 - 314

μmol/kg DM). The copper concentration in the liver was also above the reference interval. The

histopathological examination also found evidence of more chronic liver damage, which may have

predisposed the condition by increasing the organs avidity for copper. Bacteriological culture of liver

tissue resulted in heavy pure isolation of non-haemolytic Escherichia coli, a lack of inflammatory

response in the liver suggests this was secondary and terminal to the liver damage itself.

Traumatic reticulo-peritonitis

A five-year old suckler cow was lethargic and recumbent in the field 24 hours prior to death. Gross findings consisted of severe subcutaneous oedema of the brisket and marked oedema of the mesocolon, in addition to ascites fluid within the abdominal cavity. Strong adhesions were present between the diaphragm and forestomachs and between the thoracic walls and the lungs and pericardium. The pericardial sac was markedly thickened and contained a large amount of foul smelling, watery, turbid exudate. Copious amounts of purulent material was attached to the epicardium and the inner layer of the pericardium (Figure 2a). No foreign body was identified within the epicardium or reticulum, however a bolus present in the lumen of the reticulum, had a two cm thin, sharp piece of metal attached to it (Figure 2b), which bore evidence that the animal had previously ingested sharp metal shards. The adhesions present between the forestomachs and

diaphragm further supports a pathogenesis which involves trauma to this area. A gross diagnosis of traumatic reticulo-peritonitis (hardware disease) was made.

Figure 2b: Sharp piece of metal found

attached to a broken bolus within the

reticulum.

Figure 2a: Pericardial sac opened and displaying a thick layer of purulent material.

Small ruminants

Visceral form of caseous lymphadenitis

An adult breeding ram with clinical symptoms of wasting and diarrhoea was euthanised and submitted for post-mortem examination. Two other rams with similar symptoms had died within a few weeks. Caseous lymphadenitis (CLA) was suspected on gross examination, and later confirmed by bacterial isolation of Corynebacterium pseudotuberculosis in pure culture from an internal abscess. The ram showed evidence of the visceral form of the disease with abscess-formation within the lungs, lymph nodes and right testicle (Figure 3b), which can readily explain the poor body condition of the animal (Figure 3a). Evidence of parasitic gastroenteritis indicated by a large number of worms discovered within the abomasum and small intestines, and a high faecal egg count of 11.650 EPG, may also have contributed to the dramatic weight loss. A large subcutaneous abscess located over the sternum may have provided entry of Corynebacterium pseudotuberculosis with subsequently systemic spread of the bacterium. No superficial lymph nodes were affected, hence a concurrent diagnosis of the more classical cutaneous form of CLA is unlikely. Corynebacterium pseudotuberculosis is highly contagious and difficult to control with antibiotics due to the abscess formation. There are no licensed vaccines to control CLA available in the UK, however the production of autogenous vaccines and importation of commercial vaccines is possible in affected flocks, although this requires a license from the Veterinary Medicines Directorate VMD. Control measures include the use of serology-testing within flocks and as part of a pre-purchase screening to identify infected animals and stop spread of the disease.

Figure 3a: Ram with poor body condition. Figure 3b: Abscess-formation within the right testicle.

Pigs

Leptospirosis outbreak

An outbreak of leptospirosis was diagnosed following submission of three jaundiced pigs for post-mortem examination (Figure 4a). Twenty, six to eight-week-old pigs died within a few days from a group of 100 growers. Post-mortem findings were variable apart from the marked yellow discolouration of the skin, mucus membranes and internal organs, and consisted of haemorrhage within the gastrointestinal tract (Figure 4b) and the renal medulla (Figure 4c). Acute leptospirosis was confirmed as the primary disease by PCR on kidneys, with concurrent infections of salmonellosis (presumptive Salmonella Typhimurium) and porcine intestinal spirochaetosis likely contributing to the severity of disease on farm. Involvement of a rodent-associated serovar of leptospires, such as L. icterohaemorrhagiae is considered likely, as rats had been seen on farm, however serology will be necessary for identification. As all serovars are potentially zoonotic, advice was given regarding avoiding zoonotic infection and controlling disease in the pigs, in particular, recommending rodent control and improved hygiene. Other causes of jaundice in pigs includes coal tar poisoning, which is the second most common cause of toxicity incidents in pigs diagnosed by the APHA over the last decade. Environmental exposure to possible toxins was high on the initial differential list of disease, as only one group of pigs on the farm were affected, which indicate a localised source. A VIO farm visit reported that toxicity was unlikely, and that the pigs in the group did not have access to sources of coal tar. The gross and histopathological findings in the pigs were also not suggestive of coal tar poisoning.

Figure 4a: Generalised jaundice of the carcass.

4c: Haemorrhage of the renal medulla.

Figure 4b: Large blood clot within the stomach.

Poultry

Lead poisoning in ducks

An 18 month-old female White-faced whistling duck with clinical signs of lethargy the day prior to death was submitted for post-mortem examination. Gross findings consisted of dark discolouration of the gizzard mucosa, which appeared thickened (Figure 6a+b) and the presence of a small, round, dark, hard object resembling a gunshot pellet or small fishing weight within the oesophageal lumen. A lead concentration of 11.70 mg/kg FT was measured in the kidney of the female duck, which exceeds the VIDA threshold of 50 μmol/kg DM and thereby confirms a diagnosis of lead poisoning. The kidney lead level result was well above the food safety cut off point of 0.5 mg/kg FT, hence caution was advised if consumption of the meat or eggs of the ducks in the flock was intended. The source of lead in this instance was likely to be the suspected shotgun pellet found in the oesophagus, hence advice was given to not use lead shot close to water.

Figure 5a+b: Thickening and

discolouration of the coilin layer and

mucosa of the gizzard.

Northern fowl mite

The northern fowl mite (Ornithonyssus sylviarum) was identified in two different submissions of backyard poultry. The clinical history and gross findings in the cases varied greatly. A one-year-old chicken was one of twenty birds in a flock which showed symptoms of diffuse scaling and thickening of the skin of the head and neck (Figure 6), a condition diagnosed as moderate/severe, chronic dermatitis by histopathological examination. A parasitic cause was suggested due to the presence of eosinophils within the lesions. A few mites which were later identified as the northern fowl mite by direct ectoparasitic microscopy was found on the carcass. A multifactorial cause was

suspected, due to the distribution of the lesions, which is unusual for the northern fowl mite, which tend to congregate near the vent and back area. A secondary bacterial infection may be present in this case, as bacteria were identified to be adherent to the epidermis by histopathological examination. Other parasites which were thought to possibly be involved included Knemidocoptes gallinae, a mite related to Knemidocoptes mutans (the scaly leg mite), which tends to affect the head and neck, and is not uncommon in backyard poultry. The other/second submission included the third bird in a small group of backyard chickens with clinical signs of stargazing and recumbency prior to death. An uncountable number of ectoparasites was seen to be crawling amongst the feathers of the bird on external examination, and the skin around the vent and legs was dark and discoloured. Ectoparasitic examination identified the mites as being Ornithonyssus sylviarum. Bacterial cultures yielded non-haemolytic E. coli in purity from heart, blood and liver, suggesting a terminal coli-septicaemia. The northern fowl mite spends its entire life cycle, which can be as short as five to seven days in ideal conditions, on the chicken. The mite feeds on blood from the bird, which can result in severe anaemia, and also make the bird more susceptible to other parasites and diseases. The mite is common on wild birds and rodents, which act as vectors, hence good biosecurity is important to prevent introduction into a flock.

Figure 6: Diffuse scaling and thickening of the skin of the head

and neck.

FARM ANIMAL PATHOLOGY AND DISEASE SURVEILLANCE TEAM

VPC Director:

Prof. Roberto La Ragione

Pathologists:

Dr. Alex Stoll

Dr Ladislav Novotny

Veterinary Investigation Officers:

Dr. Pernille Jorgensen (Service Lead)

Dr. David Harwood

Pathology Dept. Veterinary Surgeons:

Dr Benedetta Amato

Dr Carlos Gonzalez de Cara

Named Veterinary Surgeon and Pathology Rotations Coordinator: Dr. Anna Slaviero

Epidemiologists/Consultants:

Prof. Alex Cook

Pete Sewell

Surveillance Project Manager: Julia Gerhold

VPC Administrator: Louise Ryan

Receptionists: Sue Grover-Smith

Technical Services Manager: Jon Cooper

Post-mortem Facilities Manager: Tom Hussey

Technical Staff: Kat Gowan, Emily Tubb, Mike Chaplin,

Keith Hiley, Alice Robinson, Nic Scorovich

Pathology Laboratory Manager: Abbe Martyn

Histology Technical Staff: Lucia Lozano White, Katy

Walker, Ella May

Business Development Manager: Rachel Hargreaves

SURREY VETERINARY PATHOLOGY CENTRE

Surrey Veterinary Pathology Centre (left) and the main post-mortem room (right)

HOW TO FIND US

If using a Sat Nav, please follow postcode: GU2 7YW and do NOT turn left at the traffic lights

after leaving the A3

http://www.surreyvetpathology.com