Chapter 17.

Diseases of the skin and eye

Contagious pustular dermatitis (CPD, Contagious ecthyma, Scabby mouth) | Actinobacillosis |

Squamous cell carcinoma | Photosensitization | Burns | Other skin diseases | Contagious
ophthalmia, Ovine infectious keratoconjunctivitis, (Pinkeye) | Exotic diseases | Recommended
reading

Return to Sheep Health & Production Index

Contagious pustular dermatitis (CPD, Contagious ecthyma, Scabby

mouth)

The disease is caused by a parapoxvirus and is mainly seen in lambs and weaners. Infection
occurs classically on the lips but also occurs on the lower legs and on the oral mucosa.
Lesions in other sites of the body are usually trivial and of no consequence.
The lesions commence with one or more small focal areas of inflammation which develop into
vesicles and pustules then rupture, forming scabs at sites other than the oral mucosa. The
disease normally runs a course of 2 to 3 weeks before resolving completely.
Infection with the virus of CPD requires a break in the epithelium. Trauma to the skin can be
caused by rough feed, thistles or grass seeds. On the legs, lesions occur above the coronary
band, behind the pastern or on the interdigital skin. Infections are often preceded by
persistent wetting that comes from walking through very wet pasture or in flooded paddocks.
The resultant maceration of the skin provides the opportunity for the virus to enter the skin.
Infection of the site of application of ear tags can occur, leading to an enlargement of the hole
and a loss of the eartag[1].
In lambs, lip lesions can infect ewes' teats; the ewes then refuse to allow the lambs to suck.
Mastitis and necrosis of the quarter is an occasional consequence. CPD can also occur on
the scrotum. Rarely (but not in Australia), the virus has caused severe systemic infection with
significant mortality. Occasionally severe forms, but not systemic forms, are seen in Australia.
CPD is seen most commonly in summer months. The virus does not persist on sheep but can
survive for years in the environment. Scabs are a rich source of the virus.

Economic consequences of CPD

The results of infection are generally trivial but at times can be serious. The presence of CPD
lesions on sheep at particular times may lead to management complications such as delays in
shearing or sale of rams. Limb lesions can confuse a diagnosis of benign footrot as well as
causing some lameness.
Weaners with lip and mouth lesions will graze less and lose weight which, at particular times
of the year, may have serious consequences on their survival rates and/or their need for later
supplementation.
The infection has been transmitted rapidly between sheep in 'Sharlea' sheep sheds and
between sheep on ships en route to the Middle-East. The resultant inappetence can lead to
increased mortalities but, more importantly, the presence of lesions on arrival has led to the
refusal of importing countries to accept delivery.
Humans are readily infected but the disease is rarely important.

Vaccination

A commercial vaccine prepared from scab material is available. It is applied with a small,
double-pointed fork which holds a small volume of vaccine suspension and simultaneously
scratches the skin and dispenses the fluid. The usual site for vaccination is the inside of the
thigh and the operation can be done conveniently at lamb marking. It is advisable to examine
the site of inoculation on a number of sheep 3 days after treatment to ensure a successful
'take'. Pustules should be evident along the site.
Immunity after one vaccination or natural infection is strong and remains effective for 2 to 3
years.
The vaccine is prepared from fully virulent virus so is capable of causing the disease.
Consequently, any animals who miss vaccination are likely to develop the disease naturally
from the contamination of the environment caused by infected vaccinates.

Diagnosis

The diagnosis is generally made on clinical grounds but can be confirmed by the
demonstration of virus in lesion material by electron microscopy. Limb lesions can be mis-
diagnosed as strawberry footrot. Severe cases must be differentiated from bluetongue and
sheep pox, both of which have high mortalities, unlike CPD. Dermatophilosis occurs in
woolled skin only; photosensitisation is diffuse through the face and exposed skin. Sheep and
goats rarely contract vesicular stomatitis when exposed.

Treatment

There is no effective treatment. The disease resolves spontaneously after 2 to 3 weeks.

Secondary infection of the limbs of valuable animals may warrant antibiotic treatment.

Actinobacillosis

Actinobacillus lignierisi in sheep affects the skin of the face, lips, nose, lower jaw and lower
part of the neck, rather than the tongue, as it does commonly in cattle[2]. The disease, when it
affects the lips and muzzle is called 'leather lips'[3].

Squamous cell carcinoma

The increased exposure to sunlight of the vulva and bare perineal skin of ewes that have had
a radical Mules operation with a short-docked tail leads to an increased incidence of
carcinoma[4]. The carcinomas develop in ewes as young as 2 years of age and the incidence
increases with age. Affected ewes are susceptible to fly strike and are usually culled or killed
when the lesion is detected. Many affected ewes are in poor condition.
Preventive treatment involves using a modified mules technique, which leaves a V-shaped
piece of wool-growing skin on the proximal third of the dorsum of the tail and amputating the
tail at the third coccygeal joint when tailing.

Photosensitization

Hepatogenous photosensitization follows the accumulation of phylloerythrin that occurs in

animals suffering liver damage caused by toxins associated with plants or plant material.
Facial eczema and tribulosis, both associated with ingestion of sporidesmin, are typical
examples of hepatogenous photosensitization in sheep. Liver damage can also result from
ingestion of Japanese millet, lantana, ragwort (Senecio jacobaeum) and crowfoot (Erodium
cicutarium, E crinitum). An inherited congenital photosensitivity of Corriedale and Southdown
sheep has also been described in which phylloerythrin accumulation follows a defect in bile
excretion.
Primary photosensitization occurs when the sensitising photodynamic agent is ingested
directly. Plants containing such agents include St John's wort (Hypericum perforatum) and
perennial ryegrass (Lolium perenne). The pathogenesis of photosensitization associated with
lucerne and the Brassica spp canola (previously called rape) and kale is unknown.
The areas affected on sheep are the non-woolled areas, particularly the face, ears and tail.
Affected sheep become restless, shake their heads and seek shade. Oedema of the face is
often marked, and in rams, must be differentiated from Clostridium novyi infection (bighead).
Eventually, the skin sloughs leaving a raw area which is slow to heal. The tips of the ears may
also slough.

Burns

Sheep are common victims of bushfires in Australia and often large numbers are killed when
they are trapped in corners of paddocks and are unable to escape downwind. Veterinarians
are often involved in the assessment and management of sheep which survive the immediate
effects of fire. It is recommended[5] that burnt sheep be individually examined as soon as
possible after fires and allocated to groups according to their prognosis for recovery without
extensive treatment.
All sheep should be tipped up and their feet, legs, belly and udder inspected. Severe burns to
the lower leg, including the knee, hock and hooves are the most significant lesions. Severe
burns may not be obvious at first but after two days the skin appears dry, scorched and
leathery. Sheep with respiratory distress usually have a poor prognosis because they are
likely to develop lung abscessation.
Sheep classed as 'likely to survive' should placed in a paddock with soft soil (such as sand),
good feed and easy access to water and shade. Many will be inappetent for five days and
lose condition for two weeks before starting to recover. Burns to the prepuce, scrotum and
teats recover well provided they are not too severe and the passage of urine is unaffected[6].
Semen quality may be affected for up to 6 months following scrotal burns.

Other skin diseases

Distal dry gangrene caused by tall fescue (Festuca arundinacae) occurs but is rare in
Australia.

Contagious ophthalmia, Ovine infectious keratoconjunctivitis, (Pinkeye)

In sheep, pinkeye is associated with infection with Mycoplasma conjunctivae[7]. There are
possibly other infectious agents involved. Spread occurs from infected and carrier sheep by
flies and dust. Weaners are most commonly affected. Infection is characterised by swelling of
the conjunctivae, lacrimation and staining of the face and, in some cases, corneal ulceration.
Once it is established that the signs are not caused by grass seeds, affected mobs of sheep
should be left at pasture without treatment. Yarding exacerbates the condition and increases
transmission. When treatment of individual sheep is desired, antibiotic ointments are
appropriate; macrolide antibiotics, tetracyclines and chloramphenicol all have activity against
mycoplasmas.

Exotic diseases

Capripox infection (Sheep pox and Goat pox)

These two pox viruses are generally host specific although goat pox can infect sheep and
cause severe disease. The viruses do not occur in Australia but occur in North Africa, Middle
East, southern Europe, China and India. Merino and European breeds are very susceptible to
infection and much more so than native African and Middle Eastern breeds.

Epidemiology

Sheep pox is highly contagious. It is spread usually during close contact with infected
animals, through abrasions, inhalation and possibly by arthropod bites. Fomites and areas
contaminated by virus can also provide a source of infection because the virus is very
resistant in the environment. It can survive months in dry scab material and on hair and wool
out of sunlight. Skin lesions are the main source of virus. In endemic areas, the prevalence of
infection is often low for some time with periodic epidemics.

Pathogenesis

Following infection there is a viraemia after about 7 days, peaking at day 10 to 14 and
persisting for a week or two. During this time the virus is distributed widely throughout the
body, including to the skin. The skin lesions are characteristic pox lesions.
Clinical signs

The severe, acute form of the disease occurs in lambs and fully susceptible animals. There is
marked depression and prostration, high fever and ocular and nasal discharges. Affected
animals may die at this time or develop skin lesions on the non-woolled (hairy) areas of skin,
on the nares, in the mouth and on the vulval mucosa within 1 or 2 days. In susceptible
animals the disease is very severe, with a mortality rate of 50% to 100%.
In adult animals of resistant breeds, or partially immune animals, the disease is milder with no
systemic reaction. Skin lesions occur and are often concentrated under the tail. Severe losses
can occur in ewes from acute secondary mastitis if the virus invades the udder. Healing of
skin lesions is slow.

Diagnosis

Bluetongue and CPD also have buccal, nasal or skin lesions but clinical signs differ from
sheep pox. CPD lesions are usually more proliferative in type. Bluetongue lesions also differ
and have a different distribution. Clinical pathology aids diagnosis; using tests for both virus
detection and serology.

Treatment and control

There is no effective treatment. Control in endemic areas is achieved by vaccination.

Psoroptic mange (Sheep scab)

Sheep scab, caused by the mite Psoroptes ovis, was present in australia for over 100 years
until its eradication in 1896. It has been eradicated from a number of other countries but is still
present in the UK, continental Europe, Africa, Middle East, Asia, Central and South America.
The disease induces severe wool damage and causes sheep to lose much condition and
some sheep to die as a consequence of infestation.

Epidemiology

The mites complete all stages of their life cycle on the sheep although adult mites can survive
off sheep for 2 to 3 weeks. They have a short life-cycle (11 - 12 days) and can increase in
population very rapidly. They increase in autumn and winter and tend to regress in summer to
sub-clinical infections in protected body areas such as the groin, scrotum and interdigital
fossa. Spread occurs by close contact between sheep but fomites and infested premises can
be responsible for new infestations.

Clinical signs

The skin-puncturing habits of the mites cause intense irritation of the skin. Initially the lesions
are small papules, oozing serum, often noticed first on the sides of the sheep. The wool is
pulled and chewed by the sheep in response to the irritation. The lesions increase in size and
coalesce and become covered in a thin yellow scab, often bleeding from the sheep's rubbing
and biting. The wool over infected areas may contain large amounts of this scab material and
is severely matted. Parts of the fleece are shed completely and severely affected sheep
become very thin.

Diagnosis

Severe cases resemble dermatophilosis but the pruritus is more marked. Scrapie and
infestations with lice or itchmite cause pruritus but have no visible skin lesions. Definitive
diagnosis is made by demonstrating the mites in scrapings from the edge of lesions and from
scabs collected from the base of wool fibres.

Treatment and control

Treatment is carried out by prolonged dipping (2 minutes or more) in acaricide solution,

repeated after 10 to 12 days if necessary, depending on the chemical used. Regional control
programs require the planned treatment of all flocks in one area.

Recommended reading

Radostits OM, Blood DC and Gay CC (1994) Contagious ecthyma In Veterinary Medicine VIII
edition, Bailliere Tindall, p 1125
Beveridge WIB (1981) Contagious pustular dermatitis In Viral Diseases of Farm Livestock,
Australian Agricultural Health and Quarantine Service/Australian Government Publishing
Service, Canberra (Animal Health in Australia vol 1) p 52

[1] Allworth MB, Hughes KL and Studdert MJ (1987) Contagious pustular dermatitis (orf) of
sheep affecting the ear following ear tagging Aust Vet J 64 p 61
[2] Beveridge WIB (1983) Infection with Actinobacillus lignierisi In Bacterial Diseases of
Cattle, Sheep and Goats, Australian Bureau of Animal Health/Australian Government
Publishing Service, Canberra (Animal Health in Australia vol 4) p 4
[3] Brightling A (1988) Sheep diseases, Inkata Press Pty Ltd, Melbourne & Sydney, p 75
[4] Vandergraaff R (1976) Squamous-cell carcinoma of the vulva in Merino sheep Aust Vet J
52 p 21
[5] Coghill K Saving burnt livestock Department of Agriculture, Victoria, Agdex 400/29
[6] Brightling A (1988) Burns In Sheep Diseases Inkata Press, Melbourne & Sydney
[7] Surman PG (1973) Mycoplasma aetiology of keratoconjunctivitis ("Pink-eye") in domestic
ruminants Aust J Expl Biol & Med Sci 51 p 589