Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


contagious ecthyma



contagious ecthyma


  • Last modified
  • 11 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • contagious ecthyma
  • Pathogens
  • Orf virus
  • Overview
  • Contagious pustular dermatitis (CPD) is a worldwide zoonotic viral disease of sheep and goats. It has been recognized for centuries in sheep-keeping areas of the world. In many areas the infection is called ‘orf’, a w...

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Orf lesions on a sheep.
TitleOrf. Symptoms.
CaptionOrf lesions on a sheep.
CopyrightR. Paul Kitching
Orf lesions on a sheep.
Orf. Symptoms.Orf lesions on a sheep.R. Paul Kitching
Contagious ecthyma infection in foot of sheep. Separation at coronary band arrowed.
CaptionContagious ecthyma infection in foot of sheep. Separation at coronary band arrowed.
CopyrightJohn R. Egerton
Contagious ecthyma infection in foot of sheep. Separation at coronary band arrowed.
SymptomsContagious ecthyma infection in foot of sheep. Separation at coronary band arrowed.John R. Egerton


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Preferred Scientific Name

  • contagious ecthyma

International Common Names

  • English: contagious ecthyma of sheep and goats; contagious pustular dermatitis; orf; orf, contagious viral pustular dermatitis, ecthyma, in sheep and goats; orf, contagious viral pustular dermatitis, ecthyma, parapoxvirus, in sheep and goats; ovine ulcerative dermatosis, lip and leg ulceration; scabby mouth; sore mouth; strawberry footrot; ulcerative dermatosis; viral dermatitis of goats - exotic

English acronym

  • CE
  • CPD


Top of page Orf virus


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Contagious pustular dermatitis (CPD) is a worldwide zoonotic viral disease of sheep and goats. It has been recognized for centuries in sheep-keeping areas of the world. In many areas the infection is called ‘orf’, a word that derives from the Old English word ‘herof’ meaning scab.

Contagious pustular dermatitis is a common disease in sheep and most sheep farmers recognise the disease by its clinical presentation. The disease is known by many names, including contagious pustular dermatitis (Glover, 1928), contagious ecthyma of sheep (Boughton and Hardy, 1934), soremuzzle (Hardy and Price, 1952) and scabby mouth (Gardiner et al., 1967). Although CPD is usually considered of limited impact, because infection is so widespread and adventitious bacterial infections are common sequelae it can be a cause of major production and welfare losses. Occasionally the effects of outbreaks of CPD or strawberry footrot (a mixed infection with the bacterium Dermatophilus congolensis, in which Orf virus acts as the initiating infection) in a single flock may result in significant economic losses through high morbidity and not insignificant mortality.

Host Animals

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Animal nameContextLife stageSystem
Camelus dromedarius (dromedary camel)Domesticated host
Capra hircus (goats)Domesticated host, Experimental settingsSheep & Goats: All Stages
Lama glama (llamas)Domesticated host
Lama pacos (alpacas)Domesticated host
Mus musculus (house mouse)Experimental settings
Oryctolagus cuniculus (rabbits)Experimental settings
Ovis aries (sheep)Domesticated host, Experimental settings, Wild hostSheep & Goats: All Stages
Rangifer tarandus (reindeer)Domesticated host

Hosts/Species Affected

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Orf virus (Contagious pustular dermatitis virus) naturally infects only sheep, goats, reindeer (Hautaniemi et al., 2010) and people (Haig and Mercer, 1998). Wilkinson (1970) reported a case of CPD in hunting hounds fed potentially infected sheep, although the virus was not recovered from the lesions. Recently, CPD infection in cats has been reported, but with the suggestion that the three cats involved may have had an underlying immune deficiency. This, however, was not investigated further (Fairley et al., 2008).

Infection of other species has been attempted experimentally, usually with negative results. Blanc (1922) inoculated, by scarification, a goat strain of virus into the skin of dogs, guinea pigs, pigeons, rabbits and Macaque monkeys. Lesions typical of CPD were produced only in the monkeys. Other workers have shown that inoculation of Orf virus into dogs does not result in a delayed-type hypersensitivity reaction as in susceptible species, although a humoral response was demonstrated (Buttner et al., 1995). Successful experimental infections of rabbits and mice with Orf virus have been demonstrated recently (Cargnelutti et al., 2011), but the lesions were relatively mild and resolved in less than two weeks. It remains the fact, however, that dogs, cats, guinea pigs, pigeons, macaques, rabbits and mice are not considered natural hosts for the Orf virus, but under exceptional circumstances may be infected.

Systems Affected

Top of page bone, foot diseases and lameness in small ruminants
mammary gland diseases of small ruminants
skin and ocular diseases of small ruminants


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CPD is reported wherever sheep are kept.

In Western Australia, cross-sectional studies have reported that CPD was present in at least a quarter of randomly selected sheep farms supplying lambs for export (Higgs et al., 1996). Similarly, in Canada a questionnaire study also reported CPD on 24% of sheep farms (Dohoo et al., 1985).

In a survey conducted in 1995, of farmers involved in a study of zoonotic diseases in England and Wales, CPD was reported in almost half of flocks (Paiba, 1995). The high prevalence in the UK may be due to the high stocking density used on many farms and the temperate prevailing weather conditions.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


AzerbaijanNo information availableOIE Handistatus, 2005
BahrainDisease never reportedOIE Handistatus, 2005
BangladeshDisease never reportedNooruddin and Barik, 1989
BhutanDisease never reportedOIE Handistatus, 2005
Brunei DarussalamNo information availableOIE Handistatus, 2005
ChinaPresentWang et al., 1998
-Hong KongNo information availableOIE Handistatus, 2005
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaOIE Handistatus, 2005
-Madhya PradeshPresentJoshi et al., 1996
-OdishaPresentTripathy et al., 1998
IndonesiaDisease not reportedOIE Handistatus, 2005
-JavaPresentAdjid and Mangunwiryo, 1991; Adjid et al., 1995
IranNo information availableOIE Handistatus, 2005
IraqReported present or known to be presentHussain et al., 1992; Hussain, 1995; Hussain et al., 1996; OIE Handistatus, 2005
IsraelNo information availableOIE Handistatus, 2005
JapanReported present or known to be presentOIE Handistatus, 2005
JordanReported present or known to be presentOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedKim et al., 1996; OIE Handistatus, 2005
Korea, Republic ofNo information availableOIE Handistatus, 2005
KuwaitLast reported2003OIE Handistatus, 2005
LebanonNo information availableOIE Handistatus, 2005
MalaysiaPresentZamri-Saad et al., 1993; Fatimah et al., 1994
-Peninsular MalaysiaDisease not reportedOIE Handistatus, 2005
-SabahReported present or known to be presentOIE Handistatus, 2005
-SarawakNo information availableOIE Handistatus, 2005
MongoliaNo information availableWu and Sun, 1992; OIE Handistatus, 2005
MyanmarDisease never reportedOIE Handistatus, 2005
NepalNo information availableOIE Handistatus, 2005
OmanReported present or known to be presentOIE Handistatus, 2005
PhilippinesDisease not reportedOIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
Saudi ArabiaReported present or known to be presentHousawi et al., 1991; Housawi et al., 1992; Gameel et al., 1995; Elzein et al., 1998; OIE Handistatus, 2005
SingaporeDisease never reportedOIE Handistatus, 2005
Sri LankaReported present or known to be presentOIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandDisease not reportedOIE Handistatus, 2005
TurkeyNo information availableCabalar et al., 1996; OIE Handistatus, 2005
TurkmenistanLast reported2003OIE Handistatus, 2005
United Arab EmiratesDisease not reportedOIE Handistatus, 2005
UzbekistanDisease not reportedOIE Handistatus, 2005
VietnamDisease never reportedOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005


AlgeriaReported present or known to be presentOIE Handistatus, 2005
AngolaReported present or known to be presentOIE Handistatus, 2005
BeninReported present or known to be presentOIE Handistatus, 2005
BotswanaNo information availableOIE Handistatus, 2005
Burkina FasoNo information availableOIE Handistatus, 2005
BurundiReported present or known to be presentOIE Handistatus, 2005
CameroonOIE Handistatus, 2005
Cape VerdeLast reported1989OIE Handistatus, 2005
Central African RepublicNo information availableOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
ComorosPresentHamers et al., 1993
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireReported present or known to be presentOIE Handistatus, 2005
DjiboutiReported present or known to be presentOIE Handistatus, 2005
EgyptNo information availableOIE Handistatus, 2005
EritreaReported present or known to be presentOIE Handistatus, 2005
EthiopiaReported present or known to be presentOIE Handistatus, 2005
GhanaNo information availableOIE Handistatus, 2005
GuineaReported present or known to be presentOIE Handistatus, 2005
Guinea-BissauDisease not reportedOIE Handistatus, 2005
KenyaCAB Abstracts data miningOIE Handistatus, 2005
LibyaNo information availableOIE Handistatus, 2005
MadagascarDisease never reportedOIE Handistatus, 2005
MalawiNo information availableOIE Handistatus, 2005
MaliNo information availableMaiga and Sarr, 1992; OIE Handistatus, 2005
MauritiusDisease not reportedOIE Handistatus, 2005
MoroccoReported present or known to be presentOIE Handistatus, 2005
MozambiqueNo information availableOIE Handistatus, 2005
NamibiaReported present or known to be presentOIE Handistatus, 2005
NigeriaNo information availableOIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaReported present or known to be presentOIE Handistatus, 2005
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalNo information availableSarr et al., 1988; OIE Handistatus, 2005
SeychellesNo information availableOIE Handistatus, 2005
SomaliaNo information availableMoallin and Zessin, 1988; Moallin et al., 1989; OIE Handistatus, 2005
South AfricaReported present or known to be presentOIE Handistatus, 2005
SudanDisease not reportedOIE Handistatus, 2005
SwazilandDisease not reportedOIE Handistatus, 2005
TanzaniaNo information availableOIE Handistatus, 2005
TogoReported present or known to be presentOIE Handistatus, 2005
TunisiaReported present or known to be presentOIE Handistatus, 2005
UgandaDisease not reportedOIE Handistatus, 2005
ZambiaNo information availableOIE Handistatus, 2005
ZimbabweNo information availableOIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaReported present or known to be presentOIE Handistatus, 2005
-AlbertaPresentL'Heureux et al., 1996
MexicoReported present or known to be presentOIE Handistatus, 2005
USAOIE Handistatus, 2005
-CaliforniaPresentClark et al., 1993; Elliott et al., 1994
-MinnesotaPresentAmes et al., 1984
-TexasPresentHardy and Price, 1952

Central America and Caribbean

BarbadosReported present or known to be presentOIE Handistatus, 2005
BelizeNo information availableOIE Handistatus, 2005
British Virgin IslandsDisease not reportedOIE Handistatus, 2005
Cayman IslandsLast reported1999OIE Handistatus, 2005
Costa RicaDisease never reportedOIE Handistatus, 2005
CubaReported present or known to be presentOIE Handistatus, 2005
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicOIE Handistatus, 2005
El SalvadorDisease never reportedOIE Handistatus, 2005
GuadeloupeLast reported1997OIE Handistatus, 2005
GuatemalaDisease never reportedOIE Handistatus, 2005
HaitiLast reported2003OIE Handistatus, 2005
HondurasDisease never reportedOIE Handistatus, 2005
JamaicaDisease never reportedOIE Handistatus, 2005
MartiniqueReported present or known to be presentOIE Handistatus, 2005
NicaraguaDisease never reportedOIE Handistatus, 2005
PanamaDisease not reportedOIE Handistatus, 2005
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesNo information availableOIE Handistatus, 2005
Trinidad and TobagoNo information availableOIE Handistatus, 2005

South America

ArgentinaReported present or known to be presentOIE Handistatus, 2005
BoliviaNo information availableOIE Handistatus, 2005
BrazilNo information availableOIE Handistatus, 2005
-PernambucoPresentOliveira et al., 1998
ChileOIE Handistatus, 2005
ColombiaLast reported2003OIE Handistatus, 2005
EcuadorNo information availableOIE Handistatus, 2005
Falkland IslandsReported present or known to be presentOIE Handistatus, 2005
French GuianaNo information availableOIE Handistatus, 2005
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayNo information availableOIE Handistatus, 2005
PeruReported present or known to be presentOIE Handistatus, 2005
UruguayReported present or known to be presentOIE Handistatus, 2005
VenezuelaDisease never reportedOIE Handistatus, 2005


AndorraReported present or known to be presentOIE Handistatus, 2005
AustriaNo information availableOIE Handistatus, 2005
BelarusDisease never reportedOIE Handistatus, 2005
BelgiumNo information availableOIE Handistatus, 2005
Bosnia-HercegovinaNo information availableOIE Handistatus, 2005
BulgariaLast reported2001OIE Handistatus, 2005
CroatiaReported present or known to be presentOIE Handistatus, 2005
CyprusReported present or known to be presentOIE Handistatus, 2005
Czech RepublicLast reported1996OIE Handistatus, 2005
DenmarkNo information availableOIE Handistatus, 2005
EstoniaDisease never reportedOIE Handistatus, 2005
FinlandLast reported2003OIE Handistatus, 2005
FranceReported present or known to be presentOIE Handistatus, 2005
GermanyReported present or known to be presentOIE Handistatus, 2005
GreeceReported present or known to be presentOIE Handistatus, 2005
HungaryOIE Handistatus, 2005
IcelandLast reported2002OIE Handistatus, 2005
IrelandReported present or known to be presentOIE Handistatus, 2005
Isle of Man (UK)Reported present or known to be presentOIE Handistatus, 2005
ItalyNo information availableOIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
LithuaniaDisease never reportedOIE Handistatus, 2005
LuxembourgNo information availableOIE Handistatus, 2005
MacedoniaDisease not reportedOIE Handistatus, 2005
MaltaDisease never reportedOIE Handistatus, 2005
MoldovaDisease never reportedOIE Handistatus, 2005
NetherlandsReported present or known to be presentOIE Handistatus, 2005
NorwayReported present or known to be presentOIE Handistatus, 2005
PolandNo information availableOIE Handistatus, 2005
PortugalLast reported1997OIE Handistatus, 2005
RomaniaOIE Handistatus, 2005
Russian FederationNo information availableOIE Handistatus, 2005
SlovakiaLast reported2002OIE Handistatus, 2005
SloveniaDisease not reportedOIE Handistatus, 2005
SpainNo information availableOIE Handistatus, 2005
SwedenReported present or known to be presentOIE Handistatus, 2005
SwitzerlandNo information availableOIE Handistatus, 2005
UKReported present or known to be presentOIE Handistatus, 2005
-Northern IrelandReported present or known to be presentOIE Handistatus, 2005
UkraineLast reported2001OIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Reported present or known to be presentOIE Handistatus, 2005


AustraliaReported present or known to be presentOIE Handistatus, 2005
-Western AustraliaPresentGardiner et al., 1967; Higgs et al., 1996
French PolynesiaDisease not reportedOIE Handistatus, 2005
New CaledoniaReported present or known to be presentOIE Handistatus, 2005
New ZealandReported present or known to be presentOIE Handistatus, 2005
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005


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Histologically, the development of lesions following natural or experimental infection of skin with Orf virus occurs in three separate, but confluent, phases. The separate phases can be described as cellular infiltration, tissue response and recovery. Following skin abrasion, infection with Orf virus leads to a cellular response within 24 hours that cannot be differentiated from the normal response to abrasion (McKeever et al., 1988). Thereafter, a rapid increase in the number of neutrophils peaks at around 24 hours to form a band of cells located above a layer of active fibroblasts (Jenkinson et al., 1990; Jenkinson et al., 1991). T-cells and B-cells accumulate during the following 48-72 hours (Jenkinson et al., 1992). During this period of immune cell infiltration the epidermal cells begin to vacuolate and by the fifth day after infection the typical ballooning degeneration of CPD-infected epidermal cells is evident (Robinson and Balassu, 1981; McKeever et al., 1988). The epidermis continues to disintegrate over the next week resulting in a necrotic, polymorphonuclear infiltrated dermis. A scab covers the lesion by 15 days post-infection and comprises the necrotic stratum papillare, the infiltrated cells of the cellular immune response, wool fibres, fibrin, collagen and serum. Under the scab the epidermis continues to hypertrophy, so that by day 20 a complete surface is re-established. Six to eight weeks after infection the skin surface is largely indistinguishable from that pre-infection (McKeever et al., 1988). It has been suggested that the ‘papillomatous’ lesions often associated with the lips may occur due to a reduced protection to viral infection afforded by the thinner epidermal layers found in the buccal tissues (Glover, 1928).

The healing process as described above may be disrupted by a concomitant bacterial infection; a mild infection may result in debris containing lymphocytes and bacteria, whereas a severe infection may disrupt the dermis itself (Glover, 1928).


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Diagnosis usually relies upon the presenting clinical signs and within-flock epidemiology. Confirmation is performed through the identification of the Orf virus in scab material by electron microscopy, this being most likely 1-2 weeks after the first appearance of the lesion. Alternatively, the polymerase chain reaction (PCR) is now used routinely to identify the virus from scab material. Several PCR assays have been described in the literature some of which, when combined with DNA sequencing of the PCR product, can be used to differentiate between isolates of the Orf virus as well as for differentiating the Orf virus from the other parapoxviruses that cause disease in cattle and deer (Inoshima et al., 2000; Torfason and Gunadottir, 2002; Gallina et al., 2006; Bora et al., 2011). Such assays have been used to investigate outbreaks of disease in the field in an attempt to attribute source or origin of infection including differentiation between wild Orf virus and vaccinal strains. An alternative to PCR, namely a loop-mediated isothermal amplification (LAMP) assay, for resource-limited laboratories has also been described (Tsai et al., 2009).

A serum antibody test that can be used to assess exposure to the Orf virus has been described (Yirrel et al., 1989). However, since the presence of antibodies against the virus does not correlate strongly with protection the test does not predict immune status of sheep in the field.

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sheep & Goats:Lamb Diagnosis
Digestive Signs / Difficulty in prehending or chewing food Sheep & Goats:Lamb Diagnosis
Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism Sheep & Goats:Lamb Sign
Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears Sheep & Goats:Lamb Diagnosis
Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears Sign
General Signs / Dehydration Sheep & Goats:Lamb Sign
General Signs / Fever, pyrexia, hyperthermia Sign
General Signs / Forefoot swelling, mass front foot, feet Sheep & Goats:Lamb Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sheep & Goats:Lamb Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Sheep & Goats:Lamb Diagnosis
General Signs / Hindfoot swelling, mass rear foot, feet Sheep & Goats:Lamb Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sheep & Goats:Lamb Sign
General Signs / Lack of growth or weight gain, retarded, stunted growth Sheep & Goats:Lamb Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Sign
General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia Sheep & Goats:Gimmer,Sheep & Goats:Mature female Sign
General Signs / Oral cavity, tongue swelling, mass in mouth Sign
General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass Sheep & Goats:All Stages Diagnosis
General Signs / Swelling mass, vulva, clitoris Sign
General Signs / Swelling mass, vulva, clitoris Sign
General Signs / Swelling skin or subcutaneous, mass, lump, nodule Sheep & Goats:Lamb Diagnosis
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sheep & Goats:Lamb Diagnosis
General Signs / Weight loss Sheep & Goats:Lamb Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Ophthalmology Signs / Corneal swelling, mass, nodule Sign
Ophthalmology Signs / Entropion, inverted eyelid Sign
Pain / Discomfort Signs / Forefoot pain, front foot Sheep & Goats:Lamb Diagnosis
Pain / Discomfort Signs / Forelimb pain, front leg Sheep & Goats:Lamb Diagnosis
Pain / Discomfort Signs / Hindfoot pain, rear foot Sheep & Goats:Lamb Diagnosis
Pain / Discomfort Signs / Hindlimb pain, hind leg Sheep & Goats:Lamb Diagnosis
Pain / Discomfort Signs / Mouth, oral mucosal or tongue pain Sheep & Goats:Lamb Diagnosis
Pain / Discomfort Signs / Pain mammary gland, udder Sheep & Goats:Gimmer,Sheep & Goats:Mature female Diagnosis
Pain / Discomfort Signs / Pain, penis Sign
Pain / Discomfort Signs / Pain, prepuce Sign
Pain / Discomfort Signs / Pain, vulva, vagina Sign
Pain / Discomfort Signs / Skin pain Sheep & Goats:All Stages Diagnosis
Reproductive Signs / Male infertility Sign
Reproductive Signs / Mastitis, abnormal milk Sheep & Goats:Mature female Sign
Reproductive Signs / Papule, pustule, vesicle, ulcer penis or prepuce Sign
Reproductive Signs / Paraphimosis or priapism, inability to retract penis Sign
Reproductive Signs / Phimosis Sign
Reproductive Signs / Purulent discharge, penis or prepuce Sign
Reproductive Signs / Teat injury, cut, tear Sheep & Goats:Gimmer,Sheep & Goats:Mature female Sign
Reproductive Signs / Vulval ulcers, vesicles, erosions, tears, cuts, pustules, papules Sheep & Goats:Lamb,Sheep & Goats:Gimmer,Sheep & Goats:Mature female Diagnosis
Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules Sign
Skin / Integumentary Signs / Cracked skin, fissure Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Defective growth of nail, claw, hoof Sheep & Goats:All Stages Sign
Skin / Integumentary Signs / Foul odor skin, smell Sheep & Goats:All Stages Sign
Skin / Integumentary Signs / Hyperkeratosis, thick skin Sign
Skin / Integumentary Signs / Matted or dirty hair Sheep & Goats:All Stages Sign
Skin / Integumentary Signs / Purulent discharge skin Sheep & Goats:All Stages Sign
Skin / Integumentary Signs / Skin crusts, scabs Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin erythema, inflammation, redness Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Skin papules Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Skin plaque Sign
Skin / Integumentary Signs / Skin pustules Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Skin scales, flakes, peeling Sign
Skin / Integumentary Signs / Skin ulcer, erosion, excoriation Sheep & Goats:All Stages Diagnosis
Skin / Integumentary Signs / Skin vesicles, bullae, blisters Sheep & Goats:All Stages Diagnosis

Disease Course

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Contagious pustular dermatitis is usually associated with the non-woolly areas of the skin. Virus enters the skin through surface cuts or abrasions or where the erupting teeth break the gums. The Orf virus is epitheliotrophic (i.e. confined to the skin) and thus, on inoculation into the skin, does not result in virus entering the bloodstream (a viraemia) (Glover, 1928). The virus rapidly replicates in the skin, wool and hair follicles and sebaceous glands. The resulting lesions are characterized by the development of papules, vesicles and pustules. When the pustules erupt, serum oozes onto the skin surface where wool or hair may clump around the lesion sites. The maximum amounts of virus are present 5-10 days after infection (McKeever et al., 1988). These lesions mature into crusty scabs that eventually dry up and fall off. Two months after infection the skin surface is largely indistinguishable from that pre-infection. However, scabs that are rubbed off before being healed leave an elevated raw bleeding surface that is prone to secondary bacterial infection, particularly with Staphylococcus aureus. Should the lesions become secondarily infected with bacteria before complete resolution, a scar may result.

The most frequent lesions are seen in young lambs and kids and appear as raw areas or crusty scabs in and around the mouths and nares. In mild cases, lesions are most apparent at the commissures of the muzzle, but in severe cases, the buccal mucous membrane, tongue and oesophagus may also be affected (Boughton and Hardy, 1934; Lewis, 1996). In young lambs, a wet mouth and apparent excess salivation is often the first sign of infection. Infected lambs may lose considerable amounts of weight, or even starve to death, because of a reluctance to suckle. In older lambs, grazing on land with shrubs with rough or spiny foliage may exacerbate outbreaks of disease (Gardiner et al., 1967; Hawkins et al., 1991). Skin lesions may become infected with bacteria including Staphylococci, resulting in local tissue swelling, erythema, pain and irritation.


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Contagious pustular dermatitis outbreaks occur most commonly at, or shortly after lambing, but lesions may be seen at any time of year. This seasonality may occur as a result of infection with virus that has survived in scabs shed during the previous season. However, sheep carriers have been postulated, but this has not been confirmed by experiment. Other sources of infection that have been identified include non-sterilized emasculators and ear hole punches that may used for tail-docking or ear tagging, respectively.

Contagious pustular dermatits virus may also be found in lesions on the feet and legs of sheep and goats, often in association with the bacterium Dermatophilus congolensis (Roberts, 1967). These lesions are known as strawberry footrot and are characterized by necrotic, scabby lesions around the coronary band of the foot, which may, in severe cases, extend up the leg. Strawberry footrot is usually seen in finishing lambs in the autumn. Lesions may be so severe that they result in a stiff gait and lameness (Lewis, 1996).

Adult sheep may also develop lesions due to CPD infection. In ewes, lesions and scabs may develop on the udder and teats. Local pain associated with these lesions may make ewes reluctant to allow the lambs to suckle, resulting in mis-mothering. Additionally, secondary infection associated with lesions around the teat sphincter can result in mastitis. Rams may get persistent scabby lesions on the poll which results in sites that are prone to damage, particularly when sparring takes place around mating. Such sites may then become secondarily infected.

In temperate climates, viable virus particles may survive from one season to the next. The lambing accommodation, particularly the difficult-to-reach parts of the sheep accommodation and the grain of wooden hurdles or feed troughs, may harbour infectious organism from one season to the next (Lewis, 1996).

Impact: Economic

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No studies have been conducted to estimate the economic impact of CPD infection. Production losses associated with reduced growth rate or weight loss in lambs may be considerable, due to a reluctance to suckle or graze. Losses due to CPD will depend upon the severity of infection and the within-flock prevalence, which may vary considerably from below 10% to all of the flock being affected (Hardy and Price, 1952; Gardiner et al., 1967; Higgs et al., 1996). Factors resulting in stress or an increased transmission of virus, such as high stocking density or transport, may play a major role in determining the course of flock infection (Gumbrell and McGregor, 1997). Thus a significant impact will be seen in severe outbreaks where mortality may be considerable (Boughton and Hardy, 1934; Darbyshire, 1961).

Contagious pustular dermatitis lesions on the teats of ewes may be associated with an increased level of mastitis in the flock. In consequence, the udder half may be lost to milk production and the ewe culled as a result (Lewis, 1996).

Other losses associated with growing lambs may be associated with strawberry footrot. Infected lambs show a reduced growth rate and an extended time to finishing (Reid, 1993). This inevitably has a deleterious economic impact for the farm.

Zoonoses and Food Safety

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Contagious pustular dermatitis virus is zoonotic, causing skin lesions in people. These lesions are usually found on the hands and, provided they do not become secondarily infected, resolve spontaneously over a few weeks (Leavell et al., 1968). The exceptions to this may be where individuals display an underlying immune deficiency or suffer from other skin-related disorders such as psoriasis. The virus only infects through broken skin and therefore the wearing of non-porous gloves and the practise of good hand hygiene is recommended when handling infected animals, the vaccine or contaminated bedding. If bearing lesions, particularly on the hands, patients should avoid sharing towels or other items with non-infected individuals.

Diagnosis in people is usually based on the presenting history since several poxviruses produce clinically and histologically indistinguishable lesions and although confirmation of a parapox infection may be performed using electron microscopy, all parapox viruses have similar appearances when viewed this way. Diagnosis is now also routinely performed using PCR assays (see below) that can differentiate between the different parapox viruses.

The typical mid-stage human CPD lesion has a vesicular or pustular appearance, but is solid to the touch. Generally a red halo with a greyish central area is observed which may occasionally ‘weep’ a clear serum-like fluid. This ‘target’ stage contains the highest concentration of virus (Pask et al., 1951). Lesions develop a crusty scab but usually leave little or no scarring once fully resolved. They are not usually painful, but are sometimes pruritic. The majority of lesions are single, although multiple lesions have been reported (Leavell et al., 1968; Kim and Tarrier, 1977). Occasionally lymphangitis or generalised cutaneous manifestations may result from secondary bacterial infections (Moore, 1973; Erickson et al., 1975; Wilkinson, 1977). Complications were seen in almost a quarter of cases reported in a GP practice-based study of CPD in Wales (Buchan, 1996). Severe complications may occur in immunosuppressed patients including lymphadenitis, generalised malaise or bullous pemphigoid (Savage and Black, 1972; Hunskaar, 1986; Murphy and Ralphs, 1996).

In recent years persistant cases of human CPD have been treated successfully by the topical application of creams containing anti-viral drugs. In particular, Cidofovir (1%), a nucleoside analogue and Imiquimod (5%), an activator of the human immune system, have been used successfully, even in immuno-compromised individuals (Geerinck et al., 2001; Lederman et al., 2007).

The prevalence of CPD in humans is difficult to assess. Several studies have reported that between a third and half of those people working with sheep develop CPD lesions at some time during their working lives (Buchan, 1996; Paiba et al., 1999). Abattoir workers are also known to get CPD (Hodgson-Jones, 1951). Infection in people in the UK coincides with the periods of most sheep handling (PHLS, 1982; Buchan, 1996; Thomas and Salmon, 1997). Disease often occurs in spring and early summer at the end of the lambing season when tasks such as bottle-feeding and vaccinating may be responsible for transmission (Blakemore et al., 1948) and also at the end of the finishing period when lambs are sent to market. Those working in the meat trade are also at higher risk with disease possibly associated with wounding by splinters of bones or teeth from infected sheep or with knives used for cutting mutton.

Disease Treatment

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Treatment of CPD in sheep is usually unnecessary as the disease normally resolves without intervention within 5-7 weeks for a primary infection and within 2-3 weeks for subsequent infections. In cases where lambs are having obvious difficulty in suckling, bottle feeding to prevent severe weight loss and debilitation may be necessary. However, due to the zoonotic potential of the virus care should be taken when doing so. Any bottles or teats used should also be thoroughly disinfected between use.

When CPD infection does occur in livestock, the control of secondary bacterial infections by the maintenance of good hygiene practices is very important. The most frequent secondary infections result from the uncontrolled growth of skin commensal Streptococci spp. and Staphylococci spp. Antibiotic use is usually unnecessary except in the most severe cases, but the topical application of antibiotic formulations or antiseptics and in some cases systemic application may be appropriate. As with any antibiotic usage, they should be used prudently and only as directed by a qualified veterinary practitioner.

The use of antiviral agents, in both sheep and people, has been proven to be effective against Orf virus infection, although currently none of the drugs tested are licenced for such use. The antiviral drug Cidofovir has powerful anti-orf activity. When used as a cream and applied topically to human orf the lesions resolve rapidly. Similar results have been obtained using a cream containing Imiquimod (5%) (Lederman et al., 2007). A formulation of Cidofovir that can be sprayed directly onto orf lesions has been tested in sheep with good results (Sonvico et al., 2009), but in the case of flock or herd infections, the use of such drugs would, however, be impractical and prohibitively expensive.

Prevention and Control

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Immunological memory is generated by prior exposure to Orf virus either via natural infection or through vaccination. However, the nature of the immunity engendered, and its duration, is poorly understood. As with most poxvirus infections it is thought that cell-mediated immunity is most likely to have a major role in providing the mechanism of protection (Haig et al., 1996a; Haig et al., 1996b, Haig and Mercer, 1998), whilst the role of antibody (humoral) responses in protection against CPD infection is less clearly defined (Robinson and Balassu, 1981; McKeever and Reid, 1986a, Yirrell et al., 1989).

Passive acquisition of antibody via colostrum was not enough to protect lambs challenged with Orf virus 1 month later (Buddle and Pulford, 1984), although an earlier study had suggested some degree of protection in the first 3-4 weeks post-partum (Le Jan, et al., 1978). Clinically, a repeat infection with Orf virus in an animal that has recovered from a previous infection usually results in a less severe infection with a shorter time to resolution. This is the principle by which the vaccine works. The duration of such protective immunity in sheep has been reported to last from 6 weeks to at least 8 months (Glover, 1928; Boughton and Hardy, 1934; McKeever et al., 1988), although some of the vaccines claim 12 months efficacy.

Vaccines are available and where CPD is recognized as a production problem vaccination is widely practised. However, since vaccines contain live virus, vaccination is contraindicated on farms with no history of CPD infection in the flock, since environmental viral load may increase following their use. Although none of the current vaccines induce a long-lasting immunity, a continuous low level exposure of the flock to environmental virus may maintain clinical immunity by regular re-exposure to virus.

There are several vaccines registered in countries throughout the world; Scabivax Forte (UK), Ecthybel (France), Ectisan (Uruguay), Orf Freeze Dried vaccine (South Africa and Namibia), Orfvax (Kenya), Ovine Ecthyma Vaccine (USA), Vacina Leivas Leite Contra o Ectima Contagioso dos Ovinos (Brazil); Scabby Mouth Vaccine (Australia) and Scabiguard Vaccine (Australia and New Zealand). All contain live viruses that replicate disease to some extent. Due to the zoonotic nature of the virus great care should be taken when administering the vaccine, which should only be done so on advice from a veterinary surgeon.

Vaccination of ewes on farms where CPD infection causes significant morbidity is advised, particularly when predisposing factors are likely to result in widespread infection amongst the lambs. Vaccination of the ewes, however, should not be carried out less than 8 weeks before lambing as the vaccine contains live virus and replicates disease in the vaccinated animal (Lewis, 1996). Inoculation of the ewes should be carried out on clean skin away from areas where the lambs are likely to nuzzle. The preferred sites are the outside fold of the skin found on either side of the underside of the base of the tail or in the axilla of the front limb. Scabs form at the site of the inoculation before they fall off into the environment. Preferably the vaccinated sheep should not be given access to the lambing areas for the 8 weeks following vaccination. However, if the sheep do remain housed until lambing, adequate bedding should be provided in order to reduce the risk to the young lambs from the recently shed virus particles.

In the face of an outbreak, vaccination of animals of any age may assist with the control of spread, duration and intensity of the infection. Vaccination of lambs in the first week of life is recommended as that is when they are at highest risk of exposure to CPD, particularly where ewes have not been previously immunised. The vaccine should be applied to the axilla of the lambs and not in their groin. Older and finishing lambs may also benefit from vaccination where the risk of infection is high. Care should be taken when using CPD vaccine in animals since self-inoculation with the live virus will cause lesions in the operator (Nomland, 1940).

Contagious pustular dermatitis virus infections are believed to arise in many instances through infection from the environment. As a consequence, buildings that have been used to house infected animals, or when administering the vaccine, must be considered as being contaminated with the virus and should be disinfected before re-use. All potentially contaminated materials such as feeding troughs and pen divisions should also be disinfected.

Floors, walls, troughs and pens should be thoroughly cleaned to remove organic matter prior to application of disinfectant. The virus is susceptible to most disinfectants, such as 3% iodophor solution. General purpose disinfectants may be applied liberally, but it must be remembered that if hypochlorite solutions are used they rapidly lose activity in the presence of organic matter. Nowadays, bio-degradable, non-corrosive disinfectants with relatively long shelf lives are available, but users should check with the manufacturer their suitability for use against Orf virus. An alternative is to use steam cleaning as an effective way of disinfecting premises since Orf virus is susceptible to heat treatment.


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