- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
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
Pathogen/sTop of page
OverviewTop of page
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 AnimalsTop of page
|Animal name||Context||Life stage||System|
|Camelus dromedarius (dromedary camel)||Domesticated host|
|Capra hircus (goats)||Domesticated host; Experimental settings||Sheep & 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 host||Sheep & Goats: All Stages|
|Rangifer tarandus (reindeer)||Domesticated host|
Hosts/Species AffectedTop of page
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 AffectedTop of page
mammary gland diseases of small ruminants
skin and ocular diseases of small ruminants
DistributionTop of page
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 TableTop of page
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.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Congo, Democratic Republic of the||Absent, No presence record(s)|
|Eswatini||Absent, No presence record(s)|
|Guinea-Bissau||Absent, No presence record(s)|
|Kenya||Present||CAB Abstracts Data Mining|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|São Tomé and Príncipe||Absent, No presence record(s)|
|Sudan||Absent, No presence record(s)|
|Uganda||Absent, No presence record(s)|
|Bahrain||Absent, No presence record(s)|
|Bangladesh||Absent, No presence record(s)|
|Bhutan||Absent, No presence record(s)|
|Georgia||Absent, No presence record(s)|
|Indonesia||Absent, No presence record(s)|
|Kazakhstan||Absent, No presence record(s)|
|-Peninsular Malaysia||Absent, No presence record(s)|
|Myanmar||Absent, No presence record(s)|
|North Korea||Absent, No presence record(s)|
|Philippines||Absent, No presence record(s)|
|Singapore||Absent, No presence record(s)|
|Syria||Absent, No presence record(s)|
|Taiwan||Absent, No presence record(s)|
|Thailand||Absent, No presence record(s)|
|United Arab Emirates||Absent, No presence record(s)|
|Uzbekistan||Absent, No presence record(s)|
|Vietnam||Absent, No presence record(s)|
|Belarus||Absent, No presence record(s)|
|Estonia||Absent, No presence record(s)|
|Isle of Man||Present|
|Jersey||Absent, No presence record(s)|
|Latvia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|Lithuania||Absent, No presence record(s)|
|Malta||Absent, No presence record(s)|
|Moldova||Absent, No presence record(s)|
|North Macedonia||Absent, No presence record(s)|
|Serbia and Montenegro||Present|
|Slovenia||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Costa Rica||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|Dominica||Absent, No presence record(s)|
|El Salvador||Absent, No presence record(s)|
|Guatemala||Absent, No presence record(s)|
|Honduras||Absent, No presence record(s)|
|Jamaica||Absent, No presence record(s)|
|Nicaragua||Absent, No presence record(s)|
|Panama||Absent, No presence record(s)|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|French Polynesia||Absent, No presence record(s)|
|Samoa||Absent, No presence record(s)|
|Vanuatu||Absent, No presence record(s)|
|Guyana||Absent, No presence record(s)|
|Venezuela||Absent, No presence record(s)|
PathologyTop of page
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).
DiagnosisTop of page
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/SignsTop of page
|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 CourseTop of page
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.
EpidemiologyTop of page
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: EconomicTop of page
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 SafetyTop of page
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 TreatmentTop of page
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 ControlTop of page
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.
ReferencesTop of page
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