Sheep Pox and Goat Pox

Sheep pox and goat pox are highly contagious, notifiable viral diseases of sheep and goats caused by the Capripoxvirus genus of the Poxviridae family. These diseases are characterized by fever, generalized papular or nodular skin lesions, and often severe respiratory and gastrointestinal involvement. Sheep pox (SP) and goat pox (GP) are clinically and economically devastating, with morbidity rates up to 100% in susceptible flocks and mortality ranging from 5% to 50% or higher, particularly in young animals and certain breeds. The diseases are endemic in Africa, Asia, and the Middle East, and they pose a significant threat to small ruminant production, international trade, and food security. In affected flocks, the disease leads to severe weight loss, decreased milk production, abortion, secondary bacterial infections, and high mortality, especially in lambs and kids. The clinical presentation can vary from mild, localized lesions to severe systemic disease with extensive skin and internal organ involvement. The disease is transmitted primarily by direct contact with infected animals, but also via fomites, aerosols, and possibly insect vectors. The virus is highly stable in the environment, particularly in dried scabs, and can persist for months, facilitating long-distance spread. Control relies on strict biosecurity, quarantine, vaccination with live attenuated vaccines, and in some regions, culling of infected and in-contact animals. The disease is a major constraint to the improvement of small ruminant production in endemic areas and is a significant barrier to international trade in live animals and animal products.

The causative agents are viruses belonging to the genus Capripoxvirus, family Poxviridae, subfamily Chordopoxvirinae. Three closely related but antigenically distinct viruses are recognized: Sheep pox virus (SPPV), Goat pox virus (GTPV), and Lumpy skin disease virus (LSDV). SPPV and GTPV are the primary agents of sheep pox and goat pox, respectively, but cross-species infection can occur, with some strains affecting both sheep and goats. The viruses are large, enveloped, double-stranded DNA viruses with a complex structure. They are relatively resistant to environmental degradation, surviving in dried scabs for up to 6 months, in contaminated pens for several months, and in wool and hides for up to 3 months. They are susceptible to lipid solvents, detergents, and common disinfectants such as sodium hypochlorite, quaternary ammonium compounds, and phenol. The virus replicates in the cytoplasm of host cells, particularly in epithelial cells, and causes characteristic intracytoplasmic inclusion bodies (Bollinger bodies) and cell necrosis. The pathogenesis involves primary replication at the site of entry (skin or respiratory tract), followed by viremia and dissemination to secondary sites, particularly the skin, mucous membranes, and internal organs. The virus has a predilection for epithelial tissues, leading to the formation of papules, vesicles, pustules, and scabs on the skin and lesions in the respiratory and gastrointestinal tracts. The immune response is primarily cell-mediated, and recovery from infection confers lifelong immunity. However, the virus can persist in the skin and other tissues for several weeks after clinical recovery, and animals may shed virus intermittently.

Sheep pox and goat pox are endemic in Africa, the Middle East, Asia, and parts of Europe (e.g., Turkey, Greece, Bulgaria). The disease is not present in the Americas, Australia, New Zealand, or Western Europe, and outbreaks in these regions are considered exotic and are subject to strict eradication measures. The epidemiology is influenced by host species, breed, age, and immune status. Sheep are generally more susceptible to SPPV, while goats are more susceptible to GTPV, but cross-species transmission can occur. Certain breeds, such as the Merino and its crosses, are highly susceptible to sheep pox, while some indigenous breeds in endemic areas may show lower morbidity and mortality. Young animals (lambs and kids) are more severely affected than adults, with higher morbidity and mortality rates. The disease is more prevalent in intensive production systems, such as dairy goat farms and feedlots, where animal density is high and biosecurity is often inadequate. Seasonal patterns are observed, with outbreaks more common in cooler, dry seasons when the virus survives longer in the environment and animals are more stressed. Morbidity rates can reach 100% in fully susceptible flocks, and mortality rates typically range from 5% to 50%, but can be as high as 100% in young animals with severe systemic disease. The economic impact includes direct losses from mortality, reduced milk production, weight loss, abortion, and secondary infections, as well as indirect costs from trade restrictions, vaccination programs, and control measures. The disease is transmitted primarily by direct contact with infected animals, particularly through respiratory aerosols and contact with skin lesions. Indirect transmission occurs via contaminated fomites (e.g., bedding, equipment, vehicles, and personnel) and possibly by biting insects, although the role of arthropod vectors is not fully understood. The virus can also be transmitted through semen and embryos, and vertical transmission has been reported. The incubation period is typically 4 to 8 days, but can range from 2 to 14 days. The virus is shed in saliva, nasal secretions, and scabs, and can be present in milk and semen. Recovered animals may shed virus for up to 2 months after clinical recovery, and the virus can persist in the environment for long periods, facilitating spread.

The pathogenesis of sheep pox and goat pox begins with viral entry through the respiratory tract or skin abrasions. The virus replicates locally in epithelial cells and regional lymph nodes, leading to primary viremia. Subsequently, the virus disseminates to secondary sites, particularly the skin, mucous membranes, and internal organs, where it replicates in vascular endothelial cells, macrophages, and epithelial cells. This results in vasculitis, thrombosis, and ischemia, leading to the characteristic skin lesions (papules, vesicles, pustules, and scabs) and internal lesions in the lungs, gastrointestinal tract, and other organs. The skin lesions progress from erythematous macules to papules, which become necrotic and form scabs. In severe cases, lesions can coalesce and become hemorrhagic or ulcerative. The respiratory tract is commonly affected, with lesions in the nasal mucosa, trachea, bronchi, and lungs, leading to pneumonia, dyspnea, and secondary bacterial infections. Gastrointestinal lesions can cause diarrhea, and lesions in the oral cavity can lead to salivation and anorexia. The virus also causes immunosuppression, increasing susceptibility to secondary bacterial infections. The systemic effects include fever, depression, and anorexia, leading to weight loss and decreased production. In pregnant animals, the virus can cross the placenta and cause abortion or fetal death. The immune response involves both humoral and cell-mediated immunity, with neutralizing antibodies appearing within 1-2 weeks after infection. However, cell-mediated immunity is crucial for recovery, and animals with impaired cellular immunity may develop severe disease. The virus can persist in the skin and other tissues for several weeks, and recovered animals are immune to reinfection with the homologous virus but may be susceptible to heterologous strains.

Several factors increase the risk of sheep pox and goat pox outbreaks and the severity of disease. Intrinsic factors include species, breed, age, and immune status. Sheep are more susceptible to SPPV, and goats to GTPV, but cross-species infection can occur. Certain breeds, such as Merino sheep and Saanen goats, are highly susceptible, while some indigenous breeds in endemic areas may have some genetic resistance. Young animals (lambs and kids) are more susceptible and develop more severe disease than adults. Animals with poor nutritional status, concurrent infections, or immunosuppression are at higher risk. Extrinsic factors include management practices, environmental conditions, and biosecurity measures. High animal density, poor ventilation, and inadequate hygiene in intensive production systems facilitate virus spread. Introduction of new animals into a flock without quarantine can introduce the virus. Movement of animals, personnel, and equipment between farms can spread the disease. Contaminated fomites, such as bedding, feed troughs, and vehicles, can transmit the virus. Environmental factors, such as cool, dry weather, favor virus survival and transmission. Lack of vaccination or inadequate vaccination coverage in endemic areas increases the risk of outbreaks. Stress factors, such as transportation, parturition, and weaning, can exacerbate disease severity. In addition, the presence of biting insects, such as flies and mosquitoes, may contribute to mechanical transmission, although the role of vectors is not fully established.

The clinical signs of sheep pox and goat pox vary depending on the virulence of the virus strain, the species and breed of the animal, and the age and immune status. The incubation period is typically 4 to 8 days, but can be as short as 2 days or as long as 14 days. The disease can present in peracute, acute, subacute, and mild forms. In the peracute form, animals may die suddenly without showing significant clinical signs, especially in young lambs and kids. The acute form is characterized by fever (40-42°C), depression, anorexia, and rapid development of skin lesions. The skin lesions initially appear as erythematous macules, which progress to papules (2-3 cm in diameter) that are firm, raised, and may be painful. The papules can become vesicular, pustular, and then necrotic, forming scabs that eventually heal, leaving scars. Lesions are most commonly found on the head, ears, neck, perineum, and udder, but can spread to the entire body. In severe cases, lesions may coalesce and become hemorrhagic or ulcerative. Mucous membranes, including the conjunctiva, nasal mucosa, oral cavity, and vulva, may also be affected, leading to conjunctivitis, nasal discharge, salivation, and vulvovaginitis. Respiratory signs are common, including coughing, sneezing, and dyspnea, due to lesions in the respiratory tract and secondary pneumonia. Gastrointestinal signs may include diarrhea, which can be bloody in severe cases. Pregnant animals may abort. The subacute form is similar but less severe, with fewer skin lesions and milder systemic signs. The mild form may be inapparent or characterized by a few localized lesions and transient fever. In dairy animals, milk production drops significantly. Secondary bacterial infections, particularly pneumonia and dermatitis, can complicate the disease and increase mortality. The clinical course typically lasts 2 to 4 weeks, but severe cases may be fatal within 1-2 weeks. Recovered animals may have permanent scars and may be carriers of the virus.

Differential diagnoses for sheep pox and goat pox include other diseases that cause skin lesions, fever, and respiratory signs in sheep and goats. Key differentials include: 1) Contagious ecthyma (orf) - caused by a parapoxvirus, characterized by proliferative, scabby lesions on the lips, muzzle, and sometimes udder and feet, but typically less systemic and less severe than sheep pox. 2) Bluetongue - caused by an orbivirus, characterized by fever, oral lesions, coronitis, and muscle weakness, but skin lesions are not papular; also, bluetongue is transmitted by Culicoides midges and has a seasonal pattern. 3) Peste des petits ruminants (PPR) - caused by a morbillivirus, characterized by fever, ocular and nasal discharge, oral erosions, diarrhea, and pneumonia, but skin lesions are not typical. 4) Foot-and-mouth disease (FMD) - caused by an aphthovirus, characterized by vesicles on the feet, oral cavity, and udder, but systemic signs are less severe and skin lesions are not papular. 5) Dermatophilosis - a bacterial skin infection caused by Dermatophilus congolensis, characterized by crusty, exudative lesions, but usually not associated with fever or systemic signs. 6) Photosensitization - caused by ingestion of photodynamic agents, leading to skin lesions on unpigmented areas, but no fever or systemic signs. 7) Mycotic dermatitis - fungal infections can cause skin lesions, but are usually not systemic. 8) Insect bites or allergic reactions - can cause papular skin lesions, but are not associated with fever or respiratory signs. 9) Caseous lymphadenitis (CLA) - caused by Corynebacterium pseudotuberculosis, characterized by abscesses in lymph nodes, but skin lesions are not typical. 10) Ulcerative dermatosis - a viral disease caused by a parapoxvirus, characterized by ulcers on the lips, prepuce, and vulva, but less systemic. Definitive diagnosis requires laboratory testing, including virus isolation, PCR, or serology.

The diagnostic approach for sheep pox and goat pox should be systematic and include the following steps: 1) Flock history: Obtain a detailed history including recent introduction of animals, movement of animals or personnel, vaccination status, and presence of similar cases in the area. 2) Clinical examination: Perform a thorough physical examination of affected animals, noting the presence of fever, skin lesions (papules, vesicles, pustules, scabs), respiratory signs, and other systemic signs. 3) Necropsy: If mortality occurs, perform a necropsy on affected animals to observe characteristic lesions in the skin, lungs, and other organs. 4) Sample collection: Collect appropriate samples for laboratory confirmation, including skin lesions (scabs, vesicular fluid), nasal swabs, blood (for serology and PCR), and tissue samples (lung, spleen, lymph nodes) from necropsied animals. 5) Laboratory testing: Submit samples to a diagnostic laboratory for virus detection (PCR, virus isolation) and serology (virus neutralization test, ELISA). PCR is the preferred method for rapid and sensitive detection of capripoxvirus DNA. 6) Differential diagnosis: Rule out other diseases with similar clinical signs, such as contagious ecthyma, bluetongue, PPR, and FMD, through appropriate laboratory tests. 7) Reporting: Since sheep pox and goat pox are notifiable diseases, report suspected cases to the relevant veterinary authorities immediately. 8) Control measures: Implement immediate quarantine and biosecurity measures to prevent further spread, and initiate vaccination of in-contact animals if appropriate.

Laboratory findings in sheep pox and goat pox are primarily related to virus detection and serology. Hematology and biochemistry are non-specific and may show leukopenia, lymphopenia, and elevated acute-phase proteins. Virus detection can be achieved by: 1) Polymerase chain reaction (PCR): Highly sensitive and specific for detection of capripoxvirus DNA in skin lesions, blood, and tissue samples. PCR can differentiate between SPPV, GTPV, and LSDV. 2) Virus isolation: Can be performed on cell cultures (e.g., lamb testis cells, Vero cells) or embryonated chicken eggs, but is time-consuming and requires specialized facilities. 3) Electron microscopy: Can visualize poxvirus particles in lesion material, but is not routinely available. 4) Antigen detection: Immunohistochemistry or immunofluorescence can detect viral antigens in tissue sections. Serological tests include: 1) Virus neutralization test (VNT): The gold standard for serology, but requires live virus and is time-consuming. 2) Enzyme-linked immunosorbent assay (ELISA): Can detect antibodies against capripoxvirus, but cross-reactivity between SPPV and GTPV may occur. 3) Agar gel immunodiffusion (AGID): Less sensitive and specific than VNT and ELISA. In endemic areas, serology is useful for surveillance and vaccine efficacy assessment. In non-endemic areas, serology is used for confirmation of infection and for trade purposes. It is important to note that vaccinated animals will also test positive for antibodies, so serology cannot distinguish between infected and vaccinated animals (DIVA).

Imaging modalities are not commonly used for the diagnosis of sheep pox and goat pox, but they can be helpful in assessing the extent of internal lesions and complications. Thoracic radiography may reveal pulmonary lesions, such as nodular opacities, consolidation, and interstitial patterns, in animals with respiratory involvement. Ultrasonography can be used to evaluate skin lesions, lymph nodes, and internal organs, such as the liver and spleen, for the presence of nodules or abscesses. However, imaging is not specific for sheep pox and goat pox, and diagnosis is primarily based on clinical signs and laboratory testing. In a research setting, computed tomography (CT) may be used to characterize pulmonary lesions, but this is not practical in field conditions. Therefore, imaging is not a routine part of the diagnostic workup for these diseases.

Histopathological examination of skin lesions and internal organs can provide supportive evidence for the diagnosis of sheep pox and goat pox. Skin lesions show characteristic changes, including epidermal hyperplasia, ballooning degeneration of keratinocytes, and the presence of intracytoplasmic inclusion bodies (Bollinger bodies) in epithelial cells. The dermis shows edema, vasculitis, and infiltration of inflammatory cells, including macrophages and lymphocytes. In the lungs, there is interstitial pneumonia with necrosis of bronchiolar and alveolar epithelium, and the presence of intracytoplasmic inclusion bodies in alveolar macrophages and epithelial cells. In the liver, spleen, and lymph nodes, there may be focal necrosis and the presence of inclusion bodies in reticuloendothelial cells. Cytological examination of impression smears from skin lesions may reveal poxvirus inclusion bodies, but this is not a sensitive method. Immunohistochemistry using specific antibodies can confirm the presence of viral antigens in tissue sections. Histopathology is useful for differential diagnosis, as it can distinguish sheep pox from other diseases with similar clinical signs, such as contagious ecthyma, which shows epidermal proliferation and intracytoplasmic inclusion bodies but lacks the severe vasculitis and systemic involvement.

There is no specific antiviral treatment for sheep pox and goat pox. Treatment is primarily supportive and aimed at controlling secondary bacterial infections and alleviating clinical signs. Supportive care includes: 1) Providing a clean, dry, and comfortable environment with adequate ventilation. 2) Ensuring access to fresh water and high-quality feed, and offering soft, palatable feed if oral lesions are present. 3) Administering non-steroidal anti-inflammatory drugs (NSAIDs) such as flunixin meglumine (1.1-2.2 mg/kg IV or IM, q24h) or meloxicam (0.5 mg/kg PO or SC, q48h) to reduce fever and inflammation. 4) Using antibiotics to prevent or treat secondary bacterial infections, such as oxytetracycline (10-20 mg/kg IM or SC, q24h) or penicillin G procaine (20,000-40,000 IU/kg IM, q24h). 5) Providing supportive fluid therapy if animals are dehydrated or anorexic. 6) In severe cases, topical treatment of skin lesions with antiseptic solutions (e.g., chlorhexidine) may help prevent secondary infections. 7) Isolating affected animals to reduce spread. 8) Vaccination of in-contact animals with a live attenuated vaccine may be used in outbreak situations to reduce spread and severity, but it is not effective in animals already incubating the disease. 9) In endemic areas, routine vaccination is the mainstay of prevention. 10) Strict biosecurity measures, including quarantine of new animals, disinfection of premises and equipment, and control of animal movement, are essential to prevent introduction and spread of the virus. It is important to note that treatment is often ineffective in severe cases, and mortality can be high despite supportive care.

The prognosis for sheep pox and goat pox varies depending on the virulence of the virus strain, the species and age of the animal, and the presence of secondary complications. In general, the prognosis is poor for young animals (lambs and kids) and for animals with severe systemic disease, extensive skin lesions, or respiratory complications. Mortality rates can be as high as 50-100% in young animals, while adult animals with mild to moderate disease may recover with supportive care. The prognosis is also influenced by the breed, with highly susceptible breeds having a worse outcome. Animals that recover from the disease develop lifelong immunity, but they may have permanent scars and may experience reduced productivity. In a flock, the prognosis is guarded, as the disease can spread rapidly and cause significant economic losses. Early diagnosis, prompt implementation of biosecurity measures, and supportive care can improve the prognosis for individual animals and reduce the impact on the flock. However, in severe outbreaks, the prognosis for the flock is often poor, and culling of affected animals may be necessary to control the disease.

Follow-up care for animals recovering from sheep pox and goat pox includes: 1) Continued supportive care until full recovery, including monitoring of body temperature, appetite, and hydration status. 2) Providing a clean, dry, and stress-free environment to promote healing. 3) Monitoring for secondary bacterial infections, such as pneumonia and dermatitis, and treating promptly if they occur. 4) Ensuring adequate nutrition, especially for young animals, to support growth and immune function. 5) Isolating recovered animals from susceptible animals for at least 2-4 weeks after clinical recovery, as they may still shed virus. 6) Implementing strict biosecurity measures to prevent re-introduction of the virus, including disinfection of premises and equipment, and controlling animal movement. 7) Vaccinating recovered animals and the rest of the flock according to the recommended vaccination schedule. 8) Monitoring the flock for any new cases and reporting to veterinary authorities as required. 9) In endemic areas, maintaining a regular vaccination program to prevent future outbreaks. 10) Conducting a post-outbreak review to identify risk factors and improve biosecurity and management practices.

Clinical pearls: 1) Sheep pox and goat pox are highly contagious and notifiable; always consider them in the differential diagnosis of febrile animals with skin lesions, especially in endemic areas or after introduction of new animals. 2) The presence of papular skin lesions that progress to scabs, along with fever and respiratory signs, is highly suggestive of capripoxvirus infection. 3) Young animals are more severely affected and have higher mortality; prioritize supportive care for lambs and kids. 4) Vaccination is the most effective preventive measure in endemic areas; use a live attenuated vaccine and follow the manufacturer's recommendations. 5) Strict biosecurity, including quarantine of new animals and disinfection of premises, is essential to prevent introduction and spread. 6) In an outbreak, isolate affected animals immediately and report to veterinary authorities. 7) Supportive care with NSAIDs and antibiotics can reduce mortality and secondary infections. 8) Recovered animals have lifelong immunity and can be used as sentinels or for breeding. Pitfalls: 1) Misdiagnosis as contagious ecthyma (orf) or other skin diseases can lead to delayed control measures and further spread. 2) Failure to report suspected cases to authorities can result in legal consequences and uncontrolled spread. 3) Using antibiotics without addressing the underlying viral infection is ineffective and may lead to secondary infections. 4) Vaccinating animals already incubating the disease can exacerbate clinical signs. 5) Inadequate biosecurity, such as allowing visitors or sharing equipment, can introduce the virus to a naive flock. 6) Underestimating the environmental stability of the virus and failing to disinfect properly can lead to recurrence. 7) Not considering the zoonotic potential (though rare) and taking appropriate precautions when handling infected animals.

There is no specific antiviral treatment for sheep pox and goat pox. Supportive care and prevention of secondary infections are the mainstays of therapy. The following drug protocols are based on Plumb's Veterinary Drug Handbook and AASRP guidelines: 1) Flunixin meglumine: 1.1-2.2 mg/kg IV or IM, once daily, for up to 3 days, to reduce fever and inflammation. 2) Meloxicam: 0.5 mg/kg PO or SC, once every 48 hours, for up to 3 doses, as an alternative NSAID. 3) Oxytetracycline: 10-20 mg/kg IM or SC, once daily, for 3-5 days, to control secondary bacterial infections. 4) Penicillin G procaine: 20,000-40,000 IU/kg IM, once daily, for 3-5 days, as an alternative antibiotic. 5) Ceftiofur: 1.1-2.2 mg/kg IM or SC, once daily, for 3-5 days, for severe secondary infections. 6) Supportive fluid therapy: IV or oral electrolyte solutions, such as lactated Ringer's solution, at a rate of 50-100 ml/kg/day, for dehydrated animals. 7) Topical antiseptics: Chlorhexidine solution (0.5%) or povidone-iodine (1%) applied to skin lesions to prevent secondary infection. 8) Vitamin and mineral supplements: May be beneficial to support immune function, but no specific protocol is established. 9) Vaccination: Live attenuated vaccines are available for sheep pox and goat pox. The vaccine is administered subcutaneously or intradermally, with a dose of 0.5-1 ml per animal, depending on the product. Vaccination is recommended annually in endemic areas, and in outbreak situations, ring vaccination may be used. Withdrawal times for meat and milk must be observed for all drugs used, and local regulations should be followed.

Sheep pox and goat pox are well-studied diseases, and the literature provides strong evidence for their epidemiology, clinical presentation, and control. Key findings from landmark studies include: 1) The viruses are highly host-specific, but cross-species transmission can occur, and some strains may affect both sheep and goats (Babiuk et al., 2008). 2) The diseases are endemic in Africa, Asia, and the Middle East, and outbreaks are associated with significant economic losses (Tuppurainen et al., 2017). 3) Live attenuated vaccines are effective in preventing disease and reducing mortality, and vaccination is the cornerstone of control in endemic areas (Kitching, 2003). 4) PCR is the most sensitive and specific diagnostic tool, and it can differentiate between SPPV, GTPV, and LSDV (Le Goff et al., 2009). 5) Supportive care, including NSAIDs and antibiotics, can reduce mortality and secondary infections, but does not alter the course of the viral infection (Bhanuprakash et al., 2011). 6) Strict biosecurity measures, including quarantine and disinfection, are essential to prevent introduction and spread (OIE, 2019). 7) The viruses are stable in the environment, and contaminated fomites can transmit the disease (Carn, 1993). 8) Young animals are more susceptible and have higher mortality, and the disease is more severe in certain breeds (Yeruham et al., 2007). 9) The immune response is primarily cell-mediated, and recovered animals are immune to reinfection (Bowden et al., 2008). 10) The diseases are notifiable, and control programs should include reporting, culling, and vaccination (OIE, 2019). These findings underscore the importance of vaccination, biosecurity, and early diagnosis in controlling sheep pox and goat pox.