Definition
Sheep and goat pox (SGP) is an acute to chronic disease of sheep
and goats characterized by generalized pox lesions throughout the skin and mucous
membranes, a persistent fever, lymphadenitis, and often a focal viral pneumonia with
lesions distributed uniformly throughout the lungs. Subclinical cases may occur.
Etiology
The virus that causes SGP is a capripoxvirus, one of the largest
viruses (170-260 nm by 300-450 nm) (10). It is closely related to the virus that causes
lumpy skin disease; SGP virus and lumpy skin disease virus cannot be distinguished
serologically. There is only one serotype of SGP virus (SGPV). Various strains of SGPV
cause disease only in sheep, others only in goats, and some in both sheep and goats
(2,3,9).
The SGPV is very resistant to physical and chemical agents.
Host Range
Sheep and goat pox virus causes clinical disease in sheep and
goats. The virus replicates in cattle but does not cause clinical disease. The disease has
not been detected in wild ungulate populations.
Geographic Distribution
The disease is endemic in Africa, the Middle East, the Indian
subcontinent, and much of Asia.
A goat-pox-like disease was reported in the western United States
(15), but no attempt was made to indentify the agent with a reference serum against SGPV.
Serum samples from animals representing the affected group of goats were submitted to the
Foreign Animal Disease Diagnostic Laboratory (FADDL) at Plum Island, NY, and tested for
antibody to SGPV; no antibodies were found against SGPV. The serums were not tested for
antibodies to bovid herpesvirus 2 or contagious ecthyma at the FADDL. Unfortunately, the
viral isolate was not available for study. It is conclusive that what was reported in the
literature was not goat pox.
Transmission
Contact is the main means of transmission of SGPV. Inhalation of
aerosols from acutely affected animals, aerosols generated from dust contaminated from pox
scabs in barns and night holding areas, and contact through skin abrasions either by
fomites or by direct contact are the natural means of transmitting SGPV. Insect
transmission is possible. The virus can cause infection experimentally by intravenous,
intradermal, intranasal, or subcutaneous inoculation.
Incubation Period
Under field conditions, the incubation of SGP is between 4 and 8
days. Experimentally, the first sign (fever) may appear within 3 to 5 days after
inoculation. The course of the disease is 4 to 6 weeks with various stages of pox lesions
present at the same time. Full recovery may take up to 3 months.
Clinical Signs
Sheep and goat pox virus may cause subclinical infection; clinical
cases vary from mild to severe (3). The course of the disease in sheep and goats is
similar. The first signs may include fever, depression, conjunctivitis, lacrimation, and
rhinitis. Within a few days of the prodromal signs, pox lesions develop in the skin. These
are more easily observed on the wool-free or hair-free parts of the body such as the
perineum, inguinal area, scrotum, udder, axilla, and muzzle. Lesions do occur in wooled or
haired skin. Generally, more severe (extensive) skin lesions correlate with more severe
illness. The skin lesion first appears as an erythematous area (macula). This lesion
progress to a raised, slightly blanched lesion that presents erythema with edema in the
central part of the lesion (papule) (Fig. 103).
Pox lesions with a transudate, representing the vesicular stage of the lesion, may be
noted, but rarely is there any gross vesicle in the skin. The center of the lesion then
becomes depressed and gray (necrotic) and is surrounded by an area of hyperemia (Fig. 104). Late in the course of the
disease (2 to 4 weeks after the first signs), the lesion become dry, and a scab forms (Fig. 105). A characteristic feature of a
pox lesion is that lesions involve the entire epidermis and dermis and penetrate into the
subcutaneous tissue; it feels like a nodule. Depending on the severity of the skin lesion,
there may be a scar, an area devoid of wool or hair, after the lesion heals. Secondary
bacterial infection may complicate the healing process. The muzzle may be swollen, and the
nares and oral mucosa may have extensive lesions. In many cases, pneumonia may occur with
labored breathing and a respiratory rate approaching 90 per minute. Depression, anorexia,
and emaciation are common and may persist. Nervous signs may occur, but how these are
related to the SGPV infection is not clear.
Lambs and kids under 1 month of age may suffer a very severe
generalized form of SGP. The signs described above for older animals are exaggerated, and
there is an increased mortality.
Gross Lesions
At necropsy, skin lesions have congestion, hemorrhage, edema,
vasculitis, and necrosis and will be seen to involve all layers of the epidermis, dermis,
and, in severe cases, extend into the adjacent musculature. Lymph nodes draining affected
areas are enlarged up to eight times their normal size owing to extensive lymphoid
proliferation, edema, congestion, and hemorrhage.
Mucous membranes of the eye, mouth, and nose have pox lesions
that, in severe cases, may coalesce. In severe cases of SGP, the eyelids may be so
seriously affected that the proliferative lesions and inflammation cause the eyes to
close. Lesions on the muzzle and nares may coalesce, and proliferative changes and
inflammation may be extensive. Pox lesions may occur in the pharynx, epiglottis, and
trachea. These usually appear as rounded blanched areas surrounded by an area of
hyperemia. Occasionally there may be lesions in the epithelium of the rumen and omasum.
Pox lesions in the lungs may be severe and extensive; the lesions
are focal and uniformly distributed throughout the lungs as the result of hematogenous
infection (Fig. 106). Early lesions are
congested areas; these then progress to discrete areas of congestion and edema and finally
to white nodules. Areas distal to the pox lesions have lobular atelectasis. Mediastinal
lymph nodes are often enlarged up to five times their normal size and may be congested,
hemorrhagic, and edematous.
Pox lesions also may be present on the vulva, prepuce, testicles,
udder, and teats.
Morbidity and Mortality
The severity of SGP varies depending on the strain of the virus
and the age and breed of the animals affected (5). In adult sheep and goats, morbidity may
range to 80 percent with some subclinical infections. Mortality can approach 50 percent.
In susceptible lambs and kids under 1 month of age, morbidity may approach 100 percent,
and mortality may be as high as 95 perent. Factors that may complicate the course of the
disease and increase the mortality are poor nutrition, heavy parasitism, and severe
climatic conditions
Diagnosis
Field Diagnosis
A tentative diagnosis of SGP can be made on the basis of clinical
signs consisting of skin lesions, which on, palpation involve the whole thickness of the
skin, a persistent fever, lymphadenitis, and often pneumonia; mortality may approach 50
percent in adults and 95 percent in lambs and kids under 1 month of age.
Specimens for Laboratory
For laboratory diagnosis of SGP, skin biopsies of early lesions
can be used for virus isolation and histopathologic and electron microscopic studies.
Samples aspirated from enlarged lymph nodes can be used for virus isolation. Necropsy
samples should include a full set of tissues, but samples of the lungs, trachea, and rumen
containing gross lesions are especially valuable for histopathology. Samples for virus
isolation should be shipped to the laboratory under wet ice if they will arrive in 2 days
and shipped under dry ice if delivery will take longer (send in screw-capped vials with
the caps secured with electrical tape). Samples for histopathology should be preserved in
10 percent buffered formalin (DO NOT FREEZE). Serum samples should be taken from acute and
chronic cases. Followup serum samples from acute cases may be taken 2 to 3 weeks after the
first sample.
Laboratory Diagnosis
The laboratory procedures for the diagnosis of SGP include virus
isolation; observation of the virus by electron microscopy; detection of antibody by virus
neutralization, the indirect fluorescent antibody test (4), or both; and characteristic
histopathologic lesions (3).
Differential Diagnosis
Following are several diseases to consider in the differential
diagnosis for SGP:
Bluetongue — Animals are depressed and have a nonpurulent
conjunctivitis. The muzzle is swollen, congested, and edematous, and there may be a
coronitis. Deformed aborted fetuses and deformed newborn sheep and goats may be
encountered.
Peste des Petits Ruminants — Conjunctivitis, rhinitis, and
oral lesions that are white, raised, and necrotic are common. Pneumonia, diarrhea, and
mortality approaching 90 percent in lambs and kids under 1 month of age are characteristic
signs.
Contagious Ecthyma (contagious pustular dermatitis, ORF) —
This disease is most severe in lambs and kids. The proliferative pox lesions are common on
the muzzle and eyes of affected neonates; mortality may approach 50 percent. Nursing
females may have proliferative pox lesions on the teats and muzzle. This is a zoonotic
disease; lesions in attendants are not uncommon.
Photosensitization — Dry, flaky, inflamed areas are confined
to the nonpigmented parts of the skin.
Insect bites — The trauma from insect bites may cause local
inflammation, edema, and pruritus. Insects seldom bite mucous membranes.
Parasitic pneumonia — Severe signs of respiratory distress
may occur with extensive parasitic lesions; in these cases, there is no pox lesion in the
skin.
Caseous lymphadenitis — Focal, raised lesions in the skin
represent caseous abscesses; abscesses are not seen in SGP.
Streptothricosis (Dermatophilus congolensis infection)
— Lesions are superficial and often moist. Lesions are common in the skin of the
neck, axillary region, inguinal region, and perineum. The organism may be demonstrated by
Giemsa staining.
Mange - Scab-like skin lesions are seen in psoroptic mange.
Itching and scratching are not seen in SGP.
Vaccination
In endemic areas, vaccination is an effective means of controlling
losses from SGP. Killed vaccines have not proven to be practical under field conditions
because they do not provide solid lasting immunity. Several modified live virus vaccines
have been used for protection against SGP. The most widely employed vaccine is probably
the Romanian strain that has been used effectively for many years (14,16). The Kenya O 180
strain (6) is possibly the vaccine with the best safety and efficacy.
Control and Eradication
Prevention
The most likely manner for SGP to enter a new area is by
introduction of infected animals. Restrictions on the movement of animals and animal
products (meat, hair, wool, and hides) are essential to prevent introduction of SGP. Wool,
hair, and hides must be subjected to suitable decontamination procedures before entry into
nonendemic areas.
Control
If a new case is confirmed in a new area before extensive spread
occurs, the area should be quarantined, infected and exposed animals should be
slaughtered, and the premises cleaned and disinfected. Vaccination of susceptible animals
on premises surrounding the infected flock(s) should be considered.
If the disease has spread over a large area, the most effective
means of controlling losses from SGP is vaccination; however, consideration should be
given to eliminating infected and exposed flocks by slaughter; properly disposing of
animals and contaminated material; and cleaning and disinfecting contaminated premises,
equipment, and facilities.
Eradication
A carrier state has not been shown for SGPV. However, the virus
may persist for many months on contaminated premises. The imposition of quarantines on
areas and premises containing infected or exposed animals is required to prevent disease
spread. Depopulation of infected and exposed flocks should be used if limited spread has
occurred. If the disease has spread extensively, massive vaccination followed by cessation
of vaccination and control of animal movements from the area represent a strong strategy
to control and then eradicate SGP.
Public Health
There is no conclusive evidence that SGPV infects humans. A report
from India (17) that implied that goat pox caused human infection was merely based on
clinical signs. There was no attempt to isolate the causative virus or perform serology on
the convalescent serums of the three patients to differentiate the infection from
contagious ecthyma, which is a known zoonotic agent that occurs worldwide. A report from
Sweden (1) indicated that human infection occurred during an outbreak of goat pox.
Although serological studies seemed to indicate that the apparent causative agent of the
outbreak was not vaccinia or contagious ecthyma, no virus was isolated. Therefore, it
cannot be said that goat pox virus caused human infection.
GUIDE TO THE LITERATURE
1. BAKOS, VON K., and BRAG, S. 1957. Untersuchungen über
Ziegenpocken in Schweden. Nord. Vet.-Med., 9: 431-449.
2. DAVIES, F.G. 1976. Characteristics of a virus causing a pox
disease of sheep and goats in Kenya, with observations on the epidemiology and control. J.
Hyg.(Camb.), 76:163-171.
3. DAVIES, F.G. 1981. Sheep and Goat pox. In Virus diseases of
Food Animals. Vol 2., E.P.J. Gibbs ed., London:Academic Press, pp 733-748.
4. DAVIES, F.G., and OTEMA, C. 1978. The antibody response in
sheep infected with a Kenyan sheep and goat pox virus. J. Comp. Path., 88:205-210.
5. DAVIES, F.G., and OTEMA, C. 1981. Relationship of capripox
viruses in Kenya with two Middle Eastern strains and some orthopox viruses. Res. Vet.
Sci., 31:253-255.
6. DAVIES, F.G., and MBUGWA, G. 1985. The alterations in
pathogenicity of a Kenya sheep and goat pox virus on serial passage in bovine fetal muscle
cell cultures. J. Comp. Pathol., 95:565-572.
7. JUBB, K.V.F. and KENNLDY, P.C. Sheep pox In Pathology of
Domestic Animals, 3 ed., New York:Academic Press. pp 466-469.
8. KITCHING, R.P. BHAT, P.P., and BLACK, D.N. 1989. The
characterization of African strains of capripoxviruses. Epidemiology and Infection.
102:335-343.
9. KITCHING, R.P., and TAYLOR, W.P. 1985. Clinical and antigenic
relationship between isolates of sheep and goat pox viruses. Trop. Anim. Hlth. Prod.,
17:64-74.
10. MATTHEWS, R.E.F. 1982. Classification and nomenclature of
viruses. Intervirol., 17:1 -99.
11. MURRY, M., MARTIN, W.B., and KOYLU, A. 1973. Experimental
sheep pox: A histological and ultrastructure study. Res. Vet. Sci., 15:201-208.
12. PLOWRIGHT, W., and FERRIS, R.D. 1958. The growth and
cytopathogenicity of sheep pox virus in tissue cultures. Br. J. Exper. Pathol.,
39:424-435.
13. PLOWRIGHT, W., MacLEOD, W.G., and FERRIS, R.D. 1959. The
pathogenesis of sheep pox in the skin of sheep. J. Comp. Path., 69:400-413.
14. RAMYAR, H. 1965. Studies on the immunogenic properties of
tissue culture sheep pox virus. Zentralbl. Veterinarmed., 123:537-540.
15. RENSHAW, H.W., and DODD, A.G. 1978. Serological and
crossimmunity studies with contagious ecthyma and goat pox viruses isolated from the
Western United States. Arch. Virol., 56: 201-210.
16. SABBAN, M.S. 1957. The cultivation of sheep pox virus on the
chorioallantoic membrane of the developing chicken embryo. A.J.V.R., 18:618.
17. SAWHNEY, A.N., SINGH, A.K., and MALIK, B.S. 1972. Goat pox; an
anthropozoonosis. Indian J. Med. Res., 60: 683-684.
James A. House, D.V.M., Ph.D., Plum Island Animal Disease Center,
USDA. APHIS, NVSL, Foreign Animal Disease Diagnostic Laboratory, Greenport, NY
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