lumpy skin disease virus
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- lumpy skin disease virus
International Common Names
- English: Neethling virus
Taxonomic TreeTop of page
- Domain: Virus
- Group: "ssDNA viruses"
- Group: "DNA viruses"
- Family: Poxviridae
- Subfamily: Chordopoxvirinae
- Genus: Capripoxvirus
- Species: lumpy skin disease virus
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
Pathogen CharacteristicsTop of page
The early studies in South Africa showed that a transmissible agent was involved in the aetiology of LSD, and that it was not due to an allergic response to insect bites. However, early attempts to isolate the virus in tissue cultures were complicated by the isolation of three different virus groups from tissues that were taken from lesion samples. Firstly researchers isolated a herpes virus, which was subsequently shown to be bovine herpes virus group 2, subsequently known to cause Allerton or pseudo lumpy skin disease. On sub-inoculation into cattle, it produces an initial reaction, which for 1-2 days resembles that produced by LSD. This is a focal inflammation of the skin, which after 3-4 days rapidly becomes necrotic only in the very superficial epidermal and dermal layers (Alexander et al.,1957); the same virus causes bovine herpes mammilitis, which is a similar superficial necrotic disease affecting mainly the udder (Gibbs and Rweyemamu, 1977). A second herpes virus was isolated which belonged to the orphan herpes virus group 3. These are regularly isolated from the skin and other tissues of cattle and are not known to be associated with any disease problem. They do mislead diagnosticians however, who find herpes virus particles in LSD skin lesions (House et al., 1990).
A third virus isolate from the LSD lesions proved to be the one that reproduced the disease upon sub-inoculation into cattle. This was a poxvirus whose morphology and other characteristics suggested that it might be an orthopox virus. Further tests showed that the LSD virus was serologically and immunologically virtually identical with sheep and goat poxviruses of the Capripox genus (Alexander et al., 1957; Haig, 1957; Davies et al., 1971: Davies and Atema, 1981).
Capripox virus particles are ovoid in shape and both LSD and the sheep and goat isolates appear to be of similar size; 294 nm long and 262 nm wide with standard deviations of approximately +/- 20 nm. They have double stranded DNA and appear in forms covered by a membrane or mulberry-like components, similar to those described for members of the Orthopox viruses, which they closely resemble (Munz and Owen, 1966). The core has a characteristic dumbbell shape. The virus is ether- and chloroform-sensitive, it loses infectivity after 1 h at 60°C, is sensitive to sodium desoxycholate, losing infectivity after 1 h and is acid sensitive (Weiss, 1968). The virus, like most poxviruses, is stable over a wide range of temperatures and is highly resistant to desiccation in the presence of proteinaceous material. The virus can persist in the environment for long periods of time.
All strains that have been isolated are serologically and immunologically identical. All Capripox viruses are very closely related with 95.8% homology of the nucleotide sequences, but LSD is most closely allied to the African group of Capripox viruses, which include the sheep and goat poxviruses found in Africa. Other groups are from sheep or goats in other parts of the world and from either sheep or goats in Africa and the Middle East (Kitching et al., 1989). LSD virus is virtually indistinguishable from the African sheeppox and goatpox strains other than by its level of host adaptation in producing clinical LSD in cattle (Davies and Atema, 1981).
All the natural strains of LSD that have been isolated have been pathogenic, and no naturally occurring strains with modified virulence have been found. A strain from South Africa has been found to have greatly reduced virulence after 60 passages in tissue cultures and then 20 times in embryonated eggs. It is immunogenic and is extensively used as a vaccine despite the fact that it produces a granulomatous reaction at the site of inoculation (Weiss, 1968). A Kenyan LSD strain showed no modification of virulence after 70 passages in a foetal muscle cell line.
Disease(s) associated with this pathogen is/are on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's Handistatus database on disease occurrence. Please see the AHPC library for further information from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Aepyceros melampus||Experimental settings|
|Bos grunniens (yaks)||Wild host|
|Bos indicus (zebu)||Domesticated host|
|Bos taurus (cattle)||Domesticated host|
|Bubalus bubalis (Asian water buffalo)||Domesticated host|
|Capra hircus (goats)||Experimental settings|
|Gazella thomsonii||Experimental settings|
|Giraffa camelopardalis||Experimental settings|
|Oryx leucoryx||Wild host|
|Ovis aries (sheep)||Experimental settings|
Vectors and Intermediate HostsTop of page
ReferencesTop of page
Alexander RA; Plowright W; Haig DA, 1957. Cytopathic agents associated with lumpy skin disease of cattle. Bulletin Epizootic Diseases of Africa, 5:489-492.
Davies FG; Atema C, 1981. Relationships of capripox viruses found in Kenya with two Middle eastern strains and some orthopox viruses. Res. Vet. Sci., 31:253-255.
Davies FG; Krauss H; Lund LJ; Taylor M, 1971. The laboratory diagnosis of lumpy skin disease. Res. Vet. Sci., 12:123-127.
Gibbs EPJ; Rweyemamu MM, 1977. Bovine herpes viruses 2 & 3. Vet. Bull., 47:411-425.
Haig DA, 1957. Lumpy Skin disease. Bull. Epiz. Dis. Afr., 5:421-430.
House JA; Wilson TM; El Nakashly S; Karim IA; Ismail I; El Danaf N; Moussa AM; Ayoub NN, 1990. The isolation of lumpy skin disease virus and bovine herpesvirus-4 from cattle in Egypt. Journal of Veterinary Diagnostic Investigation, 2(2):111-115; 15 ref.
Kitching PR; Bhat BP; Black DN, 1989. The characterisation of African strains of capripoxvirus. Epid. Inf., 102:335-343.
Munz EK; Owen NC, 1966. Electron microscope studies on Lumpy skin disease virus type Neethling. Onderstepoort, J. Vet. Res., 33:1-8.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
Weiss KE, 1968. Lumpy skin disease. In: Virology Monographs, Vol. 3. Vienna, Austria; New York, USA: Springer-Verlag, 111-131.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
Distribution MapsTop of page
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