Lumpy skin disease

Abstract

Lumpy skin disease (LSD) is an infectious, eruptive, occasionally fatal disease of cattle caused by a virus of the family Poxviridae (genus Capripox), which is sometimes also termed as Neethling virus. LSD does not have a high fatality rate, usually less than 10%. LSD has an economical importance because of permanent damage to hides, the
prolonged debilitating effect especially in severely affected animals with consequent losses resulting from reduced weight gain, temporary or permanent cessation of milk production as a result of mastitis, temporary or permanent infertility or even sterility in bulls as a consequence of orchitis, and abortion in approximately 10% of infected pregnant cows.

Full text

Lumpy Skin Disease
Hawsar Yasin Abdulqa1, Heshu Sulaiman Rahman1,2,3*, Hiewa Othman Dyary1 and Hemn Hasan
Othman2
1Department of Clinic and Internal Medicine, College of Veterinary Medicine, University of Sulaimani, Street 11, Zone 217, Kurdistan Region,
Sulaimani New, Northern Iraq
2Department of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, University Putra Malaysia, Selangor, Malaysia
3Department of Medical Laboratory Sciences, College of Health Sciences, Komar University of Science and Technology, ChaqChaq-Qularasisy,
Kurdistan Region, Northern Iraq
*Corresponding author: Heshu Sulaiman Rahman, Department of Veterinary Clinical Sciences, Faculty of Veterinary Medicine, University Putra
Malaysia, Selangor, Malaysia, Tel: +964 772 615 9598; +964751 146 5757; E-mail: heshusr77@gmail.com
Received date: September 03, 2016; Accepted date: November 10, 2016; Published date: November 14, 2016
Citaon: Abdulqa HY, Rahman HS, Dyary HO, Othman HH (2016) Lumpy Skin Disease. Reproducve Immunol Open Acc 1:25.
Copyright: © 2016 Abdulqa HY, et al. This is an open-access arcle distributed under the terms of the Creave Commons Aribuon License, which
permits unrestricted use, distribuon, and reproducon in any medium, provided the original author and source are credited.
Abstract
Lumpy skin disease (LSD) is an infecous, erupve,
occasionally fatal disease of cale caused by a virus of the
family Poxviridae (genus Capripox), which is somemes also
termed as Neethling virus. LSD does not have a high fatality
rate, usually less than 10%. LSD has an economical
importance because of permanent damage to hides, the
prolonged debilitang eect especially in severely aected
animals with consequent losses resulng from reduced
weight gain, temporary or permanent cessaon of milk
producon as a result of mass, temporary or permanent
inferlity or even sterility in bulls as a consequence of
orchis, and aboron in approximately 10% of infected
pregnant cows.
Keywords: Lumpy skin; Viral infecon; Incidence
Introducon
Lumpy skin disease (LSD) is an exhausted viral disease that
characterised by high economic losses due to chronic debility in
aected animals, reduced milk producon, poor growth,
inferlity, aboron, and somemes death. Moreover, severe and
permanent damage can occur to hides, decreasing their
commercial value. The more suscepble breeds to LSD infecon
are related to ne-skinned breeds such as Holstein Friesian (HF)
and Jersey breeds [1,2]. In addion, the disease disrupts the
trade in cale and their products from LSD endemic countries
[3]. LSD was inially restricted to countries in sub-Saharan
Africa, although, there were unconrmed reports of the disease
in cale in Oman and Kuwait [4,5]. Since 2000, LSD outbreaks
have been reported across the Middle East and it is highly likely
the disease will become endemic at least in parts of the Region.
Incursion of LSD was reported for the rst me in Turkey and
Iraq in 2013, indicang that the disease has a potenal for
further spread to the European Union and Caucasus Region, as
well as to Asia [6].
Currently, it is widely accepted that LSD is transmied
mechanically by blood-feeding insects such as mosquitoes and
stable flies [7]. This is supported by earlier observaons that
associated most outbreaks with high abundance of bing flies
such as in areas along water courses and during wet seasons [8].
History
The clinical syndrome of LSD was rst described in Zambia in
1929. Inially, it was considered to be the result of either
poisoning or a hypersensivity to insect bites. More cases also
occur between 1943 and 1945 in Botswana (Bechuanaland),
Zimbabwe (Southern Rhodesia) and the Republic of South
Africa. A panzooc infecon in South Africa aected
approximately 8 million cale ll 1949 and consequently
incurred enormous economic losses [8-10].
LSD was rst found and diagnosed in East Africa (Kenya) in
1957, Sudan in 1972, and in West Africa in 1974. Tanzania,
Kenya, Zimbabwe, Somalia and the Cameroon, also reported an
outbreaks of epizooc LSD between 1981 and 1986 with
mortality rates of 20% in aected cale [11]. The disease was
restricted to some countries in sub-Saharan Africa between
1929 to 1986 [12].
The LSD also reported in Asian countries such as Kuwait in
1986 [13]. Later on, other countries such as United Arab
Emirates, Arab Republic of Yemen, and Democrac People’s
Republic of Yemen also conrmed or suspected some cases of
LSD [14].
Similarly, in the 1989 Israel outbreak of capripox is thought to
have been the result of infected Stomoxys calcitrans being
carried on the wind from Ismailiya in Egypt [15]. LSD virus
infecon in cale was also found in 1992 in Saudi Arabia [16].
Moreover, LSD infecon reported in Egypt in 2006, as a result of
imporng infected cale from the African Horn countries [17]
Mini Review
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and the disease spreads surprisingly swily throughout the
whole country in spite of an extensive vaccinaon program. In
the same year, LSD was again reported in Israel, and the Israel
authories speculated that the LSD virus may have already been
circulang in other Middle Eastern countries [18]. LSD outbreaks
have been reported in the Middle Eastern region since 1990.
According to the World Organizaon from Animal Health (OIE),
LSD has been found in Kuwait (1991), Lebanon (1993), Yemen
(1995), United Arab Emirates (2000), Bahrain (2003), Israel
(2006) and Oman (2010) [19].
Eology
Mature capripoxvirions have a more oval prole and larger
lateral bodies than orthopoxvirions [20]. Their average size is 320
x 260 nm [21].
The LSD virus grows and propagated to a high level in a wide
variety of cell cultures such as lamb and calf kidneys, adrenal
and thyroid glands, muscle and testes. Sheep embryonic kidneys
and lungs, rabbit fetal kidneys and skin, chicken embryo
broblasts, adult vervet monkey and baby hamster kidneys and
primary cell cultures of bovine dermis and equine lungs are also
used for that purpose [22].
The development of cytopathic eects may take up to 11 days
during primary isolaon [23]. There is only one serotype of LSD
virus which is very closely related serologically to the virus of
sheep and goat pox (SGP), in which it cannot be disnguished
easily by roune virus neutralizaon tests [24].
It has been found that LSD virus strains are essenally
idencal with each other and with a Kenyan strain (O 240/KS
sheep and goat pox virus (SGPV) using restricon endonuclease
studies of capripox virus. Other strains of SGPV from Kenya were
dierent from the O 240/KSGP strain but similar to each other
and resemble strains of SGPV from the Arabian Peninsula. The
Kenyan group of SGPV strain showed dierences when
compared with strains from India, Iraq, and Nigeria [25]. The LSD
virus is very resistant and well tolerated to most of physical and
chemical agents. The virus can remain in necroc skin for more
than 1 month, while remains viable in lesions in air-dried hides
for more than 2 weeks at ambient temperature [26].
Epidemiology and Transmission
Most of LSD virus infecons are thought to be transmied
through insects [8,26,27]. Pox viruses are highly resistant and
can remain viable in infected ssue for more than 120 days or
probably longer me. The virus is also found in blood, nasal
discharge, lacrimal secreon, semen and saliva, which
considered as main sources for LSD transmission [28].
The virus transmission is likely to be mechanical, although
there is no enough data demonstrang a parcular insect
species as a vector of LSD virus transmission. However, the virus
has been isolated from Stomoxys, Biomyia fasciata, Tabanidae,
Glossina and Culicoides species [28]. The role of all these insects
in the transmission of LSD remains to be evaluated in the
laboratory and under eld condions [29].
Cross-protecon between LSD virus and sheep or goat pox
viruses has been exploited by the use of sheep pox virus for the
immunizaon of cale against LSD in Kenya and in the Middle
East. LSD virus is remarkably stable that can be recovered from
necroc skin nodules kept at -80°C for 10 years and from
infected ssue culture stored at 4°C for 6 months.
Imported Bostaurus breeds such as Friesian cale with
necroc skin nodules usually show more severe signs of the
disease than thick-skinned indigenous breeds such as Afrikaner
and Afrikaner cross-breeds. Although, all age-groups are
suscepble, but cows in the peak of lactaon as well as young
animals show more severe clinical disease [30].
Incubaon Period
The incubaon period is ranged between 2 to 5 weeks in the
eld, while aer experimental infecon by intradermal
inoculaon, a skin lesion containing virus more probably
develops at the injecon area within 1-3 weeks [31].
Host suscepbility
Host suscepbility, dose and route of virus inoculaon aect
the severity of disease. Both male and female, all age groups
and various species and breeds of cale are considered to be at
risk and can get LSD infecon, which may followed by severe
and serious complicaons. Among more famous breeds,
Bostaurus breeds of cale are more suscepble for the disease
than Bosindicus breeds, although younger animals oen
aecng and show more severe disease than adult ones [32].
The disease is started with the onset of fever almost 1 week
aer entering the virus. It has been found that infecon with
LSD virus is not leading to the characteriscs in cale [26,33].
Pathogenesis
Intradermal or subcutaneous inoculaon of cale with LSD
virus results in the swelling at the site of injecon aer about 1
week and enlargement of the regional lymph nodes, while
generalized erupon of skin nodules usually occurs 7-19 days
aer injecon. Following intradermal inoculaon of cale with
LSDV, about 40-50% of animals will only develop a localized
lesion at the site of inoculaon or no clinical signs at all, whereas
those that have been inoculated intravenously are more inclined
to develop generalized lesions and more severe disease [2].
LSD virus in experimentally infected cale was demonstrated
in saliva 11 days aer the development of fever, in semen aer
22 days, and in skin nodules aer 33 days, while the virus not
found in urine or faeces. Viremia occurred aer the inial febrile
reacon and persisted for at least 4 days [34].
Various types of cells such as Pericytes, broblasts, epithelial
and endothelial cells can be infected by the virus. Viral
replicaon in pericytes, endothelial cells and probably some
cells in blood vessel and lymph vessel walls results in severe
vasculis and lymphangis in aected areas. In severe cases
infarcon may also result [35,36].
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Viral concentraons at the skin nodules, lymph nodes, liver,
kidneys, skeletal muscle, saliva and semen of infected animals
however, have not been determined [37,38].
Immunity aer recovery from a natural infecon is life-long in
most survivor cale; calves from immunized dam acquire
maternal anbody and are resistant to clinical disease for about
6 months [35].
Clinical signs and pathological observaons
Skin nodules about 0.5-5 cm in diameter in whole skin or
subcutaneous ssue and swollen supercial lymph nodes
especially subscapular and precrural lymph nodes are the main
symptoms of LSD infecon in most animals [39]. These nodules
can also aect the nasal, oral, ocular, and genital mucosa. Their
number may range from a few to several hundreds. Cutaneous
lesions may resolve rapidly or may indurate and persist as hard
lumps, or become sequestrated to leave deep ulcers partly lled
with granulaon ssue, which oen suppurates [40].
Papules most easily seen in hairless areas of perineum, udder,
inner ear, muzzle and eyelids [41], which leads to the
development of ulcerave lesions with excessive salivaon,
lacrimaon and nasal discharge that may contain LSD virus [42].
Some of the infected cale may develop oedematous swelling
of one or more legs and show lameness. This virus infecon is
more severe in cows at the peak of lactaon and causes a sharp
drop in milk producon due to high fever (40-41°C) and
secondary bacterial mass [39].
If extensive necrosis occurs in the upper respiratory tract,
secondary infected necroc ssue may be inhaled, resulng in
pneumonia. Stenosis of the trachea following healing of lesions
with scar ssue formaon few weeks or even months aer
infecon has been described [43].
Pathological lesions
Extensive post mortem lesions are appearing of deep nodules
in the skin that penetrate into the subcutaneous ssues and
adjacent muscles that results in vacuies, necrosis, oedema,
congeson with haemorrhage. The mucous membranes of the
oral and nasal cavies, pharynx, epiglos, tongue, nasal cavity,
trachea, lungs, tescles and urinary bladder may also contain
lesions. Enlargement of the supercial lymph nodes with
bronchopneumonia are more pronounced in infected cale
(Figures 1 and 2) [44].
Severe cases of infected cale with LSD are characterised by
edema and areas of focal lobular atelectasis in lungs; pleuris
with enlargement of the mediasnal lymph nodes. Synovis and
tendosynovis with brin in the synovial uid may also see [45].
Figure 1: Nodules in lungs (A), Lesions in the m/m throughout
the GIT (B) (CFSPH, 2011).
Figure 2: loss in income because of lower producon (deaths,
milk and meat, aborons, lowered breeding potenal, and
damage to valuable hides), and the costs of drugs to treat sick
animals.
Diagnosis
At present me, no commercial diagnosc test kits for LSD
virus detecon are available yet [19]. Thus, the tentave
diagnosis of LSD is usually based on the characterisc clinical
signs, dierenal diagnosis, and the clinical diagnosis which is
conrmed by laboratory tests using convenonal polymerase
chain reacon (PCR) techniques [46].
LSD should be suspected clinically when there are
characterisc skin nodules, fever and enlargement of supercial
lymph nodes [44]. The lumps on the skin follows within 2 days
which may appear anywhere on the body from the nose to the
tail. Same characterisc lesions appear in the mucosa of the
mouth, vagina and conjuncva. A purulent nasal and ocular
discharge are not rare [34].
Laboratory conrmaon of LSD virus can be done very rapidly
using a PCR method specic for Capri poxviruses or by the
demonstraon of typical Capri pox virions in biopsy material or
desiccated crusts using the transmission electron microscopy
(TEM) [12]. Roune diagnosc techniques are described in the
OIE Manual of Diagnosc Tests and Vaccines [44,47,48].
Capri poxvirus is disnguished from Para poxvirus, which
causes bovine popular stomas and pseudo cowpox, but
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cannot be disnguished morphologically from cowpox and
vaccine virus infecons of bovine [32].
Conrmaon of LSD in a new area requires virus isolaon and
idencaon [19]. LSD virus can propagate in bovine, caprine or
ovine cell cultures; especially lamb tess cells [51]. The
cytopathic eect and the intra-cytoplasmic locaon of inclusion
bodies can be used to disnguish LSD virus from the herpes
virus, the causave agent of pseudo lumpy skin disease.
Recently, direct immunouorescence, virus neutralizaon test,
enzyme-linked immunosorbent assay (ELISA) and immune
blong (Western blong) can be used for the idencaon of
LSD virus angens in infected animals. However, the immunity to
LSD infecon is predominantly cell mediated, thus the virus
neutralizaon test is not suciently sensive to idenfy animals
with LSD virus due to low level of neutralizing anbody
development.
Genome detecon using Capri pox virus-specic primers for
the aachment protein and fusion protein a gene has been
reported, and several convenonal and real-me PCR methods
have been established to be used on blood, ssue and semen
specimens [32].
Cross-reacons occur with bovine papular stomas and
pseudo cowpox virus when agar gel immune diusion test is
used [44].
Indirect Fluorescent Anbody Test (IFAT) demonstrated to be
suitable for use in retrospecve serological surveys in a study
carried out in Ethiopia, and it was evaluated test for accuracy
[49]. The IFAT is a serological test for Capri pox Virus. It was used
to detect serum anbody against Capri pox virus and
dierenate serological posive and negave animals.
Dierenal diagnosis
Misdiagnosis of skin lumps and misreporng of infecon have
probably been common over the years due to veterinarians not
having previous experience of the disease [51].
Although severe LSD is highly characterisc, but milder forms
can be confused and misdiagnosed with numerous diseases and
infecons such as pseudo lumpy skin disease (Bovine Herpes
virus), bovine papular stomas (Para poxvirus), pseudo cowpox
(Para poxvirus), Vaccinia virus and Cowpox virus
(Orthopoxviruses) infecons, dermatophilosis, insect or ck
bites, besnoiosis, rinderpest, demodicosis, Hypoderma bovis
infecon, photosensisaon, urcaria, cutaneous tuberculosis
and onchocercosis [52].
Economic importance of the disease
Lumpy skin disease is considered as an economically
important disease of cale; serious economic losses can follow
outbreaks that have a high morbidity and can produce a chronic
debility in infected cale [50]. The economic losses due to this
disease is due to reduced milk producon, in appete and
weight loss, poor growth, aboron, inferlity, skin damage and
pneumonia especially in animals with l mouth and respiratory
tract lesions [32].
Even though, the morbidity and mortality rates of LSD are
usually low, it is an economically important disease of cale in
Africa because of the prolonged loss of producvity of dairy and
beef cale, use of the animals for tracon, decrease in body
weight, mass, severe orchis, which may result in temporary
inferlity and somemes permanent sterility. Furthermore, LSD
induced economic losses due to reducon of wool and meat
qualies [53].
Currently, there is one project in Ethiopia (NAHDIC with
integraon of NVI and MoA) on improvement of the ecacy of
LSD vaccines. Capri pox viruses are classied as potenal agents
for agro terrorism and listed as noable diseases, since they
cause serious economic losses [54].
Treatment
Till this moment, no specic anviral treatment for LSD
infecon has been found. Sick animals should be removed from
the herd and follow supporve treatment such as anbiocs,
an-inammatory drugs, and vitamin injecons. These therapies
are usually the chances for the development of secondary
bacterial infecons, inammaon and fever, and thus improving
the appete of the animal [55].
Generally, animals infected with LSD will recover as mortality
is usually less than 3%. If secondary bacterial infecon
developed, complete recovery may takes more than 6 months or
longer [26].
Control and prevenon
The bing ies and certain ck species are probably the most
important method of transmission of the disease, control by
quaranne and movement control is generally not very
eecve. In endemic areas, control is therefore essenally
conned to immunoprophylaxis [30].
Two approaches to immunizaon against LSD have been
followed. In South Africa, the Neethling strain of LSD was
aenuated by 20 passages on the chorio-allantoic membranes
of hens' eggs, but the vaccine virus is now propagated in cell
culture [56].
In Kenya, the vaccine produced from sheep or goat pox
viruses produces a solid immunity in cale to LSD. This vaccine
has the disadvantage that it can only be used in countries where
sheep pox or goat pox is endemic as the vaccine could otherwise
provide a source of infecon for the suscepble sheep and goat
populaons.
Suscepble adult cale should be vaccinated annually to
ensure adequate protecon against LSD. Approximately 50% of
cale develop swelling that is 10-20 mm in diameter at the point
of inoculaon, and this may be accompanied by a temporary
drop in milk yield in dairy cows. The swelling disappear within a
few weeks. Calves under 6 months whose dams were either
naturally infected or immunized should not be vaccinated in
order to preclude interference from maternal anbody.
However, calves born from suscepble cows are very suscepble
and should be vaccinated to prevent outbreaks [30].
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References
1. Davies FG (1991) Lumpy skin disease, a Capripox Virus Infecon in
Cale in Africa. FAO, Rome, Italy.
2. Barnard B, Munz E, Dumbell K, Prozesky L (1994) Lumpy skin
disease. In: Coetzer J, Thomson G, Tusn R (Edn), Infecous
Disease of Livestock. Oxford University Press, Oxford, Capetown,
pp: 605-612.
3. Babiuk S, Bowden TR, Parkyn G, Dalman B, Manning L, et al.
(2008) Quancaon of lumpy skin disease virus following
experimental infecon in cale. Transbound Emerg Dis 55:
299-307.
4. House JA, Wilson TM, El Nakashly S, Karim IA, Ismail I, et al. (1990)
The isolaon of lumpy skin disease virus and bovine herpesvirus-4
from cale in Egypt. J Vet Diagn Invest 2: 111–115.
5. Kumar SM (2011) An Outbreak of Lumpy Skin Disease in a Holstein
Dairy Herd in Oman: A Clinical Report. Asian J Anim Vet Adv 6:
851-859.
6. Barnard BJH (1981-1987) Onderstepoort Veterinary Instute,
South Africa. Personal observaon.
7. Carn VM, Kitching RP (1995) An invesgaon of possible routes of
transmission of lumpy skin disease virus (Neethling). Epidemiol
Infect 114: 219-226.
8. Von Backstrom U (1945) Ngamiland cale disease. Preliminary
report on a new disease, the eological agent being probably of
an infecous nature. Jl SA Vet Med Assn 16: 29-35.
9. Thomas AD, Mare CVE (1945) Knopvelsiekte. J S Afr Vet Med Assoc
16: 36-43.
10. Diesel AM (1949) The Epizooology of Lumpy Skin Disease in
South Africa. In Proceedings of the 14th Internaonal Veterinary
Congress, London, U.K., pp: 492-500.
11. Brenner J, Haimovitz M, Oron E, Stram Y, Fridgut O, et al. (2006)
Lumpy skin disease (LSD) in a large dairy herd in Israel. Refu Vet,
61: 73-77.
12. Davies FG (1981) Lumpy skin disease. In Virus diseases of food
animals. E.P. J. Gibbs, edn. New York: Academic Press, pp:
751-764.
13. Ordner G, Lefervre PC (1978) La dermatosenodulairecontagieuse
des bovines. Etudes etsytheses de l’Instutd’Elevage et de
Medicine Veterinarie Tropicale, Maison-Alfort, Paris, pp. 92.
14. Oce Internaonal Des Epizooes (1990) World Animal Health 5:
703. 1990.
15. Yeruham I, Nir O, Braverman Y, Davidson M, Grinstein H, et al.
(1995) Spread of lumpy skin disease in Israel dairy herds. Vet Rec
137: 91-93.
16. Greth A, Gourreau JM, Vassart M, Ba-Uy N, Wyers M, et al. (1992)
Capripoxvirus disease in an Arabian Oryx (Oryx leucoryx) from
Saudi Arabia. Jl Wld Dis 28: 295-300.
17. El-Kholy AA, Soliman HMT, Abdelrahman KA (2008) Polymerase
chain reacon for rapid diagnosis of a recent lumpy skin disease
virus incursion to Egypt. Arab J Biotech 11: 293-302.
18. Brenner J, Bellaiche M, Gross E, Elad D, Oved Z, et al. (2009)
Appearance of skin lesions in cale populaons vaccinated against
lumpy skin disease. Vaccine 27: 1500-1503.
19. Tuppurainen ESM, Oura CAL (2012) Review: Lumpy Skin Disease:
An Emerging Threat to Europe, the Middle East and Asia.
Transbound Emerg Dis, 59: 40-48.
20. Munz EK, Owen NC (1966) Electron microscopic studies on lumpy
skin disease virus type 'Neethling'. Onderstepoort J Vet Res 33:
3-8.
21. Ghaboussi B (1978) Morphological and physical characteriscs of
sheep and goat pox viruses. Archiv Instut Razi 30: 107-115.
22. Alexander RA, Plowright W, Haig DA (1957) Cytopathogenic agents
associated with lumpy skin disease of cale. Bull Epizoot Dis Afr 5:
489-492.
23. Weiss KE, Geyer SM (1959) The eect of lactalbuminhydrolysate
on the cytopathogenesis of lumpy skin disease virus in ssue
culture. Bull Epizoot Dis Afr 7: 243.
24. Burdin ML (1959) The use of histopathological examinaons of
skin material for the diagnosis of lumpy skin disease in Kenya. Bull
Epizoot Dis Afr 7: 27-36.
25. Kitching RP, Bhat PP, Black DN (1989) The characterizaon of
African strains of capripoxviruses. Epidemiol Infect, 102: 335-34.3.
26. Weiss KE (1968) Lumpy skin disease. In Virology Monographs, 3,
New York: Springer Verlag, pp: 111-131
27. MacOwan KDS (1959) Observaons on the epizooology of lumpy
skin disease during the rst year of its occurrence in Kenya. Bull
Epizoot Dis Afr 7: 7-20.
28. hp://www.fao.org/docrep/u4900t/u4900t0d.htm
29. Kitching RP, Mellor PS (1986) Insect transmission of
capripoxviruses. Res Vet Sci 40: 255-258.
30. Coetzer JAW, Tuppurainen E (2004) Lumpy skin disease, in:
Infecous diseases of livestock, edited by Coetzer JAW, Tusn RC.
Cape Town: Oxford University Press Southern Africa, 2: 1268-1276.
31. Haig DA (1957) Lumpy skin disease. Bull Epizoot Dis Afr 5:
421-430.
32. OIE (2010) Terrestrial Manual of Lumpy Skin Disease, Chapter
2.4.14. Version adopted by the World Assembly of Delegates of
the OIE in May 2010, OIE, Paris.
33. Onderstepoort J (2005) Vet Res 72: 153-164.
34. Weiss WE (1968) Lumpy Skin disease. In Emerging Diseases of
Animals. FAO Agricultural Studies Bullen, 61, 179-201.
35. Prozeesky L, Barnard BJH (1981) A study of the pathology of lumpy
skin disease in cale. Onderstepoort J Vet Res 49: 167-175.
36. Capsck PB (1959) Lumpy skin disease: Experimental infecon.
Bull Epizoot Dis Afr 7: 51- 62.
37. Thomas AD, Robinson EM, Alexander RA (1945) Lumpy skin
disease-knopvelsiekte. Onderstepoort J Vet Res, Veterinary
Newsleer, pp: 10.
38. Tuppurainen ESM (2005) The detecon of lumpy skin disease virus
in samples of experimentally infected cale using dierent
diagnosc techniques. Onderstepoort J Vet Res 72: 153-64.
39. hp://c.ymcdn.com/sites/www.eazwv.org/resource/resmgr/
Files/Transmissible_Diseases_Handbook/Fact_Sheets/
039_Lumpy_Skin_Disease.pdf
40. Wainwright Sh, El Idrissi A, Maoli R, Tibbo M, Njeumi F, et al.
(2013) Emergence of lumpy skin disease in the Eastern
Mediterranean Basin countries. Emp Watch 29: 2.
41. Babiuk S, Bowden TR, Boyle DB, Wall ace DB, Kitching RP (2008)
Capripoxvi ruses: An Emerging Worldwide Threat to Sheep, goats
and Cale. Transbound Emerg Dis 55: 263-572.
Reproductive Immunology: Open Access
Vol.1 No.4:25
2016
© Under License of Creave Commons Aribuon 3.0 License 5

42. DE Boom HPA (1948) Knopvelsiekte. South African Scienc
Bullen 1: 44-46.
43. CFSPH (2008) The Central for Food Security and Public Health,
Iowa State University, College of Veterinary Medicine.
44. hp://web.oie.int/eng/maladies/Technical%20disease%20cards/
LUMPY%20SKIN%20DISEASE_FINAL.pdf
45. Tuppurainen SM (2005) The detecon of lumpy skin disease virus
in samples of experimentally infected cale using dierent
diagnosc techniques, Onderstepoort J Vet Res, 72: 153-164.
46. OIE (2011) Lumpy Skin Disease. Terrestrial Animal Ethiopian
Veterinary Associaon (EVA). Addis Health Code. OIE, Paris.
47. El-Kenawy AA, El-Tholoth MS (2011) LSD Virus Idencaon in
Dierent Tissues of Naturally Infected Cale and Chorioallantoic
Membrane of Embryonated Chicken Eggs Using Immune
uorescence Immunovperoxidase Techniques and Polymerase
Chain Reacon. Int J Virol 7: 158-166.
48. Gari GF, Biteau-Coroller C, LeGo P, Roger CF (2008) Evaluaon of
Indirect Fluorescent Anbody Test (IFAT) for the Diagnosis and
Screening of Lumpy Skin Disease Using Bayesian Method. Vet
Microbiol 129: 269-280.
49. Woods JA (1988) Lumpy skin disease: A review. Trop Anim Health
Prod. 20: 11-17.
50. Siraw B (1987) Bovine Dermatophilus Infecon in Mend You
Province: Prevalence and Relave Ecacy of Dierent Drugs
against the Disease. Onderstepoort j vet res 83: 1.
51. Yacob HB, NesanetandDinka A (2008) Part II:Prevalence of major
skin diseases in cale, sheep andgoats at Adama Veterinary Clinic,
Oromia regionalstate, Ethiopia. Rev Med Vet 159: 455-461.
52. Davies FG (1991) Lumpy skin disease of cale: a growing problem
in Africa and the Near East. World Animal Review 68: 37-42.
53. Davies FG (1982) Observaons on the epidemiology of lumpy skin
disease in Kenya. J Hyg 88: 95-102.
54. Van Rooyen P, Munz KE, Weiss KE (1969) The Opmal Condions
for the mulplicaon of Neethling-type lumpy skin disease virus in
embryonated eggs. Onderstepoort J Vet Res 36: 165-174.
55. Capsck PB, Prydie J, Coackley W, Burdin ML (1959) Protecon Of
cale against 'Neethling' type virus of lumpy skin disease. Vet Rec
71: 422.
56. Nawthe DR, Asagba MO, Abegunde A, Ajayi SA, Durkwa L (1982)
Some observaons on the occurrence of lumpy skin disease in
Nigeria. Zentralbl Veterinarmed B 29: 31-36.
Reproductive Immunology: Open Access
Vol.1 No.4:25
2016
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