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visna/maedi

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visna/maedi

Summary

  • Last modified
  • 27 July 2017
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • visna/maedi
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Identity

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Preferred Scientific Name

  • visna/maedi

International Common Names

  • English: maedi; maedi, visna, encephalitis, hard udders, progressive pneumonia, arthritis; maedi-visna; ovine progressive pneumonia; progressive pneumonia of sheep; visna; visna-maedi

Local Common Names

  • South Africa: zwoegersiekte

English acronym

  • MV
  • VM

Overview

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Visna/maedi virus was first isolated in the 1950s by Sigurdsson in Iceland (Carey and Dalziel, 1993; Pepin et al., 1998). By 1939 it had become clear that sheep in Iceland were suffering from a previously unknown condition, and this could be traced back to import of clinically healthy, infected Karakul rams from Germany in 1933. Following its discovery in Iceland, visna/maedi virus infections were detected in many other countries. The Icelandic terms for the most prominent clinical symptoms, progressive pneumonia (maedi) and progressive paralysis (visna), gave the disease its name.

The disease is categorised as a List B disease according to the Office International des Epizooties (OIE), based on its economic impact. The outbreak in Iceland is considered to have been the most severe to-date, with an estimated loss of 150,000 diseased animals and 650,000 destroyed (Carey and Dalziel, 1993). Only sheep and goats become naturally infected by visna/maedi virus. Transmission of visna/maedi virus occurs horizontally by inhalation of respiratory secretions, and vertically through colostrum and milk containing virus-infected cells and free virus (de la Concha-Bermejillo, 1997). The virus was a prototype of the virus subfamily the Lentivirinae (Narayan et al., 1997), and the pathogenesis is characterised by a long incubation period, and a slow development of disease after infection that may take months to several years. The disease may affect various organs, leading to respiratory and neurological signs, and to chronic mastitis and arthritis. Usually the disease starts with dyspnea, which becomes particularly obvious when the animal is exercised. At postmortem, the lungs are heavier and show decreased elasticity and fibrosis, which is more prominent when disease is in an advanced state. The neurological signs include affected gait, paresis of the hind limbs that progresses until paraplegia develops (Carey and Dalziel, 1993). The diagnosis of disease can be performed by detection of visna/maedi virus-specific antibodies by agar gel immunodiffusion (AGID), ELISA or immunoblot, and by detection of the virus by PCR. Virus isolation is difficult.

The prevention of visna/maedi virus infection may occur by two main methods: by detection of visna/maedi virus-infected animals and removal of the herd, and by raising newborn lambs separately from their infected mothers. There is no vaccine available. Visna/maedi virus infections are a useful animal model for other Lentivirus infections such as HIV, and in the development of antiviral drugs (Thormar et al., 1995).

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease 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.

Hosts/Species Affected

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Only sheep and goats are infected in vivo by visna/maedi virus (Carey and Dalziel, 1993).

Distribution

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After the discovery of the causative virus in Iceland, an examination of the typical clinical symptoms indicated that the disease had been previously described in the USA (Gates et al., 1978), and South Africa. Further study showed that the disease was present in sheep in Peru (Madewell et al., 1987), in Canada (Dukes et al., 1979; Campbell et al., 1994), the Czech Republic (Celer et al., 1997), Switzerland (Schaller et al., 2000), Italy (Caporale et al., 1983), the UK (Barber, 1981; Dawson and Wilesmith, 1985; Pritchard et al., 1995; Buchanan, 2001), Ethiopia (Ayelet et al., 2001), Nigeria (Belino and Ezeifeka, 1984), and the Netherlands (Houwers, 1980).

For current information on disease incidence, see OIE's WAHID Interface.

Distribution Table

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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.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanNo information availableOIE, 2009
ArmeniaDisease not reportedOIE, 2009
AzerbaijanDisease not reportedOIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshDisease never reportedOIE, 2009
BhutanDisease never reportedOIE, 2009
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
CambodiaNo information availableOIE, 2009
ChinaDisease never reportedOIE, 2009
-Hong KongDisease never reportedOIE, 2009
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaDisease not reportedOIE, 2009
IndonesiaDisease never reportedOIE, 2009
IranDisease never reportedOIE, 2009
IraqDisease not reportedOIE, 2009
IsraelPresentOIE, 2009
JapanDisease never reportedOIE, 2009
JordanDisease never reportedOIE, 2009
KazakhstanDisease never reportedOIE, 2009
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease never reportedOIE, 2009
KuwaitDisease not reportedOIE, 2009
KyrgyzstanDisease not reportedOIE, 2009
LaosDisease never reportedOIE, 2009
LebanonDisease not reportedOIE, 2009
MalaysiaDisease never reportedOIE, 2009
-Peninsular MalaysiaDisease never reportedOIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakDisease never reportedOIE Handistatus, 2005
MongoliaNo information availableOIE, 2009
MyanmarNo information availableOIE, 2009
NepalDisease never reportedOIE, 2009
OmanDisease not reportedOIE, 2009
PakistanDisease not reportedOIE, 2009
PhilippinesDisease never reportedOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaDisease not reportedOIE, 2009
SingaporeDisease never reportedOIE, 2009
Sri LankaDisease never reportedOIE, 2009
SyriaDisease not reportedOIE, 2009
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanDisease not reportedOIE, 2009
ThailandDisease never reportedOIE, 2009
TurkeyNo information availableOIE, 2009
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesNo information availableOIE, 2009
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamDisease never reportedOIE, 2009
YemenNo information availableOIE, 2009

Africa

AlgeriaDisease not reportedOIE, 2009
AngolaDisease never reportedOIE, 2009
BeninDisease not reportedOIE, 2009
BotswanaDisease not reportedOIE, 2009
Burkina FasoNo information availableOIE, 2009
BurundiDisease never reportedOIE Handistatus, 2005
CameroonDisease never reportedOIE Handistatus, 2005
Cape VerdeDisease never reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE, 2009
CongoNo information availableOIE, 2009
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireDisease not reportedOIE Handistatus, 2005
DjiboutiDisease not reportedOIE, 2009
EgyptDisease never reportedOIE, 2009
EritreaNo information availableOIE, 2009
EthiopiaDisease not reported2005Pépin et al., 1998; Ayelet et al., 2001; OIE, 2009
GabonNo information availableOIE, 2009
GambiaNo information availableOIE, 2009
GhanaNo information availableOIE, 2009
GuineaNo information availableOIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaNo information availableOIE, 2009
LesothoDisease never reportedOIE, 2009
LibyaDisease never reportedOIE Handistatus, 2005
MadagascarDisease never reportedOIE, 2009
MalawiDisease never reportedOIE, 2009
MaliNo information availableOIE, 2009
MauritiusDisease never reportedOIE, 2009
MoroccoDisease never reportedOIE, 2009
MozambiqueDisease not reportedOIE, 2009
NamibiaDisease not reportedOIE, 2009
NigeriaDisease never reportedNULLBelino and Ezeifeka, 1984; Pépin et al., 1998; OIE, 2009
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE, 2009
Sao Tome and PrincipeLast reported2003OIE Handistatus, 2005
SenegalNo information availableOIE, 2009
SeychellesDisease not reportedOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaDisease not reported2004Pépin et al., 1998; OIE, 2009
SudanDisease never reportedOIE, 2009
SwazilandDisease never reportedOIE, 2009
TanzaniaNo information availableOIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reportedOIE, 2009
UgandaNo information availableOIE, 2009
ZambiaDisease never reportedOIE, 2009
ZimbabweDisease never reportedOIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaPresentNULLDukes et al., 1979; Campbell et al., 1994; Pépin et al., 1998; OIE, 2009
GreenlandDisease never reportedOIE, 2009
MexicoDisease never reportedOIE, 2009
USARestricted distributionNULLGates et al., 1978; Pépin et al., 1998; OIE, 2009

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaDisease never reportedOIE, 2009
CubaDisease never reportedOIE, 2009
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE, 2009
El SalvadorDisease never reportedOIE, 2009
GuadeloupeNo information availableOIE, 2009
GuatemalaDisease never reportedOIE, 2009
HaitiDisease never reportedOIE, 2009
HondurasDisease never reportedOIE, 2009
JamaicaDisease never reportedOIE, 2009
MartiniqueDisease not reportedOIE, 2009
NicaraguaDisease never reportedOIE, 2009
PanamaDisease never reportedOIE, 2009
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease not reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaDisease not reportedOIE, 2009
BoliviaDisease never reportedOIE, 2009
BrazilDisease never reportedOIE, 2009
ChileDisease not reportedOIE, 2009
ColombiaDisease not reportedOIE, 2009
EcuadorDisease never reportedOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedOIE, 2009
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayDisease never reportedOIE Handistatus, 2005
PeruAbsent, reported but not confirmedNULLMadewell et al., 1987; Pépin et al., 1998; OIE, 2009
UruguayDisease never reportedOIE, 2009
VenezuelaDisease never reportedOIE, 2009

Europe

AlbaniaNo information availableOIE, 2009
AndorraSerological evidence and/or isolation of the agentOIE Handistatus, 2005
AustriaNo information availableOIE, 2009
BelarusNo information availableOIE, 2009
BelgiumDisease not reportedOIE, 2009
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaDisease not reportedOIE, 2009
CroatiaDisease never reportedOIE, 2009
CyprusPresentOIE, 2009
Czech RepublicDisease not reported2003Celer et al., 1997; Pépin et al., 1998; OIE, 2009
DenmarkAbsent, reported but not confirmedOIE, 2009
EstoniaPresentOIE, 2009
FinlandDisease not reportedOIE, 2009
FranceNo information availableOIE, 2009
GermanyPresentOIE, 2009
GreecePresentOIE, 2009
HungaryRestricted distributionOIE, 2009
IcelandDisease not reported1965Pépin et al., 1998; OIE, 2009
IrelandDisease not reportedOIE, 2009
Isle of Man (UK)Disease not reportedOIE Handistatus, 2005
ItalyNo information availableNULLCaporale et al., 1983; Pépin et al., 1998; OIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease not reportedOIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease never reportedOIE, 2009
LuxembourgPresentOIE, 2009
MacedoniaNo information availableOIE, 2009
MaltaPresentOIE, 2009
MoldovaDisease never reportedOIE Handistatus, 2005
MontenegroDisease not reportedOIE, 2009
NetherlandsPresentNULLHouwers, 1980; Pépin et al., 1998; OIE, 2009
NorwayPresentOIE, 2009
PolandPresentOIE, 2009
PortugalPresentOIE, 2009
RomaniaPresentOIE, 2009
Russian FederationNo information availableOIE, 2009
SerbiaDisease not reportedOIE, 2009
SlovakiaDisease not reportedOIE, 2009
SloveniaPresentOIE, 2009
SpainRestricted distributionOIE, 2009
SwedenPresentOIE, 2009
SwitzerlandPresentNULLPépin et al., 1998; Schaller et al., 2000; OIE, 2009
UKPresentNULLBarber, 1981; Dawson and Wilesmith, 1985; Pritchard et al., 1995; Pépin et al., 1998; Buchanan, 2001; OIE, 2009
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease never reportedOIE, 2009
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)No information availableOIE Handistatus, 2005

Oceania

AustraliaDisease never reportedOIE, 2009
French PolynesiaDisease not reportedOIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE Handistatus, 2005

Pathology

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Unlike other lentiviruses such as HIV, visna/maedi virus does not lead to severe generalised immunosuppression; secondary infections with opportunistic pathogens are not routinely seen in affected flocks .

Respiratory disease leads to a classical interstitial pneumonia. Massive numbers of mononuclear cells infiltrate the interstitial spaces in the lungs and there is smooth muscle hyperplasia. Alveoli are obliterated by these infiltrations, and interalveolar septa are thickened by accumulation of plasma cells, mononuclear phagocytes and lymphocytes. On postmortem examination, the lungs may be 2-4 times heavier than normal with decreased elasticity and fibrosis. Regional lymphnodes are enlarged and contain accompanying formation of lymphoid follicles with active germinal centres.

The neurological form of the disease is characterised by chronic and active meningoencephalomyelitis and chorioiditis with massive infiltrations of mononuclear cells around the blood vessels, microglial nodules, and astrogliosis. There is demyelination and destruction of the white matter of the brain, cerebellum and also in the dorsal and lateral columns of the spinal cord (Carey and Dalziel, 1993; Narayan et al., 1997). The predominantly inflammatory nature of the lesions in visna/maedi virus-induced disease suggests that the disease mechanism could be immunopathological in nature. Supporting evidence for this is the major increase in early nervous system lesions in immunosuppressed sheep, which occurs without a demonstrable decrease in virus replication (Nathanson et al., 1976). In particular, visna/maedi virus encephalopathy may have in part a cellular autoimmune pathogenesis (Naryan et al., 1997).

An increase in MHC-II-expressing inflammatory cells, including alveolar macrophages, can be found in the lungs of affected animals, concomitant with a release of interferon. This may indicate an over-activation of immune cells, with an increased release of inflammatory factors (Carey and Dalziel, 1993).

Diagnosis

Top of page Clinical Diagnosis

Clinical diagnosis can be made upon observation of the typical clinical signs: dyspnea after exercise, gradual progression of cachexia and neurological signs. The history of the herd may give indication on the presence of the agent in the flock.

Laboratory Diagnosis

Diagnosis of the disease can be performed by detection of visna/maedi virus-specific antibodies by agar gel immunodiffusion (AGID), ELISA (Houwers and Schaake, 1987) or immunoblot, and by detection of the virus by PCR. Virus isolation is problematic.

Serological tests are most commonly used. Most widely used is AGID, based on detection of antibodies directed against the major structural protein of the virus; the core protein p25, and the major envelope protein gp135. However, CAEV is closely related to visna/maedi virus and may be detected, yielding a false positive. Development of crude-virus ELISAs has also been hampered by false-positive reactions, and as a result western blot or radio-immunoprecipitation assays have been used to overcome specificity problems. These tests are less useful for routine testing. Development of monoclonal antibodies against the most immunogenic viral proteins p25 and gp135, and production of recombinant viral protein has produced tests with better sensitivity and specificity. Nonetheless, false-positive reactions remain a problem that cannot as yet be fully prevented. Recently, detection of nucleic acids has been explored for diagnosis of visna/maedi virus infection, leading to the creation of promising tests, which facilitate quicker detection than that obtained by serological tests, which depend on the slow process of induction of antibodies.

Variability between the lentiviruses demand that PCR tests are based on conserved regions of the genome, and in most studies conserved LTR regions and gag or pol genes are targeted. PCR can be used for direct detection of visna/maedi virus in clinical specimens, either prior to culture or after co-cultivation with susceptible cells. The latter is more sensitive because only a few PBMCs are infected by visna/maedi virus in vivo. PCR is highly sensitive when used after experimental infections. However field samples may occasionally give rise to false-negative results even in serologically positive animals. Direct PCR requires a high virus load in the animals to reveal a positive test result. PCR methods were improved by using degenerative primer sets, and by nested, semi-nested and double-nested procedures (Celer et al., 2000). Furthermore, southern-blot hybridisation with suitable probes appeared more sensitive than ethidium bromide staining, and significantly can increase the sensitivity and specificity, especially when using samples without prior in vitro culture (Pepin et al., 1998).

Virus isolation is rather difficult. Tissue samples from affected animals containing living cells must be co-cultured on sheep choroid plexus cells or goat synovial membrane cells, which also support replication of visna/maedi virus. Co-cultivation may also be performed with PBMCs or milk leukocytes. Cytopathic effects may show up after 2-3 weeks, indicating formation of giant multinucleated cells (Pepin et al., 1998).

Neutralising antibodies are formed after infection. However in sheep, antibody-escape mutants of visna/maedi virus develop subsequent to appearance of neutralising antibodies. This is a feature common to other lentiviruses such as HIV, EIAV and SIV. The genetic basis of these mutations are formed by single-base mutations and substitutions, and have been mimicked in vitro, by adding 'early' and 'late' post-infection sera from sheep to visna/maedi virus-infected cell cultures. 'Early' sera lead to induction of non-neutralising mutants, whereas 'late' sera do not, suggesting that antigenic variation does not continue indefinitely in individual animals (Narayan et al., 1997).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
General Signs / Abnormal proprioceptive positioning, knuckling Sign
General Signs / Ataxia, incoordination, staggering, falling Sheep & Goats:All Stages Diagnosis
General Signs / Dysmetria, hypermetria, hypometria Sign
General Signs / Exercise intolerance, tires easily Sign
General Signs / Fever, pyrexia, hyperthermia Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sign
General Signs / Forelimb weakness, paresis, paralysis front leg Sign
General Signs / Generalized lameness or stiffness, limping Sign
General Signs / Generalized weakness, paresis, paralysis Sheep & Goats:All Stages Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sign
General Signs / Inability to stand, downer, prostration Sign
General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Sheep & Goats:All Stages Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Stiffness or extended neck Sign
General Signs / Tetraparesis, weakness, paralysis all four limbs Sheep & Goats:All Stages Sign
General Signs / Torticollis, twisted neck Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sheep & Goats:All Stages Sign
General Signs / Weakness of one hindlimb, paresis paralysis rear leg Sign
General Signs / Weight loss Sheep & Goats:All Stages Sign
Nervous Signs / Abnormal behavior, aggression, changing habits Sign
Nervous Signs / Circling Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Nervous Signs / Head tilt Sign
Nervous Signs / Seizures or syncope, convulsions, fits, collapse Sign
Nervous Signs / Tremor Sign
Ophthalmology Signs / Blindness Sign
Ophthalmology Signs / Nystagmus Sign
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Firm mammary gland, hard udder Sign
Reproductive Signs / Mastitis, abnormal milk Sheep & Goats:All Stages Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Coughing, coughs Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sheep & Goats:All Stages Diagnosis
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sign
Respiratory Signs / Purulent nasal discharge Sign

Disease Course

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The disease is characterised by a long incubation period that may last several months to years. An incubation period of 1-3 years was noted during the initial outbreak in Iceland (Carey and Dalziel, 1993). Symptoms develop gradually and progressively. There is a gradual loss of condition and body mass leading to cachexia, and a slow development of incoordination or respiratory distress. The disease progresses over many months, with affected organs showing typical histopathological lesions (Dawson, 1987; Narayan et al., 1997). The most commonly reported symptom is dyspnea, which becomes particularly obvious when affected animals are exercised. In animals with neurological dysfunction, the gait is affected, with paresis of the hindquarters progressing until paraplegia develops.

Visna/maedi virus has also been shown to affect mammary glands. Chronic indurative mastitis may result, characterised by marked lymphoid hyperplasia and fibrosis. Arthritis is sometimes observed in visna/maedi virus-infected sheep, which is similar to that found in CAEV-infected goats (Carey and Dalziel, 1993). In vivo synergism between Jaagsiekte retrovirus (causing sheep pulmonary adenomatosis) and visna/maedi virus has been suggested, based on accelerated development of lesions when both viruses are present, but this has yet to be confirmed.

Epidemiology

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Infected animals are persistently infected and remain a source of infection for herd mates and their offspring during life. Clusters of visna/maedi virus-infected macrophage precursors have been found in the bone marrow, which may act as a reservoir for infection. Such a reservoir is essential for the continued survival of the virus in the host because blood monocytes and macrophages are relatively short lived. In vivo, the number of detectable infected target cells is low; figures of 1 in 100,000 circulating leukocytes have been quoted for visna/maedi virus (Carey and Dalziel, 1993).

Visna/maedi virus can be transmitted horizontally and vertically. The major route of transmission is horizontal spread via the respiratory route. Horizontal transmission occurs through inhalation of respiratory secretions. Close confinement, such as stabling in winter facilitates the spread of virus within a herd (Pepin et al., 1998). This may even be favoured by concomitant infections such as sheep pulmonary adenomatosis (SPA), because of increased numbers of alveolar macrophages, which facilitate visna/maedi virus-replication in the lungs of sheep with SPA. Vertical transmission from ewes to offspring occurs frequently. Virus-infected cells and free virus are passed from ewes to their lambs via colostrum and milk. The lamming season is a time of high Lentivirus expression, which facilitates the spread of the infection. Many affected ewes suffer from mastitis, and subsequent high amounts of mononuclear cells in the milk facilitate transport of virus-containing cells to suckling lambs (Pepin et al., 1998). In utero transmission is more controversial. A few unexplained cases of visna/maedi virus have been found in visna/maedi virus eradication programmes with strict lambing controls; reports on isolation of visna/maedi virus in embryos from infected ewes are conflicting. Artificial infection of foetuses by in utero injection with virus is possible, indicating that foetuses are permissive to the virus. However, because the virus is mainly cell-associated in the blood of affected ewes, infection through in utero transmission seems usually unlikely. Sexual transmission has not been documented.

Impact: Economic

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The disease is categorised as a List B disease according to the Office International des Epizooties (OIE), based on its economic impact. The outbreak in Iceland is considered to have been the most severe, with an estimated loss of 150,000 diseased animals and 650,000 destroyed (Carey and Dalziel, 1993). The effect of visna/maedi virus on the growth of lambs is significant. Lambs from visna/maedi virus-positive ewes may grow 6-12% less than lambs from visna/maedi virus-free mothers, mainly caused by udder problems . However, some studies have shown little or no significant impact of visna/maedi virus infections under certain conditions (Dungu et al., 2000).

Zoonoses and Food Safety

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Visna/maedi virus is not a zoonosis. Lentivirus infections, such as HIV occur in man but are caused by different, albeit related viruses. However, visna/maedi virus infection models may be used to study putative antiviral drugs against HIV (Thormar et al., 1995).

Disease Treatment

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No treatment exists for visna/maedi virus infections. However, antiviral drugs aimed at treatment of HIV have been described using visna/maedi virus as a model (Thormar et al., 1995; Thormar et al., 1998).

Prevention and Control

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Prevention of visna/maedi virus infection results from detection of visna/maedi virus-infected animals and subsequent removal of the herd to prevent horizontal transmission, and by raising new-born lambs separately from their infected mothers, to prevent vertical transmission (Cutlip and Lehmkuhl, 1986; Sihvonen et al., 2000).

Periodic serological testing using AGID or ELISA represents the standard method of detecting visna/maedi virus-positive animals. Otherwise, PCR may be used.

To prevent infection of lambs and kids, they can be removed from the mothers directly after birth, and raised using visna/maedi virus-free colostrum and milk. Colostrum fed to these animals may heat-treated at 56°C for 60 minutes, and milk pasteurised to inactivate the virus, or preferably colostrum and milk should be obtained from visna/maedi virus-free ewes.

There is no vaccine available for visna/maedi virus infection (Cutlip et al., 1987). The antigenic variation in visna/maedi virus, the complex mechanism of immunoprotection, and the complexity of viral persistence are major obstacles to vaccine development, and stress the importance of disease prevention. Nonetheless, despite major efforts, eradication programmes have met serious difficulties. Lack of sensitivity in the tests that have been employed have led to unexpected relapses in the occurrence of visna/maedi virus-positive animals in presumably visna/maedi virus-free herds.

Breeding of visna/maedi virus-resistance sheep may offer alternative control methods. Texel sheep, Border Leicester and Finnish Landrace breeds seem highly susceptible (Cutlip et al., 1986), whereas the Ile-de-France breed seems less susceptible (Houwers et al., 1989). It seems that there exists a genetic susceptibility to the disease rather than a susceptibility to infection per se (Pepin et al., 1998).

References

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Agnarsdottir G; Thorsteinsdottir H; Oskarsson T; Matthiasdottir S; St Haflidadottir B; Andresson OS; Andresdottir V, 2000. The long terminal repeat is a determinant of cell tropism of maedi- visna virus. J. Gen. Virol., 81(8):1901-1905.

Ayelet G; Roger F; Tibbo M; Tembely S, 2001. Survey of maedi-visna (MV) in ethiopian highland sheep. Vet. J., 161:208-210.

Barber DM, 1981. Maedi-visna in Britain. Vet. Rec., 109:23.

Belino ED; Ezeifeka GO, 1984. Maedi-visna antibodies in sheep and goats in Nigeria. Veterinary Record, 114(23):570; 7 ref.

Buchanan HF, 2001. Maedi visna infection in a flock in Yorkshire. Veterinary Record, 148(7):218-219; 5 ref.

Campbell JR; Menzies PI; Waltner-Toews D; Walton JS; Buckrell BC; Thorsen J, 1994. The seroprevalence of maedi-visna in Ontario sheep flocks and its relationship to flock demographics and management practices. Canadian Veterinary Journal, 35(1):39-44; 31 ref.

Caporale VP; Foglini A; Lelli R; Mantovani A; Nannini D; Simoni P, 1983. Preliminary observations on the presence of visna-maedi in Italy. Vet. Res. Commun., 6:31-35.

Carey N; Dalziel RG, 1993. The biology of maedi-visna virus- an overview. British Veterinary Journal, 149(5):437-454; 100 ref.

Celer V Jr; Celer V; Nejedla E; Bertoni G; Peterhans E; Zanoni RG, 2000. The detection of proviral DNA by semi-nested polymerase chain reaction and phylogenetic analysis of Czech Maedi-Visna isolates based on gag gene sequences. J. Vet. Med. B. Infect. Dis. Vet. Public Health, 47:203-215.

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