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IdentityTop of page
Preferred Scientific Name
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
OverviewTop of page
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 AffectedTop of page
Only sheep and goats are infected in vivo by visna/maedi virus (Carey and Dalziel, 1993).
DistributionTop of page
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 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.
PathologyTop of page
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).
DiagnosisTop 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/SignsTop of page
|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 CourseTop of page
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.
EpidemiologyTop of page
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: EconomicTop of page
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 SafetyTop of page
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 TreatmentTop of page
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 ControlTop of page
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).
ReferencesTop of page
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.
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.
Clements JE; Zink MC; Narayan O; Gabuzda DH, 1994. Lentivirus infection of macrophages. Immunol. Ser., 60:589-600.
Concha-Bermejillo Ade la, 1997. Maedi-visna and ovine progressive pneumonia. Veterinary Clinics of North America, Food Animal Practice, 13(1):13-33; 125 ref.
Cutlip RC; Lehmkuhl HD; Brogden KA; Schmerr MJF, 1987. Failure of experimental vaccines to protect against infection with ovine progressive pneumonia (Maedi-visna) virus. Veterinary Microbiology, 13(3):201-204; 14 ref.
Dukes TW; Greig AS; Corner AH, 1979. Maedi-visna in Canadian sheep. Can. J. Comp. Med., 43:313-320.
Dungu B; Vorster J; Bath GF; Verwoerd DW, 2000. The effect of a natural maedi-visna virus infection on the productivity of South African sheep. Onderstepoort J. Vet. Res., 67:87-96.
Gates NL; Winward LD; Gorham JR; Shen DT, 1978. Serologic survey of prevalence of ovine progressive pneumonia in Idaho range sheep. J. Am. Vet. Med. Assoc., 173:1575-1577.
Houwers DJ, 1980. [Maedi and maedi control (author's transl)]. Tijdschr. Diergeneeskd., 105:661-664.
Houwers DJ; Schaake JJr, 1987. An improved ELISA for the detection of antibodies to ovine and caprine lentiviruses, employing monoclonal antibodies in a one-step assay. Journal of Immunological Methods, 98(1):151-154; 12 ref.
Madewell BR; Ameghino E; Rivera H; Inope L; Martini Jde, 1987. Seroreactivity of Peruvian sheep and goats to small ruminant lentivirus-ovine progressive pneumonia virus. American Journal of Veterinary Research, 48(3):372-374; 17 ref.
Narayan O; Joag SV; Chebloune Y; Zink MC; Clements JE, 1997. Visna-Maedi: the prototype lentiviral disease. In: Nathanson N, Ahmed R, Gonzalez-Scarano F, Griffin DE, Holmes KV, Murphy FA, Robinson HL, eds. Viral Pathogenesis. Philadelphia, USA: Lippincott-Raven, 657-668. ISBN 0-7817-0297-6.
Nathanson N; Panitch H; Palsson PA; Petursson G; Georgsson G, 1976. Pathogenesis of visna. II. Effect of immunosuppression upon early central nervous system lesions. Lab. Invest., 35:444-451.
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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.
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
Pekelder JJ; Houwers DJ; Elving L, 1991. Effect of maedi-visna virus infection on lamb growth. Veterinary Record, 129(16):368.
Pépin M; Vitu C; Russo P; Mornex JF; Peterhans E, 1998. Maedi-visna virus infection in sheep: a review. Veterinary Research, 29(3/4):341-367; many ref.
Schaller P; Vogt HR; Strasser M; Nettleton PF; Peterhans E; Zanoni R, 2000. [Seroprevalence of maedi-visna and border disease in Switzerland]. Schweiz Arch Tierheilkd., 142:145-153.
Sihvonen L; Nuotio L; Rikula U; Hirvela-Koski V; Kokkonen U, 2000. Preventing the spread of maedi-visna in sheep through a voluntary control programme in Finland. Prev. Vet. Med., 47:213-220.
Thormar H; Georgsson G; Gunnarsson E; Naesens L; Torsteinsdóttir S; Balzarini J; Clercq Ede, 1998. Treatment of visna virus infection in lambs with the acyclic nucleoside phosphonate analogue 9-(2-phosphonylmethoxyethyl)adenine (PMEA). Antiviral Chemistry & Chemotherapy, 9(3):245-252; 16 ref.
Thormar H; Georgsson G; Pálsson PA; Balzarini J; Naesens L; Torsteinsdóttir S; Clercq EDe, 1995. Inhibitory effect of 9-(2-phosphonylmethoxyethyl) adenine on visna virus infection in lambs: a model for in vivo testing of candidate anti-human immunodeficiency virus drugs. Proceedings of the National Academy of Sciences of the United States of America, 92(8):3283-3287; 31 ref.
Distribution MapsTop of page
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