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pulmonary adenomatosis

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pulmonary adenomatosis

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • pulmonary adenomatosis
  • Overview
  • Sheep pulmonary adenomatosis (SPA) is a contagious disease of sheep produced by a tumour of type II alveolar and Clara cells in the lungs. The disease has been occasionally recorded naturally in goats and mouflon. SPA...

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Pictures

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PictureTitleCaptionCopyright
Two year-old ram with raised hindquarters and lowered head. Copious amount of foamy, whitish-mucous is observed coming from the the lungs. This is a very characteristic sign of sheep pulmonary adenomatosis.
TitleSymptoms
CaptionTwo year-old ram with raised hindquarters and lowered head. Copious amount of foamy, whitish-mucous is observed coming from the the lungs. This is a very characteristic sign of sheep pulmonary adenomatosis.
CopyrightM. de las Heras Guillamon
Two year-old ram with raised hindquarters and lowered head. Copious amount of foamy, whitish-mucous is observed coming from the the lungs. This is a very characteristic sign of sheep pulmonary adenomatosis.
SymptomsTwo year-old ram with raised hindquarters and lowered head. Copious amount of foamy, whitish-mucous is observed coming from the the lungs. This is a very characteristic sign of sheep pulmonary adenomatosis.M. de las Heras Guillamon
Lung from adult sheep showing classical sign of sheep pulmonary adenomatosis. Cranioventral and caudal areas of all lung lobules show extensive grey areas of tumour. Small tumour nodules of varying sizes can be seen in other areas.
TitleLung pathology
CaptionLung from adult sheep showing classical sign of sheep pulmonary adenomatosis. Cranioventral and caudal areas of all lung lobules show extensive grey areas of tumour. Small tumour nodules of varying sizes can be seen in other areas.
CopyrightM. de las Heras Guillamon
Lung from adult sheep showing classical sign of sheep pulmonary adenomatosis. Cranioventral and caudal areas of all lung lobules show extensive grey areas of tumour. Small tumour nodules of varying sizes can be seen in other areas.
Lung pathologyLung from adult sheep showing classical sign of sheep pulmonary adenomatosis. Cranioventral and caudal areas of all lung lobules show extensive grey areas of tumour. Small tumour nodules of varying sizes can be seen in other areas.M. de las Heras Guillamon
Sectioned lung from adult sheep showing classical signs of sheep pulmonary adenomatosis. Grey areas of tumour can be seen. Note copious amount of whitish-foamy fluid coming from the airways.
TitleLung pathology
CaptionSectioned lung from adult sheep showing classical signs of sheep pulmonary adenomatosis. Grey areas of tumour can be seen. Note copious amount of whitish-foamy fluid coming from the airways.
CopyrightM. de las Heras Guillamon
Sectioned lung from adult sheep showing classical signs of sheep pulmonary adenomatosis. Grey areas of tumour can be seen. Note copious amount of whitish-foamy fluid coming from the airways.
Lung pathologySectioned lung from adult sheep showing classical signs of sheep pulmonary adenomatosis. Grey areas of tumour can be seen. Note copious amount of whitish-foamy fluid coming from the airways.M. de las Heras Guillamon
Lung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White, hard nodules of various sizes are distributed throughout the lung.
TitleLung pathology
CaptionLung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White, hard nodules of various sizes are distributed throughout the lung.
CopyrightM. de las Heras Guillamon
Lung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White, hard nodules of various sizes are distributed throughout the lung.
Lung pathologyLung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White, hard nodules of various sizes are distributed throughout the lung.M. de las Heras Guillamon
Sectioned lung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White scattered tumor nodules are distributed throughout the section. Note the foamy fluid is not evident in this anatomical form. (Note scale bar).
TitleLung pathology
CaptionSectioned lung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White scattered tumor nodules are distributed throughout the section. Note the foamy fluid is not evident in this anatomical form. (Note scale bar).
CopyrightM. de las Heras Guillamon
Sectioned lung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White scattered tumor nodules are distributed throughout the section. Note the foamy fluid is not evident in this anatomical form. (Note scale bar).
Lung pathologySectioned lung from adult sheep showing atypical form of sheep pulmonary adenomatosis. White scattered tumor nodules are distributed throughout the section. Note the foamy fluid is not evident in this anatomical form. (Note scale bar).M. de las Heras Guillamon
Histology of a sheep pulmonary adenomatosis tumour: adenomatomus transformation of the alveolar epthelium showing the characteristic papilliform growth of the type II alveolar cells. Papillary proliferations can seen in bronchioli. (Hematoxylin-Eosin).
TitleTumour histology
CaptionHistology of a sheep pulmonary adenomatosis tumour: adenomatomus transformation of the alveolar epthelium showing the characteristic papilliform growth of the type II alveolar cells. Papillary proliferations can seen in bronchioli. (Hematoxylin-Eosin).
CopyrightM. de las Heras Guillamon
Histology of a sheep pulmonary adenomatosis tumour: adenomatomus transformation of the alveolar epthelium showing the characteristic papilliform growth of the type II alveolar cells. Papillary proliferations can seen in bronchioli. (Hematoxylin-Eosin).
Tumour histologyHistology of a sheep pulmonary adenomatosis tumour: adenomatomus transformation of the alveolar epthelium showing the characteristic papilliform growth of the type II alveolar cells. Papillary proliferations can seen in bronchioli. (Hematoxylin-Eosin).M. de las Heras Guillamon

Identity

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Preferred Scientific Name

  • pulmonary adenomatosis

International Common Names

  • English: ovine pulmonary adenomatosis; ovine pulmonary carcinoma, adenomatosis in sheep and goats; pulmonary adenocarcinoma in sheep and goats; sheep pulmonary adenomatosis

Local Common Names

  • South Africa: jaagsiekte
  • USA: ovine pulmonary carcinoma

English acronym

  • OPA
  • OPC
  • SPA

Overview

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Sheep pulmonary adenomatosis (SPA) is a contagious disease of sheep produced by a tumour of type II alveolar and Clara cells in the lungs. The disease has been occasionally recorded naturally in goats and mouflon. SPA is also known as jaagsiekte and ovine pulmonary carcinoma. The term jaagsiekte was used in South Africa where the first cases were described and it is derived from two Afrikaner words: "jaag" drive and "siekte" = disease. The term ovine pulmonary carcinoma is preferred in the USA.

SPA is caused by a type B/D exogenous retrovirus, known as jaagsiekte sheep retrovirus (JSRV); its oncogenic mechanisms are not known. SPA is widely distributed throughout several continents, except Australia and New Zealand. No accurate figures about the economic importance of the disease are available, because there are no pre-clinical diagnostic tests. The prevalence of the disease has been evaluated only by post-mortem examination in diagnostic laboratories or of lungs at the abattoir. In spite of these difficulties, in some countries such as South Africa, Scotland (UK), Peru and Spain the disease appears to be widespread and causes a high number of deaths, mainly in young adult sheep. Meat production is generally affected.

Hosts/Species Affected

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SPA is diagnosed mainly in young adult sheep but is (rarely) found in goats (Banerjee and Gupta, 1979, Sriraman et al., 1982, Metin et al., 1988), and wild mouflon, Ovis musimon (Nieddu et al., 1987). In countries where the disease is endemic, SPA may be more common in certain areas or breeds and also during the winter (Dungal et al., 1938; Tustin, 1969; Hunter and Munro, 1983). Any management condition that tends to keep animals housed for a long time promotes the spread of disease.

Distribution

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The earliest known report of sheep pulmonary adenomatosis (SPA) comes from South Africa. In 1825, a letter by AP Aucamp reported a contagious respiratory disease known as "jaagziekte", which caused an elevated number of deaths with no recovery of affected animals. In the ensuing years, further reports confirmed the contagious and neoplastic nature of the disease and described other affected flocks, not only in South Africa, but also in several European countries (Tustin, 1969).

The history of the disease in Iceland deserves special mention. Nowadays this country is free of SPA but a very important epizootic causing a large number of deaths happened in the 1930s. The disease was imported from Germany in 1933 and introduced to an Icelandic farm called Deildartunga by a 1-year-old Karakul ram with no clinical signs of SPA. This ram was used to serve ewes and was kept in separate accommodation with one ewe and her lamb throughout the winter. The disease was noticed in the ram in the spring when the animals were released on the mountains. This ram did not return. In the following years, new cases appeared in the flock and in many others around the island, eventually killing between 50-80% of the animals in the affected flocks (Dungal et al., 1938). The high mortality probably was due to the particular sheep management system in Iceland. In this system, sheep are housed through the winter (1-4 months). At other times of the year, usually in September, sheep from different farms are concentrated at the heads of the valleys, where they spend several days before returning to their original farms. SPA was eradicated in 1952 following a very restrictive policy of sanitary control by killing all animals coming from flocks that showed any animal with clinical signs of the disease.

SPA has been recognised in many other countries throughout the world and, with the exception of Australia and New Zealand, is present in all continents with a varying degree of significance (see list of countries).

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

AzerbaijanNo information availableOIE Handistatus, 2005
BahrainDisease never reportedOIE Handistatus, 2005
BhutanDisease never reportedOIE Handistatus, 2005
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
ChinaPresentCAB ABSTRACTS Data Mining 2001
-Hong KongDisease never reportedOIE Handistatus, 2005
-XinjiangPresentDeng et al., 1996
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaDisease never reportedDamodaran, 1960; OIE Handistatus, 2005
-Andaman and Nicobar IslandsPresentSriraman et al., 1982
-Indian PunjabPresentBanerjee and Gupta, 1979
-RajasthanPresentDadhich and Sharma, 1995
-Uttar PradeshPresentRajya and Singh, 1964; Sharma et al., 1975
-West BengalPresentSarkar et al., 1988
IndonesiaDisease never reportedOIE Handistatus, 2005
IranDisease not reportedNaghshineh and Sohrabi, 1972; OIE Handistatus, 2005
IraqNo information availableYoukhana, 1995; OIE Handistatus, 2005
IsraelReported present or known to be presentNobel, 1958; Nobel et al., 1969; OIE Handistatus, 2005
JapanDisease not reportedOIE Handistatus, 2005
JordanDisease never reportedOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease not reportedOIE Handistatus, 2005
KuwaitDisease not reportedOIE Handistatus, 2005
LebanonDisease not reportedOIE Handistatus, 2005
Malaysia
-Peninsular MalaysiaLast reported2003Shah et al., 1996; OIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakDisease never reportedOIE Handistatus, 2005
MongoliaDisease never reportedOIE Handistatus, 2005
MyanmarDisease never reportedOIE Handistatus, 2005
NepalDisease never reportedOIE Handistatus, 2005
OmanDisease not reportedOIE Handistatus, 2005
PhilippinesDisease never reportedOIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
Saudi ArabiaDisease not reportedOIE Handistatus, 2005
SingaporeDisease never reportedOIE Handistatus, 2005
Sri LankaDisease never reportedOIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandDisease never reportedOIE Handistatus, 2005
TurkeyNo information availableMetin et al., 1988; Kiran, 1993; OIE Handistatus, 2005
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesNo information availableOIE Handistatus, 2005
UzbekistanDisease never reportedOIE Handistatus, 2005
VietnamDisease never reportedOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005

Africa

AlgeriaDisease never reportedOIE Handistatus, 2005
AngolaNo information availableOIE Handistatus, 2005
BeninNo information availableOIE Handistatus, 2005
BotswanaDisease never reportedOIE Handistatus, 2005
Burkina FasoNo information availableOIE Handistatus, 2005
BurundiDisease never reportedOIE Handistatus, 2005
CameroonNo information availableOIE Handistatus, 2005
Cape VerdeDisease never reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireDisease not reportedOIE Handistatus, 2005
DjiboutiDisease not reportedOIE Handistatus, 2005
EgyptDisease never reportedOIE Handistatus, 2005
EritreaDisease not reportedOIE Handistatus, 2005
EthiopiaDisease never reportedOIE Handistatus, 2005
GhanaDisease not reportedOIE Handistatus, 2005
GuineaDisease never reportedOIE Handistatus, 2005
Guinea-BissauNo information availableOIE Handistatus, 2005
KenyaNo information availableShirlaw, 1959; Wandera, 1971; OIE Handistatus, 2005
LesothoDisease not reportedOIE, 1998
LibyaDisease never reportedAlsenosy et al., 1986; OIE Handistatus, 2005
MadagascarDisease never reportedOIE Handistatus, 2005
MalawiNo information availableOIE Handistatus, 2005
MaliNo information availableOIE Handistatus, 2005
MauritiusDisease not reportedOIE Handistatus, 2005
MoroccoNo information availableBouljihad et al., 1996; OIE Handistatus, 2005
MozambiqueNo information availableOIE Handistatus, 2005
NamibiaLast reported2003OIE, 1998; OIE Handistatus, 2005
NigeriaDisease never reportedOIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalNo information availableOIE Handistatus, 2005
SeychellesDisease not reportedOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaReported present or known to be presentAucamp, 1825; Tustin, 1969; OIE Handistatus, 2005
SudanDisease never reportedOIE Handistatus, 2005
SwazilandDisease not reportedOIE Handistatus, 2005
TanzaniaNo information availableWandera, 1971; OIE Handistatus, 2005
TogoDisease never reportedOIE, 1998; OIE Handistatus, 2005
TunisiaDisease not reportedAmara et al., 1994; OIE Handistatus, 2005
UgandaDisease not reportedOIE Handistatus, 2005
ZambiaNo information availableOIE Handistatus, 2005
ZimbabweLast reported1994OIE, 1998; OIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaReported present or known to be presentStevenson et al., 1980; OIE Handistatus, 2005
MexicoDisease never reportedEquiluz and De, 1981; OIE Handistatus, 2005
USASerological evidence and/or isolation of the agentMarsh, 1966; Cutlip and Young, 1982; OIE Handistatus, 2005
-ColoradoPresentCutlip and Young, 1982
-MinnesotaPresentMarsh, 1966; Cutlip and Young, 1982
-WyomingPresentCutlip and Young, 1982

Central America and Caribbean

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

South America

ArgentinaSerological evidence and/or isolation of the agentGea and González, 1992; OIE Handistatus, 2005
BoliviaNo information availableOIE Handistatus, 2005
BrazilLast reported1999OIE Handistatus, 2005
-Mato Grosso do SulPresentDrimeier et al., 1998
ChileSchultz et al., 1965; OIE Handistatus, 2005
ColombiaDisease never reportedOIE, 1998; OIE Handistatus, 2005
EcuadorDisease never reportedOIE Handistatus, 2005
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaDisease not reportedOIE Handistatus, 2005
GuyanaDisease never reportedOIE Handistatus, 2005
ParaguayDisease never reportedOIE Handistatus, 2005
PeruCuba-Caparo, 1945; Cuba-Caparo et al., 1961; Snyder et al., 1983; Ellis et al., 1993; OIE Handistatus, 2005
UruguayLast reported1982OIE Handistatus, 2005
VenezuelaDisease never reportedOIE Handistatus, 2005

Europe

AndorraCAB Abstracts data miningOIE Handistatus, 2005
AustriaDisease not reportedOIE Handistatus, 2005
BelarusDisease never reportedOIE Handistatus, 2005
BelgiumNo information availableOIE Handistatus, 2005
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaDisease never reportedEnchev et al., 1958; OIE Handistatus, 2005
CroatiaDisease never reportedOIE Handistatus, 2005
CyprusLast reported1993Toumazos, 1989; OIE Handistatus, 2005
Czech RepublicLast reported1995Halouzka and Celer, 1983; Seidl, 1990; OIE Handistatus, 2005
DenmarkLast reported2000OIE, 1998; OIE Handistatus, 2005
EstoniaDisease never reportedOIE Handistatus, 2005
FinlandDisease never reportedOIE Handistatus, 2005
FranceReported present or known to be presentAynaud, 1926; Moraillon and Yalcin, 1967; OIE Handistatus, 2005
GermanyCAB Abstracts data miningEber, 1899; Jakob and Krauze, 1965; Geisel, 1975; OIE Handistatus, 2005
GreeceLast reported2003Christodoulous and Tarlatis, 1952; Stefanou et al., 1975; OIE Handistatus, 2005
HungaryLast reported1970Glávits et al., 1996; OIE Handistatus, 2005
IcelandLast reported1952OIE Handistatus, 2005
IrelandReported present or known to be presentBasset and Sheehan, 1989; OIE Handistatus, 2005
Isle of Man (UK)Disease not reportedOIE Handistatus, 2005
ItalyNo information availableRomboli and Botti, 1957; Carrara and Gasparini, 1959; Romboli, 1959; Cerretto and Deiana, 1967; Nieddu et al., 1987; OIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
LithuaniaDisease never reportedOIE Handistatus, 2005
LuxembourgDisease never reportedOIE Handistatus, 2005
MacedoniaDisease never reportedOIE Handistatus, 2005
MaltaDisease not reportedOIE Handistatus, 2005
MoldovaDisease never reportedOIE Handistatus, 2005
NetherlandsNo information availableHouwers and Terpstra, 1984; OIE Handistatus, 2005
NorwayDisease never reportedKrogsrud et al., 1996; OIE Handistatus, 2005
PolandDisease not reportedKopczewski et al., 1986; OIE Handistatus, 2005
PortugalReported present or known to be presentMadeira, 1949; OIE Handistatus, 2005
RomaniaDisease not reportedAdamesteanu et al., 1969; OIE Handistatus, 2005
Russian FederationReported present or known to be presentOIE Handistatus, 2005
-Central RussiaPresentKostenko, 1964
-Southern RussiaPresentMitrofanov, 1963
SlovakiaDisease not reportedOIE Handistatus, 2005
SloveniaDisease never reportedOIE Handistatus, 2005
SpainNo information availableDualde, 1963; Santiago Luque, 1963; Heras et al., 1992; González et al., 1993; OIE Handistatus, 2005
SwedenDisease never reportedNilsson, 1984; OIE Handistatus, 2005
SwitzerlandReported present or known to be presentPusterla et al., 1995; OIE Handistatus, 2005
UKReported present or known to be presentMcFadyean, 1938; Hunter and Munro, 1983; Pritchard and Done, 1990; OIE Handistatus, 2005
-Northern IrelandLast reported1996OIE Handistatus, 2005
UkraineLast reported1994OIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Disease not reportedCvjetanovic and Martinic, 1962; Prasovic et al., 1991; OIE Handistatus, 2005

Oceania

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

Pathology

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Post-mortem examination of the sheep affected by SPA shows that lesions are confined mainly to the lungs. They are considerably enlarged and heavier than normal due to infiltration by areas of tumour which may vary from small discrete nodules, measuring only 0.5-2 cm, to extensive tumours involving the entire ventral half of the diaphragmatic and other lobes. Usually tumour tissue is present in both lungs although the extent on either side does vary. The lesions can be segregated into two general types:


Classical SPA


Tumours are solid, grey or light purple with a shiny translucent sheen and often separated from adjacent normal lung by a narrow emphysematous zone. The presence of frothy white fluid in the respiratory passages is a prominent feature and is obvious even in lesions as small as a few millimetres. In advanced cases, this fluid flows out of the trachea when it is cut or pendant. Histological examination of SPA lesions shows areas of lung where cuboidal or columnar cells replace the normal thin alveolar cells. Sometimes these abnormal cells form papilliform growths that project into the alveoli. Intrabronchiolar proliferation also may be present. The histological picture is classified as a bronchioloalveolar cell carcinoma. A third type of change consists of nodules of loose connective tissue in a mucopolysaccharide substance. Accumulations of large macrophage cells occur in the lung tissue around the tumours (Wandera, 1971; Sharp and Angus, 1990).


Atypical SPA


Tumours comprise solitary or aggregated hard white nodules, which have a dry cut surface and show clear demarcation from surrounding tissues. The presence of excess fluid is not a prominent feature. The histological appearance of these tumours is essentially the same as classical SPA but with an exaggerated inflammatory response (mostly lymphocytes and plasma cells) and fibrosis (De las Heras et al.,1992; Garcia Goti et al., 2000).

Pleurisy may be evident over the surface of the tumour and in some cases abscesses or gangrenous tissue are present in the adenomatous tissue.

Adult sheep, that on post-mortem examination appear to have died from acute pasteurellosis should have their lungs examined carefully, as lesions of SPA may be masked by the acute reaction to the Pasteurellae.

The tumour rarely metastasises beyond the mediastinal lymph nodes but extrathoracic tumour metastases can be found in some cases (Nobel et al., 1969).

Ultrastructural studies have shown that the cells forming the alveolar lesion are type II alveolar cells and those in the bronchiolar tumours, the cells of Clara (Nisbet et al., 1971; Perk et al., 1971).

Diagnosis

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Clinical detection of a case of classical SPA should be based on the presence, in a single mature sheep of an afebrile wasting disease, with marked respiratory signs. A useful aid to diagnosis is to raise the hindquarters and lower the head of the sheep, which causes mucoid fluid, sometimes copious in amount, to run from the nostrils. This is the key clinical sign to differentiate SPA from other sheep lung diseases that can show respiratory distress but never the emission of such amount and type of fluid. Large tumours are unmistakable in appearance at necropsy but confirmatory histology may be necessary where the amount of adenomatous tissue is small or secondary bacterial pneumonia has developed. Where tumours are not obvious, at least 1-2 samples for histological examination should be taken from each lobe. The transformed epithelial cells are the major sites of virus replication and JSRV antigens can be revealed by immunohistochemical techniques (Palmarini et al., 1995).

At present, there are no laboratory tests to support a clinical diagnosis of SPA in the live animal. JSRV has been associated exclusively with both classical and atypical forms of SPA but antibodies to this virus have not been detected in the sera of affected sheep, even with highly sensitive assays such as immunoblotting (Ortín et al., 1998).

Sequencing of JSRV and SERVs has led to the development of PCR that can detect the exogenous virus in a background of genomic DNA and endogenous sequences (Palmarini et al., 1997). Using this sensitive procedure, JSRV has been detected in the blood of unaffected in-contact sheep from flocks with SPA, as well as experimentally infected lambs. This finding suggests that infected animals can be identified during the pre-clinical stages and may offer a new way to diagnose SPA.

List of Symptoms/Signs

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SignLife StagesType
General Signs / Exercise intolerance, tires easily Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Sign
General Signs / Generalized weakness, paresis, paralysis Sign
General Signs / Reluctant to move, refusal to move Sign
General Signs / Sudden death, found dead Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Diagnosis
General Signs / Weight loss Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Diagnosis
Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Dull areas on percussion of chest, thorax Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Sign
Respiratory Signs / Mucoid nasal discharge, serous, watery Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male Diagnosis
Respiratory Signs / Purulent nasal discharge Sign

Disease Course

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In naturally infected sheep, the incubation period appears to be long, so that the disease is not usually seen until sheep are about 2-4 years old. However, tumours have been seen exceptionally in lambs as young as 2 months and in a sheep as old as 11 years of age (Hunter and Munro, 1983; Sharp and Angus, 1990). Clinical signs of the disease only appear when the tumours are sufficiently large to interfere with normal lung function resulting in respiratory embarrassment, which is most obvious following exercise. Abattoir studies have revealed small SPA lesions in clinically normal animals (De las Heras et al., 1992). Experimentally, tumour formation occurs 5-12 months after the intra-tracheal inoculation of tumour tissue or lung fluid extracts containing JRSV into lambs several months old (Wandera, 1971; Martin et al., 1976; Herring et al., 1983). However, when neonatal lambs are inoculated with these extracts or virions from the infectious molecular clone, the tumours can be reproduced in several weeks (Sharp et al., 1983, Palmarini et al., 1999).

The mechanisms of oncogenesis by JSRV are unknown and can only be speculated. The natural course of the disease suggests a very long incubation period, which would be compatible with oncogenenesis by retroviruses that lack oncogenes and induce tumours by insertional mutagenesis. This hypothesis is supported by the absence of recognisable oncogenes in the sequence of JSRV (York et al., 1992). However, the rapid induction of tumour in neonatal lambs is more characteristic of the tumours induced by acute transforming retroviruses that encode oncogenes. Other factors, such as viral dose and the age of the inoculated lamb, may be important and may account for the different types of disease response (Palmarini et al., 1997). JSRV establishes a disseminated infection in SPA-affected sheep (Palmarini et al., 1996b) and can be detected in lymphoid tissue before the onset of neoplasia (Holland et al., 1999). The dissemination of the virus is less intense in atypical SPA than in classical SPA (see types of lesions of SPA described in Pathology section) and in this form the number of tumour infiltrating cells and fibrosis is more intense, suggesting that in some animals the response to the virus is different (Garcia Goti et al., 2000). Although little is know about this area, the interaction between the JSRV and host immune system may be important in the pathogenesis of the disease.

Epidemiology

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SPA has been recognised for many years to be naturally and experimentally transmissible by the respiratory route. It is probable that an infected sheep, even before it develops obvious respiratory signs, excretes virus-containing droplets as it breathes. Later, as the disease progresses, it will discharge quantities of infective respiratory fluid, especially during feeding when the head is lowered. This causes the sheep to snuffle and doubtless creates an aerosol of infected droplets. Close confinement of a flock obviously increases the probability of transmission so that housing with trough feeding and watering may allow the infection to spread.

SPA is generally introduced into flocks by the acquisition of infected sheep. Losses from classical SPA can be high when the disease is first introduced. During the epidemic of SPA in Iceland the estimated time from the introduction of the disease and the appearance of the first clinical cases in other sheep was between 6 and 8 months (Dungal et al., 1938). All of the existing epidemiological information has been based on clinical diagnosis and pathology, and the extent of infection by jaagsiekte retrovirus (JSRV) in affected flocks is unknown.

Impact: Economic

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There are no data available in terms of the real cost of SPA but there is some information about the percentage of animals that have died of the disease and of animals that show SPA-associated lesions at slaughterhouses. In endemic areas such as South Africa or Scotland the percentage of sheep killed by SPA is about 2-4% annually (Tustin, 1969; Hunter and Munro, 1983). However, in countries or farms where the disease has been recently introduced, the mortality, depending on management conditions, could reach 30-80% in the first two years (Dungal et al., 1938; Shirlaw, 1959; Enchev et al., 1958). Where the prevalence has been estimated as a proportion of the number of sheep slaughtered, the percentages can be as low as 0.1-0.2% in Chile or Germany (Schultz et al., 1965), 0.5-0.6% in India (Banerjee and Gupta, 1979), 0.6-1.7% in Perú (Ellis et al., 1993), 0.4-1.6% in Spain (De las Heras et al., 1992) or 0.7% in Italy (Cerretto and Deiana, 1967).

Zoonoses and Food Safety

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A protein related antigenically to JSRV has been demonstrated in approximately 30% of three forms of human primary pulmonary carcinoma and not in other tumours or diseases (De las Heras et al., 1997). This observation supports the view that the antigen in the human tumours may be a retrovirus protein and that a retrovirus may be associated with the neoplastic process in some tumours or represent reactivation/upregulation of an endogenous retrovirus. Although there is no epidemiological evidence to implicate JSRV as a cause of disease in man, recent demonstration of a receptor for JSRV on human cells warrants a cautious reappraisal of any potential zoonotic role.

Disease Treatment

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No method of treatment is recognised or advised. Once the disease is detected there is no possibility of cure. Antimicrobial therapy only reduces the intensity of clinical signs for a short time.

Prevention and Control

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Control should be based on regular inspection of adult sheep in affected flocks. Any animal showing weight loss or signs of respiratory disease should be isolated and veterinary advice sought. Prompt culling of any suspicious animal is advisable, as well as the offspring of affected ewes, which frequently develop SPA. While these methods are unlikely to eradicate SPA from a flock in which the disease is endemic, reduction in the prevalence of infection may be obtained.

Embryo transfer has been reported as one way to obtain animals free of SPA, based on clinical and pathological evidence (Parker et al., 1998). It would be worthwhile to re-evaluate this approach with the more sensitive PCR techniques to confirm that the offspring were free of JSRV infection.

References

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