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A histological and immunohistochemical study of the lesions observed in desert warthogs (Phacochoerus africanus) and bushpigs (Potamochoerus porcus) following experimental challenge with CSF virusGers, Sophette 19 October 2011 (has links)
English: Common warthogs (Phacochoerus africanus) and bushpigs (Potamochoerus larvatus), were
experimentally infected with classical swine fever virus (CSFv) following the diagnosis of classical
swine fever (CSF) subtype 2.1 in 2005 in domestic pigs in South Africa. At that time, no data
regarding their susceptibility or the potential lesions in these wild suids were available. Seven
sub-adult warthogs and six bushpigs were captured, taken to the high containment facilities of the
Transboundary Animal Diseases Programme of the Agriculture Research Council (ARC) -
Onderstepoort Veterinary Research Institute, and infected intranasally with the South African
isolate. In each experiment, two in-contact control animals of the same species verified intraspecies
transmission, while two domestic pigs were used to demonstrate virus virulence and
viability. Surviving animals were euthanized 44 days post infection. Formalin-fixed tissue samples
collected from all experimental animals were evaluated for histological lesions. The warthogs,
which remained clinically normal throughout the study, developed histological lesions that were
inconsistently present and sometimes subtle. Three warthogs, including one in-contact control,
developed distinct perivascular lymphoplasmacytic cuffing in their brains. Subtle lesions included
scant lymphoplasmacytic infiltration of various organs, occasionally accompanied by perivascular
cuffing. In contrast, the bushpigs developed overt clinical signs similar to CSF in domestic pigs.
Four animals out of six, including two in-contact controls, died or were euthanized during the trial.
On post mortem examination, intestinal necrosis and ulceration, purulent rhinitis and pneumonia were present. Acutely affected animals developed lymphoid necrosis and depletion whilst
surviving individuals showed perivascular lymphoplasmacytic cuffing in multiple organs.
Immunohistochemical demonstration of CSFv antigen using a commercially available mouse
monoclonal antibody, WH303, revealed intense, widespread labelling in most tissues of all the
warthogs and bushpigs as well as the four domestic pigs used as controls during the trial. A wide
range of cell types and tissues reacted with the antibody. These included: mononuclear cells
(monocyte-macrophages, lymphocytes and plasma cells), follicular reticular cells, epithelial cells,
vascular endothelial cells, mesothelial cells, smooth muscle cells and fibroblasts.
Tissues that were labelled included tonsil, lymph nodes, spleen, third eyelid, adrenal gland,
urinary bladder, skin, liver, kidney, lung, certain cells within central nervous tissue like the choroid
plexus, various parts of the gastro-intestinal tract as well as glandular tissue like the pancreas
and salivary gland.
The tonsils were the most consistently labelled tissue, while no labelling was noted in myocytes of
skeletal or cardiac muscle.
From the present work, it was concluded that these wild Suidae are susceptible to CSFv and
intra-species transmission under experimental conditions can occur. / Afrikaans: Wilde Afrika varke, nl. vlakvarke (Phacocoerus africanus) en bosvarke (Potamochoerus larvatus)
was eksperimenteel infekteer met europese varkpes virus nadat die siekte in kommersiële mak
varke diagnoseer is in 2005 (dit was tipeer as subtipe 2.1). Geen inligiting oor die vatbaarheid of
potensiële letsels weens europese varkpes infeksie in hierdie wilde varke was beskikbaar nie.
Sewe wilde onvolwasse vlakvarke en ses bosvarke is gevang, na die isolasie eenheid van die
Onderstepoort Veterinêre Instituut se oor-grens siekte afdeling geneem en intranasal geïnfekteer
met die Suid-Afrikaanse isolaat van 2005. Twee in-kontak kontrole diere van dieselfde spesie is
gebruik in elke eksperiment om intra-spesie oordraging vas te stel en twee mak varke om virus
lewensvatbaarheid en virulensie te demonstreer. Oorlewende diere is uitgesit na 44 dae.
Formalien gefikseerde weefsel monsters is versamel van hulle, sowel as van diere wat uitgesit is
tydens die eksperiment. Die vlakvarke was klinies normal regdeur die eksperiment, maar het wel
histologiese letsels ontwikkel wat subtiel was en ook nie altyd teenwoordig in alle gevalle nie.
Drie vlakvarke, waarvan een ‘n in-kontak dier was, het prominente limfo-plasmasitiese
perivaskulêre flensing in hul breine ontwikkel. Subtiele letsels het klein hoeveelhede limfoplasmasitiese
infiltrasies in verskeie organe en somtyds perivaskulêre flensing ingesluit. In teenstelling, het die bosvarke uitgesproke kliniese tekens soortgelyk aan Europese varkpes in
mak varke, ontwikkel. Vier uit die ses diere, insluitend twee in-kontak diere is dood of uitgesit
tydens die eksperiment. Met nadoodse ondersoek is daar intestinale nekrose en ulserasie,
purulente rinitis en pneumonie gevind. Diere wat dood is, het limfoïede nekrose en limfoïede
uitputting getoon, terwyl die oorlewende bosvarke perivaskulêre flensing met limfo-plasma selle in
verskeie organe ontwikkel het.
Immunohistochemiese demonstrasie van Europese varkpes virus antigen deur gebruik van ‘n
kommersieël beskikbare muis monoklonale teenligaam, WH303, het duidelike wydverspreide
kleuring in meeste weefsel van die die vlakvarke, bosvarke en mak varke getoon. ‘n Wye reeks
van weefsel en sel tipes het met die teenliggam reageer naamlik: mononukliêre selle (monosietmakrofage
en limfo-plasma selle), follikulêre retikulêre selle, epiteel, vaskulêre endoteel,
mesoteel, gladde spier selle en fibroblaste.
Weefsel wat gemerk is met die teenliggaam het ingesluit: mangels, limfknope, milt, derde ooglid,
adrenaal klier, urienblaas, vel, lewer, nier, long, sekere selle in die sentrale senuwee stelsel, soos
die koroïed pleksus, verskeie dele van die gastro-intestinale stelsel sowel as klier weefsel soos
die pankreas en speekselklier.
Die mangels was die mees konsekwent gemerkte weefsel, terwyl geen kleuring gevind is in
miosiete van skelet of hartspier nie.
Uit hierdie werk kon daar afgelei word dat vlakvarke en bosvarke vatbaar is vir Europese varkpes
en dat intra-spesie oordraging plaasvind onder eksperimentele omstandighede. / Dissertation (MMedVet)--University of Pretoria, 2011. / Paraclinical Sciences / Unrestricted
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The role of wild deer in the epidemiology and management of bovine tuberculosis in New Zealand.Nugent, Graham January 2005 (has links)
The eco-epidemiology of bovine tuberculosis (Tb) in wild deer (mainly red deer Cervus elaphus) in New Zealand was investigated. Bovine Tb is caused by Mycobacterium bovis. Specific aims were to clarify the likely routes of infection in deer, and to determine the status of deer as hosts of Tb, the likely rates and routes of inter- and intra-species transmission between deer and other wildlife hosts, the role of deer in spreading Tb, and the likely utility of deer as sentinels of Tb presence in wildlife. As the possum (Trichosurus vulpecula) is the main wildlife host of Tb, the research also included some investigation of transmission routes in possums.
Patterns of infection were measured in 994 deer killed between 1993 and 2003. Tb prevalence varied between areas (range 836%). Few deer had generalised infection, with 2168% of infected deer having no visible lesions, depending on the area. The retropharyngeal lymph nodes and oropharyngeal tonsils were commonly infected. No dependent fawns less than 0.75 years old were infected, indicating intra-species transmission is rare in wild deer. Where possums were not controlled, the net (cumulative) force of infection in young (14 y) deer was 0.100.24 per year in males and 0.090.12 per year in females, but much lower in older deer (less than 0.05 per year). Possum control reduced the net force of infection quickly, and eventually to zero. However, Tb persisted in possum-controlled areas through immigration of infected deer and, for almost a decade, through the survival of resident deer infected before possum control. Tb was lost from infected deer at an exponential rate of 0.13 per year, mostly as a result of deer recovering from infection rather than dying from it. Wild deer do die of Tb, but there was no discernible effect on age structure. The occurrence of infection in deer was not linked to the local deer or possum density at their kill sites (i.e. in their home range), but the area-wide prevalence of Tb in deer was closely correlated with Tb levels in possums, which were in turn correlated with area-wide measures of possum density. For wild deer in New Zealand, Tb is a persistent but usually inconsequential disease of the lymphatic system. It is acquired mainly by young independent deer, usually orally via the tonsils, and probably as a result of licking infected possums.
Many species fed on deer carrion, including possums. Most possums encountering carrion did not feed on it, but a few fed for long periods. Other scavengers such ferrets (Mustela furo), hawks (Circus approximans), and weka (a hen-sized flightless native bird; Gallirallus australis) fed in a way that probably increased the infectivity of carrion to possums. Commercial deer hunting may have facilitated the historical establishment of Tb in possums. Scavenging (including cannibalism) and interactions with dead and dying possums are identified for the first time as potentially important routes for transmission of Tb to possums, and I develop new hypotheses involving peri- and post-mortem transmission in possums that explain many of the epidemiological patterns that are characteristic of the disease in possum.
In continuous native forest, deer home range size averaged 250 hectares for six young females, and over twice that for two males. Over 90% of infected deer are likely to die within 2 km (females) or 6 km (males) of where they acquired Tb, but deer could occasionally carry Tb up to 30 km. Deer will be useful as sentinels, but only where other sentinels are rare, because the force of infection for a deer with a single infected possum in its home range is only 0.004 per year, compared to greater than 0.2 per year for deliberately released pigs. Deer are occasionally capable of initiating new cycles of infection in wildlife, but deer control is not essential to eradicate Tb from wildlife.
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The role of wild deer in the epidemiology and management of bovine tuberculosis in New ZealandNugent, Graham January 2005 (has links)
The eco-epidemiology of bovine tuberculosis (Tb) in wild deer (mainly red deer Cervus elaphus) in New Zealand was investigated. Bovine Tb is caused by Mycobacterium bovis. Specific aims were to clarify the likely routes of infection in deer, and to determine the status of deer as hosts of Tb, the likely rates and routes of inter- and intra-species transmission between deer and other wildlife hosts, the role of deer in spreading Tb, and the likely utility of deer as sentinels of Tb presence in wildlife. As the possum (Trichosurus vulpecula) is the main wildlife host of Tb, the research also included some investigation of transmission routes in possums. Patterns of infection were measured in 994 deer killed between 1993 and 2003. Tb prevalence varied between areas (range 8–36%). Few deer had generalised infection, with 21–68% of infected deer having no visible lesions, depending on the area. The retropharyngeal lymph nodes and oropharyngeal tonsils were commonly infected. No dependent fawns less than 0.75 years old were infected, indicating intra-species transmission is rare in wild deer. Where possums were not controlled, the net (cumulative) force of infection in young (1–4 y) deer was 0.10–0.24 per year in males and 0.09–0.12 per year in females, but much lower in older deer (less than 0.05 per year). Possum control reduced the net force of infection quickly, and eventually to zero. However, Tb persisted in possum-controlled areas through immigration of infected deer and, for almost a decade, through the survival of resident deer infected before possum control. Tb was lost from infected deer at an exponential rate of 0.13 per year, mostly as a result of deer recovering from infection rather than dying from it. Wild deer do die of Tb, but there was no discernible effect on age structure. The occurrence of infection in deer was not linked to the local deer or possum density at their kill sites (i.e. in their home range), but the area-wide prevalence of Tb in deer was closely correlated with Tb levels in possums, which were in turn correlated with area-wide measures of possum density. For wild deer in New Zealand, Tb is a persistent but usually inconsequential disease of the lymphatic system. It is acquired mainly by young independent deer, usually orally via the tonsils, and probably as a result of licking infected possums. Many species fed on deer carrion, including possums. Most possums encountering carrion did not feed on it, but a few fed for long periods. Other scavengers such ferrets (Mustela furo), hawks (Circus approximans), and weka (a hen-sized flightless native bird; Gallirallus australis) fed in a way that probably increased the infectivity of carrion to possums. Commercial deer hunting may have facilitated the historical establishment of Tb in possums. Scavenging (including cannibalism) and interactions with dead and dying possums are identified for the first time as potentially important routes for transmission of Tb to possums, and I develop new hypotheses involving peri- and post-mortem transmission in possums that explain many of the epidemiological patterns that are characteristic of the disease in possum. In continuous native forest, deer home range size averaged 250 hectares for six young females, and over twice that for two males. Over 90% of infected deer are likely to die within 2 km (females) or 6 km (males) of where they acquired Tb, but deer could occasionally carry Tb up to 30 km. Deer will be useful as sentinels, but only where other sentinels are rare, because the force of infection for a deer with a single infected possum in its home range is only 0.004 per year, compared to greater than 0.2 per year for deliberately released pigs. Deer are occasionally capable of initiating new cycles of infection in wildlife, but deer control is not essential to eradicate Tb from wildlife.
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