An investigation of moose calves from females with Moose Wasting Syndrome (Alces alces L.)
Moose Wasting Syndrome in moose (Alces alces) was first discovered in Sweden in the 1980’s. It was characterised by atrophied lymphoid organs, ulcers and erosions of the mucus membranes of the digestive tract, e.g. glossitis, gingivitis, esophagitis, rumenitis and abomasitis. Clinical signs seen i...
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| Formato: | H3 |
| Lenguaje: | Inglés sueco |
| Publicado: |
SLU/Dept. of Anatomy, Physiology and Biochemistry (until 231231)
2019
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| Materias: |
| _version_ | 1855572551902691328 |
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| author | Kallunki Nyström, Jonas |
| author_browse | Kallunki Nyström, Jonas |
| author_facet | Kallunki Nyström, Jonas |
| author_sort | Kallunki Nyström, Jonas |
| collection | Epsilon Archive for Student Projects |
| description | Moose Wasting Syndrome in moose (Alces alces) was first discovered in Sweden in the 1980’s.
It was characterised by atrophied lymphoid organs, ulcers and erosions of the mucus membranes of the digestive tract, e.g. glossitis, gingivitis, esophagitis, rumenitis and abomasitis.
Clinical signs seen in affected moose were diarrhoea, dehydration, alopecia, weakness, anorexia, impaired vision, emaciation and central nervous system disturbances. The etiology of the
wasting syndrome is still unknown. There are many hypothesis as to the cause of the disease;
however, none have been definitively proven.
In this project, an experimental study of seven moose calves born by mothers suspected of being
affected with MWS is compiled and reviewed. The calves were born between May 15 and June
15, 1992. They were captured in the south of Sweden where MWS was known to occur. The
calves were stabled in a specific-pathogen-free surrounding as laboratory animals between 7 to
11 months and any diseases contracted by the calves were treated. They were given controlled
deer milk formula and feed with known ingredients. Extra minerals and vitamins were given at
a regular basis and they had constant access to saltstones and water. The calves were observed
daily to detect any abnormalities. Investigations for blood biochemistry, hematology, gross pathology and histopahology were done. Results show that the calves developed some clinical,
gross pathological and histopathological findings similar to those found in MWS affected
moose. Some of the clinical signs shown by the calves were diarrhoea, alopecia, inappetence
and lesions in the mouth. No pronounced neurological disturbances were shown by the calves.
Gross pathology showed enlarged and congested liver and spleen, hemorrhages in the adrenal
cortex, lung consolidation, hyperemic trachea, discolouration of the renal cortex and medulla
and lesions in the mouth, myocardium, lungs and cerebral meninges. In the intestinal tract congestion, discolourations, bleedings, flaccidity of the intestinal walls and thin Peyer’s patches
were seen. Histopathology revealed hyperplasia of lymph nodes, alveolar emphysema, mononuclear cell infiltration in the myocardium and mucosa of some areas of the intestinal tract
among other findings. The brain did not display any histopathological lesions indicating classical spongiform encephalopathy. Hematology and biochemistry showed increases and decreases in total leukocyte, lymhocyte, neutrophil and eosinophil count but no uniform changes
were seen. In conclusion, there were indications that MWS was contracted by the calves via
their mother’s directly or transplacentally, suggesting an infectious cause of MWS. It is possible
that other, more severe MWS characteristic clinical and gross pathological lesions would have
appeared if the calves had been stabled for a longer time and been investigated when the disease
had progressed further. No evidence of classic prion disease (BSE) was shown in this study,
however, with the long incubation period for prion diseases like CWD, as Benestad & Telling
(2018) declare, it is possible that more pronounced lesions would have developed in the moose
calves, given more time. Future studies are needed, using up to date technology and methods
to determine if prions is the cause of MWS. |
| format | H3 |
| id | RepoSLU15281 |
| institution | Swedish University of Agricultural Sciences |
| language | Inglés swe |
| publishDate | 2019 |
| publishDateSort | 2019 |
| publisher | SLU/Dept. of Anatomy, Physiology and Biochemistry (until 231231) |
| publisherStr | SLU/Dept. of Anatomy, Physiology and Biochemistry (until 231231) |
| record_format | eprints |
| spelling | RepoSLU152812020-01-21T10:07:46Z An investigation of moose calves from females with Moose Wasting Syndrome (Alces alces L.) Studier av älgkalvar från Moose Wasting Syndrome drabbade älgkor (Alces alces L.) Kallunki Nyström, Jonas Moose wasting syndrome spongiform encephalopathy histology pathology Moose Wasting Syndrome in moose (Alces alces) was first discovered in Sweden in the 1980’s. It was characterised by atrophied lymphoid organs, ulcers and erosions of the mucus membranes of the digestive tract, e.g. glossitis, gingivitis, esophagitis, rumenitis and abomasitis. Clinical signs seen in affected moose were diarrhoea, dehydration, alopecia, weakness, anorexia, impaired vision, emaciation and central nervous system disturbances. The etiology of the wasting syndrome is still unknown. There are many hypothesis as to the cause of the disease; however, none have been definitively proven. In this project, an experimental study of seven moose calves born by mothers suspected of being affected with MWS is compiled and reviewed. The calves were born between May 15 and June 15, 1992. They were captured in the south of Sweden where MWS was known to occur. The calves were stabled in a specific-pathogen-free surrounding as laboratory animals between 7 to 11 months and any diseases contracted by the calves were treated. They were given controlled deer milk formula and feed with known ingredients. Extra minerals and vitamins were given at a regular basis and they had constant access to saltstones and water. The calves were observed daily to detect any abnormalities. Investigations for blood biochemistry, hematology, gross pathology and histopahology were done. Results show that the calves developed some clinical, gross pathological and histopathological findings similar to those found in MWS affected moose. Some of the clinical signs shown by the calves were diarrhoea, alopecia, inappetence and lesions in the mouth. No pronounced neurological disturbances were shown by the calves. Gross pathology showed enlarged and congested liver and spleen, hemorrhages in the adrenal cortex, lung consolidation, hyperemic trachea, discolouration of the renal cortex and medulla and lesions in the mouth, myocardium, lungs and cerebral meninges. In the intestinal tract congestion, discolourations, bleedings, flaccidity of the intestinal walls and thin Peyer’s patches were seen. Histopathology revealed hyperplasia of lymph nodes, alveolar emphysema, mononuclear cell infiltration in the myocardium and mucosa of some areas of the intestinal tract among other findings. The brain did not display any histopathological lesions indicating classical spongiform encephalopathy. Hematology and biochemistry showed increases and decreases in total leukocyte, lymhocyte, neutrophil and eosinophil count but no uniform changes were seen. In conclusion, there were indications that MWS was contracted by the calves via their mother’s directly or transplacentally, suggesting an infectious cause of MWS. It is possible that other, more severe MWS characteristic clinical and gross pathological lesions would have appeared if the calves had been stabled for a longer time and been investigated when the disease had progressed further. No evidence of classic prion disease (BSE) was shown in this study, however, with the long incubation period for prion diseases like CWD, as Benestad & Telling (2018) declare, it is possible that more pronounced lesions would have developed in the moose calves, given more time. Future studies are needed, using up to date technology and methods to determine if prions is the cause of MWS. Moose Wasting Syndrome upptäcktes första gången i Sverige under 1980-talet. Det karaktäriserades av atrofierade lymfoida organ, ulceration och erosioner i digestionkanalens slemhinnor, d.v.s. glossit, gingivit, esofagit, rumenit och abomasit. Kliniska tecken noterade hos MWSdrabbade älgar var diarré, dehydrering, alopeci, svaghet, anorexi, synnedsättning, utmärgling och defekter i centrala nervsystemet. Etiologin bakom wasting syndromet är fortfarande okänd. Det finns många hypoteser om vad som orsakar sjukdomen; dock har ingen slutligen bevisats. I detta projekt sammanställs och granskas en experimentell studie av sju kalvar, födda till mödrar misstänkta att vara drabbade av MWS. Kalvarna föddes mellan 15:e maj och 15:e juni 1992. De fångades i södra Sverige där sjukdomen veterligen förekom. Kalvarna stod uppstallade i en SPF-miljö mellan 7 till 11 månader och om de uppvisade tecken på sjukdom behandlades de. De gavs kontrollerad hjortmjölk och foder med känt innehåll. Extra mineraler och vitaminer gavs på regelbunden basis och de hade konstant tillgång till saltsten och vatten. Kalvarna observerades dagligen för att upptäcka avvikelser. Undersökningar för blodbiokemi, hematologi, patologi och histopatologi gjordes. Resultaten visar att kalvarna utvecklade vissa kliniska, patologiska och histopatologiska fynd som liknar de som ses hos MWS-sjuka älgar. Några av de kliniska fynd som sågs hos kalvarna var diarré, alopeci, inappetens och lesioner i munnen. Inga uttalade neurologiska avvikelser sågs hos kalvarna. Vid obduktion sågs bl.a förstorad och stasad lever och mjälte, blödningar i binjurebark, konsolidering av lunga, hyperemisk trachea, missfärgning av njurbark och –märg samt lesioner i munnen, myokardiet, lungor och hjärnhinnor. I gastrointestinalkanalen sågs bl.a stas, missfärgningar, blödningar, slapphet av tarmväggen samt tunna Peyerska plack. Histopatologi visade hyperplasi av lymfknutor, alveolärt emfysém, mononukleär cellinfiltration i myokardiet och i slemhinnan i vissa delar av gastrointestinalkanalen m.m. I hjärnan sågs inga histologiska fynd som indikerade klassisk spongiform encefalopati. Hematologi och biokemi visade både ökade som sänkta nivåer av totalantal leukocyter, lymfocyter, neutrofiler och eosinofiler men inga ensartade förändringar sågs. Sammanfattningsvis kan sägas att det fanns indikationer på att kalvarna smittats med MWS av sina mödrar, direkt eller transplacentalt, vilket tyder på att MWS har en infektiös orsak. Det är möjligt att andra eller mer allvarliga MWS-karaktäristiska kliniska och patologiska fynd hade setts om kalvarna hade hållits uppstallade en längre tid och blivit undersökta när sjukdomen fått fortskrida längre. Inga tecken på prionsjukdom sågs i denna studie, men med den långa inkubationstid för prionsjukdomar så som ses vid CWD, som Benestad och Telling (2018) uppger, kunde potentiellt mer uttalade lesioner utvecklats efter ett längre tidsförlopp. Vidare studier, med modern teknik och moderna metoder, krävs för att avgöra om prioner är orsaken till MWS. SLU/Dept. of Anatomy, Physiology and Biochemistry (until 231231) 2019 H3 eng swe https://stud.epsilon.slu.se/15281/ |
| spellingShingle | Moose wasting syndrome spongiform encephalopathy histology pathology Kallunki Nyström, Jonas An investigation of moose calves from females with Moose Wasting Syndrome (Alces alces L.) |
| title | An investigation of moose calves from females
with Moose Wasting Syndrome (Alces alces L.) |
| title_full | An investigation of moose calves from females
with Moose Wasting Syndrome (Alces alces L.) |
| title_fullStr | An investigation of moose calves from females
with Moose Wasting Syndrome (Alces alces L.) |
| title_full_unstemmed | An investigation of moose calves from females
with Moose Wasting Syndrome (Alces alces L.) |
| title_short | An investigation of moose calves from females
with Moose Wasting Syndrome (Alces alces L.) |
| title_sort | investigation of moose calves from females
with moose wasting syndrome (alces alces l.) |
| topic | Moose wasting syndrome spongiform encephalopathy histology pathology |