Sheep measles can eat into your profit.
According to DPI monitoring programs, 36% of sheep consignments at various NSW abattoirs are affected by this parasite. On infected premises as many as one in 4 lambs have been found to have the small oval white cysts, 3 to 10mm long, in various muscles. At slaughter affected carcasses will be partly or wholly condemned. These cysts, commonly known as sheep measles, are the intermediate stage of a particular tape worm – Taenia ovis. It occurs in Australia wherever there are sheep or goats, as well as dogs.
Dogs are the final hosts of Taenia ovis. The adult tapeworm lives in its intestines, where it can grow to 2 meters long. The dog’s health is generally unaffected by the tapeworm.
Eggs are shed in the dog’s droppings and infest the pasture. Grazing sheep ingest the eggs. These eggs hatch and tiny larvae developed and migrate to the muscles where they become cysts. Dogs get infected with Taenia ovis by eating viable tapeworm cysts in sheep or goat tissues, e.g. raw meat.
Domestic dogs are the most important definitive host for Taenia ovis. Dingoes and wild dogs are only very occasionally affected.
Foxes are rarely affected with this tapeworm. They are more likely to get different species of tapeworm from rabbits (T.pisiformis and T. serialis) and less commonly the tapeworm Spirometra erinacea from eating reptiles and amphibians.
Sheep measles threaten your wealth and does not develop in humans.
Another dog tapeworm Echinococcus granulosus, or the hydatid tapeworm, is a human health hazard. The adult hydatid tapeworm is tiny – only 4 to 6mm. Its lifecycle is similar to Taenia ovis. However, if humans ingest the eggs – usually due to close contact with dogs – cysts can develop in their organs – such as the liver, lungs or even brain, with life threatening results. Cysts also develop in the organs of sheep or goats.
To control sheep measles and hydatid tapeworm one needs to break the sheep-dog lifecycle.
· Control dog movements
· Prevent dogs from eating raw sheep or goat meat or offal.
· Treat dogs regularly with an efficient tapewormer such as praziquantel (eg Droncit) which can be purchased from a vet.
Thursday, July 31, 2008
Monday, July 21, 2008
Bovine Pestivirus
Bovine Pestivirus under Extensive Farming Conditions in Australia
Cause:
Pestivirus or Bovine Viral Diarrhoea Virus belongs to the Flaviviridae family and the Pestivirus genus. Human Hepatitis C belongs to the same family of viruses, but is a member of the Flavivirus genus. Only Type 1 occurs in Australia. It is less aggressive than Type 2, which occurs in the USA and UK, amongst others.
History and prevalence:
It has been known to be present in Australia for about 40 years. Approximately 90% of herds have animals that test positive for antibodies against this disease, therefore it is widely distributed.
How does it spread:
Calves which survive in utero infection between 30 and 90 days of gestation are born persistently infected. Their developing immune systems do not recognise the virus as a foreign entity and do not produce any antibodies against the disease. Occasionally infection between day 90 and 125 can also result in the birth of a PI. These so-called PI calves are a potent and constant source of virus, excreting vast amounts in every secretion and excretion - eg saliva, urine, faeces, semen etc.
In the general population 0.5% to 1% of animals at 1 to 2 years of age may be PI's. In certain infected mobs of calves it may be as high as 50%.
PI animals often have deranged nervous systems and are more likely than other animals to be aggressive and jump fences, therefore posing a risk to neighbouring herds and farms.
In an average herd situation, in a herd of 100 calves running together and occasionally being yarded together, all should be infected by the time they are 12 months old is there is a single PI present. This in itself is not a big problem, as the disease's main impact is on the developing foetus. An animal infected before breeding under extensive conditions rarely show symptoms. Once infected, all (except the PI's) develop antibodies and are immune for life.
A problem develops when pregnant susceptible animals are exposed to the PI animal, for instance by mixing groups of cattle that were previously separated, or by a PI animal jumping a fence. The pregnant animals come into contact with the infected animal and its excretions/secretions and become infected. Bulls may also be PI's and infect the cows they mate with.
Depending on conditions the virus can survive for a few hours to a few days in the environment. If a cow aborts an infected foetus, the foetus and placenta are a source of the virus for a short period.
Animals which become infected after birth, regardless of their age, rarely show symptoms, but they are viraemic for 7 to 10 days. They secrete small numbers of virus; usually insufficient to infect other animals, though there have been instances of the Type 1 virus spreading from transiently infected animals. Type 2 is more likely to spread to in contact animals in this way.
Symptoms:
If breeding cows are infected close to the time of mating, there will be reduced conception and cows will return to service. Infection later in the 1st trimester of pregnancy causes embryonic death, abortion, stillbirth, the birth of weak non-viable calves and the birth of PI's.
Infection in the second trimester leads to congenital defects, such as eye defects and cerebellar hyperplasia.
Infection in the third trimester does not cause any problems. The foetus mounts an immune response and is born immune to BVDV and is seropositive (has antibodies in his bloodstream)
PI calves are often small, are poor do-ers and immunological cripples. They are prone to common infections such as ringworm, and are reservoirs of other infections.
A PI cow will always give birth to a PI calf.
Young animals that contact BVDV may show mild transient respiratory symptoms, but are often asymptomatic. They have antibodies 13 to 19 days after exposure and remain immune for life. The exception is animals in feedlots. They can develop severe respiratory disease and diarrhoea.
Non pregnant adult animals show no symptoms.
However, BVDV does suppress the immune system and makes animals more susceptible to other infections for up to two months after the initial infection.
Mucosal Disease:
This condition only occurs in PI's after a superinfection with a cytopathogenic strain of BVDV which arises as a mutant form of the persisting virus in a given PI animal. It causes ulceration of the buccal cavity and alimentary tract and leads to the death of the animal. As is the case with their original infection, they do not recognize the mutant virus as foreign and do not mount an immune response. This mutant strain only needs to arise in one PI in a herd and will rapidly spread to other PI's in the mob, due to their immune tolerance. This results in sudden death of clusters of PI's.
The mutant virus does not pose a risk to the rest of the herd.
50% of PI's will usually die in the first year of life. Half or more of the remainder die in the following year. Sometimes a PI will survive for a number of years. A female PI can breed successfully, but her calf will always be a PI.
sources:
www.bvdvaustralia.com
Dr. Peter Kirkland, Alison Bradford, Bruce Watt, David Gardiner and other Rural Land Protection Board District Veterinarians in NSW. E-mail communications.
Cause:
Pestivirus or Bovine Viral Diarrhoea Virus belongs to the Flaviviridae family and the Pestivirus genus. Human Hepatitis C belongs to the same family of viruses, but is a member of the Flavivirus genus. Only Type 1 occurs in Australia. It is less aggressive than Type 2, which occurs in the USA and UK, amongst others.
History and prevalence:
It has been known to be present in Australia for about 40 years. Approximately 90% of herds have animals that test positive for antibodies against this disease, therefore it is widely distributed.
How does it spread:
Calves which survive in utero infection between 30 and 90 days of gestation are born persistently infected. Their developing immune systems do not recognise the virus as a foreign entity and do not produce any antibodies against the disease. Occasionally infection between day 90 and 125 can also result in the birth of a PI. These so-called PI calves are a potent and constant source of virus, excreting vast amounts in every secretion and excretion - eg saliva, urine, faeces, semen etc.
In the general population 0.5% to 1% of animals at 1 to 2 years of age may be PI's. In certain infected mobs of calves it may be as high as 50%.
PI animals often have deranged nervous systems and are more likely than other animals to be aggressive and jump fences, therefore posing a risk to neighbouring herds and farms.
In an average herd situation, in a herd of 100 calves running together and occasionally being yarded together, all should be infected by the time they are 12 months old is there is a single PI present. This in itself is not a big problem, as the disease's main impact is on the developing foetus. An animal infected before breeding under extensive conditions rarely show symptoms. Once infected, all (except the PI's) develop antibodies and are immune for life.
A problem develops when pregnant susceptible animals are exposed to the PI animal, for instance by mixing groups of cattle that were previously separated, or by a PI animal jumping a fence. The pregnant animals come into contact with the infected animal and its excretions/secretions and become infected. Bulls may also be PI's and infect the cows they mate with.
Depending on conditions the virus can survive for a few hours to a few days in the environment. If a cow aborts an infected foetus, the foetus and placenta are a source of the virus for a short period.
Animals which become infected after birth, regardless of their age, rarely show symptoms, but they are viraemic for 7 to 10 days. They secrete small numbers of virus; usually insufficient to infect other animals, though there have been instances of the Type 1 virus spreading from transiently infected animals. Type 2 is more likely to spread to in contact animals in this way.
Symptoms:
If breeding cows are infected close to the time of mating, there will be reduced conception and cows will return to service. Infection later in the 1st trimester of pregnancy causes embryonic death, abortion, stillbirth, the birth of weak non-viable calves and the birth of PI's.
Infection in the second trimester leads to congenital defects, such as eye defects and cerebellar hyperplasia.
Infection in the third trimester does not cause any problems. The foetus mounts an immune response and is born immune to BVDV and is seropositive (has antibodies in his bloodstream)
PI calves are often small, are poor do-ers and immunological cripples. They are prone to common infections such as ringworm, and are reservoirs of other infections.
A PI cow will always give birth to a PI calf.
Young animals that contact BVDV may show mild transient respiratory symptoms, but are often asymptomatic. They have antibodies 13 to 19 days after exposure and remain immune for life. The exception is animals in feedlots. They can develop severe respiratory disease and diarrhoea.
Non pregnant adult animals show no symptoms.
However, BVDV does suppress the immune system and makes animals more susceptible to other infections for up to two months after the initial infection.
Mucosal Disease:
This condition only occurs in PI's after a superinfection with a cytopathogenic strain of BVDV which arises as a mutant form of the persisting virus in a given PI animal. It causes ulceration of the buccal cavity and alimentary tract and leads to the death of the animal. As is the case with their original infection, they do not recognize the mutant virus as foreign and do not mount an immune response. This mutant strain only needs to arise in one PI in a herd and will rapidly spread to other PI's in the mob, due to their immune tolerance. This results in sudden death of clusters of PI's.
The mutant virus does not pose a risk to the rest of the herd.
50% of PI's will usually die in the first year of life. Half or more of the remainder die in the following year. Sometimes a PI will survive for a number of years. A female PI can breed successfully, but her calf will always be a PI.
sources:
www.bvdvaustralia.com
Dr. Peter Kirkland, Alison Bradford, Bruce Watt, David Gardiner and other Rural Land Protection Board District Veterinarians in NSW. E-mail communications.
Friday, May 30, 2008
for the love of dog
I grew up with dogs in my parents' and grandparents' homes. When I was 5 years old, my dachshund died of strychnine poisoning. The only vet was out of town. I vowed there and then that I would be a vet, so that this would never happen again and in spite of scepticism and objections from family, teachers and friends over the years, never wavered in my resolve. So in a way I became a vet to avenge Woofy's cruel and senseless death.
What I never could foresee in those years was how many dogs I would have to kill in the course of my career - some to relieve suffering, but far too many were victims of "disposal dog syndrome", and were killed for the sake of their owners' convenience. Throughout the years I have struggled with the ethics and emotional issues. At times I am in tears and close to leaving the profession, at other times I manage to distance myself emotionally and rationalize - too many dogs, too few people to care, behavioural issues, disease or injury, which though treatable, exceeds the budgets of their owners. If I refused their owners would sometimes threaten to beat them to death, or shoot them or dump them by the side of the road. During a recent visit to the RSPCA someone brought in two 6 week old puppies that had been found tied shut in a bag and left in the hot sun in the bush. Some dogs I have saved and rehomed, but too many have died and are continuing to do so.
Veterinarians and veterinary nurses as a group have an unacceptably high suicide rate, which has often been related to the stress and distress caused by having to kill the very animals they dedicate their lives to saving.
Therefore I dedicate my paintings to the dogs that I and my colleagues have killed, and to my colleagues who suffer deeply every time this happens.
I have a dream to establish a no kill animal shelter, where all dogs will be welcome, and they will be rehabilitated and rehomed or housed and cared for until they die of old age. If I could become as famous and succesfull as Ron Burns,the artist who is my inspiration for this series, I will use the money to start a trust fund towards fulfilling this dream.
Tragically most existing animal shelters are compelled to kill vast numbers of unwanted pets as they are severely constrained by limited funds.
Dogs love their humans without holding back, with no guile or subterfuge and will often be loyal to the death, even throwing themselves at gun toting intruders and in the way of bullets as happened to a German Shepherd I treated in Sydney late last year. Their loyalty and devotion are technicolour bright, without shades of gray. Their love knows no compromise. All they desire is too please their owners. So I chose bright colours for my paintings, to reflect the bright bold technicolour love that dogs have for their owners, deserving or not.
These paintings have given me great pleasure and they are just the begining. I am inspired by my subject matter, their beautiful transparent eyes and the huge variety of shapes and characters they come in. I hope I can do justice to the love I have experienced from the dogs in my life, and in some way, maybe save a few lives, by making people appreciate dogs for the wonderful animals they truly are
Budgie
Veeartsenykunde is vir mal mense. Ek het in die vroee ure van Sondagoggend 'n budgie verlos van 'n eier wat vassit met sy histeriese eienares se bogpratery in my ore. Sy beweer die budgie is verlief op haar man, daarom is haar hormone deurmekaar (die budgie s'n, my lam). Daarom wil sy eiers le terwyl haar liggam nie gereed is daarvoor nie. Ek het my bes probeer om die budgie te hou en haar weg te stuur, maar sy het bly sit. Nou ja, met groot moeite, geduld en toewyding kry ek toe uiteindelik die eier uit sonder veel trauma - behalwe vir die wat die vrou op my psige uitgeoefen het. Die budgie lyk toe goed, dis 5 uur in die oggend, ek is gatvol vir die mal vrou en reken dis die beste vir die arme budgie om huis toe te gaan na 'n bekende omgewing. Soos Leon sou se "WRONGGG!!"
Gisteraand na aan middernag storm die vrou die spreekkamer binne met die budgie styf toegedraai in 'n handdoek teen haar boesem. Toe ons hom losgewikkel kry, is hy nie alleen dood nie, maar lankal stokstyf, hoewel sy oortuig is hy het gelewe toe sy by die huis weg is. Nou ja. 'n Drie jaar oue kind kan baie by haar leer oor die gooi van tantrums - huil, skreeu, rol op die vloer, stamp jou kop herhaaldelik teen die toonbank, hard. Skreeu 'n bietjie harder. Vloek - vreeslik. Dryg om jouself dood te maak, want jou lewe is nie meer die moeite werd nie en dit sal die veearts se skuld wees. (Selfs al onderdruk die veearts die innner voice wat se "Nou, vat haar kop vas op die agterkant van sy trek en help hom vorentoe - na die skerp rand van die toonbank".) Beskuldig die veearts van budgie moord. Skreeu nog harder en dreig om die veearts hof toe te neem. As die veearts steeds haar inner voice ignoreer, dreig om haar dood te maak. As dit ook nie werk nie, dreig om almal by die praktyk dood te maak. Intussen staan die man in die hoekie en skop na die muur. Hy se egter niks. Is hy ontsteld oor sy enigste ware geliefde dood is, of verbeel hy hom die muur is sy vrou? Sy broer staan hulpeloos en toekyk. Eindelik is die spul darem by die deur uit en gelukkig was daar nie ander kliente in die spreekkamer nie.
Toe se die veearts wat nog agter besig is dat dit praktyk beleid is om enige dreigemente van geweld aan die polisie te rapporteer. Dit is een ding wat my beindruk van Oz - hulle was binne 10 minute daar, hoewel ons vir hulle gese het die mense is reeds weg en ons glo nie daar is regtig enige gevaar nie. Hulle was vriendelik en professioneel en het gese hulle patrolleer heel nag in die omgewing en kan gou daar wees en moenie huiwer om te bel as daar enige verdere probleme is nie.
Nogtans, dit was 'n lang donker nag in die stil gebou en enige krake was harder as gewoonlik en die arme Amerikaanse verpleegstertjie - my enige geselskap na 12 - was maar senuweeagtig om die honde buite toe te neem om te gaan piepie.
Ek wens ek was 'n kunstenaar! Of dalk die Filipino wat om 4uur in die oggend die gebou kom skoonmaak. Behalwe vir groet, hoef hy met niemand te praat nie en na niemand te luister nie.
Gisteraand na aan middernag storm die vrou die spreekkamer binne met die budgie styf toegedraai in 'n handdoek teen haar boesem. Toe ons hom losgewikkel kry, is hy nie alleen dood nie, maar lankal stokstyf, hoewel sy oortuig is hy het gelewe toe sy by die huis weg is. Nou ja. 'n Drie jaar oue kind kan baie by haar leer oor die gooi van tantrums - huil, skreeu, rol op die vloer, stamp jou kop herhaaldelik teen die toonbank, hard. Skreeu 'n bietjie harder. Vloek - vreeslik. Dryg om jouself dood te maak, want jou lewe is nie meer die moeite werd nie en dit sal die veearts se skuld wees. (Selfs al onderdruk die veearts die innner voice wat se "Nou, vat haar kop vas op die agterkant van sy trek en help hom vorentoe - na die skerp rand van die toonbank".) Beskuldig die veearts van budgie moord. Skreeu nog harder en dreig om die veearts hof toe te neem. As die veearts steeds haar inner voice ignoreer, dreig om haar dood te maak. As dit ook nie werk nie, dreig om almal by die praktyk dood te maak. Intussen staan die man in die hoekie en skop na die muur. Hy se egter niks. Is hy ontsteld oor sy enigste ware geliefde dood is, of verbeel hy hom die muur is sy vrou? Sy broer staan hulpeloos en toekyk. Eindelik is die spul darem by die deur uit en gelukkig was daar nie ander kliente in die spreekkamer nie.
Toe se die veearts wat nog agter besig is dat dit praktyk beleid is om enige dreigemente van geweld aan die polisie te rapporteer. Dit is een ding wat my beindruk van Oz - hulle was binne 10 minute daar, hoewel ons vir hulle gese het die mense is reeds weg en ons glo nie daar is regtig enige gevaar nie. Hulle was vriendelik en professioneel en het gese hulle patrolleer heel nag in die omgewing en kan gou daar wees en moenie huiwer om te bel as daar enige verdere probleme is nie.
Nogtans, dit was 'n lang donker nag in die stil gebou en enige krake was harder as gewoonlik en die arme Amerikaanse verpleegstertjie - my enige geselskap na 12 - was maar senuweeagtig om die honde buite toe te neem om te gaan piepie.
Ek wens ek was 'n kunstenaar! Of dalk die Filipino wat om 4uur in die oggend die gebou kom skoonmaak. Behalwe vir groet, hoef hy met niemand te praat nie en na niemand te luister nie.
Nitrate Poisoning in Livestock
Significant Stock Losses caused by drought feeding.
Last week two farms suffered significant livestock losses. Deaths were caused by drought feeding of millet silage in one case and millet hay in the other. Approximately 10% of cattle died apparently overnight after being fed the millet products.
Laboratory tests confirmed that the cause was nitrate/nitrite poisoning in both cases.
Nitrates in fodder are converted to nitrites in the rumen. Nitrates in stored fodder can also be converted to nitrites when plant materials heat up or are attacked by bacteria or fungi. Normal levels of nitrite are converted to ammonia in the rumen by bacterial action. However excessive levels of nitrate or nitrite are poisonous.
Certain soil and environmental conditions facilitate nitrate uptake and accumulation by plants, eg.:
Use of nitrogen containing fertilizers
Low soil sulfur and molybdenum
Areas where stock have congregated and urinated and defecated (stock yards)
Drought
Cloudy or cold weather
Herbicide application, esp 2.4-D
Wilting
Plant species
Stage of maturity of plant
Part of plant
Young plants have higher nitrate concentrations and most plant nitrate is located in the bottom third of the stalk.
Hays made from cereal crops, especially those grown under drought conditions and cut while "sappy" can develop toxic nitrite levels when they heat up.
Hays contain almost the same level of nitrate as the parent crop. Silage normally contains significantly less due to the fermentation process.
Sheep are less susceptible to nitrite poisoning than cattle, but can also be affected.
Stressed animals in poor health or poor condition are more susceptible and hunggry animals are more likely to eat large amounts.
The risk of poisoning can be reduced by
Having feeds and forages analysed for nitrate levels.
Gradually introducing any new feeds by feeding small amounts frequently and diluting with known safe feeds.
Cattle can become acclimatized to relatively high levels of nitrate this way.
Frequent observation of stock, especially when changing food or grazing.
Don't overstock.
Prevent hungry stock from grazing on high risk fodder.
Do not graze high nitrate pastures for 7 days after rainfall, cloudy weather, frosts or high temperatures causing wilting.
Do not harvest pastures under these conditions either.
Graze these pastures during sunny afternoons above 15 degrees Celsius and remove livestock at night.
Never feed mouldy hay.
Harvest crops close to maturity and raise the cutter head selectively to avoid the bottom part of the stalk.
Keep in mind that rapidly growing weeds after rainfall may also contain excessive levels of nitrate as well as cyanide (prussic acid).
Last week two farms suffered significant livestock losses. Deaths were caused by drought feeding of millet silage in one case and millet hay in the other. Approximately 10% of cattle died apparently overnight after being fed the millet products.
Laboratory tests confirmed that the cause was nitrate/nitrite poisoning in both cases.
Nitrates in fodder are converted to nitrites in the rumen. Nitrates in stored fodder can also be converted to nitrites when plant materials heat up or are attacked by bacteria or fungi. Normal levels of nitrite are converted to ammonia in the rumen by bacterial action. However excessive levels of nitrate or nitrite are poisonous.
Certain soil and environmental conditions facilitate nitrate uptake and accumulation by plants, eg.:
Use of nitrogen containing fertilizers
Low soil sulfur and molybdenum
Areas where stock have congregated and urinated and defecated (stock yards)
Drought
Cloudy or cold weather
Herbicide application, esp 2.4-D
Wilting
Plant species
Stage of maturity of plant
Part of plant
Young plants have higher nitrate concentrations and most plant nitrate is located in the bottom third of the stalk.
Hays made from cereal crops, especially those grown under drought conditions and cut while "sappy" can develop toxic nitrite levels when they heat up.
Hays contain almost the same level of nitrate as the parent crop. Silage normally contains significantly less due to the fermentation process.
Sheep are less susceptible to nitrite poisoning than cattle, but can also be affected.
Stressed animals in poor health or poor condition are more susceptible and hunggry animals are more likely to eat large amounts.
The risk of poisoning can be reduced by
Having feeds and forages analysed for nitrate levels.
Gradually introducing any new feeds by feeding small amounts frequently and diluting with known safe feeds.
Cattle can become acclimatized to relatively high levels of nitrate this way.
Frequent observation of stock, especially when changing food or grazing.
Don't overstock.
Prevent hungry stock from grazing on high risk fodder.
Do not graze high nitrate pastures for 7 days after rainfall, cloudy weather, frosts or high temperatures causing wilting.
Do not harvest pastures under these conditions either.
Graze these pastures during sunny afternoons above 15 degrees Celsius and remove livestock at night.
Never feed mouldy hay.
Harvest crops close to maturity and raise the cutter head selectively to avoid the bottom part of the stalk.
Keep in mind that rapidly growing weeds after rainfall may also contain excessive levels of nitrate as well as cyanide (prussic acid).
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