Photo Of The Month

From Washington State
The goats are doing great and adjusting just fine! They have been sleeping in the house the past week and we just moved them to a small outdoor pen yesterday. They love roaming around with us and we all enjoy the sounds of these little maaaaaaaaas! My daugter took one of them to dog agility the other day and had a blast, she might do goat pack agility at fair. River is learning all sorts of new things and loves every second with the babies!
Just thought I would give you an update! Thanks!

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Home » Articles » Diseases, Injuries, Parasites and More

Diseases, Injuries, Parasites and More

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Articles/Diseases, Injuries, Parasites and More
Author:Administrator
  Diseases of the Respiratory System     Sheep pneumonia is especially common in newborn lambs and in feedlot lambs, it can also occur in the mature ewe flock with milder clinical signs. Pneumonia is caused by a complex interaction between the environment which produces stress, microorganisms, and the sheep's immune response. Pneumonia occurs in all ages of sheep, in all breeds, in every country of the world. As the management practices become more intensive the level and risk of pneumonia become much greater. Close contact allows for rapid spread of infectious organisms from one lamb to the next. Intensive management also leads to a buildup of pathogens in the environment. Manure in sheds also leads to the production of ammonia which irritates and damages the respiratory mucosa and reduces the sheep's ability to fight the infection. In shed or semi-confinement lambing operations the pneumonia will peak towards the end of the lambing season in many operations.     In acute outbreaks of pneumonia, Pasteurella haemolytica is the organism most frequently isolated from the affected lung tissue, but only rarely is it the primary organism. P. haemolytica is a common inhabitant of upper respiratory and tonsils of normal healthy sheep. Very young lambs less than 48 hours old with acute pneumonia and septicemia are often due to biotype A pasteurelia pneumonia. Death losses from newborn pneumonia can be as high as 50% in some flocks. Death is only a part of the actual losses: treatment expense, poor chronic doing lambs, reduced feed efficiency, reduced average daily gains also result from newborn pneumonia infections. Farms that have yearly pneumonia problems in their newborn lambs need to address the lambs environment and the stresses on the lamb at birth. We have had very limited success using any of the vaccination products available. The use of TSV 2 (also called Nasalgen) has been proven to booster the immunity levels in lambs for viral pneumonia, however it by itself will not stop or prevent an outbreak of pneumonia if environmental factors are poor. The use of a long acting (48 hour) antibiotic given on days 1 and 3 have helped stop lamb death losses on some farms. On farms with a history of severe newborn lamb pneumonia and high losses it can be advantageous to treat the entire ewe flock with water soluble antibiotics several times prior to the lambing season to reduce the shedding from the ewes to the newborn lambs.     "Barn cough" is a term used to describe a non-productive hacking cough in growing and finishing lambs. We do not know which organism causes the cough but we do know that certain antibiotics can relieve the clinical cough for 2 to 3 weeks. Barns cough does not cause large death losses or acute deaths, however, the incidence of rectal prolapses increases in direct proportion to the irritating cough. Factors such as crowding, dust, damp humid weather, or stress all can increase the amount of barn cough. Treating the entire group of lambs with antibiotics will reduce the cough, but the producer must be very careful of drug withdrawal times in lambs that are going to be slaughtered. In many cases we have to treat every 2 weeks to control the coughing. Once a lamb tears the supporting muscles and connective tissue around the rectum it will eventually prolapse and require treatment. Lambs that are coughing will develop immunity and eventually become resistant and not cough anymore. Frequently we hear producers referring to this as “the lambs outgrow the cough”. In Minnesota when the fall weather begins and temperatures become colder the incidence of “barn cough” is greatly reduced. The cough is most likely caused by a combination of organisms such as viruses and bacteria working together to weaken the lambs' respiratory system. In our experience we have had good response to treatment with Albon (sulfadimethoxine) in the water for 3 days every two weeks. Tylan, injectable and feed grade, has also worked in some flocks. Other antibiotics that have been used with some success are tetracyclines and Naxcel.     When treating sheep for pneumonia we have very few approved drugs from which to choose and these are approved at sub-therapeutic levels. You will need to work with your veterinarian to determine which drug will work most effectively and then be careful to follow the proper drug withdrawal times. Most times we need to concentrate on the environment and reduce the exposure. The answer for sheep pneumonia does not come from vaccine or the syringe and bottle. We also know that some breeds have varying degrees of innate ability to reduce the severity of clinical signs. J. D. Bobb, D.V.M. International SheepLetter Vol. 19 No. 3, April 1999 Back
Friday, 21 August 2009 | 3594 hits | Print | PDF |  E-mail | Report
Articles/Diseases, Injuries, Parasites and More
Author:Administrator
  Integrated Parasite Management (IPM) in Small Ruminants by Susan Schoenian Area Agent, Sheep and Goats Western Maryland Research & Education Center Maryland Cooperative Extension Internal parasites are the #1 health problem affecting small ruminants. Sheep and goats are more susceptible to internal parasites than other livestock, due to their grazing behavior and poor immunity. In the past, producers relied heavily on anti-parasitic drugs, called "anthelmintics" to control internal parasites in their goat herds. Unfortunately, parasites have become increasingly resistant to many of the anthelmintics. In addition, few anthelmintics are FDA-approved for use in goats, and due to the costs involved in developing new drugs, it is not likely that any new products are going to come onto the market anytime soon. As a result, producers can no longer rely on anthelmintics alone to control parasites in their herds. A more integrated approach will be necessary. On the plus side, internal parasites are a major area of study among scientists in Australia, New Zealand, South Africa, and the United States and new discoveries will likely be made in years to come. Major parasites of concern - stomach worms (roundworms, nematodes) The parasite that causes the most problems to small ruminants is Haemonchus Contortis, better known as the "barber pole" worm. The barber pole worm is a blood-sucking parasite that pierces the lining of the abomassum, causing blood plasma and protein loss to the host. The symptom most commonly associated with barber pole infection is anemia, characterized by pale mucous membranes, especially in the lower eye lid; and "bottle jaw," an accumulation of fluid under the jaw. Diarrhea (scours) is not the usual symptom of barber pole infection. The barber pole worm is a prolific egg producer with a short, direct life cycle. Severly parasitized lamb The parasite of secondary concern is Ostertagia Circumcinta, better known as the small brown stomach worm. It also burrows itself into the lining of the abomassum. But instead of causing blood and protein loss, it causes digestive disturbances such as diarrhea and weight loss. Both the barber pole worm and brown stomach worm can cause substantial death losses in goat herds, if left unchecked. Worm larvae (eggs) love warm, moist conditions, but can survive winter by going into a dormant or arrested state and not resuming their life cycle until the spring when environmental conditions have improved. When environmental conditions are ideal, the life cycle of the barber pole worm can be as short as 7 days. In normal climatic years, the number of worm larvae on pasture peaks in mid-summer (July-August). The peak may occur in the fall, if a dry summer is followed by a wet fall. In drought years and in dry climates, parasites tend to be less of a problem. Other parasites of concern Other parasites of concern are tapeworms, lungworms, liver flukes, and coccidia. Tapeworms have an indirect life cycle, requiring pasture mites to complete their life cycle, and are generally considered to be non-pathogenic. In extreme cases, tapeworm infestations can cause diarrhea, weight loss, and even death in goats. Not all anthelmintics (only the benzimidazoles) kill tapeworms. Goats become infected with lungworms when they consume the larvae in feces. The larvae then travel to the lungs where they can cause respiratory problems in severe cases. Normally, there aren't any obvious clinical signs associated with lungworms. In addition, parasite control programs for stomach worms usually control lung worms. Liver flukes are generally not considered to be a problem in the Mid-Atlantic states. They have an indirect life cycle and require open water and snails to complete their life cycle. The only anthelmintic that is effective against adult liver flukes is Albendazole (Valbazen®). Coccidia are single-cell protozoa that can wreak havoc in a sheep and goat herd. Young lambs and goats are especially susceptible to coccidia. What's important to note is that each species of livestock is affected by different species of coccidia. In addition, the drugs that are effective against stomach, tape, and lungworms are not effective against coccidia. Coccidiosis is treated with sulfa drugs and Amprolium (Corid®) and prevented with Monensin (Rumensin®), Lasalocid (Bovatec®), and Decoquinate (Deccox®) Another parasite that can be of concern in some areas is the meningeal worm or deer or brain worm. It is a parasite of the White Tail Deer, and small ruminants are an abnormal host. The deer worm has an indirect life cycle and requires snails and slugs to complete its life cycle. Once ingested, the larvae travels from the goat's intestinal tract to its spinal cord, eventually reaching its brain, resulting in paralysis and death. Early indications of a meningeal worm infection are gait abnormalities and lameness. There is no way to diagnose the condition in a live animal. Successful treatment involves heavy doses of anthelmintic drugs and use of anti-inflammatory drugs. Integrated Parasite Management (IPM) Parasite control starts with good management, with a healthy dose of common sense. Good sanitation will go a long way in controlling parasites, especially coccidia. Feed should not be fed on the ground. Feeders that minimize waste and contamination should be used. Water should always be clean and free from fecal matter. Pens and pastures should not be overstocked. All new arrivals to the farm should be isolated for at least 30 days and dewormed. Lamb with "Bottle Jaw." The use of clean or safe pastures will help to control parasite problems. A clean or safe pasture is one in which sheep or goats have not grazed for 6 to 12 months. A pasture grazed by cattle and/or horses is also considered safe, since sheep/goats and cattle/horses do not share the same parasites. Pastures that have been renovated or rotated with row crops are clean, as are pastures in which a hay or silage crop has been removed. Rotational grazing generally does not help to control internal parasites unless pasture rest periods are long enough (> 70 days). In fact, management intensive grazing (short duration, high intensity grazing) may exacerbate parasite problems in goats. Goats that browse have fewer parasite problems, though woodland grazing may increase the risk of meningeal worm infection. There are some forages that may have anti-parasitic effects. These include Birdsfoot Trefoil, Chicory, Sericea Lezpedeza, and other forages containing condensed tannins. Sheep and goats on a higher plane of nutrition and/or with a higher body condition score are better able to withstand parasite challenges. Nutrition in early pregnancy increase fat stores and has been shown to increase the immune response to parasites. Ewes receiving increased protein levels during late gestation are better able to mount an immune response to parasites. Since worms need grass to develop, sheep and goats raised in confinement have fewer parasite (stomach worm) problems and those put in confinement are less likely to get re-infected. Genetics affect an animal's ability to resist infection, as well as withstand infection. Resistance is defined as the animal's ability to resist infection. It is measured by fecal egg counts (FEC) and is 20 to 30 percent heritable. Resilience is defined as the animal's ability to withstand infection. It is measured by blood hematocrit or packed cell volume (PCV). It is less heritable than resistance. It is important to manage both resistance and resilience in a herd. In a herd, since only a small number of animals shed the majority of worm eggs, ideally, these animals should be identified and removed from the herd. Animals which require frequent treatment should also be removed from the herd. Some sheep and goat breeds are more resistant (and resilient) to parasites. These include hair sheep, the common brush goat, Spanish goat, and Myotonic. The Kiko may also be resistant to parasites due to its New Zealand background (wet climate). Dairy goats are more susceptible to parasites as are Boer goats, due to their South African ancestry (hot, dry climate). Anthelmintics There are three families of drugs which are used to treat internal parasites in livestock: 1. Benzimidazoles - Fenbendazole, Albendazole, Oxybendazole, Thiabendazole 2. Nicotinics - Levamisole, Pyrantel, Moratel 3. Macrolytic Lactones - Ivermectin, Doramectin, Moxidectin The Benzimidazoles (Safeguard®, Panacur®, Valbazen®, Synanthic®), also called "white dewormers" are broad spectrum and safe to use. They are effective against tapeworms. Albendazole is effective against adult liver flukes, but should not be used in pregnant or lactating females. Levamisole (Tramisol®), also called a "clear dewormer" is broad spectrum and effective against arrested larvae. However, it has a narrower margin of safety, especially in the injectable form. Pyrantel (Strongid®) is only effective against adult worms. Moratel (Rumatel®) is an oral feed additive and is only effective against adult worms. The Macrolytic lactones or "avermectins" (Ivomec®, Dectomax®, Quest®, Cydectin®) are the newest family of drugs. They are broad spectrum and have a wide margin of safety. They are also effective against external (biting) parasites, including nose bots. Moxidectin is a persistent-activity dewormer that continues to kill worms after it is administered. In a sheep trial in Virginia, treatment with Moxidectin (Cydectin) at 8 week intervals was more effective than treatment with Ivermectin at 4 week intervals. Ivomec, Valbazen, and Tramisol drench are approved for use in sheep. Only Fenbendazole and Rumatel are FDA-approved for use in goats. Use of any product which is inconsistent with its label constitutes "extra-label" drug use and requires a veterinary prescription and valid veterinarian-patient-client relationship. Exaggerated withdrawals should be used when administering drugs extra-label. Currently, there are no non-chemical dewormers (including herbs and diatomaceous earth) which have been shown to be effective at controlling worms in livestock. Hopefully, research will soon be able to identify effective, natural methods of parasite control. Anthelmintic use Anthelmintics should not be used indiscriminately. Frequent deworming is costly. It accelerates the development of anthelmintic-resistant worms and leads to a false sense of security, which may result in unnecessary production losses and animal deaths. The routine use of anthelmintics is prohibited under the new National Organic Standards. Strategic deworming will help to control parasite burdens in the animals and on pastures. The most important time to deworm a sheep or goat is prior to lambing/kidding (2-4 weeks prior). This will help to prevent the "periparturient rise" in worm eggs that generally occurs around lambing/kidding time. It will also reduce the number of eggs that the ewe/doe sheds into her environment that could potentially infect her newborn lambs/kids. Other strategic times to treat with anthelmintics is prior to moving animals to a safe or "cleaner" pasture, at the start of the grazing season when the grass first starts to green up, in the mid-summer when worm larvae numbers are typically the highest, and in the fall after the first frost. Anthelmintic treatments should be targeted to the most susceptible animals in the herd. This would include lambs/kids, lactating ewes/does, and high producers. Leaving some animals untreated will help to slow anthelmintics resistance. It is important to maximize the effect of a single treatment. Underdosing is a leading cause of anthelmintic resistance. Animals should not be underdosed. Ideally, animals should be weighed or measured with a tape to determine the proper dosage. When deworming a group of animals, the dose should be set for the heaviest animals in the group, not the average. Anthelmintics should be administered orally, over the tongue of the animal. Research has shown that benzimidazoles are more effective when the animals are fasted 12 to 24 hours before treatment or when two treatments are given 12 hours apart. Goats metabolize anthelmintics differently (it clears their system faster) than sheep and cattle and require higher doses. Producers should consult with their veterinarian to determine the proper dosage for goats. Anthelmintic resistance Anthelmintic resistance is when the drug no longer works because the worms have developed a tolerance or resistance to it. Anthelmintic resistance is determined by a fecal egg count reduction test (FECRT). Animals are weighed and treated with the anthelmintics and fecal egg counts are conducted at the time of treatment and 7 to 14 days after treatment. If the anthelmintic kills 90 percent or more of the worm eggs, it is considered to be effective. If it kills 60 to 90 percent of worm eggs, it is considered to have a moderate level of resistance. Anthelmintics killing less than 60 percent of worm eggs are considered to have severe resistance. Resistance to anthelmintics in the benzimidazoles is considered to be widespread and a world wide problem. Resistance to Ivermectin is widespread. Resistance to Levamisole is reported worldwide, but preliminary studies in Virginia, showed Levamisole to still be reasonably effective. Moxidectin is still considered to be an effective dewormer. In addition, anthelmintics in which widespread resistance has been reported may still be effective your farm. This lamb has a very pale eyelid due to anemia. FAMACHA© score of E (fatal) You can slow anthelmintics resistance on your farm by not introducing anthelmintics resistance to your farm. New arrivals should be isolated and dewormed with products from at least two families of drugs. Care should be taken not to underdose animals. Combinations of products may slow down resistance. Anthelmintics should be rotated annually or a product should be used until it is no longer working. Leaving some animals untreated and focusing treatments on susceptible animals will slow down resistance. Two tools for integrated parasite management There are two tools that producers can use to more effectively control internal parasites: fecal egg counting and FAMACHA©. Fecal egg counts can be used to determine the level of pasture contamination and the need for anthelmintic treatment. FAMACHA© is a system whereby you examine the lower eyelid of the sheep and administer treatment only if signs of anemia are present. In order to do fecal egg counts, you need a microscope, flotation solution, plastic or paper cuts, spoon or something to mix fecal slurry with, a straining device, slides, and cover slips. A microscope with 200x magnification is sufficient. Some producers use the Intel Play microscope, which connects to a computer, for doing fecal egg counts. Commercial flotation solutions are available or you can mix your own saturated salt or sugar solution. A McMaster slide has chambers that allow you to count the number of eggs in order to calculate eggs per gram whereas regular slides can be used to determine general worm loads - high, medium, or low. FAMACHA© is a technique developed in South Africa in which a color eye chart depicting varying degrees of anemia is used to determine the need for anthelmintic treatment. It was developed as a tool for anthelmintics resistance management and integrated parasite management. It only works for the barber pole worm. It was developed for sheep, but should work with goats with slight modifications. The FAMACHA© technique reduces the number of treatments because only animals showing physical signs of infection are dewormed. It identifies worm susceptible animals for culling and slows anthelmintics resistance, as worms have less exposure to the drugs. Famacha© Scores Score PCV Dose A Optimal > 30 No dose B Acceptable 25 No dose C Borderline 20 ? D Dangerous 15 Dose E Fatal 10 Dose © Copyright 2003.  Maryland Small Ruminant Page. Related Articles General Health Care of Sheep and Goats Meningeal Worm (Paralaphostrongylus tenius) Drugs (Anthelmintics) Used to Control Internal Parasites in Livestock (table) Products Used to Treat and/or Prevent Coccidiosis in Livestock (table) Disease Image Gallery Enterotoxemia in Lambs Web Resources Internal Parasites of Sheep - University of Sidney Southern Consortium for Small Ruminant Parasite Control Controlling Goat Parasites: Is It a Losing Battle? - Virginia Tech Integrated Parasite Management For Livestock - NCAT/ATTRA Parasite Control in Sheep: Biologic Approaches for the New Millennium - Ohio State University The need for alternative methods to control nematode parasites of ruminant livestock in South Africa
Monday, 06 July 2009 | 3608 hits | Print | PDF |  E-mail | Report
Articles/Diseases, Injuries, Parasites and More
Author:Administrator
  Integrated Parasite Management (IPM) in Small Ruminants by Susan Schoenian Area Agent, Sheep and Goats Western Maryland Research & Education Center Maryland Cooperative Extension Internal parasites are the #1 health problem affecting small ruminants. Sheep and goats are more susceptible to internal parasites than other livestock, due to their grazing behavior and poor immunity. In the past, producers relied heavily on anti-parasitic drugs, called "anthelmintics" to control internal parasites in their goat herds. Unfortunately, parasites have become increasingly resistant to many of the anthelmintics. In addition, few anthelmintics are FDA-approved for use in goats, and due to the costs involved in developing new drugs, it is not likely that any new products are going to come onto the market anytime soon. As a result, producers can no longer rely on anthelmintics alone to control parasites in their herds. A more integrated approach will be necessary. On the plus side, internal parasites are a major area of study among scientists in Australia, New Zealand, South Africa, and the United States and new discoveries will likely be made in years to come. Major parasites of concern - stomach worms (roundworms, nematodes) The parasite that causes the most problems to small ruminants is Haemonchus Contortis, better known as the "barber pole" worm. The barber pole worm is a blood-sucking parasite that pierces the lining of the abomassum, causing blood plasma and protein loss to the host. The symptom most commonly associated with barber pole infection is anemia, characterized by pale mucous membranes, especially in the lower eye lid; and "bottle jaw," an accumulation of fluid under the jaw. Diarrhea (scours) is not the usual symptom of barber pole infection. The barber pole worm is a prolific egg producer with a short, direct life cycle. Severly parasitized lamb The parasite of secondary concern is Ostertagia Circumcinta, better known as the small brown stomach worm. It also burrows itself into the lining of the abomassum. But instead of causing blood and protein loss, it causes digestive disturbances such as diarrhea and weight loss. Both the barber pole worm and brown stomach worm can cause substantial death losses in goat herds, if left unchecked. Worm larvae (eggs) love warm, moist conditions, but can survive winter by going into a dormant or arrested state and not resuming their life cycle until the spring when environmental conditions have improved. When environmental conditions are ideal, the life cycle of the barber pole worm can be as short as 7 days. In normal climatic years, the number of worm larvae on pasture peaks in mid-summer (July-August). The peak may occur in the fall, if a dry summer is followed by a wet fall. In drought years and in dry climates, parasites tend to be less of a problem. Other parasites of concern Other parasites of concern are tapeworms, lungworms, liver flukes, and coccidia. Tapeworms have an indirect life cycle, requiring pasture mites to complete their life cycle, and are generally considered to be non-pathogenic. In extreme cases, tapeworm infestations can cause diarrhea, weight loss, and even death in goats. Not all anthelmintics (only the benzimidazoles) kill tapeworms. Goats become infected with lungworms when they consume the larvae in feces. The larvae then travel to the lungs where they can cause respiratory problems in severe cases. Normally, there aren't any obvious clinical signs associated with lungworms. In addition, parasite control programs for stomach worms usually control lung worms. Liver flukes are generally not considered to be a problem in the Mid-Atlantic states. They have an indirect life cycle and require open water and snails to complete their life cycle. The only anthelmintic that is effective against adult liver flukes is Albendazole (Valbazen®). Coccidia are single-cell protozoa that can wreak havoc in a sheep and goat herd. Young lambs and goats are especially susceptible to coccidia. What's important to note is that each species of livestock is affected by different species of coccidia. In addition, the drugs that are effective against stomach, tape, and lungworms are not effective against coccidia. Coccidiosis is treated with sulfa drugs and Amprolium (Corid®) and prevented with Monensin (Rumensin®), Lasalocid (Bovatec®), and Decoquinate (Deccox®) Another parasite that can be of concern in some areas is the meningeal worm or deer or brain worm. It is a parasite of the White Tail Deer, and small ruminants are an abnormal host. The deer worm has an indirect life cycle and requires snails and slugs to complete its life cycle. Once ingested, the larvae travels from the goat's intestinal tract to its spinal cord, eventually reaching its brain, resulting in paralysis and death. Early indications of a meningeal worm infection are gait abnormalities and lameness. There is no way to diagnose the condition in a live animal. Successful treatment involves heavy doses of anthelmintic drugs and use of anti-inflammatory drugs. Integrated Parasite Management (IPM) Parasite control starts with good management, with a healthy dose of common sense. Good sanitation will go a long way in controlling parasites, especially coccidia. Feed should not be fed on the ground. Feeders that minimize waste and contamination should be used. Water should always be clean and free from fecal matter. Pens and pastures should not be overstocked. All new arrivals to the farm should be isolated for at least 30 days and dewormed. Lamb with "Bottle Jaw." The use of clean or safe pastures will help to control parasite problems. A clean or safe pasture is one in which sheep or goats have not grazed for 6 to 12 months. A pasture grazed by cattle and/or horses is also considered safe, since sheep/goats and cattle/horses do not share the same parasites. Pastures that have been renovated or rotated with row crops are clean, as are pastures in which a hay or silage crop has been removed. Rotational grazing generally does not help to control internal parasites unless pasture rest periods are long enough (> 70 days). In fact, management intensive grazing (short duration, high intensity grazing) may exacerbate parasite problems in goats. Goats that browse have fewer parasite problems, though woodland grazing may increase the risk of meningeal worm infection. There are some forages that may have anti-parasitic effects. These include Birdsfoot Trefoil, Chicory, Sericea Lezpedeza, and other forages containing condensed tannins. Sheep and goats on a higher plane of nutrition and/or with a higher body condition score are better able to withstand parasite challenges. Nutrition in early pregnancy increase fat stores and has been shown to increase the immune response to parasites. Ewes receiving increased protein levels during late gestation are better able to mount an immune response to parasites. Since worms need grass to develop, sheep and goats raised in confinement have fewer parasite (stomach worm) problems and those put in confinement are less likely to get re-infected. Genetics affect an animal's ability to resist infection, as well as withstand infection. Resistance is defined as the animal's ability to resist infection. It is measured by fecal egg counts (FEC) and is 20 to 30 percent heritable. Resilience is defined as the animal's ability to withstand infection. It is measured by blood hematocrit or packed cell volume (PCV). It is less heritable than resistance. It is important to manage both resistance and resilience in a herd. In a herd, since only a small number of animals shed the majority of worm eggs, ideally, these animals should be identified and removed from the herd. Animals which require frequent treatment should also be removed from the herd. Some sheep and goat breeds are more resistant (and resilient) to parasites. These include hair sheep, the common brush goat, Spanish goat, and Myotonic. The Kiko may also be resistant to parasites due to its New Zealand background (wet climate). Dairy goats are more susceptible to parasites as are Boer goats, due to their South African ancestry (hot, dry climate). Anthelmintics There are three families of drugs which are used to treat internal parasites in livestock: 1. Benzimidazoles - Fenbendazole, Albendazole, Oxybendazole, Thiabendazole 2. Nicotinics - Levamisole, Pyrantel, Moratel 3. Macrolytic Lactones - Ivermectin, Doramectin, Moxidectin The Benzimidazoles (Safeguard®, Panacur®, Valbazen®, Synanthic®), also called "white dewormers" are broad spectrum and safe to use. They are effective against tapeworms. Albendazole is effective against adult liver flukes, but should not be used in pregnant or lactating females. Levamisole (Tramisol®), also called a "clear dewormer" is broad spectrum and effective against arrested larvae. However, it has a narrower margin of safety, especially in the injectable form. Pyrantel (Strongid®) is only effective against adult worms. Moratel (Rumatel®) is an oral feed additive and is only effective against adult worms. The Macrolytic lactones or "avermectins" (Ivomec®, Dectomax®, Quest®, Cydectin®) are the newest family of drugs. They are broad spectrum and have a wide margin of safety. They are also effective against external (biting) parasites, including nose bots. Moxidectin is a persistent-activity dewormer that continues to kill worms after it is administered. In a sheep trial in Virginia, treatment with Moxidectin (Cydectin) at 8 week intervals was more effective than treatment with Ivermectin at 4 week intervals. Ivomec, Valbazen, and Tramisol drench are approved for use in sheep. Only Fenbendazole and Rumatel are FDA-approved for use in goats. Use of any product which is inconsistent with its label constitutes "extra-label" drug use and requires a veterinary prescription and valid veterinarian-patient-client relationship. Exaggerated withdrawals should be used when administering drugs extra-label. Currently, there are no non-chemical dewormers (including herbs and diatomaceous earth) which have been shown to be effective at controlling worms in livestock. Hopefully, research will soon be able to identify effective, natural methods of parasite control. Anthelmintic use Anthelmintics should not be used indiscriminately. Frequent deworming is costly. It accelerates the development of anthelmintic-resistant worms and leads to a false sense of security, which may result in unnecessary production losses and animal deaths. The routine use of anthelmintics is prohibited under the new National Organic Standards. Strategic deworming will help to control parasite burdens in the animals and on pastures. The most important time to deworm a sheep or goat is prior to lambing/kidding (2-4 weeks prior). This will help to prevent the "periparturient rise" in worm eggs that generally occurs around lambing/kidding time. It will also reduce the number of eggs that the ewe/doe sheds into her environment that could potentially infect her newborn lambs/kids. Other strategic times to treat with anthelmintics is prior to moving animals to a safe or "cleaner" pasture, at the start of the grazing season when the grass first starts to green up, in the mid-summer when worm larvae numbers are typically the highest, and in the fall after the first frost. Anthelmintic treatments should be targeted to the most susceptible animals in the herd. This would include lambs/kids, lactating ewes/does, and high producers. Leaving some animals untreated will help to slow anthelmintics resistance. It is important to maximize the effect of a single treatment. Underdosing is a leading cause of anthelmintic resistance. Animals should not be underdosed. Ideally, animals should be weighed or measured with a tape to determine the proper dosage. When deworming a group of animals, the dose should be set for the heaviest animals in the group, not the average. Anthelmintics should be administered orally, over the tongue of the animal. Research has shown that benzimidazoles are more effective when the animals are fasted 12 to 24 hours before treatment or when two treatments are given 12 hours apart. Goats metabolize anthelmintics differently (it clears their system faster) than sheep and cattle and require higher doses. Producers should consult with their veterinarian to determine the proper dosage for goats. Anthelmintic resistance Anthelmintic resistance is when the drug no longer works because the worms have developed a tolerance or resistance to it. Anthelmintic resistance is determined by a fecal egg count reduction test (FECRT). Animals are weighed and treated with the anthelmintics and fecal egg counts are conducted at the time of treatment and 7 to 14 days after treatment. If the anthelmintic kills 90 percent or more of the worm eggs, it is considered to be effective. If it kills 60 to 90 percent of worm eggs, it is considered to have a moderate level of resistance. Anthelmintics killing less than 60 percent of worm eggs are considered to have severe resistance. Resistance to anthelmintics in the benzimidazoles is considered to be widespread and a world wide problem. Resistance to Ivermectin is widespread. Resistance to Levamisole is reported worldwide, but preliminary studies in Virginia, showed Levamisole to still be reasonably effective. Moxidectin is still considered to be an effective dewormer. In addition, anthelmintics in which widespread resistance has been reported may still be effective your farm. This lamb has a very pale eyelid due to anemia. FAMACHA© score of E (fatal) You can slow anthelmintics resistance on your farm by not introducing anthelmintics resistance to your farm. New arrivals should be isolated and dewormed with products from at least two families of drugs. Care should be taken not to underdose animals. Combinations of products may slow down resistance. Anthelmintics should be rotated annually or a product should be used until it is no longer working. Leaving some animals untreated and focusing treatments on susceptible animals will slow down resistance. Two tools for integrated parasite management There are two tools that producers can use to more effectively control internal parasites: fecal egg counting and FAMACHA©. Fecal egg counts can be used to determine the level of pasture contamination and the need for anthelmintic treatment. FAMACHA© is a system whereby you examine the lower eyelid of the sheep and administer treatment only if signs of anemia are present. In order to do fecal egg counts, you need a microscope, flotation solution, plastic or paper cuts, spoon or something to mix fecal slurry with, a straining device, slides, and cover slips. A microscope with 200x magnification is sufficient. Some producers use the Intel Play microscope, which connects to a computer, for doing fecal egg counts. Commercial flotation solutions are available or you can mix your own saturated salt or sugar solution. A McMaster slide has chambers that allow you to count the number of eggs in order to calculate eggs per gram whereas regular slides can be used to determine general worm loads - high, medium, or low. FAMACHA© is a technique developed in South Africa in which a color eye chart depicting varying degrees of anemia is used to determine the need for anthelmintic treatment. It was developed as a tool for anthelmintics resistance management and integrated parasite management. It only works for the barber pole worm. It was developed for sheep, but should work with goats with slight modifications. The FAMACHA© technique reduces the number of treatments because only animals showing physical signs of infection are dewormed. It identifies worm susceptible animals for culling and slows anthelmintics resistance, as worms have less exposure to the drugs. Famacha© Scores Score PCV Dose A Optimal > 30 No dose B Acceptable 25 No dose C Borderline 20 ? D Dangerous 15 Dose E Fatal 10 Dose © Copyright 2003.  Maryland Small Ruminant Page. Related Articles General Health Care of Sheep and Goats Meningeal Worm (Paralaphostrongylus tenius) Drugs (Anthelmintics) Used to Control Internal Parasites in Livestock (table) Products Used to Treat and/or Prevent Coccidiosis in Livestock (table) Disease Image Gallery Enterotoxemia in Lambs Web Resources Internal Parasites of Sheep - University of Sidney Southern Consortium for Small Ruminant Parasite Control Controlling Goat Parasites: Is It a Losing Battle? - Virginia Tech Integrated Parasite Management For Livestock - NCAT/ATTRA Parasite Control in Sheep: Biologic Approaches for the New Millennium - Ohio State University The need for alternative methods to control nematode parasites of ruminant livestock in South Africa
Friday, 02 October 2009 | 3616 hits | Print | PDF |  E-mail | Report
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  Hit BACK on your browser to return to Copper Deficiency What diseases are associated with Copper? A short course designed by Murdoch University and The University of Sydney. Sponsored by Grant 1034/25 from the Committee for the Advancement of University Teaching (CAUT)1995. WHAT DISEASE STATES OCCUR WITH DEFICIENCY? OF COPPER? In Australasia, copper deficiency could almost be regarded as producing the Ă’classicĂ“ trace-element deficiency diseases, involving a range of differing species, organs involved and ages of animals affected. The nutritional biochemstry is complex, and deficiency states may be primary and absolute or secondary and conditioned. Harmful effects may eventuate in the foetus/neonate , the young actively growing animal and in the adult . In Australasia the ruminant species are most at risk.  What happens in the foetus/neonate and young growing animal? Copper deficiency during pregnancy can result in the birth of offspring with congenital disease of the nervous system. This situation is most common in lambs. In addition neonatal lambs, apparently normal at birth, often express neurologic disease at any time between 1 week and several months of age. This delayed effect is still an expression of the copper-deficient state of the dam. In goat kids and piglets, such delayed disease is well documented, but congenital disease is rare. The terms swayback and enzootic ataxia are frequently used in reference to these diseases. Young animals may also suffer osteoporosis (bone fragility) and anaemia. Basic cellular disturbance         1) There are a number of severe effects on nerve cells and myelin, in which destructive changes range from degeneration of neurons and axons within intact supporting tissues, to wholesale loss of all nervous tissue components, with resulting cavitation (in lambs) of some areas of cerebral white matter. Neural degeneration may extend widely throughout the brain, spinal cord and peripheral nerves. The fundamental biochemical defects remain undefined, but it is suspected that the role of Cu2+ as a component of the enzymes superoxide dismutase and cytochrome oxidase may be significant.     2) Defective crosslinking of collagen and elastin is the result of the role of Cu2+ in the activity of the enzyme lysyl oxidase. This may be the basis of is reduced production of osteoid in growing bones.  3) Defective production of red blood cells by the bone marrow. The basic cause remains undefined. Pathologic consequences 1) In congenital disease, affected lambs often have gelatinous softening and/or cavitation in the white matter of the cerebral hemispheres (JKP Fig. 3.72). In addition they have the changes described below for the delayed disease  2) In the delayed disease there are no macroscopically visible changes, but the microscope reveals swollen and dying nerve cells in many parts of the brain and spinal cord (JKP Fig. 3.16), together with disintegrating myelinated axons in parts of the brain and cord (JKP Fig. 3.22A) and in spinal motor nerves (JKP Fig. 3.21). The changes in goat kids and piglets are essentially similar, but with some differences which need not concern us here.  In the bones, there is production of thin trabeculae, with abnormally fragile and thin metaphyseal and diaphyseal bone. This state is called osteoporosis and can result in bowing of long bones, metaphyseal enlargement, and spontaneous fractures  In the bone marrow there is ineffective production and output of red blood cells in spite of an increased number (hyperplasia) of precursor cells. Consequentially there will be reduced numbers of circulating erythrocytes, and a reduced concentration of haemoglobin in the blood, producing a state of anaemia. Functional/clinical effects 1) In regard to nervous disease, congenitally affected animals may be blind and unable to stand In general, affected animals are ataxic (unable to control balance), and have a staggering gait.     2) In regard to skeletal disease, there may be lameness and deformity.  3) In regard to bone marrow disease, there will be fatigue, listlessness and pale mucous membranes. What happens in older and mature animals ? The outcomes of copper deficiency in older and mature animals may reflect the effects on bone and bone marrow, as described above, and can also be manifested by changes in the hair coat. This last-mentioned effect is a consequence of Cu2+ being: 1) an essential component of the enzyme tyrosinase, which is active the the production of melanin and 2) of having a role in the process of keratinization during hair growth. There is hypopigmentation (deficient melanization) of hair or wool, and a change in the quality of the fiber.  Thus in affected cattle, normally dark-brown or black hair will become pale, especially around the eyes, producing a spectacled appearance. In black sheep, the wool is characteristially banded , reflecting periods of differing copper status during wool growth. (JKP Fig. 5.24). WHAT DISEASE STATES OCCUR WITH AN EXCESS OF COPPER? Although the oral intake of ionic copper may produce acute severe gastroenteritis, due to directly irritant effects on the mucosa of the alimentary tract, such events are rare, and usually the result of Ă’management accidentsĂ“. By far the commonest problem is the steady accumulation of copper stores in the liver, due either to high dietary levels, or to two associated factors which cause hepatic copper storage. These are, low levels of dietary molybdenum, which results in enhanced absorption of Cu2+ from the gut, and a genetically-based tendency to store copper in the lysosomes of liver cells. Key Point: Genetic factors are very important in relation to a tendency to store copper in the liver. Thus disease related to this phenomenon is seen mainly in sheep, in particular British breeds, which will store copper readily on normal levels of intake. Copper storage is also a problem in the Bedlington terrier and West Highland White dog.  Hepatic copper storage is a long-term chronic process ( taking months rather than days). As will be described below, it can eventually produce liver damage, but more dramatically, in sheep, it results in sudden release of copper from the liver into the plasma, with acute and disasterous consequences. Key Point:Although hepatic copper storage in sheep eventually explodes as an acute catastrophe for the red blood cells, the disease is conventionally referred to as chronic copper poisoning.  What happens when there is HEPATIC copper storage in sheep? Basic cellular disturbances A key factor is the ability of the liver to produce new cells by mitosis. Copper is stored, complexed to protein, within the lsyosomes of hepatocytes. When the concentration exceeds about 300 ppm, some damage is done to the storing hepatocytes, and many undergo apoptosis, and release their stored copper.     If the released copper can be taken up by new cells produced by increased mitosis, the situation can be kept in hand, even when the liver concentration exceeds 1000 ppm. If the mitotic activity cannot supply new cells at a sufficent rate, copper begins to leak into the plasma, and the stage is set for the real disease. Critical elevation of plasma copper places severe oxidative stress on red blood cells, exhausts their antioxidant systems and results in denaturation of globin. Key Point: If the sheep is concurrently affected by an agent which inhibits mitosis in the liver, the threshold for release of copper into the plasma is greatly reduced. Two common plant-derived toxins which have this effect are the pyrrolizidine alkaloids and the phomopsins.  Pathologic consequences Denaturation of globin in red blood cells causes massive intravascular haemolysis and acute anaemia. The anaemia causes further anoxic damage to the liver, and its capacity to take up, conjugate and excrete bilirubin is overwhelmed.. A massive load of free haemoglobin and red cell fragments is filtered through the kidneys, which suffer acute tubular injury. There is intense icterus, and dark brown-red discolouration of the kidneys and the urine. Functional/clinical consequences Severe anemia, hepatic necrosis and renal damage result in shock, prostration and frequently death, although animals may surive acute haemolytic crises. What happens when there is HEPATIC copper storage in cattle or pigs? Key Point: Key Point: In these species, genetic predisposition to store copper on normal intakes is not a problem, so disease is the result of high copper intake.  The hepatic and haematologic outcomes are similar to those in sheep, but there is far less tendency for massive acute haemolysis. Generally the major effect is chronic liver damage, with fibrosis in the portal tracts reflecting continual loss of hepatocytes. What happens in dogs genetically predisposed to storing copper? In the Bedlington and West Highland White terrier breeds, susceptibility to copper storage is inherited as an autosomal recessive trait in some breeding lines.     The disease differs from that in sheep,cattle and pigs, in that haemolysis is never a prominent clinical feature. The dominant change is chronic progressive hepatic atrophy and fibrosis, which at the end-stage results in a small, nodular and tough liver. The affected animals have a chronic wasting disease which reflects the progressive destruction of the liver.     Betty Walsh (e_walsh@cleo.murdoch.edu.au) 6 October 1995   Hit BACK on your browser to return to Copper Deficiency
Friday, 21 August 2009 | 3664 hits | Print | PDF |  E-mail | Report
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  Cryptosporidiosis and Kid Care Gary Fredricks Cooperative Extension Agent, Washington State University I became aware of Cryptosporidiosis when I worked with a dairy farmer who lost a large number of young calves with diarrhea (scours) that didn't respond to the usual treatments. Even though they ate, they lost weight and dehydrated as diarrhea continued. Nothing worked to keep them from dying in a few days. Later, the disease was diagnosed as Cryptosporidiosis. Veterinarians confirmed that herds in Washington and Oregon were having problems with Cryptosporidiosis. The Organism There are eleven species of Cryptosporidia, intestinal protozoan parasites similar to coccidia. None of the eleven are host-specific and can infect different species. Discovered in mice in 1907, it has since been detected in calves, lambs, pigs, goats, mice, rabbits, chickens, cats, dogs, geese, most undomesticated animals, and humans. There are still many unanswered questions about how Cyrptosporidium attacks the host animal, although its life cycle starts with the oocyst. The oocyst, kind of like an egg, is formed on the lining of the intestinal wall. Once oocysts are shed in the feces, the cells inside divide until eight small organisms, called sporozoites, are present. Outside the animal, the oocyst is dormant but becomes active when it is eaten. Oocysts are able to infect other animals within 48 hours after being shed from the host animal. After ingestion, they break open and release the sporozoites in the rumen or stomach. Sporozoites attach themselves between the cells lining the intestine where they continue to grow and multiply into merozites. Merozites form into either more oocysts or sporozoites. The formation of sporozoites from merozoites allows Cryptosporidium to continue its life cycle inside the animal. Thus, oocysts that die outside the host animal will not limit Cryptosporidium from multiplying inside infected animals. The exact mechanism of how Cryptosporidium affects the animal is still unknown. It is thought that the sporozoite interacts with and receives nutrients from the intestinal cell it lives next to. This disrupts and kills the cell. As the intestinal cells die, nutrients, such as water and minerals, are rapidly excreted into the intestinal cavity. The organism does not kill the host animal - death occurs due to the severe diarrhea that results. Secondary infections in animals weakened by cryptosporidiosis can also result in death. Symptoms and Diagnosis Symptoms of acute cryptosporidiosis include lack of appetite, weight loss, and diarrhea which is usually yellow to yellowish-brown in color and of a creamy texture. The rapid loss of nutrients and fluids during diarrhea results in severe dehydration. Since instestinal tract cells are disrupted, absorption of feed nutrients is restricted, and the animal loses more nutrients through the digestive tract than it takes in. This also disrupts the kid's immune system and makes it more susceptible to infection by other bacteria (secondary infection). When body stores of nutrients such as minerals and protein are used up, death quickly follows. Kids between five and twenty-one days old are the most susceptible. Once kids become infected, they pass oocysts in their feces in about five days. The primary mode of transmission is by fecal-oral spread. Animals eating fecal-contaminated material (food, water or bedding) can become infected. For example, an infected kid can contaminate the walls and floor with fecal matter. If the next kid coming into the same housing area licks on the contaminated walls, it can become infected. Oocysts are thought to survive for long periods of time outside the animal. Some animals do not develop into chronic cases and become carriers. After infection, animals either resist the organism, develop a mild infection that is self limiting, or soon sicken and die. Self-limiting infections run their course and clear up in a few days similar to the flu in humans. Some animals may exhibit fevers or signs of respiratory distress, but these may be secondary conditions from opportunistic microorganisms that have infected the animal in its weakened condition. The extent to which a kid is infected seems to be dependent on its age and immune status. Younger animals are much more susceptible to infection than adults. In studies done with lambs, five-day-old lambs had diarrhea for 9-10 days and suffered from a high rate of mortality. Sixty-day-old lambs showed no symptoms when they were infected, and adult sheep completely resisted infection. There is an indication that adults develop an immunity to Cryptosporidium, yet this immunity does not seem to be passed to their offspring. Immune-depressed animals are very susceptible to the disease. This refers to the total immune status, not just protection from cryptosporidiosis. Many situations can cause animals to lack immunity. Animals with severe infections are more susceptible to secondary infections. Feeding animals a balanced diet is essential in maintaining a proper immune response. Clean housing, clean bedding and proper ventilation all contribute to the ability to fight any infection more quickly. The most common problem with kids is receiving a deficient amount of colostral antibodies following birth. Whether caused by disease, an imbalanced ration or improper management, animals lacking adequate immunity are much more susceptible to cryptosporidiosis. Cryptosporidium can be detected in stool specimens during fecal flotation analysis. Failure to find it mayoccur because these oocyst are very small and difficult to identify. Lack of the investigator to look for Cryptosporidium can allow it to go undetected. Treatment A significant number of drugs have been tested and found ineffective for treating cryptosporidiosis, including most drugs normally used to treat coccidia. So far, no treatment has been found. Once an animal has been diagnosed, supportive treatment is the only alternative at this time. Solutions of electrolytes and other nutrients given IV compensate for dehydration. Using a medicine to slow the scouring, such as Pepto Bismol, has shown some success in helping kids survive until the disease is no longer life-threatening. Kids should be kept warm and separated from other kids to prevent transfer of infection. Animals will recover in about 10 days if they survive the diarrhea. Prevention The best control of cryptosporidiosis in goats comes from kids getting adequate immunity through colostrum soon after birth. Kids are born with no immunoglobulin (antibodies) in their blood. Colostral antibodies are absorbed and provide the necessary immune protection until the kid's own immune system begins to function. The kid's health is dependent on the amount of antibodies it receives through colostrum. Just because a kid receives inadequate colostral antibodies does not mean it will die. Proper management and sanitation on the farm also protect the kid. Yet, when a kid is exposed to disease, there is a greater chance of death if the kid does not have adequate immune protection. A research study showed that dairy calves receiving no immunity from colostrum are four times more likely to die and twice as likely to become sick as calves receiving adequate colostral antibodies. How soon after birth should a kid receive colostrum? As soon as possible! As everyone knows, kids lose the ability to absorb antibodies with time. The longer it waits to eat, the fewer antibodies are absorbed. A study with dairy calves showed that when they were fed colostrum at 6 hours after birth, they absorbed only 65% of available antibodies. Turning our attention to the doe, the concentration of antibodies in her colostrum also decreases with time. Studies show that the doe reabsorbs antibodies after kidding. The longer the colostrum stays in her udder, the smaller the concentration of colostral antibodies. After 16 hours, less than 10% of the original concentration of antibodies remains in the doe's colostrum. Facilities and Sanitation As previously mentioned, sanitation is very important to kid health. Kidding and housing areas must be clean and dry. These areas must be completely cleaned after a kid leaves - just letting things dry out won't get the job done. Kids need dry, draft-free shelter and adequate ventilation. High levels of ammonia can cause respiratory problems in kids. It is essential that buckets and bottles be cleaned between feedings. There is some evidence that Cryptosporidium can be found in saliva. During feeding, saliva from a contaminated kid can be left in a bottle or bucket. If kid feeding equipment is not cleaned between feedings, transfer of Cryptosporidium to other kids can occur. Summary Cryptosporidiosis kills kids. Once symptoms appear, there is a good chance they will end up dead. The best way to control the disease is to be sure all kids receive an adequate amount of immune protection through the colostrum. References Anderson, B.C., Cryptosporidiosis: A Review. Journal of American Vet Medicine Assn, Vol. 180:1455-1457, 1982. Gay, C. & Bessor, T., Discussion on Feeding Colostrum, WSU, 1990. Navin, T.R. & Juranek D.D., Cryptosporidiosis: Clinical,Epidemiologic, and Parasitologic Review, Reviews of Infectious Diseases Vol. 6:313-327, 1984. Svatos, G., Pro-Immune 99 Adds Predictability to E. Coli Scours Control Programs, Topics in Veterinary Medicine, Vol, 1:12-19, 1990.   Related Reading Cryptosporidiosis - Centers for Disease Control Cryptosporidium parvum FDA/DSFAN Bad Bug Book Home      Articles      Links   © Copyright 1994 Updated 2002 All rights reserved  
Saturday, 22 August 2009 | 3671 hits | Print | PDF |  E-mail | Report
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  Dealing with Urinary Calculi   Before you read on please understand that we are NOT Veterinarians. We are simply sharing with you what we have found in our journey along the road within "herd management of goats". The treatment shared below is not 100% successful. Some animals still die. We do know that some goats have lived when this treatment was used. Maybe they would have lived anyway, with no treatment or with another treatment. All we can share is what we have experienced using THIS meathod. Currently we do know that the balance of Calcium and Phosphorus is an important factor to the prevention of UC. The problem with this is that even though you may have a balanced feed and mineral supplement you can't always figure for your hay and pasture or the fact that certain minerals in the water that your stock is drinking can bind out various elements. That along with the fact that some animals are worse than others about picking out their favorite ingredients from their feed often make the prevention of UC a real challenge. We also know that UC can be brought on by stress, especially the stress of transportation. It is not uncommon for animals to have reduced fluid intake during times of travel which seem to increase the potential of UC. It seems we are hearing from more and more breeders that are experience UC problems and need to know what they can do to TREAT a buck or wether that has an active case of UC. During the past year we have had the opportunity to interact with several different breeders that have been experiencing UC within their herds and to follow the treatment of several individual animals. In the following text we will attempt to share with you the procedure used on the animals we were involved with in a hope that this information my prove helpful to you and your veterinarian. Please note- WE ARE NOT VETERINARIANS and urge you to consult YOUR OWN LOCAL vet for assistance in treating UC and any other illness you are experiencing in your herd. How to identify a buck with UC: The first signs of UC are normally noticed when the breeders sees the animal stretched out attempting to urinate, usually either dripping what appears to be urine from the end of the penis or forcefully straining with NO urine appearing at all. Sometimes the breeder's first thought is that the animal is constipated - but constipation is not very common in goats and UC should be your FIRST thought when you see a male goat of any age stretched out in the 'urinating position' and you do not see a stream of urine flowing. Sometimes you may even see the buck 'pulsing' a bit and curling his upper lip . On occasion you will find a buck (kid or adult) that seems to just lay down all the time and upon closer inspection you will find that the belly around the penis area is wet or damp. This is usually caused from urine leaking while the animal is laying down and should be considered a SERIOUS cause for concern.   The next question is WHAT TO DO??? The first thing is to take a closer look. Catch up the buck and LOOK at the penis. Easy to say - but not always so easy to do! Depending on the size of the animal (might be necessary to have some help on hand here) the best way we have found to expose the penis is as follows; Standing behind the buck , set him on his rump with his spine resting against your legs. Having him slightly 'slouched' over - bend over him and reach directly behind the scrotum (this is between the scrotum and the tail) at the base of the scrotum, there is a 'magic' spot that you can put pressure on and when doing can 'extend' the penis. At this point you should be able to see the HEAD of the penis. A healthy penis head will be smooth and a healthy pink color and you should see small blood vessels on it. If the head is purple, gnarled or angry looking you have trouble and we suggest at this point a trip to your veterinarian is advised. Removal of the urethra process has proven to be helpful in treating UC. Ideally letting your veterinarian do this and having his assistance and direction in treating the animal is our first choice. The urethra process is the string or worm like extension on the end of the penis that the buck uses to 'spray' urine with. The removal of the urethra process doe not normally effect the bucks fertility. It is helpful to have a damp washcloth (not 'wet' but just good and damp) to hold onto the penis with and a sharp pair of suture scissors (small manicure scissors work well and I was just told that a large pair of toenail / fingernail clippers will also work) cut off the urethra process as close to the head of the penis as you can. There is no advantage of leaving any of the urethra process in place. The urethra process is VERY narrow and one of the first places that stones and grit will accumulate and plug up the plumbing. AGAIN - having you veterinarian to do this is the recommend. Once the urethra process is removed sometimes you will get a good urine flow, sometimes just a dribble and sometimes no relief at all. Ideally your veterinarian will have a sonogram machine and can check the bucks bladder to see how full it is. Quite frequently by the time you have noticed there is a problem the bladder is full enough that is in danger of rupturing. Your VETERINARIAN can 'TAP' the bladder, using an 18-19 gauge spinal needle AFTER anesthetizing the animal. PLEASE -- DO NOT attempt to 'TAP' the bladder yourself . The animals needs to be immobilized COMPLETELY and an anesthetic is required to do this. Also, a comprehensive understanding of the anatomy and the procedure is needed and your veterinarian will also understand which anesthetics may exacerbate the problem. Understand that tapping the bladder is done to BUY TIME for further treatment to work. Tapping the bladder by itself will NOT cure the problem because the problem is BLOCKAGE. We have found that by drenching the animals with an effective ACIDIFIER, along with the proper antibiotics to address possible infection and possibly special drugs to help relax the urethra many animals have been saved . You need to monitor the fluid intake and OUT FLOW of the buck while you are IN TREATMENT with your veterinarian so that you can keep a close eye on the bladder. We find that having the veterinarian check the bladder every 36 hours by sonogram is advised, this lessen the chance of rupture. The ACIDIFIER we have used is mixed in a heavy concentration at first and the animal is drenched with with an appropriate amount depending on the age and weight of the animal. Then the acidifier is added to the goats daily water rations for several months at the least and better yet as an on going attempt at prevention. *PLEASE NOTE: Vinegar will NOT work as an acidifier! Acid Pack 4-Way 2x is available through Tri-Quest and is listed in our NUTRITION section under Product Listing. If your Veterinarian would like to know more about this procedure please have him/her contact us at 417 754-8135 and we will put them in touch with our veterinarian. *** Please note that the company that makes the Acid Pack 4-Way 2x does not manufacture this product nor endorse it as a treatment or prevention of UC. The suggestion to use this product to treat UC was made to us by our nutritionist and treatment was deemed successful. We are simply sharing with you what has worked in the field. ***   The following was shared by Donna of Safehaven Nubians *Subject: anionic salts used to prevent stones Apple cider vinegar does not work to prevent urinary stones. No way, no how. The "acidifying agent" of vinegar is acetic acid. The bacteria in a goat's rumen make tons of acetic acid as a part of digestive process. What you are feeding them is literally a drop in the bucket compared to what they naturally make themselves. Here are a couple of the many testimonials we have had from folks that have used the Acid Pack: - Please send me three more packets of the Acid Pack 4-Way 2x. I really appreciate this medication. It has literally saved his life.I HIGHLY recommend it over the ammonium Chloride. The improvement time was So much faster. ThanK you so much, again. L.K. from PA   - Please send me three packets of the acidifier Acid Pack 4-Way 2x My buck continues to do well. Check enclosed.. D.C. from OK   If you arrived at this page from a DIRECT link click here to access our entire website. If you click here and get a double frame use the back button on your browser   EMAIL US          
Monday, 12 October 2009 | 3718 hits | Print | PDF |  E-mail | Report
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A Quick Guide to Goat Health A Quick Guide to Goat Health By Peter J Lee Goats acquire many of the same diseases that occur in any dairy animal so great attention must be paid to goat health. The best way to keep your goats disease free is to keep everything clean and sanitary. Make sure that you have a veterinarian check the health of your herd frequently and keep any necessary vaccinations up to date. One of the things you must do that is critical to goat health is to establish a plan to control parasites. Have your goats wormed frequently and protect them from external parasites, such as ticks, lice, mosquitoes, and all kinds of flies--house, horn, stable, horse and deer. Any of these insects which bite and suck can affect the condition of your goats, sometimes causing diarrhea and affecting milk production. You should talk to your local county agricultural agent to see what are the best ways to eliminate these parasites. Mastitis is a disease which affects dairy goats as well as dairy cows. All it really means is that there is inflammation of the udder. When you examine the udder it can look to be tense, hard, hot and cause tremendous discomfort to the goat. Whether acute or chronic, mastitis is treated with antibiotics. The first line of defense against mastitis is cleanliness during milking. The organisms which cause mastitis can be present in the environment. Manure most be removed frequently. All of the milking equipment, whether you use your hands or machines, must be sanitary at all times. A solution made with Clorox™ bleach should be used to clean teats. Udder edema is another goat health problem. This usually occurs in dairy goats near the end of their dry period. It is treated by controlling the amount of sodium, potassium, and corn meal in the goat's food. Abscesses (caseous lymphadenitis) can be a problem in adult goats and can even lead to death should the abscesses surround an internal organ. They are most often on the neck, shoulders or head. The condition can be treated by draining the abscesses, cleaning the area and giving the goat penicillin. If this problem develops, the affected goat or goats have to be isolated to prevent it spreading to the rest of the herd. If your goats live in an area that is frequently very wet, foot rot is a possibility. There will be a gray, smelly discharge, and the goat will be lame and in pain. It's treated by trimming off the rot and applying a copper sulfate solution or ointment. Proper trimming of hooves can help avert this problem. The best plan for goat health is to observe your goats daily so that you can quickly notice any changes in posture or behavior that might be an indication that something is wrong and a vet needs to be called. The better you know your animals, the easier it is to immediately see that something is off or just not right. Learn about alpaca shearing, angelfish care and other information at the Interesting Animals site. Article Source: http://EzineArticles.com/?expert=Peter_J_Lee http://EzineArticles.com/?A-Quick-Guide-to-Goat-Health&id=3125629
Sunday, 25 October 2009 | 3799 hits | Print | PDF |  E-mail | Report
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Lyme Disease - General Information and FAQ Lyme disease is an illness caused by a spirochete bacteria, Borrelia burgdorferi, which is transmitted to animals and man through the bite of infected ticks. The disease is reported worldwide and throughout the United States. The states of New York, Massachusetts, Connecticut, Rhode Island and New Jersey account for the majority of cases in the United States. However, cases are reported from all geographic regions of the country. Different ticks are carriers in the different regions. Ixodes dammini (the deer tick) in the Northeast and midwest, Ixodes scapularis (the black-legged tick) in the South, Ixodes pacificus (the western black-legged tick) in the West and Amblyomma americanum (the lone star tick) found in several regions are all considered vectors. The is growing concern that Dermacentor variabilis (the American dog tick) may also be capable of transmitting the disease. Transmission by biting insects (flies, fleas, mosquitos) is speculated but appears to be quite rare. Not all ticks are infected. Infection rates in tick populations vary by tick species and geographic region from as few as two percent to 90 percent or more. THE DEER TICK Ixodes dammini is responsible for most of the cases of Lyme disease in the northeastern United States. These ticks are found in grassy areas (including lawns), and in brushy, shrubby and woodland sites, even on warm winter days. They prefer areas where some moisture is present. The tick has three life stages: larva, nymph and adult. Each stage takes a single blood meal. They feed on a variety of warm blooded animals including man, dogs, cats, horses and cows. The bite is painless so most victims do not know they have been bitten. The nymphal stage appears to be responsible for most Lyme disease cases. Both the larval stage (about the size of a grain of sand) and nymphal stage (about the size of a poppy seed) attach to a variety of small mammals, but prefer the white-footed mouse, the main reservoir of the Lyme disease bacteria. The adult ticks (about the size of a sesame seed) prefer to feed on white-tailed deer. The entire life cycle requires three separate hosts and takes about two years to complete. Larval and nymphal deer ticks also attach to birds. Indeed, birds may be a primary means by which the ticks (some infected) are spread from one area to another. Some species of birds also function as a reservoir of infection. LYME DISEASE SYMPTOMS IN MAN In about 50% of the cases a characteristic rash or lesion called erythema migrans is seen. It begins a few days to a few weeks after the bite of an infected tick. The rash generally looks like an expanding red ring. It is often described as looking like a bull's-eye with alternating light and dark rings. However, it can vary from a reddish blotchy appearance to red throughout. And can be confused with poison ivy, spider or insect bite, or ringworm. At about the same time that the rash develops, flu-like symptoms may appear with headache, sore throat, stiff neck, fever, muscle aches, fatigue and general malaise. Some people develop the flu-like illness without getting a rash. Seek prompt medical attention if any of these symptoms appear, especially after being bitten by a tick or visiting an area where Lyme disease is common. If possible document the presence of the rash by taking a picture because it may disappear before a physician can see it. A picture in this case is worth 10,000 words! If ignored, the early symptoms may disappear, but more serious problems can develop months to years later. The later symptoms of Lyme disease can be quite severe and chronic. Muscle pain and arthritis, usually of the large joints is common. Neurological symptoms include meningitis, numbness, tingling, and burning sensations in the extremities, Bell's palsy (loss of control of one or both sides of the face), severe pain and fatigue (often extreme and incapacitating) and depression. Heart, eye, respiratory and gastrointestinal problems can develop. Symptoms are often intermittent lasting from a few days to several months and sometimes years. Chronic Lyme disease, because of its diverse symptoms, mimics many other diseases and can be difficult to diagnose. TREATMENT Lyme disease is treated with antibiotics. Timely treatment increases chances of recovery and may lessen the severity of any later symptoms in both animals and man. The most effective treatment will be recommended by your physician or in the case of your animals by your veterinarian and will depend on the stage of the disease. Treatment for later stages is more difficult often requiring extended and repeated courses of antibiotic therapy. In animals and man treatment failures and relapses are reported. HOW TO AVOID TICK BITES When out of doors several precautions can minimize your chances of being bitten. Tuck your pant legs into your socks and your shirt into your pants. Wear light colored clothing. Dark ticks are more easily spotted against a light background. Inspect clothes often for ticks. Have a companion inspect your back. Apply repellents according to label instructions. Applying directly to clothing appears to be most effective. Upon returning to the home remove clothing and wash or put it in the dryer for 30 minutes to kill any ticks. When you get in from the field shower and inspect your body thoroughly. Especially check groin, navel, armpits, head and behind knees and ears. Have a companion check your back, or use a mirror. Inspect children at least once daily for ticks. When in heavily infested areas inspect children every three to four hours. When hiking stay in the middle of trails. Do not bushwhack. Clear brush from around your premises and keep grassy areas mown. Avoid plantings that especially attract deer and other animals. Limit watering of lawns. Judicious use of environmental insecticides to kill ticks may be necessary in some areas. LYME DISEASE IN DOMESTIC ANIMALS Lyme disease has been described in dogs, cats, horses cows and goats. Symptoms can include fever, lameness and soreness, listlessness, loss of appetite, swollen glands and joints. Heart, kidney, liver, eye and nervous system problems are also described in animals. Laminitis is reported in horses and cows, as are poor fertility, abortions and chronic weight loss. Temperament changes have been reported in dogs and horses. Untreated animals can develop chronic progressive arthritis. Symptoms can be intermittent and vary in intensity from mild to quite severe and can mimic many other conditions. If you suspect Lyme disease in your animals consult your veterinarian as soon as possible. WHERE TO FIND TICKS ON ANIMALS Ticks are most commonly found around the head and neck. They can also be found between the toes, on or in the ears, and in the armpit and groin areas. Because the ticks are so small, you must look very carefully. In animals the symptoms of illness may not develop for several weeks or months following tick bite. If you travel into tick infested areas with your animals, it is possible to bring home on the animals ticks that can infest your premises. If animals in your area develop Lyme disease it should alert you that you are also at risk. TICK CONTROL ON ANIMALS As much as possible keep animals out of tick habitat. Check animals daily for ticks and remove any found promptly. Dogs and cats can be brushed as soon as they come in. Brush over a light colored surface so any ticks removed can be seen and discarded. The most effective method to protect animals from infection and to keep those that travel from bringing ticks home is the regular use of tick repellent and control products. Permethrin, sold under many brand names, is very effective for tick control. Veterinary assistance is important in selecting safe and effective tick control products and designing a control program. HOW TO REMOVE ATTACHED TICKS Prompt removal of ticks decreases the chances of getting Lyme disease. The proper and easiest method is to grasp the tick with fine tweezers, as near the skin as you can, and gently pull it straight out. Be careful not to squeeze the tick when removing it which could result in more bacteria being injected. Do not try to remove the tick with your fingers or attempt to remove with lighted cigarettes, matches, nail polish, or vaseline. Once removed save the tick for identification. Accurate identification becomes very important if you or your animals develop disease symptoms. Proof of tick bite and the kind of tick doing the biting is especially important to document in areas where Lyme disease is not considered prevalent and doctor suspicion is low. In most areas, ticks can be submitted for identification through local or state health department offices. Many physicians and veterinarians will also submit ticks. Put the tick in a tightly closed container with a small amount of alcohol (rubbing alcohol will do). Mark it with your name, address and phone number, date collected, host collected from (animal or man) and recent travel history. NOTES The diagnosis of Lyme disease must generally be made on the basis of clinical signs and by ruling out other possible diseases. Animal ownership does not directly increase a person's risk of Lyme disease. However, allowing your animals to roam in tick habitat or venturing into tick habitat with your animals does increase your risk of exposure to ticks. Lyme disease is not considered to be contagious between people or directly from animals to man. Although some deaths have been attributed to Lyme disease, it is not generally considered to be fatal. Once an animal or person has apparently recovered from the disease it appears to be possible to be reinfected. Blood testing is available for animals and man. A positive test can be diagnostic when appropriate symptoms are present. However, it is possible to have a negative test during the course of the disease or following antibiotic therapy and still have Lyme disease. A negative test following treatment does not indicate cure. Miscarriage, premature births, still births, birth defects and transplacental infection of the fetus have been reported in animals and man. Vaccination for dogs is now available. Consult your veterinarian for advice about your dog's need for vaccination. A vaccine for people appears to be several years away. FOR ADDITIONAL INFORMATION State and local health departments Your veterinarian or family physician Local Lyme Disease support and informational groups can be found in many areas Contact: Lyme Disease Foundation, Inc. 1 Financial Plaza, 18th Floor, Hartford, CT 06103. (800) 525-2000 The Lyme Disease Electronic Mail Network publishes the "LymeNet Newsletter" once every 10-15 days. The Newsletter contains timely news about the Lyme disease epidemic. Medical abstracts, treatment protocols, prevention information, and political happenings are all included. In addition, subscribers may ask questions to the patients, doctors and researchers on the net. To subscribe, send a memo to Internet address: listserv@Lehigh.EDU In the first line of the message, write: subscribe LymeNet-L To retrieve the archives, write: get LymeNet-L/Newsletters 1-N Where N is between 01 and 12 Brochure by: Lloyd E. Miller, DVM, Troy, New York   jake@cs.cmu.edu
Friday, 21 August 2009 | 3804 hits | Print | PDF |  E-mail | Report
Articles/Diseases, Injuries, Parasites and More
Author:Administrator
The Internal Parasites That Affect Sheep and Goats Download printer-friendly versions of table: PDF or MS Word. Genus and species Common name Site Life cycle Ideal Conditions for Development Clinical signs Haemonchus contortis Barberpole worm Wire worm Abomasum Direct 18 to 21 days warm, moist summer rainfall Blood loss (Anemia) Edema ("Bottle Jaw") Weakness Wool breaks Sudden death Ostertagia circumcincta Medium or brown stomach worm Abomasum Direct 20 days cool, moist Production loss Lack of appetite Diarrhea Weight loss Decreased wool production Trichostrongylus   Bankrupt worm Hair worm Abomasum Small intestine Direct < 21 days warm, moist Black scours Reduced appetite Production loss Ocassional death Strongyloides papillosus  Common threadworm Small intestine Direct 7-9 days   warm, moist Weight loss Diarrhea Inflamation between toes Coopera spp. small intestinal worm Small intestine Direct 20 days cool, wet winter rainfall Loss of appetite Diarrhea Weight loss Decreased wool growth Nematodirus spp. threadneck worm Small intestine Direct 20 days cool, wet Usually sub-clincial Diarrhea, loss of appetite, weight loss Dictyocaulus filaria Muellerius capillaris lungworm hair lungworm Trachea and bronchi Direct Indirect (snails, slugs) 5 weeks cool, wet Usually no signs of infection. Coughing, fluid in lungs if disease is severe. Pneumonia Moniezia spp. tapeworm Small intestine Indirect (pasture mites) 6 weeks  wet Heavy infestations may result in unthriftiness and GI disturbances Eimeria spp. coccidia Small intestine Direct < 21 days cool, wet Overcrowding Liquid diarrhea Off feed, depression Death Trichuris ovis whipworm Caecum Direct 6-12 weeks Dry  Diarrhea Bunostomum phlebotomum hookworm Small intestine Direct 1-2 months  warm, most Unthriftiness, Diarrhea Blood loss, Anemia Sore feet Oesophagostomum   nodule worm Large intestine Direct 5 weeks   cool, wet winter rainfall Damage lining of small intestines Paralaphostrongylus tenius meningeal worm deer worm brain worm central nervous system Indirect (snails, slugs) 82-91 days cool, wet Hindquarter weakness Ataxia, Paralysis Blindness Fasciola hepatica liver fluke Liver Indirect (snails, slugs)  8-12 weeks wet production losses Death Organ condemnation   Created 03-May-2005 by Susan Schoenian. ©Copyright 2005. Maryland Small Ruminant Page
Thursday, 02 July 2009 | 3831 hits | Print | PDF |  E-mail | Report
Articles/Diseases, Injuries, Parasites and More
Author:Administrator
      JOHNE'S DISEASE: IT’S NOT JUST FOR CATTLE ANYMORE!*  Article by Deb Frost Meadow Lakes, Alaska     ALSO SEE THE SPRING PROMISE HERD & JOHNE'S DISEASE The goat industry has made good progress in recognizing and controlling a number of important infections.  We must apply the same approach to another infection that many do not consider a problem for goats: Johne’s disease. Johne’s disease is more prevalent in goats than many people realize and once it is established in a herd it can be difficult to eradicate. The organism can infect any ruminant species, so if you keep sheep or cattle too, they are all equally at risk.  Caused by a mycobacterium in the same family as those successful pathogens that cause tuberculosis and leprosy in humans, this fatal infection is not treatable and can be challenging to detect until late phases of the disease.  Goats get infected as kids but stay healthy for months to years which is why it is easy to sell a goat and have no idea it was infected until the new owner calls you a few years later.  Goats eventually starve to death when the organism and the immune cells fighting the organism pack the gastrointestinal tract and prevent the goat from getting any nutrition from its feed.  Goats in the clinical phases of Johne’s disease look thin, scruffy, might (or might not) have diarrhea, are hungry, eat eagerly but waste away.  The infected goat is contagious throughout its life, even while free of clinical signs of the infection.  The infection is usually spread by fecal-oral contact, meaning that anything that has been contaminated by pellets from an infected goat (water, feed, teats, mineral blocks, etc.) that might be licked or mouthed by a kid may spread the infection.  A doe does not have to have Johne's disease for her kid(s) to get it – she just has to lie down in a barnyard or pasture housing infected animals, thus getting the Johne's bacteria on her udder for the kids to suck off. Other methods include kids nibbling grain, hay, berries (you know how goat kids are!) or other interesting "goodies" off contaminated ground.  BABIES are the most susceptible age group for this disease – and you won’t know if they’ve been infected until months or years later.  The infection can spread silently in your herd as goats without symptoms contaminate your premises.  The organism is very hardy and can remain for months, although it does die off eventually and adult goats can be exposed to a low dose of the organism and not become infected.  Using disinfectants labeled as “tuberculocidal” as directed (meaning wash the mangers and non-porous surfaces such as metal feeders and fencing etc. first) helps get rid of the organism faster. These products are not of any use for your pastures or dirt barn floors, however.  There are as many methods to managing this infection as there are goat owners.  The approach will be very different for owners that have had multiple cases of the disease vs. those that have had just one case or who want to establish that their herd is free of the infection.  Some people “take no prisoners” and aggressively test, cull, and sanitize.  Some owners move test-positive goats to a separate paddock, stop breeding them, ensure that there is no contact with other animals and let them live out their lives. The best approach for you is the one that balances the resources (time, land, and money) you have, the reasons you own goats, the amount of animal exchange you do, other herd health issues and the level of M. paratuberculosis infection in the herd.  That being said, how do you determine if your herd is infected?  Not everyone needs to test but you might consider it if you have ever introduced a goat into your herd without knowing the Johne’s disease status of the source herd and have had a goat die with the vague signs of weight loss and perhaps diarrhea.  The first case of Johne’s disease usually comes as a surprise.  Think back ? have any of your goats just wasted away?  These cases are not all due to parasites, although that’s what we usually think it is.  It is always a good idea to determine the cause of any death, especially when the cause might be a slowly developing herd problem like Johne’s disease.    There are a number of diagnostic tests that are helpful in establishing the presence of the infection in adult goats (don’t bother testing until kids reach 18 months or so).  They include blood tests (AGID, ELISA) and a culture test that can be used to isolate the organism from fecal pellets or tissue samples.  Each test has its strong points and its deficits because of the biology of the infection, and be aware that there may be times that a truly infected goat may be test-negative.  Your veterinarian can help you pick the best testing protocol for your herd, and can then help you use the results to set up a management program focusing on sanitation and biosecurity that can improve herd health from the standpoint of other diseases as well, not just Johne’s disease.  Methods to keep the infection from spreading once introduced into a herd are all based on one concept: keep kids away from anything contaminated by the organism, realizing that you may not know which adult goats are doing the contaminating.  This may include using feeders that keep pellets out of food and water, pasteurization of milk (the organism can be shed into milk by infected does) for bottle-feeding, separating test-positives from test-negatives at kidding time, etc.  Testing without intending to make management changes to limit the spread of the infection will just be a waste of time for you.  Of course, the best approach of all is to keep the infection out of your herd.  If Johne's disease gets a strong grip on your herd, controlling it can be a major task. This is where we as an industry can help each other out by encouraging folks to establish their freedom from infection so we can trade animals with confidence instead of trepidation.  We can limit the spread of the infection by encouraging open discussions, just as we do with CL and CAE and by encouraging testing.  If you are lucky enough to live in Wisconsin, Alaska or one of a very few other states, you can get the costs of diagnostic tests reimbursed to you by the state’s Johne’s control program! In some states, the testing is entirely free to the breeder.  Encourage your state to include goats in its Johne’s disease control program instead of just cattle.  You are better off buying a goat from a herd that knows its Johne’s disease status even if they have had a case or two than from one that has never tested.  Ignoring the subject will not make it all go away – in fact the opposite will happen just as has occurred for the Holstein industry where the prevalence of Johne’s disease is now estimated at 80% of herds. This infection is not going to go away by our ignoring it. HEADS UP, PEOPLE!  It is time to “come up for air” and talk about it since it's safe to say no one wants Johne's disease in his or her herd.  And I believe as well that no one wants to inadvertently pass Johne's along to other herds. The only way to prevent this is to know the status of your own herd and the status of those from whom you buy.  Have necropsies done when a goat dies of an unexplained cause.  Watch the clinical status of your animals, keep Johne’s disease “on your radar screen” and test if you have any suspicions.  If you know your herd has had cases in the past and kids were in contact with those infected animals, test your herd annually.  Do your part to keep this disease from becoming as prevalent in goats as it already is in cattle.  As goat breeders we can limit the spread of this infection and the heartache it can cause if we open our eyes to the problem now.  Deb Frost Spring Promise Pygmies Test Negative for Johne's annually sinec 2002! Meadow Lakes, AK Dfrost@customcpu.com ALSO SEE THE SPRING PROMISE HERD & JOHNE'S DISEASE     *This article was checked for veterinary accuracy and approved by:  Becky Manning, MPH, MBA, DVM   Senior Scientist   Johne's Testing Center, School of Veterinary Medicine   University of Wisconsin   2015 Linden Drive   Madison, WI  53706   608-265-4958; 608-263-9754 fax   http://johnes.org     Return to Serious Goat Stuff  Joyce Lazzaro/Saanendoah DairyGoats presented for information purposes only.
Tuesday, 18 August 2009 | 3843 hits | Print | PDF |  E-mail | Report

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