Dewormers – Are They An Extremely Valuable Non-Renewable Resources?                 April 25 2018

– Michelle Arnold, DVM (Ruminant Extension Veterinarian, UKVDL), University of Kentucky

A “non-renewable” resource is a resource with economic value that cannot be readily replaced on a level equal to its consumption. Petroleum and coal are two familiar examples of valuable non-renewable products used daily but known to exist in limited supply, and formation of new product takes billions of years. Dewormers, on the other hand, are products that can be purchased from almost any farm or veterinary supply store and online. There are many different kinds, fairly inexpensive, and seemingly effective at killing parasites in the digestive tract of cattle and certain types also control flies, ticks and lice. They come in many forms and can be delivered to cattle by mouth as a liquid, paste or in block form, by injection, or simply by pouring it down the topline. Given this situation, how could dewormers ever be classified as “extremely valuable non-renewable resources”? In a recent veterinary continuing education meeting at the UKVDL, Dr. Ray Kaplan, an internationally-known veterinary parasitologist from the University of Georgia, used that very phrase to describe the dewormers used every day in cattle operations.

Dr. Kaplan is considered a leading expert on the rapidly developing problem of “anthelmintic resistance” which means the dewormers available are losing their effectiveness in the field with no new products on the horizon to take their place. He explained that although new drug “classes” entered the market every decade from the 1950s to the 1980s, it has now been over 30 years since ivermectin was introduced in 1981. Basically ‘we have what we have’ which is 3 major chemical classes or families of dewormers known as the Benzimidazoles (SafeGuard®/Valbazen®/Synanthic®), the Macrocyclic Lactones (Ivomec®/ Cydectin®/ Eprinex® & LongRange®/Dectomax®) and the Imidazothiazoles/ Tetrahydropyrimidines (Rumatel®/ Strongid®/ Prohibit® or Levasol®). “Resistance” is the term used for the ability of a parasite to survive after treatment with a dewormer given at the right dose, at the right time and in the right species. What was once a sheep and goat problem is now a growing cattle concern. The first case in US cattle was reported in 2004 and serious problems are now recognized worldwide. Resistance is most common in Cooperia, but increasingly reported in Haemonchus, Ostertagia and Oesophagostomum. Resistance to chemical dewormers is caused by a slow buildup of “resistance genes” in parasites from repeated drug treatment over many years. These genes accumulate undetected over time until the point when so many resistant worms survive there is an obvious treatment failure. Resistant worms are not more aggressive or deadly but they simply survive in high numbers after deworming, causing disease. So why, if livestock has been raised for hundreds of years and dewormers have only been around for the last 50 of those, are such dramatic effects seen if drugs fail? Unfortunately, this reliance on chemical deworming has allowed selection of bulls and replacement females with high production numbers but ignored their genetic inability to resist parasite issues. As Dr. Kaplan explained, we have developed “wimpy” animals when it comes to fighting parasites. Additionally, chemical deworming has allowed neglect of husbandry and pasture management factors that keep worm burdens naturally low. For example, overstocking a pasture means more feces, more worm eggs and larvae after egg hatching, shorter grass and more parasites in animals. This is a management problem and not the fault of the animal or the dewormer.

Parasites are a normal part of the ecosystem and it is also normal for grazing animals to be infected with parasites. “Infection” in this sense means there are worms in the digestive tract and is not the same thing as “disease”. In cattle, “clinical disease” from parasites includes signs of diarrhea, anorexia (“off feed”), rough hair coat and, depending on the parasites involved, anemia (low number of red blood cells) and hypoproteinemia (low blood protein). However, the bigger concern is often “subclinical disease” where there are no overt signs of a problem yet there is actually decreased intake and decreased nutrient utilization resulting in severe reductions in weight gain. Most animals develop good protective immunity from parasites but this can only happen if the immune system gets stimulated by worms inside the animal (similar to how a vaccine works). Development of immunity to parasites largely depends on age of the animal. Calves under a year of age have poor immunity so clinical disease is possible and production losses are certain from Cooperia and Ostertagia without proper control. Two-year olds have moderate immunity so clinical disease is less of a problem but production losses likely without good control as more Ostertagia (the brown stomach worm) are active in this age group. Three-year olds and above have good immunity with little clinical disease and only slight production losses from parasites. This immunity can be maintained throughout their productive lifespan as long as nutrition is satisfactory. Those without good immunity formed early in life are at higher risk for disease. “Premunition” is the term used for this immunity that is stimulated by a resident population of worms and actually restricts the establishment of new worms. Treatment too often in young animals removes worms and eliminates the state of premunition.

How is it possible to know if dewormer resistance is a problem in a herd? The best way to test is a Fecal Egg Count Reduction Test (FECRT) based on the premise that dead worms don’t lay eggs. Fecal samples are taken from 20 animals before deworming then the same 20 are re-sampled in 2-3 weeks (depending on which dewormer was used). The number of parasite eggs should be reduced by >95% between pre- and post- treatment samples. If <90% reduction, resistance to that family of dewormers is certain. The test is best run in weaned animals under 16 months old and is not as reliable in adult cattle. Once parasites become resistant to a drug family, they never go back to being susceptible. For this reason, it is wise to do a FECRT on any newly purchased/leased breeding stock to avoid contamination of the farm with resistant parasites before allowing them to mix with the rest of the herd.

How can we slow the development of resistance to dewormers? Reducing unnecessary treatment with dewormers, making sure the dewormers used are effective, and strategic culling all contribute to fewer resistant genes in parasites. The following are Dr. Kaplan’s recommendations:

1. Reduce treatment frequency and/or modify treatment strategies. In cattle, treat only 80, 90 or 95% of adult population of the herd, leaving heaviest and best-looking untreated. In practical terms, if you deworm twice a year (spring and late summer/early fall), limit the slick, fleshy cows to just one time per year. This leaves a proportion of the worm population untouched by a dewormer (including the worms in untreated animals and also any eggs and larvae on pasture at the time of treatment). Parasitologists refer to this proportion of worms unexposed to the chemical effects of the dewormer as “refugia”. The greater the proportion in refugia (protected or “in refuge” from chemicals), the slower the development of resistance. Unfortunately, the common recommendation for many years has been strategic parasite control by deworming when environmental contamination is at a minimum in the summer. This practice actually promotes resistance because very few worms are in refugia.
2. Ensure the treatments we administer are very effective. Given the common state of dewormer resistance, use of drug combinations is essential. Combinations slow resistance because they kill more resistant worms! An example of this is using LongRange® injectable and using a drench dewormer (SafeGuard®/ Valbazen®/Synanthic®) at the same time. The purpose of the second drug is to kill any worms that survived the first drug, resulting in much fewer worms left to reproduce. Conversely, if drugs are underdosed or administered in a manner with reduced bioavailability or absorption, then partially resistant worms are more likely to survive and mate to produce fully resistant worms.
3. Culling the “wormiest” animals. The 80/20 Rule is in effect when it comes to parasites in cattle. Approximately 20-30% of animals in the herd have 80% of the parasites. Culling the wormiest-looking animals removes a significant number of parasites and stops the passing of genetic “wimpy-ness to parasites” to their offspring.

In summary, it is impossible to eradicate parasites and, the harder we try, the faster resistance develops. The goal is not to eradicate parasites but to keep them at a level that does not cause detrimental health effects. Reliance on less chemical control and incorporating strategies based on our knowledge of parasites in the pasture (see box below) will help preserve the effectiveness of current dewormers. Viewed this way, dewormers meet the definition of “extremely valuable non-renewable resources.”

Author: Jackie Lee; lee.7186@osu.edu Editor: Kathrine Yunker; yunker.29@osu.edu The Ohio State University

College of Veterinary Medicine DVM Candidates 2019

Hypothermic Lambs: How to defrost before they’re in the freezer

Winter has already been harsh this year, making it only fitting to write about hypothermia in lambs. Even with the best management, this is bound to be an issue for many sheep producers. Hypothermia has many causes and can affect lambs at different ages. In newborn lambs less than five hours old, hypothermia often occurs due to prolonged exposure to cold temperatures.

Difficult or premature births can cause weak lambs which contributes to hypothermia because these lambs do not get up and nurse warm colostrum as readily as lambs that have a normal birth. Poor mothering can also lead to hypothermia if an ewe fails to thoroughly lick her lambs dry or if she abandons a lamb. If the ewe has poor body condition and there was a lack of adequate nutrition during gestation the risk for hypothermia increases as lambs born from these ewes are often weak and colostrum production is decreased.

Hypoglycemia, or low blood sugar, often accompanies hypothermia in newborn lambs because they have not ingested colostrum which is both a source of immunity and glucose. Lambs are born with brown fat that provides an energy source prior to colostrum ingestion but this fat is gone around five hours after birth. Therefore, lambs that have not nursed colostrum within five hours after birth are at a higher risk for hypoglycemia and will need glucose supplementation before warming. Lambs that failed to receive enough good quality colostrum in a timely manner are also at risk of sepsis associated hypothermia which occurs secondary to lack of maternal immunity. Lambs that are septic will not respond to basic hypothermia and hypoglycemia treatment and should be seen by a veterinarian as soon as possible.

Diagnosis of hypothermia in any age lamb is straightforward. The number one clinical sign of hypothermia is a subnormal body temperature of 100°F or less. As a reminder, the normal body temperature of a lamb is 102-103°F. Always have a clean, functioning thermometer on hand to take the body temperature of a lamb at the first suspicion of hypothermia. These lambs are will be very weak and lethargic. In severe cases, they may lack a suckle response and will be unable to hold their head up.

Treatment of hypothermia varies based on the severity and the age of the lamb. A lamb with mild hypothermia, a body temperature of 99-100°F, should first be thoroughly dried off before receiving colostrum via a stomach tube. It is a better option to tube hypothermic lambs since they often lack a suckle response. Giving colostrum via bottle without a suckle reflex may result in aspiration pneumonia and subsequent death of the lamb. Contact your veterinarian or experienced shepherd to learn how to tube a lamb. If warm, fresh colostrum cannot be obtained from the ewe, use a commercially available colostrum replacer. Do not use a colostrum supplement because it does not have a high enough concentration of antibodies as a replacer.

Often these replacers are made for calves but will work well for lambs also. Mixing instructions will be the same for calves and lambs but obviously a lamb does not need as much volume as a calf. A lamb should receive 10% of its body weight in colostrum over at least a few meals during the first six hours of life. Another option is to keep fresh-frozen colostrum on hand. Fresh-frozen

bovine colostrum can be used but try to make sure it comes from a healthy herd since Johnes disease transmission through the milk to lambs is possible. Some producers will choose not to use cow colostrum or ewe colostrum from other flocks due to this risk, so consider retaining fresh-frozen colostrum from your own ewes.

Lambs that are severely hypothermic with a body temperature of less than 99°F require more aggressive treatment. A lamb that is less than five hours old and severely hypothermic needs to be dried and warmed before giving colostrum via stomach tube. Warming can be accomplished using commercially available warming boxes or simply using blankets or towels. It is especially helpful if these materials can be warmed in a dryer prior to use. Another method is to place warm jugs of water or heating pads under the lamb. Do not use a hair dryer to attempt to dry and warm lambs as the high-pressure air will result in evaporative cooling rather than warming.

Lambs that are severely hypothermic and greater than five hours old must receive colostrum first before drying and warming. Lambs more than five hours old do not have any brown fat reserves left. If these lambs are warmed before receiving glucose in the colostrum, they will convulse and likely die. Again, a stomach tube should be used to give colostrum.

However, if the lamb cannot hold its head up, tubing can be a challenge and there is an increased risk for aspiration pneumonia since it is more likely for the tube to enter the trachea and lungs instead of the esophagus and stomach. In this case, Karo corn syrup can be rubbed on the gums of the lamb because absorption of sugar across the gums occurs rapidly. Alternatively, an intraperitoneal glucose injection can be given if the producer is comfortable doing this.

However, inexperienced shepherds should not attempt intraperitoneal injections without instruction from a veterinarian since there can be severe complications with incorrectly injecting any solution into the abdomen of any animal. After these lambs have been given some energy, begin the drying and warming process. It is recommended to tube these lambs again after their body temperature has increased.

Overall, it is important to remember that the best treatment for hypothermia in lambs is prevention. Ensure that lambs are born in clean and dry environments such as a well bedded lambing pen. Knowing when an ewe will lamb will help a producer predict when to move ewes into an appropriate lambing area since most of the time ewes are sheltered in colder environments such as a three-sided shed on pasture. Careful observation of breeding dates and aging fetuses at the time of pregnancy diagnosis will aid in knowing due dates. Neither of these methods are perfect so frequent monitoring for signs of parturition is necessary. The lambing area should also be free from drafts. Heating lamps are a common recommendation but make sure that they are secured to reduce fire risk. Most of the time though, the heat from the dam and her colostrum will be enough for a lamb to maintain body heat if the lamb is born in a well- insulated and appropriately ventilated barn. Wishing everyone the best of luck during this lambing season.

CLUB LAMB FUNGUS   (Ringworm)

From: Tim Barnes Ohio Extension Educator

Ovine dermatophytosis, lumpy wool, sheep ringworm, woolrot, was first recognized in the late 1980’s. It occurs most commonly in sheep exhibited at fairs and other shows. The disease is contagious to humans and other animals.

Cause of the Disease

Disease occurs when the fungus, a Trichophyton, invades the skin and hair follicles. Similar fungi cause ringworm in humans, cattle, horses, dogs, cats, and other animals. Nicks and cuts from shearing, handling, or environmental hazards allow the fungus to enter the skin. Slick shearing, repetitive washing, and stress make animals more susceptible to infection. Washing removes protective oils (primarily lanolin) that are part of the animal’s natural defenses against fungal infection. Long or frequent travel, shows, and changes in diet are stressful and reduce the animals immunity and resistance to disease.

Spread of the Disease

The spread of disease occurs mostly at shows, sales, and exhibitions. Susceptible lambs are infected by contact with other lambs, contaminated equipment, surroundings (pens, stalls, etc.), and humans. Trichophyton spores can survive several years on animals and in the environment – in barns, trucks, trailers, tack, grooming tools, wool, feeders, and in bedding, soil, and manure. Spores resist destruction, particularly if lodged in cracks or hidden from direct sunlight. Shearing equipment is very important in spreading disease between sheep. Humans can be infected from contact with the fungus on the sheep. If human infection is suspected, contact a physician and inform them that there has been contacted with infected sheep.

Diagnosing the Disease

It is much easier to identify the disease in shorn sheep. Lesions can appear anywhere, but are most common on the head, neck, and back. The skin is initially thick, red, and “weeping,” and later, there is the appearance of crusty and scaly skin, and usually in circular lesions. Sometimes the wool appears “clumped,” as well. Hairs break easily and are usually lost beginning in the center of the lesion. The “spots” are first seen in 4-8 weeks and the infection usually heals spontaneously in 8-16 weeks. Hair may regrow black in the affected areas. All stages of the fungal infection are contagious until the skin surface appears normal and growth of hair or wool has begun.

Culturing the Trichophyton species confirms the diagnosis. However, a presumptive diagnosis is based on clinical signs and history. Secondary bacterial infections often contaminate cultures because the lesions are open and exposed to the environment. Contact your veterinarian for proper diagnostic procedures.

Treatment of the Disease

There is no specific treatment for club lamb fungus. Antifungal medications inhibit fungal growth and reduce the spread of infection. Using antifungal medication in sheep is considered an extra-label drug use and requires a valid veterinary-client-patient relationship. Most cases of club lamb fungus recover over time if give the proper nutrition, rest, and appropriate treatment.

Prevention and Control

 Clean facilities and equipment with antifungal disinfectants.

 Keep facilities free of sharp edges and exposed wires.

 Minimize stress on animals.

 Use separate equipment for each lamb.

 Isolate infected animals.

 Wear rubber gloves and long sleeves when handling infected animals.

 Use different equipment and clothes for infected and non-infected animals.

Source: California Department of Food and Agriculture May 2016