LEADING ANIMAL HEALTH PRODUCTS DISTRIBUTOR

Writer: Dr. Shmulik Zamir, Small ruminants Veterinary Specialist Preeclampsia in the flock and "nectar for the flock" Preeclampsia is a metabolic disease that affects goats and sheep in normal physical condition, fat or thin, carrying several fetuses in their womb, in advanced pregnancy. The "disease" usually affects the second pregnancy or more in breeds with high fertility. (In sheep: Apek, Assaf, Romanov, Finny and all their pens). The clinical signs usually appear after a period of negative energy balance, which causes (HYPOGLYCEMIA, a drop in the blood sugar level), an increase in the metabolism of fat tissue - (KETONEMIA, the appearance of ketone bodies in the blood) and KETONURIA (the appearance of ketone bodies in the urine). Preeclampsia is an interface nutritional disease whose causes are: 1. Increase in nutritional requirements in advanced pregnancy. The more births there are, the higher the demands on the food. 2. A decrease in the ability to fill the stomach / volume of the stomach. The abdomen is pushed by the uterus and the fetuses physically occupy more space in the abdominal cavity as the pregnancy progresses. 3. Inappropriate nutrition \ insufficient in quantity and in terms of composition \ eating disorder. 4. Stress factors related to the interface. Vaccinations, transfers (from place to place and/or from group to group, weather, entry of unfamiliar dogs ("predators"), etc. 5. Associated diseases. 6. Genetic susceptibility of an individual animal to "preeclampsia". The clinical signs of "preeclampsia": In the initial stages: difficulty walking, walking as if on eggs, eating little, disorientation in space, signs of blindness, constipation and grinding of teeth. In the advanced stages: numbness, apathy, convulsions, increased breathing rate, pressing the head on hard objects, convulsions, head turned upwards - "GAZING STAR", death. The diagnosis of the disease: is usually made according to: the clinical signs, and the presence of ketone bodies in the urine. The treatment: the treatment of preeclampsia is difficult and complex and must be adapted to the ewe. The purpose of the treatment: correcting the negative energy balance, raising the glucose level in the mother's blood and stimulating her appetite. The treatment that was accepted for preeclampsia basically consisted of the ingestion of "precursors" (starting materials) for glucose such as propylene glycol and glycerin, subcutaneous/intravenous glucose administration and appetite stimulants. In addition, it is customary to give a subcutaneous calcium solution. "Nectar to the Flock" A solution containing sugars and other ingredients that, when given to a sheep/goat orally (by swallowing) every 6-8 hours, quickly (within about 20 minutes) raises the blood glucose level and manages to maintain this level for 6-8 hours. (Raising the blood glucose level with the help of other glucose sources, such as propylene glycol and glycerin, takes between 4-6 hours). The great advantage of "Nectar for the Flock" is that sheep treated with this solution have a much higher chance of having a normal litter with live births than sheep treated in other ways. The more we anticipate and treat, as soon as the suspicion of "preeclampsia" appears (a ewe 3 weeks before the expected calving date showing signs of walking difficulties, for example) the better. Of course, the earlier the problem is identified, the better the sheep or goat's chances for recovery. Another advantage of "Sheep Nectar" is its long shelf life, being in powder form before use, the preparation is very easy, simply adding tap water according to the instructions and in addition the sheep and goats drink the solution willingly. If we made a mistake in the diagnosis and there was no need for embolization, no damage will be caused, (except for the price of the treatment). Hot recommendations: 1 . Prevention is always better than treatment. 2. If adding ingredients to the ration before the expected calving works, great! 3. Introduce interface methods that help in troubleshooting. A. Distributing the ration twice a day - at the time of serving, they should all fly to the manger. B. Any sheep / goat that does not get up to eat is suspect. third. Any sheep \goat that walks slowly is suspicious. d. If there is any doubt, there is no doubt! Any suspicious behavior must be dealt with. God. In order to make the diagnosis more accurate, it is advisable to use "Ketostick" for the diagnosis of ketone bodies in the urine. and. The treatment of "preeclampsia" will be done with the help of "nectar for the flock" G. If you know for sure the duration of the pregnancy, you can consult a doctor for speeding up the calving.

Toxicokinetics of Mycotoxins: Absorption, Distribution, Metabolism and Excretion (ADME) March 6, 2024 From the BIŌNTE Technical Department introduction This article describes the toxicokinetics of the most important mycotoxins in farm animal pathology. The information presented is sufficient An overview of the chemical properties of mycotoxins and their absorption, distribution, metabolism and excretion processes accordingly in farm animals and delves into the differences found between the species. Aflatoxins chemical properties Aflatoxins have a common structure of four rings, a feature that gives them a rigid and flat geometric structure. The important aflatoxins Most are B, G and M, which is a metabolite of B. The difference between B and G lies in the six ring ketones. Besides, the difference between classification 1 and 2 lies in the oxidation of the double bond. As for the other aflatoxin metabolites, aflatoxin (AFL) is obtained by oxidation of a The ketone, AFP1 is formed when the ether group is converted to an alcohol, and AFQ1 has an alcohol group in the cyclopentanone group. Figure 1. Chemical structure of the main aflatoxins and their metabolites. absorption The main absorption of aflatoxin B1 occurs in the small intestine and depends largely on its molecular weight and lipophilic properties his (Schrenk et. al, 2020). distribution According to distribution, metabolism and secretion, the organ that is mainly affected by the effect of aflatoxins is the liver. Moreover, it can also to accumulate in the muscle (Popescu et.al, 2022). metabolism Aflatoxin B1 is metabolized during its passage through the digestive tract, but the main site where it causes metabolism Its extent has not yet been clarified. Hepatic exposure to aflatoxin is closely related to AFB1 concentration and intestinal absorption rate, in addition to flow the portal in the liver (Schrenk et.al, 2020). In the liver, aflatoxins are substrates of CYP monooxygenases, including CYP3A4, 3A5, and 1A2. An important step in AFB1 activation is formation of AFB1-exo-8,9-epoxide, which is its reactive form. Only AFB1, AFG1 and AFM1 can be activated by CYPs in such a reactive way. AFB1 has many other metabolites that are obtained by different reactions. For example, Aflatoxicol is A molecule obtained from the reduction of AFB1 via NADPH-dependent reductase in the liver. Other important metabolites are: AFM1 and AFQ1 (obtained by hydroxylation), AFP1 (formed by the demethylation process) and the oxidation products (AFQ1 and AFM1). One of the processes The important enzymes the body has to reduce the reactive form of AFB1 to a less reactive metabolite such as AFB1-dialcohol carried out by a family of NADPH-dependent aldo-keto-reductases. Among the metabolites mentioned: AFM1, AFP1, AFQ1 and aflatoxin-dialcohol can be conjugated with glucuronic acid and excreted in feces or urine. Unlike AFB1, the information on The metabolism of the other types of aflatoxins is limited, with only limited literature identified on the metabolism of AFB2. (Schrenk et al, 2020). the affair AFB1 and its metabolites are excreted mainly through bile, followed by urine. Mammals may excrete some AFB1 which is ingested in the form of AFM1 and other metabolites through milk (Eaton & Groopman, 1994). Deoxynivalenol chemical properties Deoxynivalenol (DON) is a mycotoxin belonging to the trichothecene family. Trichothecens are characterized by a common structure of three rings and epoxide at carbon 12. Within this group of compounds there are four types: C, B, A and D. The most common types in nature are A and B. DON is a type B trichothecane that is characterized by having a ketone group at the 8-carbon position. Figure 2. Chemical structure of deoxynivalenol (DON). absorption The absorption and metabolism of DON in the intestine varies greatly between different domestic animals and is highly dependent on regional pH, intestinal segments and activity germs. It is the microbial location that affects the bioavailability of DON and its metabolites upon ingestion (Knutsen, 2017). Moreover, DON absorption varies according to the type of animal, age and even sex. In addition, the appearance of DON in the blood after oral ingestion It is fast for most mammal species (Payros et.al, 2016). distribution The distribution of this toxin occurs in several organs, without its concentration being uniform. After oral administration, DON has high plasma values, in the liver and kidneys after 30 minutes, and then, its concentration becomes higher in the intestinal tract after an hour. This can be explained in the sense that DON is rapidly absorbed in the gastrointestinal tract and briefly circulates in the plasma, moving to multiple organs. By liver enzymes, DON passes Metabolized efficiently and excreted through urine, reducing its concentration in plasma, liver and kidneys. With this, DON which is not absorbed, remains In the digestive system and because the intestinal movement is much slower than the plasma cycle, it accumulates. To finish the issue of distribution, DON It has also been detected at low levels in the brain, suggesting the possibility of movement of this toxin across the blood-brain barrier, causing brain inflammation. (Sun et al, 2022). metabolism The primary metabolism of deoxynivalenol focuses on two main pathways: phase II metabolism and intestinal biotransformation. Phase II metabolism includes the formation of glucoside, glucuronic acid and sulfates. On the other hand, biotransformation is related to the transition from DON to DOM-1. The use of both metabolic processes varies depending on the species. For example, in pigs and humans, between 70 and 94% of the DON undergoes glucuronidation, while a small fraction is eliminated by gut microbiota (Sun et.al, 2022). Phase II metabolism is quite versatile in different animals. Birds usually exhibit sulfate conjugation, while other animals do not The glucuronidation pathway is used. A relevant fact is that pigs and humans share the metabolite DON-12GlcA (which is obtained by phase II metabolism), therefore this animal is used as a model for the study of human toxicokinetics and metabolism (Sun et.al, 2022). Transformation of intestinal bacteria from DON to DOM-1 is another important detoxification pathway. In chickens, it is suggested that track This metabolism is one of the main reasons for their resistance to DON and although there is no extensive evidence, studies have confirmed that the level of the toxin decreases as it progresses through the intestinal tract of birds. However, DOM-1 is not the only metabolite product of transformation biologically, but the conversion of DON to DON-3S was detected in broiler chickens (Sun et.al, 2022). the affair The excretion of DON and its metabolites in pigs, mice and humans occurs exclusively in the urinary tract; Unlike chickens and rats, where the rate of DON in feces can be higher than that found in urine (Sun et.al, 2022). Zearalenone chemical properties Zearalenone is a mycotoxin with an acidic and resorcyclic lactone structure. The main metabolites of zarlenone are α and β-zarlenol, formed by oxidation of the ketone group to alcohol. α and β-zearelenol are isomers that differ in the chirality of the carbon to which it is attached The hydroxyl group is attached. Figure 3. Chemical structure of zarlenone and its metabolites. absorption Zearalenone is a mycotoxin with rapid and extensive absorption after oral administration in rats, rabbits, pigs and humans (EFSA, 2011). One of the special characteristics of zarlenone absorption is that after absorption in the intestine, part of ZEA returns through bile secretion for a second absorption (Han et al, 2022). distribution Zarlenone and its metabolites can be detected both in animal tissues and in their products. Detection of ZEA is quite limited in the liver, kidneys, and muscle and in plasma. Its metabolites α and β-zearelenol are better distributed. It is worth mentioning that these metabolites have a huge affinity to albumins, which is why they remain widespread in plasma (Liu & Applegate, 2020). Other organs involved are organs Reproduction (uterus, testicles and ovaries) and adipose tissue (Han et.al, 2022). metabolism The metabolism of zarlenone has been studied in vivo in both animals and humans. Consequently, three important biological pathways have been reported in animals (EFSA, 2011). First, there is the enzymatic reduction of zarlenone, catalyzed by 3α and 3 hydroxysteroid dehydrogenase (HSDs)β-, which produces α and β-zearelenol and a small group of zearalanols. The main reduced forms of the toxin have different estrogenic activities, And the toxic reactivity of α-zearelenol is greater than meso-zearelenone and β-zearelenol. In mammalian species, the transformation The hepatic disposition of zarlenone is completely different for reduced metabolites and glucuronides. For example, pigs convert zaralenone primarily into zarlenol, while ruminants convert it to β-zarlenol, which explains greater sensitivity on the part of pigs (EFSA, 2011). The second metabolic process is monohydroxylation. Reported in humans via cytochrome P450 (CYPs) and liver microsomes. Christian catechists by aromatic hydroxylation and these metabolites are then oxidized to compounds that develop a redox cycle and covalently modify Biological macromolecules. The estrogenic properties of these catechols remain unknown (EFSA, 2011). As the last metabolic process, phase II conjugation of zaralenone and its reduced metabolites with glucuronic acid and sulfate occurs, mediated by catalysts such as Uridine diphosphate-glucoronosyltransferases (UGTs) and sulfotransferases (SULTs). Based on In vitro studies, zarlenone and its metabolites are rapidly glucuronidated in the liver and intestine, but can also be metabolized in extrahepatic organs both in humans and in some animal species (EFSA, 2011). the affair Most mammals use biliary and enterohepatic circulation to excrete zaralenone. The glucuronide derivatives of zarlenone are collected in the bile and again are reabsorbed and metabolized in the intestinal mucosa. This reabsorption process contributes to the retention time of ZEA in the body, extending the Its toxic effect inhibits its elimination (Han et.al, 2022). Ochratoxin chemical properties Ochratoxins consist of the union of a phenylalanine group with dihydroscoumaric acid through a peptidic bond, in which a the carboxyl (-COOH) and the amino group (-NH2). There are mainly two types of ochratoxins, A and B, which differ in the presence of a group Chloride in the form of A. Ochratoxins can be hydrolyzed, and the metabolites OTalpha and OTbeta with low toxicity can be obtained More. Figure 4. Chemical structure of the main ochratoxins and their metabolites. absorption Ochratoxin is rapidly absorbed after oral ingestion, and it reaches high levels in the blood for several hours. passive diffusion through The stomach, and especially the proximal region of the jejunum, causes systemic entry of ochratoxin. At the same time, this process is facilitated by the high affinity of plasma proteins to this toxin. The systemic bioavailability of the toxin varies depending on the species (Schrenk et al, 2020). distribution Regarding distribution, OTA is particularly relevant due to its strong non-covalent binding to serum proteins, especially albumin, which explains How difficult it is to eliminate afterwards and its long half-life in the body. OTA has its distribution in all body organs, however, The concentration that the toxin presents in each organ will depend on the animal species, the dose given and how it is studied (kinetic study design). Most studies or Reports indicate that high concentrations of OTA are often expressed in the kidney, followed by the liver and muscle. Furthermore, Redistribution and deposition of this toxin can occur in fat-rich organs. Regarding the transfer of ochratoxin through the placenta, Transport is minimal, as some in vitro studies have indicated. Furthermore, evidence suggests that OTA transmission is assocd for placental discharge or development. The transfer of the toxin can also occur through the uterus or through breast milk in both animals and humans. Studies in dairy cows have found traces of ochratoxin in milk, suggesting that the minimum concentration of the toxin in the product can be attributed This is due to the efficient pre-systemic breakdown created by the brome microflora (Schrenk et.al, 2020). metabolism The main metabolite of OTA is OTalpha, which is formed when the amide bridge between phenylalanine and dihydroisomeric acid undergoes hydrolysis. This molecule is produced by the gut microbiota in non-ruminant animals, including humans, and in turn, In the rumen microbiota of cows, sheep and other ruminants. OTA degradation is carried out by many hydrolases, such as carboxypeptidase A, which is the most active. The formation of OTalpha is considered an important step in the detoxification process and once formed This metabolite, it does not accumulate in the kidney and is quickly excreted in the urine, as a glucuronide (Schrenk et.al, 2020). the affair The complex binding of OTA to albumin results in reduced elimination of the toxin by glomerular filtration. Tubular secretion is responsible for the elimination of OTA by using organic anion exchangers. Unfortunately, the toxin can be reabsorbed at the tubular level and this phenomenon partially responsible for its accumulation in the body. In addition, various in vivo studies have established that the toxin has the ability to be reabsorbed in any part of the nephron, via active transport or passive diffusion depending on pH. Biliary excretion of OTA and its metabolites is the important pathway most through the fecal route. Similar to the urinary tract, OTA can be reabsorbed after hydrolysis by the bacterial microflora and continue in the enterohepatic circulation, then it is slowly eliminated from the body. Finally, there is evidence that OTA can contaminate and be excreted in milk, when there is a direct relationship between OTA consumption and its concentration in milk (Koszegi & Poor, 2016). T-2 toxin chemical properties T-2 toxin is a mycotoxin that belongs to the trichothecene type A family. T-2 toxin is characterized by having two ester groups in the carbons 4 and 8 in its molecular structure. Its main metabolite is the toxin HT-2, which is formed by hydrolysis of the ester at the 4-carbon position to the hydroxide group. Figure 5. The chemical structure of T-2 toxin and its main metabolite HT-2. absorption T-2 toxin is rapidly absorbed after ingestion in most animal species, and is distributed throughout the body with little or no accumulation in a specific organ. It is a lipophilic toxin that, in addition to being absorbed through the digestive tract, can penetrate the respiratory mucosa (Janik et al., 2021). distribution T-2 toxin rapidly moves from plasma to tissues or organs, with a plasma half-life of less than 20 minutes. It is distributed in organs such as liver or kidney without significant accumulation. At the same time, T-2 has the ability to cross the placenta and fetal tissues (CONTAM, 2011). metabolism The metabolism of T-2 toxin occurs in the intestine, liver and other tissues (CONTAM, 2011). The main metabolic pathways of This toxin includes hydrolysis, hydroxylation, conjugation and deoxidation. The predominant metabolite of T-2 toxin in all species is HT-2, obtained as a result of the hydrolysis of the toxin. This metabolite is considered an important biomarker because it can detect the exposure of Animals and humans to T-2 toxin (Janik et al., 2021). Most metabolites, especially T-2 toxin, are extensively conjugated with Glucuronides, which is one of the most relevant mechanisms of detoxification (CONTAM, 2011). the affair The urinary and biliary tracts are the routes used to excrete T-2 toxin and its metabolites. The discharge is fast, with a higher rate in feces Enterohepatic circulation of T-2 toxin and its glucuronide-conjugated metabolites is known to occur (CONTAM, 2011). Fumonisins chemical properties Fumonisins display a molecular structure similar to a lipid chain. There are four types of fumonisins, with type B1 being the most toxic most, and differ in the presence of alcohol groups in positions 5 and 10 of the chain. In addition, they have branching through asters in positions Carbons 14 and 15. Figure 6. Chemical structure of the main femonisins. absorption Fumonisins are mycotoxins characterized by low bioavailability due to their structural charge and the limited expression of a specific receptor for their transportation at the enteric level. In several species, reports indicate that fumonisins undergo a series of hydrolytic reactions Continued mainly in the intestine, forming partially fumonisin A and fumonisin B and finally HFB1 or aminopentol. In exposed animals can be found Metabolites in liver, kidneys and to a lesser extent in muscle (Schrenk et al., 2022). distribution In many animal species, the distribution of fumonisin B1 after absorption in the gastrointestinal tract occurs mostly in the liver, kidneys, and muscle. Through According to various reports, it is known that the liver and kidney show a certain sensitivity to fumonisin B1, which may be due to or correlated with the concentration of the toxin in the tissue after absorption (Knutsen et al., 2018). metabolism The main sites for the metabolism of fumonisin are the liver and the digestive tract, where the basic metabolic pathways are hydrolysis, Acylation and transamination. The main metabolite of fumonisin B1 is HFB1 or also called AP1. It is formed by the hydrolysis of tricarbylic acid side chains at carbons 14 and 15, which are then substituted with hydroxyl groups (Wang et al., 2015). the affair Most studies in experimental animals and farm animals report that after oral ingestion of FB1 and FB2, these are excreted unchanged in the feces, and to the extent less, in urine. Toxin excretion occurs in the first 12 and 48 hours through the urine and feces, respectively (Knutsen et al., 2018).

Lameness in sheep and goats Dr. Shmulik Zamir, expert in sheep medicine Lameness, whatever the cause, causes a decrease in sheep/goat productivity. First, it must be determined whether it is a lameness that originates from a pathological process in a muscle, bone, or joint or that originates from damage to the peripheral or central nervous system. In young animals the main causes of lameness are joint problems. In adult animals, most lameness is due to problems with the teleps. Uneven growth of the papillae and factors such as moisture that soften the papillae, may increase the sensitivity to infectious agents. The most important step to prevent lameness in the herd is routine and correct culling. Clinical examination to identify the source of the lameness: the animal will be examined at rest and in motion paying attention to weight bearing, standing, prominent wounds and swellings, etc., structure and shape, and a telepal examination. A detailed examination should locate the place of the lameness by cleaning and picking up the lameness if necessary, palpation and manipulations. Additional measures: X-ray. Non-infectious diseases of the telepathies: White line disease (the cemented junction between the wall and the heel, therefore it is a weak area). It is about the separation of part of the corneal material in the outer wall from the laminae that is under it in the area of the white line. In cases of slight to complete separation, a pocket is formed that creates pressure on the laminae. Trauma to the area, such as gravel and stones, can cause damage that worsens with dirt ingressing into the carpet. Moisture softens the fabric, which increases the chance of damage. Picking up and removing a loose horn will prevent lameness. Separation of the horn will occur in most cases as a result of the white line disease. Separation is also possible as a result of trauma to the septal wall. Trauma to the calf can be caused by the insertion of a foreign body such as a stone / nail, which is immediately manifested by lameness. Neglect can cause an abscess. The treatment will include removal of the foreign body, drainage, antibiotics, immersion and washing with antiseptic agents. Another component of the trauma is heel abscesses (not common), probably due to trauma to the heel. The treatment of the abscess will include instillation, drainage and cleaning, injection of antibiotics and washing with antiseptic agents. Granulomas in the heel are caused by trauma and ulceration. The treatment will include cutting the granulation tissue and lysing. Fibroma between the telepals. The treatment will include surgical lowering. Distal phalanx fractures cause acute lameness. The diagnosis will be made using an X-ray, the treatment will be fixation. Laminitis is a metabolic disease of the corium and the germinal layer of the calf, caused by the degeneration of the blood supply to the corium. Notice in: Acute laminitis, as a result of the release of endotoxins in toxic eggs such as acidosis and endometritis. Subclinical laminitis, caused by overeating over a long period of time Chronic laminitis, which develops when the previous two are not treated. Treatment of acute laminitis: weaning the sheep from feeding a mixture, giving only straw and hay, lining the beating site with straw, treating with anti-inflammatory drugs, giving antibiotics, heating in the first hours to maintain blood flow to the area. In chronic cases, Tilof to reduce the pressure on the Tilof. Prevention will be done through a proper interface. A lack of zinc may cause damage to the skeleton and the pelvis. An animal is standing with its back bent, pain in the palps on palpation, transverse thickenings are formed on the palps. Infectious diseases of the wolf: Interdigital dermatitis and Foot rot. The prerequisites for the formation of these two syndromes are: wet and muddy yards, overcrowding, introduction of clinically or subclinically infected animals, incorrect treatment or lack of treatment of the litter and incorrect structure of the litter. The reasons for this are: Fusobacterium necrophorum - an environmental bacterium that penetrates the skin between the palms after the skin has been damaged by prolonged wetting and causes inflammation in the skin between the palms. Dichelobacter nodosus - has keratolytic activity that destroys the pulp. It is found in carrier animals, and together with F. necroforum causes the leaf rot. The bacterium Treponema is found in cases of severe rot in sheep and goats, but its role is unclear. Interdigital dermatitis (inflammation of the skin between the digits): Clinical signs: Goats show more severe clinical signs than sheep due to longer telepals and a deeper area between the telepals. Mild / severe lameness in one or more legs, walking on the knees (in goats), weight loss, decrease in milk yield, the skin between the legs is inflamed/swollen with a characteristic smell, the inflammation does not cause damage to the legs. Foot rot Clinical signs as in inflammation between the feet, but with foot rot. In addition, horn separation occurs - pus accumulates under the horn and necrotic tissue with a characteristic odor is formed. Secondary complications may result from suffocation or tetanus. Treatment and prevention: routine examination and vaccination for the entire herd. Inflammation between the telepals - removal from a wet area to a dry one, spraying with iodine containing antibiotics, dipping in bleach or halamide. Decayed rot - ablation and removal of rotten tissue, treatment with systemic antibiotics (penicillin / streptomycin / tetracyclines) Immersion in Zinc sulphate 10%, once a day for 5 days and then weekly immersion. There is currently a zinc sulphate paste that can be applied between and on the lips once a day for 5 days, and it should solve the problem. In severe cases, the tape can be bandaged over the ointment. Abscesses in the palms: Causes: hit by stones in the tarp, excessive tarp, inflammation between the tarps and tarp caries, White line disease, cracks in the tarp wall, Bacteria penetrate the instep due to one of the above factors and cause abscesses in the heel or in the front part. The abscess can break out in the connection between the skin and the horn or between the insteps. Clinical signs: swelling, pain, bloody purulent discharge between the eyelids or in the connection between the skin and the eyelid. Treatment: drainage of the pus, immersion in an antiseptic solution, systemic antibiotics and, in severe cases, amputation of the finger.

- Dr. Shmulik Zamir, expert in sheep medicine Medicine has never been an exact science, symptoms of one disease are part of the symptoms of another disease, clinical signs of one syndrome can be part of another syndrome, so here comes the experience of the doctor in combination with what is at his disposal such as laboratory tests in order to diagnose any disease in a person or in a "H in order to offer a suitable treatment for the disease if such exists. Clinical signs presented by AH may correspond to a number of diseases and here comes the differential diagnosis, namely: Among several diseases characterized by similar/identical clinical signs, the doctor must, with the help of the means at his disposal, decide what is the cause of the clinical signs and hence the definition of the disease, therefore when a farmer from one of the northern Negev settlements called me a few days ago (mid-November) and told me that in his flock of sheep for meat, several sheep had started About two weeks ago and they have difficulty walking, last week several sheep appeared with swollen heads and two of them died. A number of factors came to m ind that may cause the syndrome that combines swollen heads and lameness, and it will suffice if I mention here syndromes such as: snake bite (Israelite viper) hypersensitivity to light, and blue tongue disease. On second thought, I ruled out the possibility of hypersensitivity to light, since this herd does not go out to pasture, the possibility of a snake bite was also ruled out, since it does not make sense that more than ten sheep would be bitten by one snake, I was left with the more likely possibility of blue tongue disease. At my request, the breeder transferred the bodies of the two dead sheep to the pathology department of the veterinary institute for po st-mortem examination. Upon examination of the sheep, their heads were found to be swollen, the cause of which was edema that had formed in the lips, inside of the eyelids, and prominent submandibular edema that progressed toward the neck, the skin of the lips and the snout, the permis (red due to congestion) on the lips and inside the oral cavity, and especially on the papillae (papillae), were visible bleeding (as if were cut with a razor blade). The heparemia was also noticeable in the groin area of the sheep. Blood streaks were found in the corona area (the connection between the skin and the skin) of the four legs. In the post-mortem examination, the most striking findings were: edema, bleeding in the head and neck area, prominent visible edema, bleeding was seen on the heart and the pericardium contained bloody fluid, extensive bleeding was found at the base of the sagittal artery, and the spleen was enlarged with many bleedings found on its casing. These findings are pathognomonic (most typical) findings for bluetongue disease. The spleen of those sheep was sent to a virology laboratory to isolate the virus that causes the disease. So what is bluetongue? It is a viral disease of sheep and other ruminants caused by a virus transmitted by insects. The disease is not contagious from one sheep to another, it is an acute disease characterized by high fever (40.5°C - 42°C), prominent swelling in the head area, bleeding in the oral cavity and corona, and muscle inflammation. The disease mainly affects sensitive sheep breeds, (in Israel these are mainly the Merino, other meat breeds such as Dorfer and Spolk), and the Asaf breed (for meat and milk). The disease in Oasi is rare but exists. The disease is caused by an Orbivirus from the Reoviridae family. 24 serological types (serotypes) of bluetongue are known today. Virus types have been diagnosed in Israel to date: 2, 4, 6, 10, 16 - with the most common being 4 and the least common being 16. The disease in Israel is distinctly seasona l and limited to the period between the months of July and December. The virus that causes bluetongue is transmitted by arthropods and mainly by weevils (Culicoides). which are biological transmitters. Experiments have shown that ticks may als o trans mit the bluetongue virus mechanically or biologically, but their role in the epidemiology of the disease is probably minimal. The virus can be transmitted from viremic mothers to the developing fetus in the womb. The virus can be found during the viremia period in the semen of rams. The main carrier is the weevil, and in the country the Culicoides imicola. The epidemiology of the disease is mainly determined by three components: 1. The life cycle and activity of the transferor. 2. The pathogenicity, infectivity and antigenicity of the type of virus involved. A. Susceptibility of the host. Limiting the carrier's activity to specific periods of the year is the most significant factor and therefore the disease is clearly seasonal. The cattle is a host for the virus and it even reproduces in it. The flock is probably an "accidental victim" of the virus. The weevils bite the sheep mainly at night due to their preference for low areas. The female weasel, whose life span is about 70 days, feeds on a blood meal every 3-4 days. The virus multiplies in the salivary glands of the female heifer and 7-10 days later it is excreted in the saliva. 5-8 days after the bite the viremia (the presence of the virus in the blood) begins and it may continue 20-25 days after the infection. The first sign of infection is the increase in body temperature which reaches its peak 7-8 days after infection. The temperature may reach up to 42°C, the heat period lasts about 6 days. About two days after the onset of the fever, the skin of the face, nose, lips and mucous membranes of the mouth become inflamed, edema appears in the head area (which makes the head look swollen) mainly in the area of the lips, face, eyelids and ears. The edema is most noticeable in the submandibular area and may progress to the neck area. Spotty and poor bleeding appear on the lips, gums, tongue and especially on the nipples (papillas) in the oral cavity. The tongue may become doughy and swollen and protrude beyond the oral cavity. In extremely rare cases it becomes cyanotic (blue) and hence the name of the disease "blue tongue". A watery discharge appears from the nose which becomes mucopurulent, dries up and forms scabs in the area of the nostrils making it difficult to breathe. The sheep show signs of lameness in all four legs due to obvious coronitis when bleeding is noticed in the area of the corona (the connection between the skin and the fleece). The bleeding appears in the form of characteristic streaks above the temples. The pain is so great that the sheep walk on their knees or cannot walk at all. The sheep show a syndrome of general weakness and depression, to the point of death. Exposing sick sheep to sunlight and heat worsens the signs of the disease. The duration of the disease may last 10-15 days. In the post-mortem, the prominent findings are edema in the head and neck area, visual edema, bleeding on the heart and finding fluid in the pericardium, necrosis

Pior Agencies is very grateful to all the participants of the first forum for sheep breeders in Israel. A small and intimate event led by Dr. Shmulik Zamir and Dr. Dror Reznikov. A kind of networking, a space where problems and issues related to growth can be raised. To hear and internalize useful knowledge and acquaintances with the other breeders in Israel. This time the topics for discussion were: - Preeclampsia - The telef problems We at Pure Agencies will always look for ways to improve and help the success of growers in the State of Israel. See you in the next forum!!! Thanks!!

MYCOTOXIN BIOSORBENTS: A promising alternative in the control of mycotoxins BIŌNTE Technical Department February 6, 2024 The use of substances that suppress or reduce mycotoxin absorption, increase excretion or change their mechanisms of action are the main strategies for detoxifying mycotoxins in animal husbandry. As part of these characteristics, absorbent materials are widely used as feed additives, such as aluminosilicates, bentonites, zeolites, sepiolites, diatomite, polyvinylpyrrolidone, cholestyramine and activated carbon. However, the use of these materials has certain limitations and most of them do not degrade when released into the environment. The emerging alternatives are natural adsorbents, which have been proven to be simple, fast, environmentally friendly and less expensive than conventional ones. Biosorption is therefore a new and secondary concept of adsorption, where the sorbent is a component of biological origin. Several studies have reported successful results in vitro using biological materials such as agro-industrial waste for mycotoxin adsorption. Some of the residues are effective in binding mycotoxins in vivo, reducing their bioavailability and allowing their efficient excretion through feces. Therefore, the use of agro-industrial residues seems to be a promising alternative in the control of mycotoxins (Aguilar et.al, 2021). The most common agro-industrial remains are: leaves, tubers, roots, bark, pulp, seeds, skins, stones and others. In addition to their valuable nutrient content, these products have pores and multilayered structures with cavities and channels that provide a large surface area for the binding of multiple molecules. Agro-industrial residues such as fibers, pomace, fruit peel and seeds have been shown to play a role as binding agents for mycotoxins in both in vitro and in vivo studies (Aguilar et.al, 2021). Some of the agro-industrial wastes used as biosorbents are listed below. Agro-industrial waste 1. Dietary fiber Dietary fiber is that part of the plants that consists of soluble and insoluble carbohydrates, indigestible and starch, which is not digested and absorbed in the small intestine, during full or partial fermentation in the large intestine. Complete fiber can be found in food, such as vegetables, whole grains, fruits, cereals and flour. There are several classifications and elements that go into the concept of fiber. One classification is usually based on solubility. According to this characteristic, soluble fibers are mainly non-cellulosic polysaccharides, e.g. galactomannan, pectin, mucilage and β-glucan; While insoluble fibers make up the plant cell wall, and include cellulose, wood and hemicellulose (Aguilar et.al, 2021). Since 1980, dietary fiber has been studied as a mycotoxin binder in the gut of animals, and its consumption has been reported to reduce the incidence of mycotoxicosis in animals. In 2011, a group of researchers patented the use of very fine plant fibers to reduce the bioavailability of mycotoxins in animals (Tangni et.al, 2011). It was reported that micronized wheat fibers had the potential to reduce the bioavailability of AFB1 and OTA. In addition, the researchers also found that dietary fiber use increased stool excretion by 15-35%. Despite the effect of dietary fibers as biological substances, their action may be impaired by the appearance of certain factors, such as bacteria. In vivo digestion models have been applied to simulate the physiological conditions of the digestive tract, including digestive enzymes, pH, salt concentration, and digestion time. Using this system, it was observed that bacteria (mainly in the large intestine) have the ability to ferment certain fibers, which causes a greater exposure of the intestine to mycotoxins and increases their bioavailability. On the other hand, fibers with low fermentation (such as cellulose) are more resistant to the action of bacteria. Other fibers such as chitosan and β-(1,3)-glucan also reduce the biological access of mycotoxins through the colon and prevent bacterial fermentation. It is worth mentioning that some of the probiotic lines have a toxin-harvesting effect, therefore, the combination of these probiotic organisms with non-fermentable fibers may reduce the bioavailability of mycotoxins in the intestines (Aguilar et.al, 2021). 2. Pomades Fumes are by-products of fruit and vegetable processing. They are usually remnants of cell walls, seeds or stems. Grape and olive skins have been widely used in mycotoxin adsorption. Grape pomace is a result of the vinification process and consists of the remains of the pulp, seeds or skins after pressing or fermentation (Vázquez et.al, 2022). These residues usually contain phenolic compounds, carbohydrates, fibers, fats, proteins, vitamins and minerals. Results from in vitro studies conducted on mycotoxins, grape skins showed promising results in the adsorption of ZEN, AFB1 and OTA (Greco et.al, 2019. This adsorption property of the grape residues is not due to the amount of tannins present in their composition, but to the phenolic components and fibers included, which are effective more in the adsorption of aflatoxins (Vázquez et.al, 2022). The application of these biological agents is affected by several parameters such as pH conditions, the presence of enzymes, bile salts and contact time, which affect the adsorption of toxins. For example, changes in pH when using grape powder can to reflect mycotoxin absorption process: AFB1 and ZEN adsorption by grape pomace was stable in the pH range of the monogastric digestive system, while pH changes can affect FB1 and OTA adsorption to some extent (Aguilar et.al , 2021). Finally, the adsorption of mycotoxins such as AFB1 and ZEN from grape fruits occurs through multiple hydrophobic interactions at similar affinity sites. This adsorption mechanism varies depending on the material used, and the absorption of mycotoxins may also vary depending on the original type of grape from which the residues are derived, for example white grape skins are the most effective in absorbing mycotoxin toxins compared to red grape skins. . Other types of pomace that have been studied for their in vitro mycotoxin adsorption capacity include olive, blueberry and cherry pomace (Aguilar et.al, 2021). 3. Adsorbent dose According to reports on the adsorption of AFB1, ZEN and OTA, increasing the dose of the biosupernatant or residues improves the adsorption of the mycotoxin, which results Increased toxin adsorption sites (Aguilar et.al, 2021). 4. The role of pH Environmental pH is a key factor that directly affects mycotoxin adsorption. The pH parameter changes the charge distribution over a surface absorption, thereby affecting the equilibrium and kinetic reactions of the adsorption process. As a result of the frequent pH changes that occur Throughout the digestive system of animals and humans, the biosorbent must be effective in retaining mycotoxins in several cells during the food aisle. Due to pH characteristics or conditions, as well as contact time, the gut is where most mycotoxin absorption occurs. (Aguilar et al, 2021). 5. Exposure in time Toxin absorption increases with exposure time. However, rapid and balanced adsorption of mycotoxins presented by agro-residues Industrialization indicates the potential of using this matrix to reduce the bioavailability of toxins in the gastrointestinal tract (Aguilar et al, 2021). A study conducted on banana peel found that the adsorption process occurred in less than 10 minutes, with maximum adsorption occurs within 15-30 minutes, however, there was no change in adsorption after 30 minutes of interaction (Shar et.al, 2016). In conclusion, the use of agro-industrial residues as natural adsorbents shows promising results In the control of mycotoxins in animal production. However, it is important to consider factors that may affect adsorption capacity, such as particle size, dosage, pH and contact time. Furthermore, you can improve the The absorption capacity of these substances by physical or chemical processes, which offer potential solutions to reduce the harmful effects of mycotoxins.