LEADING ANIMAL HEALTH PRODUCTS DISTRIBUTOR

What is the advantage of giving medications to poultry during their growth until slaughter and consumption ?

During the industrial raising of poultry, they are sometimes given different medications. These medications are given in calculated and precise doses according to veterinary instructions, and they bring several important advantages:

1. Maintaining the health of the poultry

The medications help prevent diseases and infections that can spread quickly in crowded coops. When the chicken is healthy, it grows better, stronger, and reaches the desired weight faster.

2. Preventing disease outbreaks in the entire flock

If one chicken gets infected, the disease can spread to all the others. Giving medications (for example, preventive drugs or antibiotics when needed) helps prevent widespread infections that could cause signific

ant economic damage and even high mortality.

3. Protecting public health

When chickens reach slaughter while they are healthy, the meat they provide is of better quality and safer to eat. If a chicken is sick, the disease or bacteria may be transferred to the person who eats its meat, so it is important to keep them healthy during growth.

4. Improving meat quality

A chicken that grows while it is sick or weak might have lower meat quality. Healthy

chickens produce better, tastier meat that also stays fresh longer on store shelves.

5.Maintaining the farmer’s profitability

In the end, the health of the poultry also affects the farmers’ financial situation. When medications keep the chickens healthy, fewer die, and the farmer does not lose money on chickens that did not reach market size.

In summary:

Giving medications to poultry during their growth is done to keep them healthy, prevent diseases, ensure high-quality and safe meat for consumers, and maintain the farmer’s profitability. All medication use is under veterinary supervision, with strict waiting periods before slaughter to make sure no medication residues remain in the meat we eat.

Urinary tract disorders in goats and sheep are not uncommon veterinary problems, especially in males (especially castrated males), due to the anatomical structure of the relatively narrow urinary tract. Below is an overview of the main disorders:

Common types of disorders

1. Urolithiasis (urinary tract stones)

Very common, especially in castrated rams and goats.

The stones are caused by a diet rich in grains, calcium-phosphorus imbalance, magnesium deficiency or insufficient drinking.

The stones mainly get stuck in the thin penis and in the urethral process area.

Signs: lack of urination, difficulty urinating/in drops, restlessness, kicks in the abdomen, bladder distension or rupture → peritonitis and death.

2. Urinary tract infection (UTI)

More rare, usually in females.

Caused by bacterial infection (E. coli, Corynebacterium, Proteus).

Signs: cloudy urine, unusual odor, fever, decreased appetite.

3. Urinary tract injuries and trauma

Can be caused by attempts to milk stones or after amputation/manipulation of the penis.

4. Other obstructions

Sometimes tumors or birth defects in the urinary tract can cause urinary disorders.

General clinical signs

No urination or scanty/urgent urination.

Restlessness, abdominal kicks, bladder neck swelling.

Decreased appetite, weakness, stooped posture.

In severe cases: abdominal swelling, bladder rupture, tremors and death.

Treatment

In the case of stones – emergency treatment: removal of the stones by amputation of the urethral process or surgical procedures (tube cystostomy).

Medications: painkillers, anti-inflammatories, antibiotics if necessary.

In phosphate stones – drinking acids (ammonium chloride) to change the pH of the urine.

Prevention

Maintaining the correct calcium:phosphorus ratio (2:1) in the diet.

Adding salt (NaCl) to encourage drinking.

Limiting grains in the diet, providing quality forage.

Providing clean, constantly available water.

Preventive use of ammonium chloride in grain-rich feed.

1. Urolithiasis (urinary tract stones)

This is the most common disorder, especially in neutered males.

Signs: difficulty urinating, dribbling only, restlessness, abdominal kicks, hunched posture, abdominal distension. In severe cases – bladder rupture and death. Treatment: Release of obstruction by amputation of the urethral process, sometimes surgery (tube cystostomy), painkillers and anti-inflammatory drugs. In some cases, ammonium chloride is added to the solution. Prevention: Correct balance of calcium-phosphorus ratio (2:1), reduction of grains, always providing clean water, adding salt to encourage drinking, and sometimes ammonium chloride as a permanent supplement.

2. Urinary tract infections (UTI)

Less common, more common in females.

Signs: cloudy urine, unusual odor, pain when urinating, decreased appetite, sometimes fever. Treatment: Appropriate antibiotics (according to culture), anti-inflammatories, maintaining hygiene. Prevention: Maintaining a clean environment, clean water, avoiding stress and overcrowding in the cage.

3. Trauma and injuries

Can be caused by manipulation of the penis, external injuries, or unsuccessful attempts to release stones. Signs: Bleeding, swelling, severe pain, difficulty urinating.

Treatment: Rest, painkillers, sometimes surgical repair.

Prevention: Careful treatment, prevention of injuries.

4. Congenital obstructions or tumors

Relatively rare, but does exist. Signs: Similar to stones – difficulty urinating, lack of urine, swelling. Treatment: Usually surgical. Prevention: There is no real prevention, other than monitoring and early diagnosis.

In short – the main and most dangerous problem is urinary tract stones, and all other disorders are much less common.

Here is a guide to first aid in the field in case you see a goat or ram that is unable to urinate (suspected urinary tract obstruction):

What to do immediately:

1. Separate the animal from the herd – keep it quiet, as restlessness makes the stress worse.

2. Check vital signs – is it hunched over, trying to urinate in vain, is there any swelling in the abdomen or genitals.

3. Prevent access to dry or concentrated food – do not give grains or high-protein food, as this will make it worse. Always have water available.

4. Do not try to push a catheter into the urethra – in sheep and goats the urethra is very narrow, and attempting to do so can cause damage and rupture.

5. You can give a painkiller if you have one (for example, a veterinary NSAID that is used in the farm – flunixin, meloxicam, in surgery with a veterinarian). This does not open the blockage, but reduces suffering and inflammation.

6. Call a vet immediately – this is a life-threatening problem. If the bladder ruptures, the chances of saving the animal are greatly reduced.

What not to do:

Do not push a tube or metal object into the urethra to try to open it.

Do not wait until “it will go away on its own” – it will never resolve on its own.

Do not give laxatives or “popular” substances – they will not help and may be harmful.

What the vet will do:

Will check if it is possible to amputation the urethral process (the very narrow tip of the penis where stones usually get stuck).

In more severe cases – will perform a tube cystostomy (catheterization of the bladder through the abdominal wall).

Will give anti-inflammatory treatment, antibiotics and nutritional correction afterwards.

The prevention of urinary tract stones (the number 1 cause of urinary tract problems in goats and sheep) depends mainly on the composition of the diet. Here are guidelines for a preventive daily diet:

Nutritional principles

1. Correct calcium:phosphorus ratio – always maintain a ratio of at least 2:1 in favor of calcium. Excess phosphorus (which comes mainly from seeds and centers) greatly increases the risk of stones.

2. Preference for roughage – high-quality hay (alfalfa/clover/cereals) as the basis of the diet.

3. Limit grains and concentrates – if they must be given (e.g. for fattening), no more than 0.5–1% of body weight per day.

4. Clean, always available water – lack of drinking increases the risk of crystal formation.

5. Added salt (NaCl) – about 2% of the feed ration or spreading a salt lick → causes the animal to drink more.

6. Ammonium chloride (NH₄Cl) – a particularly important supplement in rams/goats, as it acidifies the urine and dissolves phosphorus crystals.

Preventive dose: 0.5%–1% of the concentrated feed (approximately 2–4 grams per day for an adult goat).

Example of a daily preventive diet (adult lamb/ram weighing 60 kg)

Alfalfa hay or high-quality grain: free (ad libitum).

Grains/concentrates: up to 300–400 g per day (no more), preferably a balanced mixture.

Salt (NaCl): sprinkle on a salt shaker or mix in food (about 5–10 g per day).

Ammonium chloride: 2–4 g per day for prevention, mix in concentrates.

Fresh water: free access 24/7.

Other important points

It is advisable not to castrate very young males – castration causes the urethra to remain narrower, which increases the risk of blockages.

In fattening diets (with a lot of grains) it is mandatory to add ammonium chloride.

Alfalfa alone (rich in calcium) can cause calcium stones – so it is better to also combine cereal hay.

The nutritional requirements are truly different between dairy goats and fattening herds (sheep/goats), so the strategy for preventing urinary tract stones should also be adapted.

Dairy Goats

Dairy goats consume much more energy and protein, so the food must be very balanced.

Daily basis: High-quality alfalfa hay – free range (an excellent source of calcium).

Cereal hay (such as dry green wheat/barley) – to maintain the correct calcium:phosphorus ratio. Milk mixture – adjusted according to milk yield (between 0.5 and 1.5 kg per day per goat, depending on yield). Free salt (NaCl) supplement – ​​in the lick or feed.

Ammonium chloride – 2–4 grams per day for an adult goat, especially if receiving a lot of mixture. Plenty of clean water – very essential for excreting excess minerals.

Important note: In dairy herds, the problem is usually less severe in females (short and wide urethra), but males raised in dairy herds may suffer if they receive a milk mixture without the correct balance.

Fattening herds (sheep and goats for fattening)

Here the risk is much higher, because the diet is rich in grains to achieve rapid weight gain.

Daily basis:

High-quality cereal hay – fiber must be maintained for proper rumen function.

Grains and mixtures – 1.5–2% of body weight per day (for example: a 40 kg lamb will receive about 0.8 kg of mixture per day).

Ammonium chloride – regularly added to concentrates (about 0.5–1% of the mixture, about 5–10 grams per day for an adult lamb/goat).Free salt – either in a liquid or in a mixture.

Fresh water is always available.

Important note: In fattening herds, castrated males are at the highest risk of stones, due to the combination of many testicles + a narrow urethra.

Brief Summary

In dairy goats – the emphasis is on balancing protein and minerals, while maintaining a calcium:phosphorus ratio and preventing excess phosphorus.

In fattening herds – the emphasis is on grain restriction, adding fixed ammonium chloride, free water, and salt blik.

*It is always advisable to consult a qualified veterinarian.

Sheep and goats have quite a few digestive system disorders, some more common and some rare but life-threatening. I will list the main ones by group:

1. Fermentation disorders and gas accumulation (bloat)

Acute rumen tympany: gas accumulation in the anterior stomach, especially after eating green legumes (alfalfa, clover).

Signs: swelling on the left side, difficulty breathing, drooling, restlessness.

Emergency – may result in rapid death.

2. Rumen acidosis

Caused by excessive consumption of concentrated grains (corn, barley).

Causes damage to the rumen flora, severe diarrhea, dehydration, lameness (due to laminitis).

3. Intestinal parasites

Coccidiosis: Common in lambs and young calves, causes bloody diarrhea, dehydration and growth retardation.

Roundworms (Strongyles, Haemonchus): Cause anemia, weight loss, edema in the jaw (“bottle jaw”).

Requires preventive deworming and regular fecal examinations.

4. Stomach and intestinal infections

Enterotoxemia ("rich feed disease"): An acute disease caused by Clostridium perfringens after a sudden dietary change. Causes sudden death. There is a preventive vaccine.

Salmonella / E. coli: Can cause acute diarrhea, especially in young goats.

5. Obstructions and mechanical disorders

Foreign body ingestion ("hardware disease") - sometimes by swallowing metal objects.

Intestinal obstruction - relatively rare but does exist.

6. Liver and gallbladder diseases

Liver damage due to parasitic load (fasciola hepatica).

Causes weight loss, anemia and weakness.

7. Nutritional and functional problems

Lack of fiber in the diet → decreased rumen activity, decreased rumen elevation.

Excess protein → foamy diarrhea, decreased milk quality.

General prevention and treatment:

Maintaining a balanced diet: combining fiber with concentrates.

Gradual transition from one type of food to another.

Routine vaccinations against clostridia.

Regular deworming according to the region and infestations.

Clean, fresh water at all times.

1. Acute fermentation and gas accumulation (bloat)

Signs: swelling on the left side, difficulty breathing, drooling, restlessness.

Causes: eating green legumes (alfalfa, clover) or a very rich mixture.

Prevention/treatment: giving dry hay before grazing, anti-foam additives, in case of emergency – a veterinarian to release gases.

2. Acidosis

Signs: Acidic diarrhea, weakness, lack of appetite, sometimes lameness.

Causes: Excess grain consumption (corn, barley) or sudden transition from a hay-based diet to concentrates.

Prevention/Treatment: Gradual transition in diet, administration of bicarbonate/baking soda, balance between fiber and grains.

3. Intestinal parasites

Coccidia: bloody diarrhea, weight loss, weakness in young animals.

Worms (such as Haemonchus): anemia, pale conjunctiva, swelling of the jaw ("bottle under the jaw"), decreased milk production.

Prevention/treatment: regular deworming according to stool tests, proper pasture management (rotation, drying).

4. Gastrointestinal Infections

Enterotoxemia (Clostridium): Sudden death or acute diarrhea after a sudden change in diet.

Salmonella / E. coli: Acute diarrhea, dehydration, fever.

Prevention/Treatment: Clostridium vaccination, good water and food hygiene, supportive care and fluids.

5. Obstructions and Mechanical Disorders

Foreign body ("Hardware disease"): pain, decreased appetite, decreased output.

Intestinal obstruction: lack of bowel movements, abdominal pain (colic).

Prevention/Treatment: Avoid exposure to metal debris, urgent veterinary care in case of obstruction.

6. Liver Disease

Fasciola: Weight loss, anemia, edema, general weakness.

Prevention/Treatment: Antiparasitic treatment appropriate for the area, prevention of grazing in infected wetland areas.

7. Nutritional and Functional Problems

Deficiency of fiber: decreased rumen elevation, improper digestion.

Excess protein: foamy diarrhea, decreased milk quality.

Prevention/Treatment: Balanced diet with sufficient dry hay, adding minerals and vitamins as needed.

"What to do in the field" guide

1. Swelling on the left side + difficulty breathing

Probably bloat (gas buildup in the stomach)

What to do immediately: stop feeding, move the animal, massage the left side. If it doesn't get better – call the vet (it may be necessary to release gas with a tube or trocar).

2. Acidic diarrhea, pungent odor, sudden weakness

Probably acidosis

What to do immediately: stop concentrates, give lots of dry hay, add baking soda to water/food. If severe – veterinary treatment.

3. Bloody diarrhea in lambs or young goats

Probably coccidia

What to do immediately: Isolate the patient, maintain dryness and hygiene, treat with anti-coccidia medication (as recommended by a veterinarian).

4. Pale conjunctiva + swelling under the jaw ("bottle") + weight loss

Probably worms in the intestines (mainly Haemonchus)

What to do immediately: Immediate deworming (in consultation on the type of preparation), examination of the entire herd, proper grazing management.

5. Sudden death or acute diarrhea after a change in food

Probably Enterotoxemia (Clostridium)

What to do immediately: In acute cases – it is difficult to save. Therefore, it is most important to routinely vaccinate the entire herd.

6. Acute diarrhea + fever + weakness

Possible Salmonella / E. coli

What to do immediately: Isolate, provide fluids and support, call the vet for antibiotic treatment.

7. Gradual weight loss + pallor + edema

Possible liver disease (malaria)

What to do immediately: Appropriate anti-parasitic treatment, avoiding grazing in swamps/infected areas.

8. Decreased rumen elevation, irregular digestion, decreased milk production

Probably lack of fiber in the diet

What to do immediately: Add good quality dry hay, balance the concentrate menu.

General field tip:

If there is acute swelling → suspect bloat.

If there is bloody diarrhea in young animals → coccidia.

If there is anemia + "bottle" in the jaw → worms.

If there is sudden death after a new mixture → Clostridium.

Respiratory disorders in goats and sheep are a relatively common problem in dairy farms and barns, especially in young animals or in situations of overcrowding, poor sanitation, crowding, weather changes and stress.

They can be acute (a rapid and life-threatening illness) or chronic (a long-term problem).

Main causes:

1. Infectious diseases (bacteria, viruses, parasites):

Pasteurellosis (Pasteurella multocida, Mannheimia haemolytica) – acute pneumonia, very common, sometimes accompanied by high mortality.

Mycoplasma ovipneumoniae – causes chronic pneumonia, persistent cough, weight loss.

Parainfluenza type 3 (PI3), Adenovirus, RSV – viruses that weaken the respiratory system and prepare the ground for bacterial infections.

Parasitic pneumonia – mainly caused by lungworms (Dictyocaulus filaria). Causes chronic cough, weight loss and performance impairment.

Toxoplasma and Chlamydia can rarely cause lung damage.

2. Environmental factors:

Poor ventilation, high humidity, wet bedding and high ammonia.

Sharp temperature changes (transitions from heat to cold).

High animal density.

Poor nutrition and nutritional deficiencies (e.g. vitamin A deficiency, selenium).

3. Additional non-infectious factors:

Inhalation of a foreign body (e.g. food entering the respiratory tract).

Traumatic injuries to the chest.

Allergies or environmental sensitivities are rarer.

Clinical signs:

Hard breathing, sometimes with mouth open.

Cough (dry or moist).

Nasal discharge (clear → purulent).

Fever, depression, loss of appetite and weight.

Wheezing, wheezing or abnormal noises from the lungs.

In chronic diseases – slow growth, dull coat, low performance.

Diagnosis:

Clinical examination (lung auscultation).

Blood count, cultures and pathogen isolation.

Chest X-ray/ultrasonography in some cases.

Stool tests for lungworms.

Treatment:

Broad-spectrum antibiotics (tetracyclines, macrolides, flurbiconazole – according to sensitivity).

Anti-inflammatories to reduce fever and improve feeling.

Antiparasitic treatment (e.g. ivermectin) if lungworms are involved.

Improving housing conditions – ventilation, dryness, reducing crowding.

Providing supportive vitamins and minerals.

Prevention:

Vaccines – available against Pasteurella, PI3 and other diseases (depending on the region).

Proper management: good ventilation, dry bedding, reduced load, avoiding sudden changes.

Preventive worming treatment according to a veterinary program.

Isolation of sick animals to prevent infection.

Pasteurella / Mannheimia (acute bacterial pneumonia):

Signs – fever, cough, purulent nasal discharge, labored breathing, rapid mortality.

Treatment – ​​broad-spectrum antibiotics, anti-inflammatories, improved housing conditions.

Mycoplasma ovipneumoniae (chronic pneumonia):

Signs – persistent cough, labored breathing, weight loss, and poor growth.

Treatment – ​​antibiotics (usually macrolides or tetracyclines), improved nutrition, and ventilation.

Respiratory viruses (PI3, RSV, Adenovirus):

Symptoms – mild fever, cough, clear runny nose → may become secondary bacterial infection.

Treatment – ​​supportive only (no antibiotics against viruses), prevention by vaccination and stress reduction.

Lungworms (Dictyocaulus filaria):

Symptoms – prolonged dry cough, weight loss, weakness, sometimes wheezing.

Treatment – ​​antiparasitics (ivermectin, levamisole), improved grazing and reduced environmental pollution.

Environmental factors (poor ventilation, wet bedding, crowding, temperature changes):

Signs – slight coughing, nasal irritation, labored breathing, especially in large groups.

Treatment – ​​improving conditions: drying the bedding, good ventilation, reducing animal crowding.

Nutritional deficiencies (vitamin A, selenium):

Signs – tendency to recurrent infections, general weakness, slow development.

Treatment – ​​supplementing with vitamins and minerals as needed

A list of practical steps to prevent respiratory disorders in goats and sheep:

Proper ventilation: Ensure there is good air circulation in the pen, without direct wind on the animals.

Dry and clean bedding: Frequent replacement of straw/sawdust to prevent moisture and ammonia.

Low density: Do not crowd too many goats/sheep in a small space – this reduces stress and infection.

Vaccinations: Carry out a vaccination program against Pasteurella and respiratory viruses (according to the recommendation of the veterinarian in the area).

Lungworm prophylaxis: Administer regular antiparasitic medications according to a schedule.

Stress reduction: Avoid unnecessary transportation, clipping/treatments during extreme heat or cold.

Isolate sick animals: Immediately remove individuals with a cough or fever to prevent infection.

Balanced diet: Provide quality feed, clean water, and vitamin-mineral supplements (especially vitamin A and selenium).

Regular monitoring: listen to breathing, check nasal discharge and cough, especially during transitional seasons.

A quick protocol for identifying and responding when you encounter a goat or sheep with signs of respiratory distress:

Step 1 – Early Detection

Watch for coughing, heavy breathing or chest noises.

Check for nasal discharge (clear or purulent).

Measure temperature – above 40°C is considered fever.

Look at general condition: appetite, alertness, weight loss.

Step 2 – Isolation

Move the animal to a separate, ventilated area.

This prevents infection and allows for easier tracking.

Step 3 – Initial Treatment (under the direction of a veterinarian)

If there is fever/inflammation – administer broad-spectrum antibiotics (as recommended).

If lungworms are suspected – administer antiparasitic (ivermectin/levamisole).

Supportive care – water available, vitamin supplements, stress prevention.

Anti-inflammatories/pain relievers if necessary.

Step 4 – Monitoring

Daily check of breathing, appetite and temperature.

If there is no improvement within 48 hours → return to the vet.

If acute signs appear (open-mouth breathing, collapse, blood in the discharge) → immediate emergency treatment.

Step 5 – Group Prevention

Check the rest of the flock – respiratory disease sometimes breaks out in groups.

Improve ventilation, bedding and nutrition for all.

Consider vaccination or preventative treatment if there is more than one case.

Newborn lambs (and in the first few days of their lives) are very susceptible to disease – mainly due to an underdeveloped immune system and dependence on colostrum (first milk from the mother). Here are the main diseases and problems:

Common diseases and problems in soft patches:

1. Failure of passive transfer

If the lamb does not suckle enough colostrum in the first 24 hours, it is vulnerable to infections.

A major cause of premature mortality.

2. Sepsis (Septicemia)

Bacterial infection of the blood, usually due to immunodeficiency or poor hygiene conditions.

Signs: weakness, fever, unwillingness to breastfeed, sometimes diarrhea or arthritis.

3. Neonatal diarrhea (“Scours”)

Caused by E. coli, rotavirus, cryptosporidium.

Signs: watery diarrhea, dehydration, weight loss, rapid death if untreated.

4. Neonatal Pneumonia

Is sometimes caused by exposure to cold, dampness, or bacterial/viral infections.

Signs: Shortness of breath, cough, loss of appetite.

5. Tetanus

Infection with Clostridium tetani, especially after umbilical cord cutting or castration.

Causes severe muscle spasms and death.

6. Infectious myositis (Blackleg / Clostridial myositis)

Rare but fatal. Occurs due to Clostridium bacteria that attack the muscle.

7. Necrobacillosis Umbilical (“Navel ill”)

An infection of the umbilical cord that does not heal properly.

May develop into sepsis or arthritis.

8. Hypothermia and Hypoglycemia

Non-infectious but critical problems. Weak lambs, in low temperatures or with a lack of milk, quickly cool down and lose energy.

Prevention is especially important:

Giving quality colostrum within the first few hours.

Disinfecting the umbilical cord with iodine.

Maintaining hygiene during birth and in the barn.

Vaccinating the mothers against clostridia before calving.

Warm and dry conditions are good for the lambs.

Congenital diseases in sheep and goats are health problems that manifest at or near birth, and are often caused by genetic defects, poor maternal nutrition during pregnancy, or problematic environmental conditions. Some diseases are genetic and hereditary, and some result from nutritional imbalances or exposure to toxins during pregnancy.

Here are some of the most common and well-known:

Congenital genetic diseases and syndromes

1. Enzootic ataxia / swayback

Caused by copper deficiency in the fetus.

Manifested by severe weakness, walking problems, tremors, and paralysis of the limbs.

2. Hereditary spongiform encephalopathy – rare, affects the nervous system.

3. Dwarfism

A genetic defect that causes short bones, skull and limb deformities.

4. Cryptorchidism

One or both testicles that do not descend into the scrotum.

Affects the ram’s fertility.

5. Cleft palate

A deformity in the structure of the jaw and palate.

Causes difficulty in sucking and recurrent respiratory infections.

6. Skeletal anomalies – such as deformities of the limbs, spine or joints (arthrogryposis).

Congenital diseases due to nutritional or environmental imbalance

1. Selenium / Vitamin E deficiency (white muscle disease)

Causes muscle atrophy, severe weakness, and sometimes sudden death.

2. Iodine deficiency

Goats and sheep are born with an enlarged thyroid gland ("goiter").

Lambs may be born dead or very weak.

3. Vitamin A deficiency during pregnancy

Can cause congenital blindness or skull and bone defects.

4. Intrauterine poisoning (i.e. due to the mother's consumption of poisonous plants)

causes deformities in the bones, limbs, and nervous system.

Diagnosis and Prevention

Diagnosis: Clinical examination of the newborn, dietary history of the mother, and sometimes laboratory or pathology tests.

Prevention:

Providing mineral and vitamin supplements to the mother during pregnancy (mainly copper, selenium, iodine, and vitamin E).

Avoiding poisonous plants in the pasture.

Using healthy breeding stock and avoiding close mating (consanguineous).

In organic chicken farming, there are very clear restrictions on medication, especially around the use of antibiotics and synthetic substances. The idea is to maintain the health of the birds through natural preventative methods, and to avoid as much as possible drug treatments that interfere with the "organic" standard.

The main principles:

1. Prevention before treatment – ​​great emphasis on proper living conditions: space for movement, good ventilation, balanced organic diet, clean water, permitted vaccinations, and natural supplements (herbal remedies, probiotics).

2. Antibiotics – usually completely prohibited in organic farming. In exceptional cases of life-threatening conditions for the chicken, antibiotics can be given, but then the chicken is no longer considered “organic”.

3. Other veterinary drugs – some of them are permitted in limited use, provided there is no natural or homeopathic alternative. It is important to check each substance against local organic regulations (in Israel – according to the Ministry of Agriculture and the “Agrior” label).

4. Vaccines – permitted and even recommended, especially against common diseases in chickens (such as Newcastle, Gumboro, Mark).

5. Waiting period – For any permitted drug treatment, there is a “waiting period” twice that of conventional chickens, before the eggs or meat can be marketed as organic.

6. Common natural supplements – garlic, oregano, apple cider vinegar, natural minerals, plant-based vitamins – all of which are used to improve immunity and reduce the need for medication.

The bottom line: In organic chicken farming, medications are a last resort, and almost always when a synthetic medication is required, the chicken is no longer considered organic.

Feeding schedule for dairy calves (general recommendation)

Day 1:

Give colostrum (first milk) – at least 4 liters in the first 6 hours.

Until 24 hours of age – another 2–3 liters of high-quality colostrum.

Week 1–2:

Milk/milk replacer: 4–6 liters per day (in two meals).

Fresh water always available.

Offer dry “starter” (calf mixture) in small quantities.

Week 3–4:

Milk/replacer: 6–8 liters per day.

Free calf mixture (target – 0.3–0.5 kg per day).

Good quality dry hay in small quantities.

Week 5–6:

Milk: 6 liters per day.

Mixture: 0.7–1 kg per day.

Free hay.

Week 7–8 (weaning phase):

Milk – gradually reduce until completely stopped around 8 weeks of age.

Mixture: at least 1.5–2 kg per day before full weaning.

Free hay.

Important points:

Fresh water is always available.

Weaning is done according to mixture consumption (and not just by age).

Do not switch too quickly – to avoid digestive problems.

What are the early signs of viruses in a chicken coop and what are the suggested solutions?

Industrial poultry farming is conducted in a disease-prone environment, where various viruses can quickly break out and affect the entire flock. Early identification of disease symptoms is critical to prevent widespread spread and minimize economic and health damage.

Early signs of viruses in the chicken coop

In the initial stage, you can notice a decrease in the chickens' general activity, lack of appetite, and a tendency to withdraw. Later, physical changes such as ruffled feathers, swelling in various areas of the body, watery or red eyes, and respiratory tract discharge are discovered.A decrease in weight gain, decreased egg production, and a higher than normal mortality rate are also suspicious signs. Viruses often affect the respiratory or digestive systems, so breathing problems, coughing, diarrhea, or blood in the feces are observed.

Proposed solutions

Treatment begins with the rapid isolation of an infected or suspected flock to prevent widespread spread to other coops. Vaccinations are a key line of defense, with a vaccination program tailored to the type of viruses prevalent in the area. In addition, maintaining high sanitation conditions in the coop – frequent cleaning, continuous disinfection, temperature regulation and ventilation – reduces the level of exposure to viruses.

At the same time, nutritional supplements and vitamins strengthen the birds' immune system and help them cope with pathogens. In the event of a serious outbreak, a professional veterinarian should be involved to determine the course of action, and sometimes controlled destruction of an infected flock is necessary to protect the entire farm.

Mandatory vaccinations for poultry and what happens in the event of infection

Maintaining the health of the flock is a necessary condition for the success of a poultry farm and the main tool in preventing diseases is the provision of mandatory vaccinations against viruses and bacteria that may cause health and economic damage.

Mandatory vaccinations in Israel

Newcastle Disease – a serious virus that affects the respiratory, digestive and nervous systems. Mandatory vaccination with booster doses

Infectious bronchitis IB – a respiratory virus that also affects fertility. Usually vaccinated together with Newcastle

Gambora IBD – damage to the immune system in young birds. Vaccination at 2–3 weeks of age

Brook – causes tumors and paralysis. Vaccination on the day of hatching

Fowl pox – a virus spread by mosquito bites or direct contact Vaccination at 6–8 weeks of age

Salmonella – a bacterium that is also dangerous to humans Vaccination in several doses, mainly in laying hens

If the flock contracts a disease

Despite vaccinations, flock infections may occur due to virulent viruses, outdated vaccinations, or poor housing conditions.

In such cases, a sharp decrease in weight and egg production is observed, and in severe diseases, mortality rates may be high. Quarantine and isolation should be carried out to prevent spread, and in viral diseases, only supportive care can be provided. In particularly severe cases, the flock may need to be destroyed.

How does morbidity in dairy cows affect the amount of milk production?

Disease in dairy cows is considered one of the main problems in the dairy industry, with a direct and significant impact on milk production levels. When a cow is sick – whether it is mastitis, digestive diseases, fever or problems with the functioning of the reproductive system – her body invests many resources in dealing with the disease, instead of producing milk.

During illness, the immune system is hyperactive, and the cow may eat less, leading to a decrease in energy and protein intake – two essential components for milk production. The result is a significant decrease in milk yield, which can sometimes persist even after the cow recovers.

In addition, there are diseases that directly affect the quality of milk – such as bacterial infections in the udder – and cause the milk to be rejected for marketing. On many dairy farms, chronic disease even leads to premature removal of cows from the herd, which leads to ongoing economic loss.

In conclusion, maintaining the health of dairy cows is not only a matter of animal welfare, but also a critical component of a stable, high-quality and profitable milk supply. Regular monitoring, balanced nutrition, sanitary conditions and preventive veterinary care are all essential to reducing morbidity and maintaining high milk yields.

Common Diseases in Chickens and Effective Treatments

Chickens are vulnerable to various diseases that affect their health and productivity. Marek's disease, for example, is a virus that causes paralysis mainly in chicks and can be prevented with a vaccine given immediately after hatching. Newcastle disease is highly contagious, causes breathing difficulties and reduced egg production, and is preventable with regular vaccinations.

Other common diseases include infectious bronchitis, which affects the respiratory system, and coccidiosis, which causes severe diarrhea and is treated with medications in water or feed. Fowlpox is also common, spread by mosquitoes, but can be prevented with vaccination and mosquito control.

Bacterial diseases like salmonella require strict hygiene and antibiotic treatment as prescribed by a veterinarian. The best way to keep chickens healthy is timely vaccination, regular cleaning, clean food and water, and close monitoring by a vet.

The Mortality Rate in Chicken Coops With and Without the Use of Medication

In the poultry industry, the use of medication during the growing cycle is highly significant.

These medications are often administered to treat various diseases or to prevent outbreaks of contagious illnesses in the coops.

When chickens receive appropriate medical treatment, the mortality rate in the coop decreases significantly, due to the body’s ability to cope with diseases and harmful bacteria.

Medications maintain the health of the flock, prevent widespread infections, and preserve the overall quality of life of the birds.

On the other hand, when no medication is used at all, especially in cases where there is a disease or a risk of infection, the mortality rate in the coop can rise sharply.

This occurs because, without proper medical treatment, diseases spread rapidly among the chickens, leading to the weakening of the entire flock and, eventually, widespread mortality.

Therefore, veterinary supervision and the prudent use of medication, according to need and the severity of the health situation in the coop, are of great importance in order to maintain low mortality rates and to ensure the welfare and health of the chickens.

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.

- 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!!

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.

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).

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.