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31

Book / Characteristics of Various Drugs used in Avian Species

« Last post by LamiyaJannat on May 27, 2021, 01:20:42 PM »

Characteristics  of  Various  Drugs used in Avian Species

http://avianmedicine.net/wp-content/uploads/2013/03/18.pdf

32

Antiprotozoal or Anticoccidial / Antiprotozoal Drugs

« Last post by LamiyaJannat on May 27, 2021, 12:48:50 PM »

Antiprotozoal

Antiprotozoal defines as drugs acts on protozoa which are single-cell organisms. several types of protozoa causing disease in poultry. Coccidiosis is the most common protozoal disease in poultry.
The life cycle of avian coccidia and the effects of anticoccidial drugs on the life cycle. All drugs are effective during the asexual cycle only, except that diclazuril is also effective during the sexual cycle.
Second generation schizonts seem to play an important role in gut damages; drugs affecting this stage can be used to treat an outbreak.

Application

Poultry is the most of the anticoccidial drugs discussed in this section and is used in chickens.
(a) Broilers are not vaccinated against coccidia because the latent infection may retard growth.
(b) Layers are vaccinated against coccidia. Outbreaks are usually treated with a sulfonamide or diclazuril on an as-needed basis.

Drugs List

Maduramycin For Poultry

Maduramycin
Maduramicin ammonium is a monovalent monoglycoside polyether ionophore that consists of 90% ammonium salt that is a fermentation product of Actinomadura yumaense. It can be grade as two types Alpha meduramycin & beta maduramycin from its definition.

Chemical Properties
Alpha meduramycin defined as that consisting of 90% ammonium salt of a polyether monocarboxylic ionophore with -OH3 at the C5 of the ring Beta maduramycin define as that consisting of the ammonium salt of a polyether monocarboxylic ionophore with –OH group at C5 of the ring.
It is (alpha & beta) does not adversely affect egg production or egg quality.  Its causes adverse effect on growth and feathering may occur at higher doses >6mg/kg (≥6 ppm).

Mode of Action
Its interfering with the transport of K+ & Na+ ions through cell membrane → influx of positively charged ions (H+) → upset of osmotic balance  Causing disturbances mitochondrial function of intracellular coccidian (Selective E. spp.)
Endogenous at sages’ effect of Emeria species
It induces anticoccidial effect on asexual stages sporozoite, trophozoite & merozoite of selective Emeria spp of poultry.

Indication
It used as a coccidiostat for the prevention & control of coccidiosis thereby increased feed efficiency, improved weight gain, reduced the number of gut lesions & mortality in poultry. It is moderately active against gram-positive bacteria.

Pharmacokinetics
Maduramycin ionophores are metabolized in the liver and are excreted mostly into bile and feces as parent compounds and metabolites in all species. It rapidly eliminated from body two-third metabolites excreted within 2 days & total 90-95% excreated within seven days that show on the animal study.

Dosages
Meduramycin is effective for the prevention of coccidiosis @ 5mg/kg body weight.  But in higher dosages, e.g 15 mg/kg body weight may cause significant weight gain depression & 8-14 mg/kg causes reduced feed efficiency in poultry. It may cause fatal toxicity in oral dosages.
For the control & prevention of coccidiosis, it may use in replacement pullets up to 16 weeks of age; turkey poults up to 12 weeks of age.

Toxicity
Maduramycin not teratogenic, Foetotoxic, carcinogenic in an animal study. It may incompatible with Tiamulin at a higher dosage above >15-20 mg/kg body weight.

Contraindication
It is used only for the prevention of coccidiosis in broiler only not use in laying birds. It does to mix with other ionophores that causing mixing error & Ionic imbalance. It does not provide horse or other equine species which causing fatal toxicosis or somehow happened mortality.

Withdrawal period
For egg & meat 5 days. It is suggested that maduramicin is acceptable without risk for use in the poultry feed @ 5mg/kg body weight for the prevention & control of coccidiosis & fattening poultry subject to mention withdrawal period.

Storage
Maduramycin should be stored under 15 degrees Celsius. Protect from direct sunlight which became causes decreased activity of maduramycin.

Available for form
It’s available as 1% & 5% as feed coccidiostat in the market.

Salinomycin in Poultry

Salinomycin
Salinomycin is a monovalent polyether ionophore anticoccidial drugs & antibacterial properties that is a fermentation product of Streptomyces albus & carries sodiam ion (Na+). Salinomycin does not adversely affect egg production or egg quality.

Spectrum
Its act against coccidiosis associated Emeria spp & several gram-positive bacteria eg methicillin-resistant Staphylococcus aureus, staphylococcus epidermidis, Mycobacterium tuberculosis. Its acts as a anticanceral agent now a days. But not active against Fungi & mold.

Mode of action
salinomycin Na+ facilitate the transport of Na+ and H+ into cells, elevating intracellular Na+ and H+ concentrations. As a result, certain mitochondrial functions (e.g.substrate oxidations) and ATP hydrolysis are inhibited. Excess intracellular Sodium ion (Na+) concentrations accompanied by water can damage organelles as well of coccidia.

Endogenous stages effect of Emeria species
Salinomycin Na+ ionophores attack the first generation of trophozoites and schizonts.  Its active against sporozoites and early and late asexual stages of chicken.

Pharmacokinetics
Salinomycin Na+ ionophores are metabolized in the liver by cytochrome P450 enzymes, and are excreted mostly into bile and feces as parent compound and metabolites in poultry.
Following oral administration, residues are present only at very low concentrations in liver and muscle that fall below the limit of decision of the assay within 2 days in poultry.

Dosages
For prophylaxis treatment of coccidiosis 4-66g (0.004–0.0066%)/ton used in medicated poultry feed. But It is not for use with pellet binders such as bentonite clays causing severe toxicity in poultry.

Tiamulin Incompatibility
Tiamulin may interfere with the metabolism of salinomycin in chickens and cause weight suppression but not produce cardiovascular & skeletal muscle weakness in poultry. Tiamulin may interfere with the metabolism of salinomycin in chickens and cause weight suppression.

Toxicity
Salinomycin is highly toxic to turkeys at levels greater than 15g/ton and causes excessive mortality at the level recommended for use in chickens (60 g/ton).

Withdrawl Period
For meat & eggs o days.

Lasalocid in poultry

Lasalocid
Lasalocid is a not only carboxylic divalent polyether ionophore but also antibacterial & coccidiostst that is a mold fermentation product of Streptomyces lasaliensis. Its commonly used as a feed additives named lasalocid sodium (C34H53Nao8) in poultry worldwide.

Mode of action
Lasalocid Ionophores upset the osmotic balance of the protozoan cell by altering the permeability of cell membranes for alkaline metal cations. It also transports big cation called dopamine.

Endogenous stages affected of Emeria spp
Lasalocid sodium Ionophores act on against extracellular sporozoites, early tropozoite and merozoites.

Spectrum
Its acts as a broad spectrum antibacterial & coccidiostsat in poultry. It has a selective antibacterial activity in gram positive bacteria but Enteriobacteriace may naturally resistant. But it is many used coccidiostat in poultry.

Absorption
Lasalocid Ionophores absorbed orally but absorption is slower in from intestine in poultry. It is rapidly & extensively metabolized in liver & metabolites excreted through faces & bile.

Doasages
75-125g (0.0075–0.0125%)/ton medicated feed for prophylaxis of coccidiosis in poultry.

Adverse effect
Lasalocid sodium will stimulate water consumption and excretion resulting in a wet litter. With slight overdoses, it may cause depress weight gain in poultry.

Withdrawl period
For meat & eggs 3 days.

Polyether Ionophores: Resistance | Toxicity in poultry

Polyether Ionophores
It’s defined as natural & biologically active compound/ substances produced by fermentation of streptomyces or actinomadura. It destroys Emeria spp by inferring balance od most important ion specially sodium & potassium.

The polyether ionophore antibiotics were first discovered in the early 1950s and their anticoccidial activities were recognized in the late 1960s. Because of their broad spectrum of activity and the development of drug resistance to other agents, the ionophores gained widespread usage in the poultry industry soon after their introduction. by this time gradually Polyether ionophores showing their resistance & toxicity in poultry

Resistance
Because of the unique mode of action of ionophores, development of anticoccidial resistance to ionophores was difficult to produce under experimental conditions and slow to develop after clinical use in the field. In the mid to late 1980s, ionophore-resistant strains of chicken Eimeria spp & ionophore resistance is now common.
Cross-resistance between ionophores is common, although strain differences in coccidial response to specific ionophores have been demonstrated in poultry.
In general, resistance to a monovalent polyether ionophore confers some cross-resistance to other monovalent polyether ionophores, but susceptibility to monovalent monoglycoside and divalent polyether ionophores may be retained now a days.

Toxicity
Ionophores are potentially toxic for highly susceptible species in animal studies. Horses appear to be the most sensitive species, with a monensin LD50 of 1.4 mg/kg, compared with goats (LD50 26.4 mg/kg) and chickens (LD50 214 mg/kg).
Clinical signs occur from acute myocardial and muscle degeneration. Sweating, colic, and ataxia with hindlimb paresis/paralysis are also noted are commonly observed in poultry. Pathologically, focal degenerative cardiomyopathy, skeletal muscle necrosis, and congestive heart failure may be noted.
Ionophore toxicosis can be potentiated with concurrent administration of tiamulin, chloramphenicol, macrolides, sulfonamides, and cardiac glycosides in poultry.
Exposure of horses to ionophores is usually accidental, or resulting from horses gaining access to medicated feed, particularly through feed mill errors. Care should always be taken to prevent highly susceptible animals from gaining access to feeds containing these products.

Polyether Ionophores In Poultry

Polyether Ionophores
Polyether Ionophores defined as a natural & biologically active compounds/ substances produced by fermentation of streptomyces or actinomadura. It destroys Emeria spp by inferring balance of most important ion especially sodium & potassium. There are some drugs included in this class. It’s also called coccidiostat in an earlier time. It’s only used via poultry for controlling coccidiosis in poultry.

It was first discovered in the early 1950s, and their anticoccidial activities were recognized in the late 1960s. Because of their broad spectrum of activity and the development of drug resistance to other agents, the ionophores gained widespread usage in the poultry industry soon after their introduction. Most commonly used polyether ionophores generic name given below
Classification
It is classified by two class

a) Monovalent ionophores
It’s defined as Ionophoes that have valency one called Monovalent ionophores. eg monensin, narasin and salinomycin & Monovalent glycosidic ionophores (maduramicin and semduramycin)
Monensin
Salinomycin
Narasin
Maduramycin
Samduaramycin

b) Divalent ionophores
It’s define Polyether as Ionophoes that have valency two called Divalent ionophores
for example -Lasalosid
FDA approval
Polyether Ionophores
Monensin - 1971
Lasalosid - 1976
Salinomycin - 1983
Narasin - 1988
Maduramycin - 1989
Samduaramycin - 1995

Approved Dosages
Polyether Ionophores
In here % means drugs 100 gm feed, PPM means Parts per million
Monensin - 0.01–0.0121 %
Lasalosid - 0.0075–0.0125%
Salinomycin - 0.004–0.0066%
Narasin - 54–72g/T
Maduramycin - 5–6 ppm
Samduaramycin - 25ppm

Withdrawal Period
Polyether Ionophores
Monensin -00 days
Lasalosid -03 days
Salinomycin -00 days
Narasin -00 days
Maduramycin -05 days
Samduaramycin -00 days

Adverse Effect
Polyether sodium (Na+)  ionophores Increased intracellular Na+ concentrations will damage mitochondria and Golgi body into the host.
Intracellular Na+ further exchanges for extracellular Ca2+ (calcium ion), thereby increasing intracellular Ca2+ concentrations ([Ca2+].
this higher calcium ion in cardiac & skeletal muscle responsible for inducing the main toxicity of these drugs. It also increases catecholamine secretion of chromaffin cells caused jeopardize cardiac arrhythmia. It increases various hormone secretions in endocrine cells.

Source: PoultryMania

33

Anti-stress & Anti-heat / Preventing Heat Stress in Poultry

« Last post by LamiyaJannat on May 26, 2021, 05:51:13 PM »

When does heat stress occur?

Heat stress occurs when the bird’s core body temperature increases to fatal temperatures because of poor heat loss and limited coping means. Environmental temperature and humidity play a role in heat stress. Thus it is key to measure both the temperature and humidity in the barn.

Temperature

The thermoneutral zone is the range of environmental temperatures that an organism can maintain their body temperature. For most poultry, the thermoneutral zone is between 60 and 75 F. This zone represents the temperature range where heat production is lowest. As temperatures increase towards 85 F, the birds will adjust their behavior and decrease feed intake and production. These changes help prevent the bird’s core body temperature from increasing.

When air temperature increases towards 100 F, the birds’ core body temperatures will increase to lethal temperatures unless relief is provided.

These temperatures can shift depending on humidity, care and building conditions.

Humidity

High humidity decreases poultry heat loss from the lungs, which makes the birds more prone to heat stress. For older turkeys, temperatures at 85 F with humidity above 50 percent places turkeys in the danger zone. At 90 F and 50 percent humidity the risk increases to extreme.

If misting or fogging at low humidity, monitor relative humidity to prevent excess moisture in the air that can worsen heat stress conditions.

Signs of heat stress

As air temperatures increase towards 85 F,  the bird will try to lose heat through evaporative cooling, panting. Panting creates more heat through muscle activity. As a result, the bird will increase its water intake, but not enough to keep up with the losses through respiration and urine excretion. Without relief, the changes will worsen and the bird may die.

Keeping birds cool

Providing ventilation

In most cases, you can manage heat in your flock through air flow. Airflow at the birds’ level is key to removing bird heat. Increasing ventilation to remove heat from the birds should be your first priority. However, some cases exist where ventilation is limiting.

Naturally-ventilated barns are at risk of heat stress if the air is calm and supplemental fans are not present. Mechanically-ventilated barns can also be at risk if barns lack ventilation capacity and air mixing for the size and number of birds present.
Feeding

Most often, birds are hungriest in the morning and will tend to fill up. This will make them more prone to heat stress in the afternoon. Withdrawing feed birds six hours before peak warm temperatures in the afternoon can lower the risk of heat stress.

You can reintroduce the feed after peak temperatures have started to decline. Birds can then feed during night time hours when we expect cooler temperatures to occur. Have the feeders full when lowering the feedline. You can use lighting during nighttime (midnight) feeding to allow intake.

You may notice some body weight loss depending on how often you use this feeding method. Thus only follow this feed method when you expect heat stress temperatures.

Managing water

During heat stress, birds will increase their water intake by 2 to 4 times their normal intake. Sufficient water space, operating waterers and cool water temperatures will encourage the birds to drink. Flush water lines and waterers routinely to keep the water fresh and cool.

Using electrolytes

You can add electrolytes to your flock’s drinking water for up to three days. Heat stress causes increased loss of several minerals including potassium, sodium, phosphorus, magnesium and zinc. Potassium chloride electrolytes appear to increase water intake when provided in drinking water at 0.6 percent concentration. It has been generally more effective than other potassium and sodium salts.

You should start providing electrolytes prior to the heat stress period.

Providing sodium bicarbonate

Sodium bicarbonate in the feed or use of carbonated water is especially useful for hens in egg production. Panting and carbon dioxide release can change the acid-base balance in poultry, but also the bicarbonate available for egg shell formation. Thus sodium bicarbonate can help lessen these changes.

Supplementing vitamins

Supplementing drinking water with vitamins (A, D, E and B complex) can be effective at tackling heat stress mortality in broilers. In breeding poultry, vitamin C can effectively moderate warm temperature declines in egg production and eggshell quality in laying hens, and sperm production in breeder males.

Other practices

    Delay activity in the barn such as moving of birds or litter conditioning.

    Provide shade for pastured poultry or decrease sun exposure in the barn.

Written By-
Sally Noll, Extension poultry scientist
University of Minnesota

34

Anti-stress & Anti-heat / Stress - The silent killer

« Last post by LamiyaJannat on May 26, 2021, 05:00:39 PM »

Birds, like humans, do not like stress. It should be understood that stress in birds hampers the function of the immune system and may have a dramatic impact on bird performance. Reasons enough to prevent stress.

So much has been written and discussed about stress and yet this familiar and little understood hazard remains one of the greatest challenges to modern day poultry management. Yes, stress has come to stay as a silent threat to the well-being and performance of chickens. I call it silent because when birds are under stress, they seldom display dramatic signs and therefore, both the problem as well as the losses that result from it go unrecognized and unaccounted for. I am afraid, it will continue to remain so, until we have understood the dynamics of this complex disorder or grow insensitive to it.

What is “stress”?

The Oxford dictionary defines stress as ‘Pressure, burden or compulsion when much energy is required’. All living beings have a limited amount of stored up resources at all times. These resources help them to adapt or adjust themselves to unstable conditions which at times may pose as a challenge or even as a threat. In chickens, for example, extreme weather conditions, vaccination, beak trimming, insufficient housing space and many such disturbing conditions are known to result in a greater demand for these resources.

As long as these challenges are minor and passing or are within tolerable limits, the animal or bird manages to make use of its reserves, adjust itself to the difficult situation and come out of it with little or no damage. It is only when these challenges come in more intense forms or in greater numbers at any given time, that serious chemical and physical changes take place within the bird with far reaching consequences. This could result in immune suppression, poor weight gain, high FCR and depression in egg production - in short, reduction in the general well-being as well as performance. This happens as a result of the bird’s response in trying to cope with the unfavorable factors which pose a threat to its very existence.

Triggering chemical reactions
The factors which interfere with the well- being of the bird are called stressors or stress factors, and the result of the response or the effort that costs the chicken while trying to cope with the stressor is what constitutes stress. Interestingly, during a training session, I asked the participants to express in their own words what the term stress meant to each one of them. Some of the notions that came to their minds were: tension, anxiety, worry, fear, uncertainty, problem, threat, discomfort, pressure, strain, torture, challenge, difficulty, distress, hardship, burden, effort and struggle.

Surely, these are concepts that are related to human experience, but not entirely. We are aware from experience as well as from medical science that certain emotions like fear, anxiety and frustration work not only on the mind, but can also produce physical ailments as well. To mention a few, today experts attribute medical problems like skin disorders, peptic ulcers, cardiac complaints and other health related issues in some patients to psychological disturbances which trigger off a chain of chemical and physical reactions within the body. If this is true in us, humans, it is also in some ways applicable to animals. This is more easily noticeable in larger animals like cattle and canines whose response to stress and the behavior resulting from it is more pronounced than that of birds.

Chicken too are subject to negative stimuli like fright, shock, discomfort, deprivation, pain and so on. As a result, their response (a must for survival) to such stimuli is also negative. This is very evident from the number of occasions you would have experienced poor performance of your flocks in any number of ways for no obvious reasons.

Chicken are not mere egg machines
We often wrongly reduce chicken to creatures of the lower order thinking that they have a very low threshold for pain and feelings. It is not so, as chicken, like other animals have reasonably well developed physical senses. Unfortunately, chicken, unlike human beings do not have the faculty to ‘reason out’ and imagine a future where things could change for the better. They live only for the present and experience the immediate.

For this reason, they are unable to ‘reconcile to’ or ‘accept’ any negative experience, even if it happens to be a life-saving procedure like vaccination or beak trimming as something that will do them good. They remain victims of the situation and the only recourse they have in order to survive and cope with such traumatic situations is with the aid of those physical and chemical processes about which I mentioned earlier. In short, this is done with the release of corticosterone, a steroid from the adrenal gland whenever the chicken’s system, in an effort to survive, struggles to prepares itself to face any challenge.

Different types of stresses:

For practical purposes, we could make a distinction between what we know as unavoidable and avoidable stresses - those that form a necessary part of poultry operations such as vaccination, beak trimming, handling for the purpose of weighing or moving, high production or rapid rates of growth, etc. and those which we unnecessarily impose on the birds either through neglect or due to wrong management practices such as overcrowding the birds, making abrupt or sudden changes, providing faulty ventilation, exposing them to harsh environmental conditions, like extreme temperatures and so on. Good management sense should dictate that we altogether prevent any kind of avoidable stress and at the same time alleviate the unavoidable ones.

What does stress do to chickens?

Technically speaking, the hormone corticosterone, is released by the adrenal glands when the bird’s body prepares for the ‘flight or fight‘ syndrome. This actually helps the bird deal with stress, but at the same time takes a heavy toll. I would like to compare stress and it’s mechanism to our familiar ATM card which provides us with ready money but not without depleting our cash reserves! Whenever a bird is under stress there is a rapid release of glucose into the blood resulting in the depletion of glycogen which is a form of sugar that is stored up as a reserve in the liver and muscles. The respiratory rate gets altered. This hormone also causes chemical changes like alteration of the pH levels in the intestines which in turn upsets the balance of micro-flora in the gut.

Results are that these changes provide a suitable environment for certain types of bacteria and fungi. Gastrointestinal diseases can follow. Several studies have shown that this stress hormone can encourage the formation of, as well as the increase of, free radicals inside the body. Free radicals are substances which once produced in the system can be extremely destructive. They react with oxygen in the body and reduce its supply. In addition to this, they constantly turn hostile to several normal processes within the body. Stress causes damages even to the growing embryo as much as it can affect a grown up bird. In practical terms, this hormone can upset several vital systems in the chicken and gnaw into productivity. Chicken have limited resources drawn mainly from daily nutrition for purposes of maintenance, growth, response to environmental changes, support of the defence mechanism and reproduction. Whenever they undergo stress, there is a redistribution or diversion of these resources which include energy and protein, thus sacrificing health, growth, reproduction and other vital functions.

Growth pattern in birds as well as reproduction show declining trends. The percentage of dropouts and culls keeps rising. Depression of the immune system with lowered resistance to viral, bacterial, protozoan and fungal infections is another natural fall out of the stress syndrome. Metabolic malfunctions can also be experienced during periods of stress. We have more than enough evidence of all this happening in humans and it is equally true in animals, including chicken. What is even more relevant in chicken is the fact that more often than not, the number of stress factors and their combinations present at any given time can often be multiple and disastrous. It is also evident that the meat of birds and animals that have undergone stress before slaughter is low in quality in many ways. In short, stress could threaten the very reason for which we grow chicken.

Best way to handle stress?

1. The most important requisite for the farm manager when it comes to stress is to be aware whenever birds are in trouble or are likely to experience it. This includes planning for the occasions when birds have to be handled or subjected to difficult times, although they may happen to be necessary or natural. Let whatever has to be done, be done by always keeping the bird’s comfort and welfare in mind.

2. It is important to quickly recognize signs of stress, like abnormal feathering, constant preening of feathers even in the absence of external parasites, increased aggression like feather pecking or cannibalism and even aimless and restless pacing of birds that are housed on the floor. Delay in laying eggs is also an indication since birds under stress are believed to hold their eggs longer in the shell gland. It is also suggested that colored egg laying birds under stress begin to lay eggs with pale colored shells. The hatchability of these eggs is also lower when compared to normal colored eggs.

3.Today, given the abundant availability of therapeutic formulations in the market, the manager should learn to judiciously pick just the right ones that will do his flock good. Many managers need to be educated in this area because the use of vitamin, mineral and herbal formulations on farms to fight stress is very often misunderstood or indiscriminate and in fact stressful for the birds and therefore counter-productive.

While the priority of poultry farming is the business consideration, we have the obligation of balancing it with humane methods of achieving it. Animal welfare in some countries is controlled by legislation which protects animals and birds from being subjected to unnecessary pain or distress. Even where we are not bound by law, without sounding sentimental, we owe our birds the quality of handling and care which they deserve for serving our business ends. Besides, everyone knows that the performance of chicken, like all living beings, is directly proportionate to a reasonable level of their well -being and comfort. As long as we stay ignorant or insensitive to any form of hardship that birds go through, stress will continue to remain a silent killer.

Source: POULTRY WORLD

35

Liver Tonic / Healthy liver, healthy birds

« Last post by LamiyaJannat on April 28, 2021, 02:53:05 PM »

Commercially grown birds process large amounts of feed. The liver plays a crucial role. Natural stimulants may help in keeping the liver in a good condition, thus ensuring healthy birds.

With poultry farming profits becoming marginal because of the increasing price of feedingredients, enhancing farm productivityby improving feed utilisation has become a core issue. The liver, being one of the most vital organs of the body, constitutes the lifeline system of animal. This organ also plays a major role in the digestion, metabolism and utilisation of feed nutrients.

Being the centre of a number of digestive, metabolic and productive activities, the liver is ever endangered by microbial and chemical toxins. These toxins may cause varying degrees of damage to the liver and affect its functions, thereby resulting in poor health and production.

The liver and its functions

The liver consists of a right lobe and a left lobe. The left lobe in the chicken and turkey is sub-divided into lateral and medial parts. In large birds, it may be possible to palpate the liver beyond the edge of the sternum. After hatching, the liver lobes have a bright yellow colour because of the pigments they absorb along with the lipids of the yolk. The colour gradually changes to the mahogany-brown between 8-14 days.

The liver is also one of the busiest organs in body. It carries out a large number of important digestive, metabolic and excretory activities, all of which have a significant role on the health and productivity in poultry. The functions of liver are detailed below.

Detoxification - Toxic substances of feeds, as well as the toxins produced in the body, are detoxified by the liver.

Protein metabolism - Dietary proteins are hydrolysed in the intestine by the action of numerous proteases and peptidases, resulting in production of free amino acids. These amino acids are absorbed by the intestinal cells and passed into the portal vein. They then enter the liver and are transported via systemic circulation to other tissues and organs. Excess amino acids, which are not utilised for the synthesis of tissue proteins, hormones, enzymes etc., are catabolised by the liver. The catabolism of amino acids involves deamination whereby ammonia and keto-acids are formed. Ammonia is toxic for the birds. The released ammonia is converted into uric acids in the liver and excreted through the kidneys. Plasma proteins (like albumin, fibrinogen and prothrombin) are formed in the liver.

Fat metabolism - The liver produces bile, which plays a very important role in the digestion of fat. With the assistance of choline, the liver is able to transform the depot fats into tissue fats so that the tissues can utilise them for energy.

Carbohydrate metabolism - Glycogen is synthesised and stored in the liver. Excessive carbohydrates that are ingested by the bird are converted into lipids and are stored as fat in the body. The liver, with the assistance of pancreas, maintains a constant level of blood glucose. In urgency, glucose is synthesized from proteins and fats in the liver, i.e. gluconeogenesis.

Vitamin metabolism - The liver helps in the absorption of fat-soluble vitamins A, D, E and K. Vitamin A is stored in the liver and released when the tissues require it. Vitamin K is utilised in the liver for the formation of prothrombin, which is required for clotting of blood in haemorrhages. Some members of the vitamin B group, especially B1, B2 and Niacin are metabolised in the liver, where they may also be stored.

Iron metabolism - The lifespan of erythrocytes in chickens is 20-30 days. After this period, the erythrocytes are destroyed in the liver and the minerals (iron, copper and cobalt) released are stored in liver for the use by the body.

Erythropoiesis - The formation of red blood cells (RBC) is called erythropoiesis. In birds, the liver is the site for erythropoiesis. Haemoglobin is synthesised in the liver.

In the event of liver hypo-functioning, birds may suffer from many recurring problems. A healthy liver will certainly help to ensure a healthy bird, and therefore this organ needs special care.

A variety of growth and production enhancers have come to be employed in poultry production to enhance poultry productivity. Herbal liver tonics act by protecting the liver from toxins and stimulating the liver function and thus, enhance growth and production performance. The use of a liver tonic liquid or powder varies from farm to farm, depending on the farmers’ preference. In general, liquid liver tonics for water administration are preferred for the curative purpose as during liver disorder, feed consumption decreases significantly. As a regular plan to prevent liver disorder and as an aid to improve productivity, powder forms of liver tonic, as feed additive is more convenient and also more cost effective. Nevertheless, irrespective of the preference for powder or liquid form, poultry farming has a natural scope for employing both forms of liver tonics, even if under particular conditions.

Beneficial plant extracts

With the increasing demand for organically grown poultry, the use of naturally occurring ingredients could be of economic importance to improve health and farm productivity. Nature provides many herbs that are shown to exert beneficial actions on the liver, thus helping improve farm productivity. Some important herbs, having major activity on the liver for its protection and to enhance functions are described below.

Phyllanthus niruri:
Plants of the genus Phyllanthus have been used widely by traditional medical practitioners for the treatment of jaundice and other liver disorders. The plant extract consists of phyllanthin, triacontanel and related compounds that have stomachic, hepato-protectiveand anti-hepatotoxic activities. Phyllanthusniruri also possesses anti-viral activity, which is believed to reduce the viral replication. Phyllanthus niruri is known by the common name “Stone-breaker”, as it is also used as an herbal remedy for urinary calculi (it reduces urinary calcium). Hence, in poultry, in addition to its use as liver tonic, the plant may also have great economic importance to prevent and control one of the most common diseases – Gout.

Andrographis paniculata:
The dried aerial parts, preferably leaves and stems of Andrographis paniculata, are used. Here, the major chemical constituents are Andrographolide and diterpene lactone. Andrographolide and related diterpenes are hepato-protective and hepatic stimulant agents. These compounds also possess choleretic (stimulate bile secretion), anti-inflammatory, anti-diarrhoeal, immuno-stimulant and anti-oxidant activities. Besides the use as liver tonic, being a potent immuno-stimulant, it can also be used to improve immune response to vaccination and infections.

Eclipta alba:
The whole plant of Eclipta alba will be used. The leaf extract is considered a powerful liver tonic and rejuvenative.
It is an established hepato-protective. The plant extract exhibits anti-mycotoxic and anti-haemorrhagic activities. It also has profound anti-hepatotoxic activity, which is attributed to wedelolactone and demethylwedelolactone, which are the major chemical constituents of Eclipta alba.

Boerhavia diffusa:
The drug used from this plant will make use of the dried, mature whole plant of Boerhavia diffusa. Major chemical constituent of the plant is Punarnavoside, an antifibrinolytic glycoside. This plant possesses potent anti-fibrinolytic and anti-inflammatory properties. The plant extract also exhibits diuretic and hepato-protective activities.

Picrorhiza kurroa:
Dried rhizome and roots of Picrorhiza have been traditionally used for many beneficial actions. Major chemical constituents include iridoid glycosides, picroside I and kutkoside. This plant is known to possess hepato-protective, anti-hepatotoxic, choleretic, anti-oxidant and anti-inflammatory activities. In addition, the plant is a potent immuno-stimulant of both cell mediated and humoral immunity.

Chicorium intybus:
This is also known as Chicory. It acts as apotent anti-hepatotoxic, hepato-stimulant and cholagogue. It is known to be useful in the treatment of jaundice, fatty liver, depression of liver, biliary stasis as well as enlargement of spleen and liver.
Maximisation of animal production as per the genetic potential is essential for profitability. The liver plays many vital roles for the maintenance of health and efficient utilisation of feed ingredients. Combinations of the herbs (as described above) are available for use in poultry, which can be used as feed additives to prevent liver disorders, and as an aid to improve feed utilisation, thereby improving farm productivity. Hence, nature’s boon, herbal liver tonic can play an integral role in poultry farming to bring about maximum productivity as per the genetic potential.

Source: Poultry World

36

Toxin Binder / Selecting the most effective toxin binder

« Last post by LamiyaJannat on April 28, 2021, 02:38:15 PM »

As mycotoxin concerns arise, more and more toxin binder products are commercially available on the market.
This can be confusing when selecting a product. Which technical and objective criteria could be used to select the most adapted product?

Mycotoxins are small and stable metabolites produced by fungi which can contaminate a wide variety of crops. The contamination of food and feed by mycotoxins is a global safety issue due to their adverse effects on human and animal health.

For example, one main concern is the presence of aflatoxin M1 in dairy products, a highly nutritious food in developing countries. Aflatoxin M1 is classified by the International Agency for Research on Cancer as potentially carcinogenic to humans (Group 2B). In livestock, mycotoxins lead to important decreases in performance (growth, feed efficiency or reproduction issues) and consequently losses of revenue for farmers.

Tools to decrease mycotoxin bioavailability

A wide range of products is available on the market to counteract the negative effects of mycotoxins in the livestock industry. These products range from single mycotoxin adsorbing agents to more complete and elaborate products. One common point between these products is, at least, their capacity to ‘adsorb’ or ‘bind’ mycotoxins, in order to decrease mycotoxin bioavailability within the animals and to reduce their absorption in the systemic circulation.

Objective and reliable criteria to select products

Over the past few years, there has been an increasing knowledge on mycotoxins pathogenic potential (co-contamination, impact on animal health and productivity, interaction in gut). In the meantime, the abundance of available products on the market, with variable physicochemical and biological properties, brings complexity and sometimes confusion for the selection of products. It appeared necessary to find objective and reliable criteria to select products with the best potential to limit mycotoxins effects on animals. After years of research on the subject, Mixscience highlighted five key criteria to evaluate the efficacy of the products:

1.   Adsorption capacity towards a wide range of mycotoxins, in various pH conditions
2.   Adsorption capacity towards other toxins
3.   Specificity
4.   Velocity
5.   Strict control plan of products.

These criteria are mainly based on in vitro analysis, which are powerful tools to screen products before in vivo studies.
Adsorption capacity toward a mycotoxin.

Toxin binding capacities can differ significantly between one product to another, due to the complex and diverse structure of adsorbing materials and the variety between the different mycotoxins. Aflatoxins have received much attention due to their frequent occurrence in agricultural commodities and health issues in a wide variety of animals. However, the occurrence and negative impact of various other mycotoxins and the reality of co-contamination strengthen the consideration that a product should bind a wide number of mycotoxins. Moreover, the conditions of the action site of the product are important to consider. For example, pH values vary greatly along the digestive tract of animals, from acidic conditions (pH 3 or 4) to more basics ones (pH 6 or 7). Binding capacities of products may be influenced by pH changes, leading to the risk that the toxins are adsorbed at one part but released at another part of the digestive tract.

Adsorption capacity toward other toxins

Some products have also demonstrated the capacity to bind more than toxins produced by fungi, which may help the animal to fight against various stress occurred in their environment. Bacterial toxins, which can be involved in various diseases such as colibacillosis, necrotic enteritis in poultry or neonatal diarrhoea in piglets, may also be bound by some products. This is interesting in a context of bacterial resistance because the targets are the metabolites of the bacteria and not the bacteria themselves. It is also recommended to test these compounds (endo and exotoxins), in order to provide maximum protection to animals.

Highest toxin adsorption capacity

As far as possible, in vitro studies should verify the adsorption capacity of a product on several types of microbial toxins, in different pH conditions. Figure 1 illustrates the mycotoxin adsorption capacity of two commercial products, tested at maximum recommended dosage (product 1 = Multiprotect at 0.3% and product 2 at 0.2%), on five mycotoxins : aflatoxin B1 (AFB1), zearalenone (ZEA), fumonisin (FUM), T2-toxin (T2), ochratoxin (OTA) and toward bacterial toxins at pH7. Considering mycotoxins and bacterial toxins, product 1 showed the highest toxin adsorption capacity and the widest spectrum of activity.

Specificity
One objection to the use of toxin binders is their potential side effects on feed components. It is true that some materials have been reported to be relatively unspecific adsorbents which may adsorb essential nutrients. As an example, activated charcoal demonstrated adsorption capacity toward a broad range of mycotoxins in vitro, but also toward some vitamins and minerals. It is recommended to verify that the in vitro adsorption of macro and micro-elements of the product is minimal before selecting it.
Respective adsorption percentages of vitamin B6 and phosphorus were less than 5% and 0% for the commercial product and 40% and 2% for activated charcoal

A study aiming at evaluating the binding properties of a commercial product (product 1 = Multiprotect at 0.2%) and activated charcoal toward vitamin B6 and phosphorus at pH 7, used a vitamin and minerals model. Respective adsorption percentages of vitamin B6 and phosphorus were less than 5% and 0% for the commercial product and 40% and 2% for activated charcoal. Multiprotect showed minimal risk of interaction with important elements from feed, conversely to activated charcoal.

Velocity of adsorption

The bioavailability of mycotoxins, correlated to their absorption on the digestive tract of the animal, is very diverse according to the type of mycotoxin and the animal species. In monogastrics, AFB1 and ZEA are rapidly absorbed in the proximal part of the digestive tract while other mycotoxins such as FUM are poorly absorbed. For the mycotoxins which are quickly absorbed, it is necessary to select a product which acts in a few minutes. An in vitro study aiming at verifying the binding properties toward AFB1 (1000 ppm) and ZEA (1000 ppm) of a commercial product (Multiprotect at 0.2%) after 1 min, 5 min and 10 min at pH 4, have shown that Multiprotect was efficient for speed of mycotoxins adsorption. Indeed, nearly 98% and 68% of AFB1 and ZEA were adsorbed with the commercial product after only 1 min.

A quality certificate is essential and represents a guarantee of product safety

Strict control plan of products

Finally, it is important to verify that the products are safe for animals, consumers and the environment. A strict control plan policy is mandatory with toxin binders which usually includes natural clays which are not risk-free, notably because of contamination to heavy metals or dioxins for example. A quality certificate is essential and represents a guarantee of product safety.

Making an informed decision

The five criteria which have been identified should be considered when selecting a mycotoxin binder product. These criteria participate to a better knowledge of the products, which are essential to satisfy feed manufacturer expectations i.e. a product with adsorption capacity toward a wide range of toxins, with fast adsorption, without desorption properties and which are safe for the animals. Also, economical aspects and favourable effects on animal health are considered.

Source: ALL ABOUT FEED

37

Growth Promoter / Steroid Hormones

« Last post by LamiyaJannat on April 17, 2021, 07:12:49 PM »

Steroid Hormones

In general, the principle that dictates which type of hormone to be used is the need to supplement or replace the particular hormone type that is deficient in the animals to be treated. Females produce estrogens normally, so better results are obtained from the administration of androgens, eg, trenbolone acetate (TBA). Estrogens should not be used in animals to be retained for breeding purposes.

Manufacturers’ instructions must be followed to ensure proper implant placement and dose administration. Anabolic hormones should not be administered by IM injection for growth-promoting purposes. Additionally, steroid hormones must not be used for anabolic or other purposes unless the indication is specifically approved by the appropriate regulatory body. The EU has banned the use of hormonal growth promoters in meat production. Appropriate surveillance programs have been established to ensure compliance by producers.

Endogenous Steroids

The steroidal compounds used for anabolic purposes in food animals are estradiol, progesterone, and testosterone. Gender and maturity of an animal influence its growth rate and body composition. Bulls grow 8%–12% faster than steers, have better feed efficiencies, and produce leaner carcasses. Superior performance of bulls is due to the steroids produced in the testes (mainly testosterone but also estradiol, which in ruminants is also anabolic and is produced in relatively large quantities). Testosterone, or one of its physiologically active metabolites, binds to receptors in muscle and stimulates increased incorporation of amino acids into protein, thereby increasing muscle mass without a concomitant increase in adipose tissue. Estradiol, on the other hand, may act by stimulation of the somatotropic axis to increase growth hormone and thus IGF-1 production and availability by modulation of the IGF binding proteins. Naturally produced endogenous steroids are not orally active, require picogram concentrations of estradiol and nanogram concentrations of testosterone in blood for physiologic effects, and can transiently affect the behavior of treated animals.

Estradiol:

A potent anabolic agent in ruminants at blood concentrations of 5–100 pg/mL, estradiol is administered as an ear implant, either as compressed tablets or silastic rubber implants. When estradiol is formulated as compressed tablets, a second steroid (usually testosterone, TBA, or progesterone) is typically present when administered to feedlot cattle fed a high-energy diet, in a ratio of ~1 part estradiol to either 5 or 10 parts of the other, androgenic, steroid. The release of hormones from compressed pellets is biphasic, with a relatively rapid rate lasting 2–7 days after insertion (50–100 times greater than baseline), followed by a slower rate of release for the next 30–100 days (5–10 times greater than baseline). Hormone concentrations gradually decline up to day 80–100, when concentrations are no different from those in control animals.

Estradiol formulated in silastic rubber enhances the effective life span of the implant relative to pelleted formulations. The pattern of release includes a short-lived spike in plasma estrogen concentration for 2–5 days after insertion, followed by a stable but modest increase (5–10 times greater than baseline). Toward the end of the effective life span of the implant, there is a gradual decline to estradial concentrations found in control animals.

Estradiol, on its own, increases nitrogen retention, growth rate by 10%–20% in steers, lean meat content by 1%–3%, and feed efficiency by 5%–8%. It can be used in steers to best advantage, but it also has anabolic effects in heifers and veal calves. It works best in lambs in conjunction with androgens. It is not effective as an anabolic agent in pigs.

Testosterone:

A potent anabolic agent at the relatively high concentrations of 1–5 ng/mL in peripheral circulation, testosterone is not used on its own as an anabolic agent in farm animals, because it is very difficult to achieve the effective physiologic concentrations for long periods (up to 100 days) with current delivery systems. It is generally used as a propionate formulation in conjunction with 20 mg estradiol benzoate (EB) in a compressed tablet implant; its major role in the compressed pellet may be to slow down the release rate of estradiol. In high concentrations in blood, testosterone induces male sexual behavior (eg, aggression and mounting), but this is not seen with the concentrations delivered by compressed pellets in the ear (1 ng/mL). Behavior resulting from use of 20 mg EB and 200 mg progesterone is not different from that seen after the use of 20 mg EB and 200 mg testosterone propionate.

Progesterone:

Unambiguous data suggesting progesterone is anabolic in farm animals does not exist. Its major use is to slow the release of estradiol from compressed pellet implants.

Synthetic Steroids

Synthetic steroids are commercially available in some countries because of their efficacy, their relatively mild androgenicity, and because they cause few behavioral anomalies (see Synthetic Steroid Hormones for Consideration as Growth Promoters). Commercial synthetic steroids are androgenic (TBA) or progestogenic (melengestrol acetate [MGA]).

Synthetic steroidal androgens are not commonly used as anabolic agents except for TBA. TBA is currently the only synthetic androgen approved for use for growth promotion in cattle; it is used to a lesser extent in sheep and not in pigs or horses. It has weak androgenic activity but has greater anabolic activity than testosterone. When administered repeatedly during the feedlot phase when cattle are fed a high-energy diet, TBA can alter the physical appearance and behavior of steers, causing them to look and act like bulls. TBA has significant anabolic effects on its own in female cattle and sheep, but in castrated males it gives maximal response when used in conjunction with estrogens. It is administered as a pellet-type implant containing 140–200 mg TBA for heifers and cull cows, and it can be used with estradiol in doses ranging from 140–200 mg TBA as either combined or separate implants.

MGA is an orally active synthetic progestagen. It is fed at dosages of 0.25–0.5 mg/day per heifer in the feed. It suppresses recurrent estrus in feedlot heifers and increases growth rate and feed efficiency (see Table: Synthetic Steroid Hormones for Consideration as Growth Promoters). It is not effective in pregnant or spayed heifers or in steers. Its mode of action is to suppress ovulation, presumably by suppressing luteinizing hormone (LH) pulse frequency; however, large follicles develop, which can increase concentrations of estradiol and growth hormone, and hence growth. MGA is permitted for use in the USA but not in the EU. When used in the absence of a growth-promoting implant, MGA increases growth rate through the increased estradiol released by the follicles; however, when used in conjunction with either estradiol or combination estradiol/TBA implants in the feedlot, the growth-promoting benefits of MGA are primarily derived from suppression of the excess, unproductive, and potentially harmful activities associated with recurrent estrus.

Synthetic Nonsteroidal Estrogens

Two major classes of synthetic nonsteroidal estrogens have been used as production enhancers in food animals. Stilbene estrogens (either diethylstilbestrol [DES] or hexestrol) have been banned in most countries as anabolic agents because of residue and food safety concerns.

The discovery of a naturally occurring estrogen, zearalenone (produced by the fungi Fusarium spp), led to the development of the synthetic analogue zeranol. Zeranol is estrogenic and has a weak affinity for the uterine estradiol receptor. It is used in animal production as a SC ear implant at a dose of 36 mg for cattle and 12 mg for sheep, with a duration of activity of 90–120 days. In steers, zeranol increases nitrogen retention, growth rate by 12%–15%, and feed conversion by 6%–10%. However, lower responses are seen in heifers. Its effects are additive to those of androgens (generally TBA).

Use in Cattle

Calves have a high conversion of feed into animal tissue compared with young growing swine or poultry. Therefore, their responses to anabolic agents are variable. Responses of 0–10% have been obtained when zeranol was given to 3-mo-old castrated male calves. Bull calves in an intensive bull beef system can be given an estrogen implant at 1–2 mo of age to suppress testicular development, which may lead to subsequent reduction in mounting and aggression. A growth response of ~5%–8% is also obtained from this implant. Reimplantation every 80–100 days is necessary if compressed pellet implants are used.

A major limitation to the use of anabolic agents in lightweight weaned calves is the low liveweight gain they may achieve because of poor nutritional status. Hence, anabolic agents should be considered only if the weanlings are expected to gain >0.25 kg/day. Zeranol, estradiol, and TBA can be used in male castrates. Dairy heifer replacements cannot be given steroid implants as weanlings.

Greater and more consistent responses are obtained in yearling and older cattle than in calves or weanlings, due primarily to greater intake and to the higher plane of nutrition. In the case of pellet-type implants with effectiveness of 90–120 days, consideration can be given to reimplanting cattle midway through the grazing season, provided gains >0.5 kg/day are maintained. Silastic implants of estradiol are effective for 200–400 days, depending on dose used. Daily gains in feedlot cattle fed a high-energy diet may be increased 20%–30% after implantation with an estrogen and an androgen; daily gain in pasture cattle is typically improved by 10%–15%.

Responses to growth promotion are good when animals are on a high plane of nutrition. Feed conversion efficiency is improved, and lean meat content of the carcass is generally increased. Although less clear, conformation of implanted cattle tends to improve. Negative impacts of implants on marbling content of the loin muscle can be minimized by finishing cattle to a fat-constant endpoint.

In steers and heifers in the feedlot and provided a high-energy diet, use of an androgen plus an estrogen hormone combination is common. Pellet-type implants are effective for as long as 150 days; reimplanting cattle after 70–100 days should be considered because of decreasing response from the pellet-type implants over time.
Results from large-pen studies (>25 animals/pen) show that heifers benefit from a combination of estradiol, TBA, and MGA. In small-pen research, however, when fed in combination with growth-promoting implants, MGA use results in reduced gain, feed efficiency, and ribeye area, as well as increased fatness. These contrary findings suggest that although progesterone may have an “anti-growth promoting” effect, the growth-promotion benefit realized from suppression of estrus overcomes the minor negative physiologic impact of progesterone in conventional large feedlot pens.

In some studies in which bulls were treated with estrogens, growth rate increased by 2%–10%, and testicular growth was suppressed with a subsequent reduction in mounting and aggression. This should make the bulls easier to manage on the farm and less subject to “dark cutting” after slaughter. The mechanism involved appears to be the reduction of the gonadotropic hormones LH and follicle-stimulating hormone (FSH) from the pituitary gland by estrogen, which has a strong negative feedback effect on LH and FSH secretion. This reduction in LH and FSH results in decreased testicular size and lower testosterone levels, with a consequent reduction in aggressive behavior. However, there appears to be sufficient testosterone secreted to maintain an anabolic effect. Therefore, the repeated use of estrogens in bulls beginning at 1–3 mo of age may lead to a hormonal castration effect with increased growth rate.

Use in Horses

The use of anabolic agents in horses is not recommended because of adverse effects on the reproductive system. Administration of a steroid hormonal androgen analogue decreases testicular size in stallions. Decreased hormonal concentrations, especially LH, testosterone, and inhibin, adversely affect testicular histology and spermatogenesis and transiently decrease sperm output and quality. One of the most commonly used compounds is 19-nortestosterone for therapy in debilitated and anemic horses. However, use of these compounds is contraindicated, and longterm treatment or large doses have serious adverse effects on reproductive tract function.

Use in Other Species

In pigs, the growth responses from the use of estradiol, progesterone, and zeranol are variable but generally low. TBA seems to increase lean meat content of pig carcasses.
In sheep, the responses to anabolic agents parallel those obtained in cattle. The most consistent responses have been obtained in lambs finished on high-concentrate diets; a 10%–15% increase in daily gain can be expected. Anabolic steroids should not be used in lambs to be retained for breeding. Also, implantation with zeranol reduces testicular development in ram lambs and delays the onset of puberty and reduces the ovulation rate in female sheep. Moreover, the short finishing period and the extensive nature of some production systems militate against widespread practical use of growth promotants in sheep on economic grounds.

In poultry, responses to estrogens include increased fat deposition. Androgens, however, have given conflicting responses. Hence, their use is of no practical significance at this time.

In fish, methyl testosterone can induce sex reversal in rainbow trout, thereby promoting growth and improved feed conversion efficiency.

Possible Complications

Any hormonal implant has a negative feedback effect on pituitary gonadotropins, thereby reducing LH and FSH secretion. Therefore, they can affect the onset of puberty and the regularity of estrous cycles, as well as reduce conception rate in females and testicular development (and thus sperm output) in males. Hormonal growth promotants should never be used in animals that are or may be used for breeding purposes, nor should they be used before puberty to increase growth in yearling thoroughbreds or young pedigree bulls for show purposes. If given to pregnant heifers, TBA results in increased incidence of severe dystocia, masculinization of female genitalia of the fetus, increased calf mortality, and reduced milk yield in the subsequent lactation.

The major problem thought to be associated with estrogenic implant use in the feedyard has been a transient increase in mounting behavior and aggression, commonly referred to as buller syndrome (see Buller Steer). However, it is also believed that the estrogen in the implant alone is not sufficient to cause bullers. The "buller" is the animal being pursued by one or more pen mates that repeatedly attempt to mount the buller throughout the day and several days. Buller syndrome generally affects 2%–3% of the feedyard steer population, but this rate can double or triple during the late summer and early fall months. An increase in yearling steers off native grass pasture (which are usually given a high-dose implant immediately on arrival), diurnal temperature fluctuations (hot days and cool nights that shift social activity to early evening hours), dusty pen conditions (exacerbated by evening social activity), feeding corn or hay that may be moldy, and incomplete fermentation on freshly harvested silage can also contribute to increases in buller syndrome. Feedlot pens with a greater number of animals experience a greater incidence of buller activity, and the incidence of bullers increases linearly with increasing number of animals within a pen above 80–100 animals per pen. This suggestes the agonistic behavior is a population phenomenon, requiring a critical mass of both the dominant, mounting animals and the animals they are attempting to mount. Bullers have been shown to have greater circulating concentrations of monoamine oxidase and reduced circulating concentrations of progesterone than non-buller pen mates. These effects generally last for 1–10 days after implantation and then subside. However, there have been a few reports of undesirable behavior in steers that lasted for 4–10 wk. The cause of this unpredictable adverse behavior is not clear; it may be a function of rearing and socialization climate. It is generally more severe in dairy cattle used for beef production. If the problem is severe, the buller steers should be identified and removed; if very severe, removal of the implants or administration of 50–100 mg of progesterone in oil for a number of days to suppress behavior should be considered.

In addition to buller syndrome, estrogenic implants may increase the size of rudimentary teats.

Factors Affecting Response
A number of factors affect the response to growth-promoting implants, including genetic makeup, plane of nutrition, and the sex and age of the animal.

Animals should be gaining a minimum of 0.25 kg/day before an economic response is obtained. Implants are best used in animals on a high plane of nutrition and under good husbandry conditions. They are an aid to, but not a substitute for, good husbandry. Consequently, there is little economic incentive in implanting cattle destined for a 3- to 4-mo “store period,” during which time animals are fed to gain little or no weight Responses are reduced in calves (based on health condition and diet), and responses are good in yearlings.

Prior implantation does not affect the response to the next implantation. Also, once the implant effect has ceased, the rate of gain reverts to the rate that would be expected in nonimplanted animals, assuming the level of feeding is the same. Also, extra weight induced by implants in early life is transferred through to extra carcass weight at slaughter.

By - Christopher D. Reinhardt, BS, MS, PhD,
Animal Sciences and Industry, Kansas State University

38

Growth Promoter / Overview of Growth Promotants and Production Enhancers

« Last post by LamiyaJannat on April 17, 2021, 07:08:03 PM »

Overview of Growth Promotants and Production Enhancers

Achieving increased efficiency of conversion of feed into human food products of high quality, without posing any significant risk to the consumer, is an important goal of livestock producers worldwide. The physiologic mechanisms involved in converting feed into muscle, fat, and bone by animals are increasingly being elucidated. Recently, consumer concerns about additives for food production have focused on animal safety, organoleptic quality, and the potential human health hazards of the food we eat.

A number of approaches may be taken to improve conversion of animal feed into meat; two of the more practical approaches are hormonal treatments and antimicrobial feed additives. The hormonal approach includes administration of anabolic steroid hormones, use of growth hormone (GH) or insulin-like growth factor (IGF-1) to augment endogenous GH levels, and use of β-adrenergic agonists (βAAs) to preferentially increase nutrient partitioning to muscle (see Natural Steroid Hormones for Consideration as Growth Promoters). The antimicrobial feed additives approach includes feeding of antibiotics to decrease populations of pathologic bacteria in host GI tracts, use of compounds to manipulate ruminal fermentation by changing the ruminal microflora population in healthy animals, and use of probiotics to promote beneficial microflora in the GI tract.
The use of hormonal treatments and antimicrobial feed additives in production animals is currently under debate in many areas and is banned in some because of concerns surrounding their possible effects on people.

The EU has banned beef produced using growth-promotant implants since 1981. Despite subsequent findings by the European Economic Community's own panel of scientific experts, referred to as the "Lamming Committee," by the World Trade Organization, and by the international Codex Alimentarius Commission indicating that appropriate use of approved growth-promoting hormones poses no human health risk to consumers, the EU has continued its ban.

More recently, use of βAAs for growth promotion in swine and beef production has come under scrutiny in the international meat trade community. Some countries, including the EU, Russia, and China, have placed a total ban on beef and pork from nations that allow the use of βAAs, whereas other countries have adopted the maximum residue limits (MRLs) for the compounds as established by the Codex Alimentarius Commission. The FDA applies a greater MRL in the USA than the Codex standard.

The use of antimicrobial compounds specifically for growth-promotion purposes, as opposed to their use for control or treatment of bacterial infection, has also come under increased attention internationally because of rising concerns over antimicrobial resistance by pathogenic bacteria of concern in human medicine. Direct cause-effect evidence of antimicrobial use in livestock leading to bacterial resistance in human medicine is virtually nonexistent, requiring more complicated epidemiologic study. However, numerous studies have linked use of specific drugs in livestock, either for disease therapy or for growth-promotion purposes, to increased prevalence of drug resistance in target bacterial species. Results of these investigations are equivocal and have been the focal point of intense scrutiny and debate. In the absence of resoundingly clear cause-and-effect data, and because preservation of the continued efficacy of existing antimicrobial compounds is paramount, the cautionary principle has prevailed and will likely lead to greater restrictions on the use of antimicrobials for growth promotion in livestock and for therapeutic purposes as well.

By - Christopher D. Reinhardt , BS, MS, PhD,
Animal Sciences and Industry, Kansas State University

39

Global Challenges / Incidence and Impact of Foodborne Diseases

« Last post by LamiyaJannat on April 17, 2021, 07:02:08 PM »

Incidence and Impact of Foodborne Diseases

The global burden of foodborne diseases is difficult to assess, because no overarching estimation has yet been performed. The World Health Organization has initiated this process but reports that efforts are limited by regional lack of funding, public health infrastructure, and political will. However, despite specific data, the burden seems obvious; diarrheal diseases, many of which are foodborne in origin, kill approximately 1.9 million children worldwide.

In the USA, the foodborne diseases are not generally reportable, so their burden likely is significantly underestimated. Contributing to this underestimation is that many foodborne illnesses lack the severity, duration, and specific diagnosis required for definitive identification and intervention. Recent estimates by the CDC indicate that foodborne pathogens cause approximately 9.6 million illnesses, 57,500 hospitalizations, and 1,500 deaths each year in the USA.

In an effort to maintain awareness of foodborne disease events and trends, CDC conducts the Foodborne Diseases Active Surveillance Network (FoodNet), which monitors the incidence of nine foodborne pathogens in ten USA cities, covering approximately 15% of the American population.

CDC reports that this epidemiologic situation has not changed appreciably since 2006, suggesting that there are gaps in the current food safety system and a need for better, more effective interventions.

Factors in Emerging Foodborne Illness Trends

Pathogenic organisms that contaminate food and result in foodborne illness are dynamic in that they adapt to new foods, processes, and human behaviors. The following categorical factors contribute to foodborne illness trends.

Human Demographics and Behavior:

The proportion of the USA population that is immunocompromised is increasing because of factors such as advancing age, underlying disease, and therapeutic drug regimens. Additionally, people consume more fresh fruits and vegetables, which may be more contaminated than processed or prepared foods, and consume an increasing number of meals outside the home. Finally, “organic” foods have not been shown to be microbiologically safer and in some cases may even increase the risk from certain foodborne pathogens.

Technologies Within the Food Industry:

Increasing concentration and vertical integration of many food production sectors have resulted in foods of higher quality and greater consistency but with certain inherent vulnerabilities. Foods (and constituent ingredients) are transported in larger batch sizes, over longer distances, and are processed into an increasing number of end products. This means that refrigeration breakdowns and cross-contamination incidents can result in more widespread effects of food recalls and illness outbreaks.

International Travel and Commerce:

The concept of “traveler’s diarrhea” is expanding because, increasingly, bulk food shipments cross international borders at least as often as people. Therefore, foodborne illnesses acquired from foreign foods can be contracted without leaving home. Additionally, when people travel, they frequently take cultural foods with them to share with extended family. Despite prohibitions against such importation practices, ~4,000 pounds of meat products are confiscated from travelers each month from Haiti to the USA. Undoubtedly, this represents only a fraction of the amount actually crossing the border.

Microbial Adaptation:

Foodborne pathogens have inexorably adapted to traditional preservation techniques. Others may even be selected by various techniques. Finally, antimicrobial resistance patterns change constantly, requiring correspondingly dynamic interventions.

Economic Development and Land Use:

USDA reports a continuing decrease in the number of farms in the USA, with the average number of livestock animals on remaining farms increasing. This concentrates the number of animals that may be affected, both by contagious pathogens and by interventions such as quarantines and depopulation efforts. Increases in ocean water temperature have been associated with increases in the number and scope of foodborne illnesses from certain seafood products such as oysters.

Lack of Food Safety Education:

Health classes at the intermediate and high school levels rarely, if ever, cover food safety in favor of topics such as sexually transmitted diseases, drug abuse, and teen pregnancy. With the increasing fraction of two-worker and single-parent homes, time demands may also preclude education of children in food safety principles and further contribute to the lack of awareness.

By
Donald L. Noah , DVM, MPH, DACVPM, Lincoln Memorial University;
Stephanie R. Ostrowski , DVM, MPVM, DACVPM, Department of Pathobiology, College of Veterinary Medicine, Auburn University

40

Probiotic & Immunity Enhancer / Types of Vaccines for Animals

« Last post by LamiyaJannat on April 17, 2021, 06:56:26 PM »

Types of Vaccines for Animals

Nonliving Vaccines

Vaccines may contain either living or killed organisms or purified antigens from these organisms. Vaccines containing living organisms tend to trigger the best protective responses. Killed organisms or purified antigens may be less immunogenic than living ones because they are unable to grow and spread in the host. Thus, they are less likely to stimulate the immune system in an optimal fashion. On the other hand, they are often less expensive and may be safer. Living viruses from vaccines, for example, infect host cells and grow briefly. The infected cells then process the viral antigens, triggering a response dominated by cytotoxic T cells, a type 1 response. Killed organisms and purified antigens, in contrast, commonly stimulate responses dominated by antibodies, a type 2 response. This type of response may not generate optimal protection against some organisms. As a result, vaccines that contain killed organisms or purified antigens usually require the use of adjuvants to maximize their effectiveness. Adjuvants may, however, cause local inflammation, and multiple doses or high doses of antigen increase the risks of producing hypersensitivity reactions. Killed vaccines should resemble the living organisms as closely as possible. Chemical inactivation should cause minimal change to their antigens. Compounds used in this way include formaldehyde, ethylene oxide, ethyleneimine, acetylethyleneimine, and beta-propiolactone.

Subunit Vaccines

Although vaccines containing whole killed organisms are economical to produce, they contain many components that do not contribute to protective immunity. They may also contain toxic components such as endotoxins. Thus, depending upon costs, it may be advantageous to identify, isolate, and purify the critical protective antigens. These can then be used in a vaccine by themselves. For example, purified tetanus toxin, inactivated by treatment with formalin (tetanus toxoid), is used for active immunization against tetanus. Likewise, the attachment pili of enteropathogenic Escherichia coli can be purified and incorporated into vaccines. The antipilus antibodies protect animals by preventing bacterial attachment to the intestinal wall.

Antigens Generated by Gene Cloning

The cost of physically purifying a specific antigen may be prohibitive. In such cases it may be more appropriate to clone the genes coding for the protective antigens into a vector such as a bacterium, yeast, baculovirus, or plant. The DNA encoding the desired antigens may be inserted into its vector, which then expresses the protective antigen. The recombinant vector is grown, and the antigens encoded by the inserted genes are harvested, purified, and administered as a vaccine. An example of such a vaccine is one directed against the cloned subunit of E coli enterotoxin. The cloned subunits are antigenic and function as effective toxoids. A purified subunit antigen, called OspA, encoded by a gene from Borrelia burgdorferi, effectively protects dogs against Lyme disease.

It is possible to clone viral antigen genes in plants. This has been successfully achieved for viruses such as transmissible gastroenteritis virus and Newcastle disease virus. The plants used include tobacco, potato, and corn. These plants contain very high concentrations of antigen, and protection may be achieved by simply feeding the plants to animals.
Some recombinant structural proteins may be assembled into virus-like particles (VLPs). One or more viral proteins may make up the VLP, and the particles may be either non-enveloped or enveloped. VLPs present viral antigen in a manner that more closely resembles the infectious virus. VLPs are potent immunogens and may not require adjuvants. Because VLPs contain no viral genetic material they cannot replicate in the recipient animal. A similar type of vaccine may be developed through the use of bacterial “ghosts,” bacteria that have been emptied of their contents, especially their DNA.

DNA Plasmid Vaccines

Animals may also be immunized by injection of DNA encoding viral antigens. This DNA is inserted into a bacterial plasmid, a piece of circular DNA that acts as a vector. When the genetically engineered plasmid is injected, it is taken up by host cells. The DNA is then transcribed, and mRNAs are translated to produce the vaccine protein. The transfected host cells thus express the vaccine protein in association with major histocompatibility complex class I molecules. This results in the development of not only neutralizing antibodies but also cytotoxic T cells.

This type of DNA plasmid vaccine is used to protect horses against West Nile virus infection. This approach has been applied experimentally to produce vaccines against:

•   avian influenza virus
•   lymphocytic choriomeningitis virus
•   rabies virus in dogs and cats
•   canine parvovirus
•   bovine viral diarrhea virus
•   feline immunodeficiency virus
•   feline leukemia virus
•   porcine herpesvirus
•   foot-and-mouth disease virus
•   bovine herpesvirus-1 related disease
•   Newcastle disease virus

Because they can produce a response similar to that induced by attenuated live vaccines, these DNA plasmid vaccines are ideally suited for use against organisms that are difficult to grow in cell culture. Some DNA vaccines are able to induce immunity even in the presence of very high levels of maternal antibody. Immunization with DNA plasmids in this way allows presentation of viral endogenous antigens in their native form.

Alphavirus Replicons

RNA vaccines also effectively induce the production of endogenous antigens. They are more stable than DNA plasmids and are more efficient because they need only enter the cell cytoplasm rather than the nucleus. RNA vaccines may also be constructed in such a way that they are self-replicating. These are usually derived from alphaviruses such as Venezuelan equine encephalitis virus. They generate large amounts of endogenous antigen when they replicate for a brief time within cells.
Modified Live Vaccines

Attenuated Vaccines

The use of live organisms in vaccines presents many advantages. For example, they are usually more effective than inactivated vaccines in triggering cell-mediated immune responses. Their use, however, also presents potential hazards. Thus, the virulence of a live organism used for vaccination must be attenuated so that it is able to replicate but is no longer pathogenic. The level of attenuation is critical to vaccine success. Underattenuation will result in residual virulence and disease (reversion to virulence); overattenuation will result in an ineffective vaccine. Rigorous reversion to virulence studies must be performed to demonstrate stability. Attenuated vaccines should not be used to vaccinate species for which they have not been tested or approved. Pathogens attenuated for one species may be over- or under-attenuated in others. Thus, they may either cause disease or fail to provide adequate protection.

Attenuation has historically involved adapting organisms to growth in unusual conditions. Bacteria were attenuated by culture under abnormal conditions, and viruses were attenuated by growth in species to which they are not naturally adapted. Vaccine viruses may also be attenuated by growth in alternative media, such as tissue culture or eggs. This has been done for canine distemper, bluetongue, and rabies vaccines. Prolonged tissue culture was, for many years, the most common method of attenuation. Attenuation of  viruses by prolonged tissue culture can be considered a primitive form of genetic engineering. Ideally, this resulted in the development of a strain of virus that was unable to cause disease. This was often difficult to achieve, and reversion to virulence was a constant hazard.

For some diseases, related organisms normally adapted to another species may impart limited immunity. Examples include vaccines against measles virus, which can protect dogs against distemper, and against bovine viral diarrhea virus, which can protect pigs against classical swine fever.

In rare circumstances, virulent organisms may be used for vaccination. The only current example of this is vaccination against contagious ecthyma (Orf, sore mouth) of sheep. Lambs are vaccinated by rubbing dried, infected scab material into scratches made on the inner thigh, resulting in local infection and solid immunity. Because vaccinated animals may spread the disease, however, they must be separated from unvaccinated stock for a few weeks. Considerable care must also be exercised in the preparation, storage, and handling of modified live vaccines to avoid temperature extremes that can reduce the viability of the organisms. Likewise, vaccines such as Brucella strain RB51 and contagious ecthyma are zoonotic and present hazards to the administrator.

Traditional methods of attenuating organisms have been by prolonged tissue culture or culture in eggs. These have relied on random mutations, an unpredictable process. Although few bacterial vaccines have been attenuated in this way (the most obvious examples are Brucella strain 19 and the Sterne strain of anthrax), the bacterial genome is usually too large to generate effectively and irreversibly attenuated mutants. It has proven much easier to attenuate viruses with their relatively small genomes. Many of the currently available viral vaccine strains were attenuated in this way. Attenuation of viruses by prolonged tissue culture can be considered a primitive form of genetic engineering. Ideally, this resulted in the development of a strain of virus that was unable to cause disease. This was often difficult to achieve, and reversion to virulence was a constant hazard. As an example of underattenuation, an MLV canine adenovirus 1 vaccine led to urine shedding, which sometimes caused corneal edema (blue eye) in naive dogs. This ended when the vaccine was changed to canine adenovirus 2.

Another relatively simple method is to adapt the vaccine virus to grow at a temperature approximately 10 degrees lower than normal body temperature. These cold-attenuated vaccines can be administered intranasally, where they can grow in the cool upper respiratory tract but not in the warmer lower respiratory tract or other organs.

Gene-deleted Vaccines

Molecular genetic techniques now make it possible to modify the genes of an organism so that it becomes irreversibly attenuated. Deliberate deletion of the genes that code for proteins associated with virulence is an increasingly attractive procedure. For example, gene-deleted vaccines were first used against the Aujeszky disease herpesvirus in swine. In this case, the thymidine kinase gene was removed from the virus. Herpesvirus requires thymidine kinase to return from latency. Viruses from which this gene has been removed can infect neurons but cannot replicate and cause disease.
Similar genetic manipulation can also be used to restrict the ability of bacteria to grow in vivo. For example, a modified live vaccine is available that contains streptomycin-dependent Mannheimia haemolytica and Pasteurella multocida. These mutants depend on the presence of streptomycin for growth. When used in a vaccine, the absence of streptomycin will eventually result in the death of the bacteria, but not before they have stimulated a protective immune response.
Additionally, it is possible to alter the expression of other antigens so that a vaccine will induce an antibody response distinguishable from that caused by wild strains. This creates a way to distinguish infected from vaccinated animals (referred to as DIVA).

Virus-vectored Vaccines

Another way to produce a highly effective living vaccine is to insert the genes that encode protective antigens into an avirulent “vector” organism. These vaccines are created by deleting genes from the vector and replacing them with genes coding for antigens from the pathogen. The recombinant vector is then administered as the vaccine, and the inserted genes express the antigens when cells are infected by the vector virus. The vector may be attenuated so that it will not be shed from the vaccinated animal, or it may be host-restricted so that it will not replicate itself within the tissues of the vaccinate. Virus-vectored vaccines are well-suited for use against organisms that are difficult or dangerous to grow in the laboratory.

The most widely used vaccine viral vectors are large DNA viruses such as poxviruses (fowlpox, canarypox), vaccinia virus, adenoviruses, and some herpesvirus. These viruses have a large genome that facilitates insertion of new genes. They also express relatively high levels of the recombinant antigen. In at least some cases, vectored vaccines appear able to induce immunity even when high levels of maternal antibody are present. Canarypox-vectored vaccines incorporating genes from canine distemper virus are now used to immunize dogs, and a similar vaccinia vector containing the gene encoding rabies glycoprotein is effective in protecting dogs and cats against rabies virus. Fowlpox virus and herpesvirus recombinant vaccines are widely used in the poultry industry. For example, one vector is fowlpox virus, into which Newcastle disease virus HA and F genes are incorporated. It has the benefit of conferring immunity against fowlpox virus as well.

An innovative example of a vectored vaccine involves the use of a yellow fever viral chimera to protect horses against West Nile virus. This technology uses the capsid and nonstructural genes of the attenuated yellow fever vaccine strain 17D to deliver the envelope genes of other flaviviruses such as West Nile virus. The resulting virus is a yellow fever/West Nile virus chimera that is much safer than either of the parent viruses.

Vectored vaccines are commercially available for:

•   avian influenza virus
•   West Nile virus and influenza virus in horses
•   feline leukemia virus
•   vaccinating wildlife against rabies virus

These vaccines are safe, stable, can work in the absence of an adjuvant, and like the gene-deleted vaccines, allow for differentiation from natural infections. Some are adaptable to mass vaccination such as in ovo vaccination of chickens.

By - Ian Tizard,
BVMS, PhD, DACVM, Department of Veterinary Pathobiology,
College of Veterinary Medicine and Biomedical Sciences, Texas A&M University