About beef cattle production

Approximately 80-90 % of beef eaten in the world comes from dairy production, where unwanted male calves are sold for beef cattle producers. About half of all calves born in a dairy farm are males. The calves stay with their mothers for some days, after which they are transferred usually to group pens with other calves. They are still fed milk, either from buckets, bottles or an automated calf feeder.

Between 10-39 days of age these young bulls leave their birth farm. In the Northern Europe, bull calves are sold to a slaughterhouse, which in fact transport the animals forward to another farm. These calf farms continue feeding the calves with milk for about six weeks. At the age of 2-4 months the calves can be considered as "teenagers" - at this stage healthy animals grow 800 - 1400 grams each day! This number varies between cow breeds. For dairy breeds the growth target is ~500 g / day, and ~700 g / day for beef breeds. When the animals weigh 120-180 kilograms (about 3-4 months of age), they may be transported to yet another farm, where they'll stay until they are slaughtered at the age of 16-19 months.

Beef cattle in the last, fattening phase.
In this case, their living conditions are abysmal.

Those farms which buy young or "teen" animals and grow them to adults have constantly a high risk of infective diseases. Animals from different farms carry different bacteria and are immune to different pathogens. It is immensely important to test the new animals especially for salmonella and BVD, and keep new animals strictly in their own sections of the barn. Each pen or section should be filled and emptied once (all in - all out), so it can be properly washed and disinfected between batches of animals. The animals are also very stressed when they arrive to a new farm. They have to get used to the new feed, barn, pen structure, feeding system etc, and yet eb able to stay healthy and grow well. This is a great challenge for the producers. Also, all medications given to cattle must be documented. When a live animal is sold, the producer must provide the buyer with information on all medications given to the animal within the last 3 months. The documentation must be done in every farm as long as the animal lives.


As mentioned, beef cattle are slaughtered at the age of 16-19 months. At this stage bulls weigh about 300-350 kg, which is half of their adult weight. Heifers should weigh over 200 kilograms.

Raising beef cattle  in America: Explore Beef
A different view by Animal Aid - Suffering of beef cattle

Pig health: common diseases and tail biting

Piglets are weaned from their mothers at the age of 28 days. Their feed, environment and pen mates change; the new pen may be colder or draftier, with different floor type etc. Weaning creates an enormous amount of stress, and many piglets get sick or die due to it. If they do make it through the weaning phase, the same stress faces them again at the age of 13 weeks, when they are moved together with the adult pigs. There even more serious diseases and behavioral problems threaten the animals.

 

Weaned pigs

Weaning diarrhea

(c) The Pig Site

Because of the stress, many pigs get diarrhea within a week of weaning. It slows down their growth, but can even be lethal. Commonly the diarrhea is caused by E. coli, in which case it may be treated with antibiotics. The medicine is added to the pig feed. In addition, electrolytes can be mixed to the drinking water, decreasing the risk of dehydration. The antibiotic treatment should last 5-7 days.

There is no preventive medication, but by reducing the stress of the weaning may have a huge impact. If at all possible, farrows should not be split in weaning. The best way is to leave the farrow to the pen they were born in, and simply lead the sow away. Good hygiene, warmth and lack of draft are essential at the time of weaning.

Swine dysentery

Swine dysentery is one of the most economically damaging diseases a farm can experience in terms of medication, mortality, non-marketable pigs and extra feed costs (The pig site). Swine dysentery is caused by the bacteria Brachyspira hyodysenteriae, which causes a severe infection in the large intestine of pigs weighing 15-70 kg (can infect also adult pigs). First pigs are usually infected by rat faeces, since rats are hosts for B. hyodysenteriae. The symptoms of dysentery are loss of weight, loss of appetite and wet and bloody faeces. The bacteria is spread with the feaces, so it spreads quite easily, and the bacteria survives in the piggery for a long time. Mortality in pig dysentery is high.

To get rid of the bacteria in the piggery, the whole piggery (or at least the sections with the infected animals) has to be emptied, washed, disinfected and kept empty for two weeks. If all the animals cannot be removed, they must be given preventive medication. All manure handling and cleaning operations must be revieved, and rats eradicated from the building. Boots must be cleaned when moving between sections in the piggery, and each section must have its own tools (such as dung shovels) to prevent any bacteria from spreading between sections.

Swine dysentery in The Pig Site.

Feces from a pig infected with dysentery. (c) http://www.pig333.com/what_the_experts_say/page_2

Brachyspira pilosicoli

Br. pilosicoli is a bacteria, which causes diarrhea to pigs a few weeks after weaning. The faeces have no blood, since the bacteria does not destroy the intestines, but the dung resembles cement (gray and lumpy). Br. pilosicoli infection decreases growth, but it can be treated with antibiotics. Mortality is lower than in swine dysentery.

It is recommended to take faeces samples if Br. pilosicoli infection is suspected. Since the bacteria dies soon when outside the animal, the sample must be taken directly from the rectum and transferred to a laboratory in a suitable culture medium.

Lawsonia intracellularis

Lawsonia is a bacteria which proliferates in the epithelial cells of the small intestine. It causes decreased growth and occassional diarrhea, which usually start two weeks after weaning. In more serious cases Lawsonia can perforate the intestinal wall, and leading into severe peritoneal infection. Mortality in Lawsonia is low, and it can be treated by mixing antibiotics to the feed. However, the infected pigs continue to spread the bacteria up to 10 weeks, so hygiene is again immensely important.

Lawsonia has a gangrenous form, which can be very severe. It causes constant, bloody diarrhea, and may cause sudden deaths. In post-mortem examinations swollen intestinal lymph nodules and thickened intestinal walls are common findings.

Pig edema disease

The pig edema disease is caused by Escherichia coli enterotoxemia. It infects pigs 1-2 weeks after weaning, and usually attacks the best grown pigs. The bacteria is first ingested by the pig, and soon the bacteria starts to create strong toxins in the guts. The toxins are absorbed and spread into the internal organs, killing the pig within  a day. The condition is described as "in the evening the pigs shiver, in the morning they're dead."

Althought the edema disease cannot be treated, it can be prevented. Before weaning the pigs must be familiarized with high-quality feed, and the amount of feed can be limited during weaning. Adding citric acid or lactic acid bacteria to the feed helps the pigs' digestion and supports the functions of the stomach.

Pig edema disease in The Merck Veterinary Manual

Gestation crates, where sows may be kept for weeks. (c) Wikipedia

Diseases of adult pigs

 

Leg and hoof injuries

Injuries in the hoof can be caused by accidents, overgrowth of the hoof, a foreign object stuck in the hoof or unfastening of the keratinous layer of the hoof. The hoof may become infected, often because of the bacteria Fusobacterium necrophorum or Arcanobacterium pyogenes. These both cause hoof infections also for cows. Due to the rather short lifespan of pigs to be slaughtered, hoof problems rarely cause severe problems. When needed, pig hooves can be trimmed just like cows' or horses'.

Swine erysipelasis.
(c) Iowa State University

Infective arithritis in pigs is often caused by streptococci, which access the joints through open wounds. Arithritis caused by other than Mycoplasma bacteria can be treated with penicillin injections.One of the causing bacteria, Erysipelothrix rhusiopathie, can cause swine erysipelasis. This disease is zoonosis, so it can affect humans. Swine erysipelasis causes clearly visible and elevated red markings in the skin and high fever.

Leg weakness or osteochondrosis (OCD) in pigs affects the surfaces of joints, causing pain when the animal moves. It is usually seen in pigs nearly ready for slaughter, even though the symptoms have developed for a long time. Osteochondrosis is partly hereditary, but strong feeding and fast growth add to the risk of getting ill. OCD can be prevented with selective breeding, soft litter in the pens, spacious pens and calm animal handling to avoid injuries. More about OCD in The Pig Site.

Tail biting

(c) The Pig Site

Tail biting is a very wide-spread and serious problem in piggeries. It is not a disease but a severe behavioral problem. This condition is so common that some producers consider is normal, while actually tail biting is a clear indication of bad animal welfare.

Tail biting means that the animals bite and chew on each others' tails. The tails are often bitten off entirely, and sometimes even the exposed spine is chewed on. This causes severe pain, and is almost impossible to stop once it becomes a habit for the animals. Several factors can induce tail biting:

• Lack of litter and stimuli (toys, chewable objects etc)
• Lack of space to avoid other animals
• Lack of space for proper social behavior
• Bad air quality
• Mixing of animal groups, disturbing their social structure
• Limited feeding or too small feeding trays, not enabling the whole group to eat and drink at the same time
• Lack of minerals or salt in the diet
• Illnesses and parasites
• Stress

Usually a small female pig starts biting the flanks of castrated boars. If the environmental conditions are not improved, more pigs pick up the behavior, and start biting the tails of others. Bitten tails are open wounds, which are prone to infection and when bleeding, encourage the pigs (omnivores as they are) to bite more. Once this becomes a habit, the pigs will not stop it even if they were transferred to ideal conditions. On the contrary, if moved to another group, the biters will only teach the habit to the new animals.

The only way to treat tail biting is to prevent it by good animal handling practices and humane animal husbandry. Docking the tails of piglets or using red lights to avoid the pigs from seeing blood are ineffective in treating the actual cause. They also make the situation worse, when the pigs cannot ease their stress even by tail biting.

(c) pig333

Piglet health

(c) Gemel's blog

Piglets, like calves, are born without any immunity at all. To survive even just the first day, they must get colostrum within a few hours after birth. The antibodies in the colostrum absorb best within 4 hours of birth, and start to weaken soon after, and stop entirely after 24 hours. The piglets also need a dry, clean, and warm environment.  New born pigs face many threats in today's production environment: diarrheas, join infections and skin problems are the most common. Good animal care can virtually eliminate the risk of piglet diseases.

Piglet diarrheas

There are several bacteria causing different types of diarrhea. Most common diarrhea causing agents are Escherichia coli, Clostridium perfringens, Coccidia, Isospora suis and the rota virus. Diarrhea is always only a symptom, never the actual cause! Piglets under three weeks of age are susceptible to diarrheas, for they have no bacteria-killing acids in their stomach, and their mucuous membranes are underdeveloped.

Vaccinating the sows is the only way to prevent some types of diarrhea. All sows must be vaccinated when they are inseminated for the first time, and again 2-3 weeks before every parturition. Diarrheas can be preventing to some extent by clean environment, protecting the piglets from cold and draft, hygienic handling of animals and by providing only clean feed and water.


E. Coli

• Coli is a common bacteria in the gut, but some strains of coli are pathogens. Commonly it infects piglets of 0-4 days of age, if they are axposed to the sow's feces. Coli diarrhea is very common, and lethal in piglets under a week old (diarrhea causes dehydration). 
• Symptoms of a diarrhea caused by E. coli are liquid, brown feces, which often are spread to the walls of the pen.
• Vaccinating the sow is the only way to prevent and treat E. coli diarrhea, since then the piglets will inherit resistance for it in the colostrum. 

Clostridium perfringens (type C)

• Cl. perfringes is a rather rare bacteria, which infects piglets 1-4 days of age. The bacteria lives in the intestine, where it secretes a strong cytotoxin, destroying the microvilli in the intestinal epithelium.
• Symptoms are bloody, foamy diarrhea, which causes high mortality
• Cl. perfringens is a sporulating bacteria, and it's spores are very durable against heat, draught etc. Destroying the spores from the piggery requires a careful and thorough disinfection of the pens.
• Vaccinating the sow is the only way to prevent and treat Cl. perfringens infections.

Rota virus

• Rota virus is a rare virus, which has strains infecting pigs and different strains infecting humans. Rota from pigs cannot thus infect humans or vice versa.
• Infects piglets 1-14 days of age, exposing the piglet to various bacterial infections (such as E. coli). Sometimes only the bacterial infection is recognized and treated, leaving the virus unharmed.
• Rota virus requires filthy surroundings and a piggery-wide decrease in immunity, but after it gets in to the piggery, it is difficult to get rid of.

Isospora suis

• Isospora suis is a protozoan, which causes coccidiosis in piglets over one week of age.
• It thrives in damp environment, so keeping the pen dry with enough clean litter is very important. Isospora suis causes creamy, yellow, possibly lumpy feces

Other piglet diseases

(c) nadis.org - Joint ill in piglets

Like calves, piglets are susceptible to join ills (arithritis) caused by bacteria. The bacteria access the body either via wounds (often in the front knees), navel or from the bases of cut teeth. Having intact and safe pen structures and clean enough litter prevents infections. Joint ills can be treated with injecting antibiotics for three days, or in severe cases by having the piglet put down.

(c) knowmycotoxins.com

Some piglets are born with very weak hind legs. Unable to stand up, they lie down with their feet spread (splay legs). This condition is partly hereditary, but slippery floors and low weight at birth add to the risk. If only the hind legs are affected, the prognosis is very good. Bandaging the hind legs together helps the piglet to control it's legs, and the animal usually heals in a few days. Piglets who have weakness in three or four legs have a bad prognosis, and should be euthanized.

(c) Flock and Herd

Greasy pig disease is caused by the common skin bacteria Staphylococcus hyicus. For weak and sensitive piglets S. hyicus can cause a severe skin infection (exudative dermatitis or exudative epidermitis). At first there are brown patches in the skin, which later becomes wrinkled, greasy and flaky. Deep scabs and lesions are seen in the skin. Greasy pig disease may be lethal, but can be treated with antibiotics if the causing bacteria is first identified. This condition has been well documented in The Pig Site.

Cow health: rumen disorders

(c) University of Minnesota

The rumen is a complex, large organ, which can hold up to 80 litres of feed. It is a sensitive organ, and any disturbances in the rumen can be lethal. Minor disturbances are quite common, and even some of the most severe cases can be solved at the farm without a vet. This text describes bloat (gas build-up in the rumen), "nail", acidic rumen and dislocation of the abomasum.

Bloat (the cumulation of gas or foam in the rumen)

The rumen contracts every 50-70 seconds, both mixing the feed and removing methane as belches. If these contractions stop or something blocks the esophagus, the gas keeps accumulating and filling up the rumen. When the rumen swells, it presses the cow's internal organs and lungs, blocking blood vessels and eventually suffocating the animal when the lungs no longer have space to expand.

(c) informedfarmers.com

Cause:  Gas can accumulate in the rumen for several reasons: the rumen stops contracting due to too low pH or nervous problems, the esophagus is blocked or the animal lies on it's side for too long. Foam can be created by the feed, often clovers or too much concentrated feed. The foam prevents the methane from being released as belches.

Symptoms: The cow's left flank swells considerably when the rumen fills with gas. The cow stops eating, and as the space for it's lungs decreases, it starts panting and gasping for breath. The condition can kill the animal in hours, depending on the severity.

Treatment: If there's foam in the rumen, the bubbles can be broken easily by giving the cow 5 desiliters of rapeseed or olive oil, or the same amount of melted butter. If the cow lies on it's side, it must be supported to the right position. Then find why the cow lies on it's side, and treat the root cause. If the rumen is swollen and the animal drools, the esophagus is blocked. The easiest way is to push the obstacle down the throat and into the rumen, thus freeing the esophagus.

Mild cases are often caused by changes in the nutrition, spoiled feed, ice cold drinking water or antibiotics given orally. In this case the cow has low appetite, and it may have pains and diarrhea. Mild cases can be treated with rumen supplements, dry hay, yeast and sugar (half a kilogram both)

An in-depth article about bloat in cattle by Alberta Agricultural and Rural Development

A sharp object in the fore-stomachs, "a nail"

Cows cannot select their feed as carefully as horses, so they may pick up and swallow foreign objects quite easily. Earlier the most common cause for this was a swallowed nail or a piece of barbwire, but luckily today those are more rare in the farms. Slaughterhouses constantly find foreign objects in the fore-stomachs: cell phones, scarves, wallets, scoops... Sometimes a coil of barbwire has fallen to the feed mill/feed wagon, got shred to small bits and been mixed with the feed, server to the whole cattle. Most often the cause is the carelessness of the people in the farm, leaving nails, hammers etc where to cows can reach them. Sometimes the animals can swallow foreign objects if they escape their pasture or barn.

Cause: When a foreign object is swallowed, it can either block the esophagus, get stuck in the digestive tract or pass through it. If the item is sharp, it may poke through the stomach walls, causing an infection. The item may become encapsulated in the digestive tract, whereupon tissue is grown around it, preventing the item from being removed or harming the organs. The reticulum is right next to a cow's heart. If a sharp object penetrates the reticulum wall, it may pierce through to the heart, causing a sudden death.

Symptoms: Symptoms vary based on the item swallowed and what it causes in the digestive tract. If the item is sharp and pierces any tissues, the animal shows signs of pain (restlessness, kicking of the abdomen). The cow may stand with it's back arched. Foreign objects in the esophagus or rumen may cause the animal to vomit, and in severe cases the cow will regurgitate even the water it drinks.

Treatment: If the foreign object is metal, the animal can be fed a magnet, which then stays in the rumen for the rest of the cow's life. The magnet catches any metal items, preventing them from pricking through the rumen walls. The animal should be tied to a stall, and it's front end should be raised. If the condition doesn't improve in 1-2 days, the foreign object must be removed surgically.
 

Acidic rumen

The pH of the rumen should always stay between 6-8. Sometimes if there's too much concentrated feed or not enough salive to buffer the contents, the pH of the rumen can drop quickly. Ruminants develop symptoms of acidic rumen when the rumen pH is lower than 5,5. Acidic rumen exposes the animal to problems with the abomasum, laminitis of the hoof, rumen wall damage and liver abscesses.

Cause: Too much starch and sugar in the feed cause very strong fermentation in the rumen, creating more acidic side products than the metabolism can handle. The feed may also require little chewing or ruminating. This condition offen occurs near calving, when the cow gets plenty of concentrated feed, but eats little roughage. Acidic rumen is also common with bulls to be slaughtered, since they are fed mostly concentrated feed.

Symptoms:  Loss of or variable appetite, wet feces, undigested feed in the feces, dropping of cuds (ruminated pieces of feed), mild bloat. The animal may lose body fat.

Treatment: Treating this condition once helps very little. Sodium bicarbonate (100-200 g / day) may relieve the worst symptoms, but the most important thing is to adjust the animal's diet to have enough hay or straw, and that the possible silage is not shredded too short. The diet must have only moderately starch and sugar, and they should not be given all at once. The animals must have access to clean water at all times.

Displaced abomasum

Abomasum is the last of the cow's stomachs, and the only which functions like the stomach of monogastric animals. As shown in the picture above, abomasum lies at the bottom of the abdomal cavity, behind the reticulum. Abomasum usually rises up to either side of the animal.

Picture adapted from The University of Missouri

Cause: The abomasum is displaced if its walls lose their tonus and the abomasum filled with gas. The cause is still uncertain, but high level of glucose and low level of calcium in the blood are contributing factors. Acidic rumen is also a risk, because it sends forward unfermented feed, which ferments even in the abomasum, creating gas and lifhting the abomasum up like a balloon. Stress and sickness near calving may also cause dislocation of the abomasum.

Symptoms: Loss of or variable appetite, no fever, slightly elevated levels of ketones. When pressing an ear against the animal's flank and tapping it with a finger, a distinct, metallic "ping" sound can be heard.

Treatment: Surgical treatment is the most effective, and can be done on-site. Gas is removed from the abomasum, and it is secured to its place with a few stitches. Another old remedy is to roll the cow over on it's back or making the animal run, but these provide often only temporary relief.

Cow health: Metabolic illnesses

Cows today produce much more milk and meat than their ancestors ever did. They are fed optimum diets and kept in maximum production the whole time, regardless of how unnatural that is to an animal. This causes many problems and illnesses to cows and calves. Most common ones are milk fever, ketosis (acetone disease) and grass staggers (grass tetany, hypomagnesemia, winter tetany).

Milk fever

Milk fever can occur in cows and pigs right or soon after calving / parturition. If not treated quickly, severe milk fever can kill the animal in one day.

Cause: Milk fever is caused by low levels of calcium in the blood. After calving the milk production starts on high efficiency, and a lot of calcium is suddenly needed. This calcium is released from the animal's bones. If calcium cannot be released quickly enough, the calcium needed for muscles to function is used instead, causing milk fever. Milk fever can be prevented by keeping the cow in very low-calcium diet during it's dry period, giving the body time to increase it's calcium release mechanism.

Milk fever can occur later in the production period if the amount of calcium in the diet suddenly drops, or absorption of calcium is decreased due to another illness. Heifers and cows with low milk yield rarely suffer from milk fever.

Symptoms: Milk fever is not actually a fever, but paralysis. First the cow stops eating, it's skin feels cool, and it's muscles of the cow may tremble. Soon the large muscles in the legs cannot support the animal's weight anymore, and it falls, unable to stand. The cow may lie on it's side, whereupon it's rumen may fill with gas, suffocating the animal. Rumen movements stop, and within a day the animal dies due to paralysis of the lungs, liver and heart.

(c) www.nadis.org.uk

Treatment: Intravenous infusion of calcium is needed to raise the level of calcium in the blood. This is done by a vet, who must also listen to the animal's heart while infusing the drug (calcium is potentially toxic, and may cause heart failure). Only enough is given for the cow to get up and start eating, so it can fill it's own calcium levels naturally. Sometimes another treatment is needed, if the diet contains too little Ca. This can be given orally by anyone.

The risk for ilk fever can be reduced by ensuring that the dry period diet is low in calcium. The diet can also be tailored to affect the cation-anion balance of the cow's body: by lowering the pH of the body (increasing anion salts) three weeks before calving, the calcium is released from the bones more effectively. This can prevent up to 50 % of the cases of milk fever.

Milk fever in The Merck Veterinary Manual

Ketosis

(c) Valley Veterinary Clinic

Cause: Ketosis is caused when the cow has too little glucose in it's blood. Cows synthetise glucose in their liver, but this creates acidic ketones. Normally rumen microbes can use them as energy. If too much glucose is formed this way (due to lack of it in the blood), the microbes cannot use all of the ketones, and the pH of the animal drops.

Earlier ketosis occurred right before milk production peak, when the cow ate less than it needed to produce milk. Nowadays ketosis occurs commonly for recently calved fat cows, because their body releases more fats for energy than their liver can handle. The liver collects fat, and can no longer produce glucose, leading to ketosis.

Symptoms: Decreased appetite especially for concentrated feeds, eating of strangle substances such as dirty straw, apathy, quietness, loss of weight, dry feces, acidic smell in the animal's breath (not all people can smell ketones). Ketone levels in the milk are elevated. Cows may drop cuds, because they are acidic and thus taste bad.

Prevention and treatment:  More important than treating ketosis is to prevent it altogether. Make sure the cows are in good shape before calving, which also makes the calving easier and reduces the following metabolic stress. Avoid cows with ultra high milk yield, because they are more prone to ketosis. Adjust the diet for each animal so that they get enough precursors for gluconeogenesis even if their appetite is low. If possible, limit milking so the cow needs less glucose for production.

Treatment for ketosis is intravenous infusion of glucose, injection of cortisone, propylene glycol given orally

Ketosis in the The Merck Veterinary Manual

Grass staggers (grass tetany, hypomagnesemia)

Grass staggers is a form of convulsion caused by acute lack of magnesium. Young grass is low on magnesium, so this disease often affects cattle which has just been let to pasture.

Cause: Grass staggers is caused by lack of magnesium. Grass in the pasture can have too little magnesium if the grass is young, or it has been fertilized with too much potassium and nitrogen and too little magnesium. Absorption of magnesium is decreased if the diet has over 20 % of protein, over 3 % of potassium or too little fiber. Appetite also affects to how much the animal eats, and how much it thus gets magnesium.

Symptoms: When the magnesium level in the blood decreases, the animal cannot no longer control it's muscles. First the animal appears overly alert and tense, it is restless and its movements are uncoordinated. Soon it's muscles convulse, and the animal gets a seizure. The cow is sweaty and it's body temperature is high due to constant muscle tension.

Treatment: Magnesium must be injected to the animal as soon as possible, for it may die at any moment. Sometimes cows with grass staggers die just from the needle prick, so even quick treatment may not save the animal. If the injection is given and the cow picks up, magnesium must be given orally for five days. The diet of the whole cattle must be checked! If the cause is low Mg levels of the pasture grass, every animal in the herd may get sick and die.

Hypomagnesemic tetany in The Merck Veterinary Manual

Cow health: Mastitis and teat injuries

Whether one keeps beef or dairy cows, the production is still dependent on the udder health of lactating cows. The udder is a delicate organ, which is very susceptible to damage and infections in today's high-stress, high-production environment. 

Mastitis

(c) http://www.agcanada.com

At every farm, approximately 30 % of cows suffer from clinical or subclinical mastitis, the infection of the udder. Since mastitis ruins the milk from the infected quarter of the udder, it causes loss of milk (loss of profit). Mastitis also increases the work load, may lower milk yield permanently and is expensive to treat because it's so common. It's symptoms therefore are the body's normal defense mechanism against viruses, tissue damage and bacteria. Therefore mastitis has very different symptoms depending on the causing agent.

Cause: Mastitis is often caused by bacteria like Escherichia coli, Staphylococcus aureus, coagulase-negative staphylococcus, Streptococcus agalactiae, Str. uberis, Str. dysgalactiae, Arganobacterium pyogenes or Corybacterium bovis. It is important to test the infection milk to find out which bacteria is causing the infection, so the correct preventive measures can be taken. E. coli for example comes usually from filty stalls, Str. dysgalactiae is found with injuries and Str. agalactiae infection is always from another cow.

Symptoms: Symptoms vary, but the most common ones are fever, swelling and warmth in the infected part of the udder, abnormal milk, reduced milk yield, loss of appetite and reluctance to give milk due to soreness in the udder.

Treatment: "Common treatment" may be costly and useless. For effective treatment the cause of mastitis must be studied. Str. agalactiae responds well to penicillin, but E. coli may need stronger antibiotics plus supportive treatment, because it often also causes severe diarrhea. C. bovis infections are best treated with teat disinfectants and drying off (stopping her from lactating until the next calving).

Prognosis: After severe mastitis the infected quarter may go dry entirely, or it must be amputated as a treatment. This leaves the cow with only three teats, decreasing its milk yield. Some cows which get mastitis often may need to be slaughtered. An epidemic of mastitis is always a cause to re-evaluate the conditions in and cleanliness of the barn.

Teat injuries

(c) http://eagleburra.com.au

Teat injuries can be problematic on their own, since they cause pain and bloody milk, but they may also lead to mastitis. Some cows may have congenital teat deformations.

Cause: The cow may step on her teats if she cannot lie down or stand up naturally due to slipper floor or other environmental problems. In a cramped barn, cows may step on each other's udders. Adult cows sucking milk from each others, fights and faulty milking machinery may also cause teat damage.

Symptoms: In chronic (long-term) teat injuries the milk channel gets thicker over time and may get clogged. Round, hard growths may be felt in the teat. Milk letting is slow. In acute (sudden) injuries the milk may be bloody, teat shows external damage.  A gangrene may develop on to the skin of the udder, and the udder may turn blue.

Treatment: Injured teats must be kept clean. The cause for the damage must be removed, if possible. Deep or long wounds in the teat should always be treated by a vet, so they heal better. Gangrenes can be left to heal on their own, but treating a possible infection and keeping the udder clean are very important. Chronic teat injuries like clogged milk channels can be surgically opened by a vet, but the prognosis is not good.

Prognosis: Prognosis depends a lot on the nature of the injury. Small acute injuries often heal well. Chronic injuries may keep getting worse if the cause isn't quickly removed, and have worse prognosis.

Animal digestion

Monogastric animals

The digestive tract of an monogastric animal (animal with only one stomach) aims at breaking down the eaten feed, splitting the compounds into nutrients, transform them into usable form and excrete the non-digestable matter as feces or urine. This is achieved with digestive enzymes and/or microbes in the digestive tract.

Picture from lecture materials,
original source unknown

Digestion has roughly three phases: chewing or mincing, digestion and absorption. After absorption it is a matter of other tissues to use the nutrients for various chemical processes. The first phase, chewing, begins as the animal picks the feed to its mouth. Chewing adds the surface area of the feed, making it easier for enzymes to attach to it. Chewing also adds the excretion of saliva, which lubricates the feed and the esophagus. Saliva includes also growth factors, which support the renewal of the digestive tract epitelium. In some species, excluding ruminants, have amylase in their saliva, which breaks starch and glycogen into smaller polysaccharides. Mouth area has also several lymp nodules, which act as a first barrier against any bacteria in the feed.

Swallowing takes the feed in small chunks to the esophagus and down to the stomach. The stomach consists of four areas: cardia, fundus, corpus and pylorus. All areas have a different structure of mucous membrane: for example, cardia excretes mucus, but fundus excrete gastric juices. Pylorus has sensory nerves, which regulate digestion. Gastric juices include HCl, a strong acid, which lowers the pH of the stomach to 1-3 and this assists the denaturation of proteins and kills bacteria. Pepsinogen is secreted by the glands in the stomach, and transformed to pepsin by the HCl. Pepsin breaks proteins to small polypeptides. In addition to HCl and pepsinogen, the gastric juice includes water, inorganic salts and mucus.
In the stomach the HCl and pepsin are mixed with the feed as the stomach wall contracts, and the food mass becomes softer, warmer and more watery.

Pyloric sphincter acts as a gate between the stomach and the small intestine. The beginning of the small intestine is called duodenum. Pancreatic juices, intestinal gland liquids, bile and bile salts are all excreted to duodenum, where the feed mass is quickly neutralized (remember it's pH was about 1-3). Intestinal glands secrete a basic liquid which neutralizes the chyme (= food mass). Bile and bile salts from the liver mix water into fats, forming fat droplets. Lipase from the pancreas is actived by bile salts, and then it breaks the fat droplets into glycerol and fatty acids. Pancreas excrete also insulin and glucagon, which are used to transfer glucose from the blood into cells (insulin) or discharge stored glycogen into the blood as glucose (glucagon).

The next part of the small intestine is called jejunum. This is where most of the nutrients are absorbed, after they have been broken down to usable compounds in the duodenum. Pancreatic amylases break down polysaccharides into disaccharides, and disaccharidases into monosaccharides. Trypsin and chymotrypsin (from the pancreas) break polypeptides into smaller pieces, which are split into amino acids by peptidases:

Picture from lecture materials, original source unknown

From the small intestine the chyme moves to the large intestine, where microbes ferment it. Only water, electrolytes and volatile fatty acids (ruminants only) are absorbed from the large intestine. In addition, some B vitamins are formed in the large intestine.

Ruminants

The  saliva of ruminants doesn't have any amylase. Instead, it is rich in mucin, phosphates and carbonates, which balance the pH of the rumen. The esophagus differs from that of the monogastric animals in that it has two kinds of contractions: peristaltic, which move the feed pieces down to the rumen, and antiperistaltic, which bring boluses back to the mouth for the animal to ruminate. 

Ruminants have four stomachs, and only the last of them (the abomasum) functions like the stomach of monogastric animals. Ruminants have three fore-stomachs: rumen, reticulum and omasum. These are sites for microbial fermentation. Rumen is the first of the fore-stomachs, and in cows it can store up to 80 liters of feed. It hosts about 10¹¹-10¹² microbes / g of feed. The rumen contracts in three stages every 50-70 seconds. The contractions mix the feed (mixing the microbes into the contents of the rumen), releases methane as burps and brings boluses back to the mouth for the animal to ruminate. Rumen and reticulum are often considered as one, and called reticulorumen. The pH in the reticulorumen must stay between 5-8 for the microbes to work, and the gases must be let out as burps. Otherwise the rumen contractions are hindered and the animal may suffocate, as the methane fills the rumen and the lungs no longer have space to expand.

From the reticulorumen, water, Na, Cl, ammonium and water are absorbed. Omasum is the last of the fore-stomachs. It is filled with leafs, which sieve the feed, and prevent too large particles from reaching abomasum. From the omasum, water, minerals, ammonium and VFA are absorbed.

The final stomach for ruminants is the abomasum. It secretes pepsin and HCl, which lower its pH to 3-4. There the dead microbes from the rumen are digested enzymatically, and the proteins and fats in the microbes can be absorbed. Some of the proteins in the feed are not absorbed until in the abomasum. Abomasum also finalizes the digestion and absorption of other particles, which may not have been fermented in the fore-stomachs.

Farm animal nutrition: Vitamins

Vitamins are essential organic compounds, which are needed for normal bodily functions. Usually animals cannot synthetize all of the required vitamins, so they must have them in the feed. Each vitamin has a task which no other compound can replace. Common tasks for vitamins are metabolism management, antioxidative activity, hormonal activity, enzyme activity and energy formation.

Vitamins can be divided to fat-soluble and water soluble compounds. K, A, D and E vitamins are fat-soluble: they are stored in fat, transferred in lymph, and are slow to excrete from the body. Vitamins B and C are water-soluble: they infuse directly to blood, circulate freely in the body, and are excreted through urine. Since they are not stored, the animal needs them daily from the feed. Most feeds do not include enough vitamins, so they must be added.

Fat-soluble vitamins: A, D, E, K

 

Vitamin: A
Required for: Important for vision, especially night vision, bone formation, renewal of epithelial tissue, fertility. Also an antioxidant.
Sources: The precursor for vitamin A are carotenoids in plants. Six micrograms of beta carotenoid creates one microgram of retinol (vitamin A).
Deficiency symptoms: Decreased vision, blindness

Vitamin: D
Required for: Immunological system, genetic expression, metabolism of phosphorus and calcium
Sources: The precursor for vitamin D exists in the skin. It turns into D-vitamin in sunlight or UV-light, and absorbs then into the body. D-vitamin can also be ingested from the feed. Non-active forms of D-vitamin are transferred to the liver and finally to kidneys, where it is transformed to calcitriol (the active form).

Deficiency symptoms: Rickets, soft bones

Vitamin: E (common name for tocopherol and tocotrienol compounds)
Required for: Acts as an antioxidant, protecting the unsaturated fatty acids in cell membranes from oxidization. Supports blood circulation, immunology and fatty acid synthesis.
Sources: Plant feeds, especially vegetable oils and whole grain products
Deficiency symptoms: Anemia, bleeding, changes in the lungs

Vitamin: K
Required for: Blood clotting
Sources: Vitamin K is formed in the large intestine. Usually animals can synthetize enough of it in any diet. The synthetic vitamin K is water-soluble, but in the liver it is transformed into a fat-soluble form.
Deficiency symptoms: Anemia, bleeding, changes in the lungs

Water-soluble vitamins: B and C 

 

Vitamin: B

• Vitamin B₁ (thiamine)
• Vitamin B₂ (riboflavin)
• Vitamin B₃ (niacin or niacinamide)
• Vitamin B₅ (pantothenic acid)
• Vitamin B₆ (pyridoxine, pyridoxal, or pyridoxamine, or pyridoxine hydrochloride)
• Vitamin B₇ (biotin, "vitamin H")
• Vitamin B₉ (folic acid)
• Vitamin B₁₂ (various cobalamins; commonly cyanocobalamin in vitamin supplements)

Required for: Coenzyme in energy-releasing reactions, coenzyme in RNA and DNA formation, neurological functions (thiamine),  redox-reactions (riboflavin, niacin), formation of phospholipids (biotin)
Sources: B vitamins are often bound to proteins, so they are metabolized as proteins. They are not stored in the body, so the animal needs to have a constant supply of vitamin B. B₁₂ is an exception, it can be stored to some extent. B-vitamins are also formed in the rumen and large intestine.
Deficiency symptoms: Symptoms depend on which vitamin B the animal is lacking. There can be  e.g. weight loss, neurological dysfunction, convulsions, skin infections, hypertension, diarrhea, lesions and anemia. Deficiency of thiamin may cause cerebro-cortical necrosis.

Vitamin: C
Required for: Acts as an antioxidant together with Fe or Cu, collagen metabolism, steroid metabolism. Increases stress tolerance. The amount needed varies greatly between species. Animal's age, production level, gestation, health, diet and nursing affect the needed amount as well.
Sources: Vitamin K is formed in the large intestine. Usually animals can synthetize enough of it in any diet. The synthetic vitamin K is water-soluble, but in the liver it is transformed into a fat-soluble form.
Deficiency symptoms: Scurvy (swollen and bleeding gums, internal haemorrhage)

Pigs and poultry 

 

Animals, which are raised indoors or fed other than plant-based feed likely need additional vitamins in their diet. Pigs and poultry commonly never see sunlight, and thus form very little or no vitamin D. Due to their concentrated, synthetic and/or animal based diet, but pigs and poultry get no vitamins A and E, which are common in plants. They may also need riboflavin, niacin, B₁₂ and pantothenic acid added to their feeds. Poultry need also vitamin K, since they are fed solely on grains and plant proteins.

Farm animal nutrition: Minerals

Minerals are inorganic compounds, which are left to the ashes after the tissue or the feed has been burned. In dog foods cans, for example, this is marked as "ash" (there is no ash added - it just means the inorganic material in the feed). There are 7 macrominerals and 15 microminerals which farm animals need to get from their feed. The animal needs over 100 mg/kg of macrominerals and less than 50 mg/kg of microminerals (trace elements) each day. In the body, minerals are used for building tissues, regulating the osmotic pressure and as catalysts. Deficiency of some minerals may be even lethal, as the important regulatory systems or metabolism fails.

For farm animals, the necessary macrominerals are C, P, K, Na, Cl, S, Mg.
Necessary trace elements / microminerals are Fe, Zn, Cu, Mb, Se, I, Mn, Co

The amount of minerals required by an animal is affected by its production level, health, amount of growth, meat quality, bone structure and feed digestability. Minerals should be in an available form in the feed. For example, phosphorus exists in plants as phytine acid, and phytase enzyme is required to sever the Ps from the acid. Pigs and poultry have no phytase enzyme in their bodies, so it must be added to the feed. Production level of the animal affects greatly to its need for minerals. Animals secrete a lot of calcium in milk and eggs, and thus need it constantly from their feed.

Mineral	Use in body	Deficiency symptoms	Poisoning symptoms
Ca Calcium	Milk production, bone structure, muscle actions, blood clotting	Rickets, bone deformations, milk fever, reduced milk yield	Calcification of soft tissues, decreased absorbance of other minerals
P Phosphorus	Bone structure, DNA, energy metabolism	Rickets, bone deformations, decreased fertility, pica (eating non-foods (soil, wood etc))	N/A
Mg Magnesium	Muscle functions, milk production, energy metabolism, nervous system	grass tetany/grass staggers, nervousness, loss of weight, Calcification of soft tissues	Diarrhea, loss of appetite, rumen damage
K Potassium	Milk production, pH balance, muscle and nervous tension	Loss of appetite, paralysis, matted fur, decreased milk yield	Milk fever, decreased absorption of Mg, mastitis
Na Sodium	Osmotic tension, pH balance, muscle functions	Loss of appetite and milk yield, pica	Swelling
Cl Cloride	Osmotic tension, pH balance, formation of gastric acid	Descrease in milk yield	Swelling, constipation
Fe Iron	Haemoglobin, biochemical reactions	Anemia	Decreased growth, liver damage
I Iodine	Essential for fertility, brain development and thyroid glands	Decreased fertility, enlarged thyroid gland	Hypothyroidism
Zn Zinc	Cell division, appetite	Loss of appetite, decreased growth and fertility, skin problems	Decreased growth, pica, liver damage
Cu Copper	Activates enzymes, bone development, growth, breeding, health of skin and fur	Anemia, decreased growth, bone deformations, colorless fur, liver damage, heart problems	Liver and muscle damage
Mn Mangan	Essential for growth and fertility	Bone deformations, decrease in fertility	Decreased growth and appetite
Co Cobalt	Component of B12 vitamin	Anemia, decreased appetite	N/A
Se Selenium	ssential for growth and fertility	Decreased fertility, muscular dystrophy	Anemia, bad fur quality, hoof problems
Cr Chrome	Connected to stress	The amount of chrome in the liver deceases during stress	N/A

More information

Salt and trace minerals by Salt Institute
The need for trace minerals by HVS Animal Health

Farm animal nutrition: Proteins

Proteins are needed for balancing pH, liquids, nitrogen and acids in the body. They are also needed for cell to cell junctions, immunology, signal transmission, genetic regulation and entzymatic reactions. Proteins are built in the cells via DNA translation, when RNA sequences are used to build chains of amino acids.

Proteins are organic compounds, built from amino acids, which are linked together with peptide bonds. So again we have basic building blocks (~20 amino acids), which can be combined to create an immense variety of peptins (short amino acid chains) and finally proteins (usually they have 100-300 amino acids). Animals need proteins form their diet to form amino acids. Out of the 20 amino acids, nine are essential for most animals (the list varies by species):

• threonine
• methionine
• isoleucine
• leucine
• valine
• tryptophan
• phenylalanine
• histidine
• lysine.

Picture from lecture materials, original source unknown

Animals can synthetize the other amino acids by deamination and transamination. Deamination means removing the amino group from the acid, and transamination means attaching it to a suitable carbon molecule. Often this doesn't create enough of the needed amino acids, so adding them to the feed may be required. The amino acids, which are presently not needed in the body, are deaminated, transferred to the liver and secreted in urine / uric acid. Thus feeding the animals too much amino acids increases the amount of nitrogen in their excrements.The carbon skeletons of the excessamino acids are stored as carbohydrates or fatty acids.

Farm animals fed with corn-based diet often have deficiency of lysine and isoleucine, but enough tryptophan and methionine. With legume-based diet there's little tryptophan and methionine, but enough lysine and isoleucine. All amino acids contain approximately 16 % of nitrogen. Thus the amino acid (or protein) amount in an animal feed can be estimated by determining the amount of nitrogen in the feed. Even after careful animal breeding, the ingested vegetable protein to animal protein ratio in farm animals is still only approximately 30 %. Most of the proteins are used in metabolism, tissue reformation and for producing offspring.

Ruminants and amino acids

Again, ruminants have their own ingenious system for creating and using amino acids. The microbes in the rumen use simple nitrogenous compounds from the feed to build amino acids for their own needs. These acids become a part of the microbe. When the microbe dies, it is transferred with the feed mass to the stomachs and to the small intestine, where the microbe is digested, and its amino acids are absorbed through the intestinal wall. This is called microbial protein or rumen degradable protein.

Animal feed may include some (mostly artificially coated) amino acids or proteins, which the rumen microbes cannot use. These particles move to the small intestine, where their coating can be broken down and the amino acids can be used. Because these proteins are not digested in the rumen, they are called bypass proteins.

Picture from lecture materials, original source unknown

Another term closely related to proteins is NPN, non-protein nitrogen. These are often created by decarboxylation of amino acids, and the NPN compounds may be toxic. Some NPN compounds form in plants, for example sinapin in rape and betaine in sugar beets. Urea and uric acid are also NPN compounds.

Farm animal nutrition: Fat

Fat for farm animals is important only when they are young, and receive most of their energy from the fat in their mother's milk. As adults, only fur animals (such as foxes and minks) are dependant on fats in their diet. For ruminants, poultry and pigs, carbohydrates are more important. Fats have twice as much energy as carbohydrates, approximately 39 MJ/kg. 

Fats int he body are used in electron transfer, reaction medium, cell membranes and as stored energy. Plants have fats in their leaves and cell membranes, where they are stored as oils. Fats are used as fatty acids, of which three are necessary: linolic acid, linoleic acid and arachidonic acid (animals can build this from linoleic acid). Linoleic acid is synthetized further into EPA (Eicosapentaenoic acid) and DHA (Docosahexaenoic acid). These three acids are the source for hormone-like eikosanoids. Eikosanoids participate to blood pressure regulation, muscle cell contractions, immunology, nervous system regulation and body temperature regulation.

Fatty acids have methyl group in the tail end, and a carboxylic group in the alpha end. They always have an even number of carbons. If the fat has double bonds between the carbons, it is an unsaturated fatty acid.

Unsaturated fatty acid

 Fats are builts from fatty acids, much like carbohydrates are built from saccharides. Plant fat has usually more unsaturated fatty acids than animal fat. Fats in general belong to lipids, which include also phospholipids, waces, terpens and steroids.

Volatile fatty acids
Ruminants again have a specific way to gain fats, which are rare in their diet. The bacteria in the rumen create volatile fatty acids (VFAs) with the energy they receive from reducing carbohydrates. VFAs are fatty acids with a carbon chain of six carbons or fewer. The most important three volatile fatty acids for ruminants are acetic acid, propanoic acid and butyric acid. Acetic acid is used to synthetize 50 % of the fats in milk.

Producing VFA creates methane gas as a side product, which the animal must remove from its rumen by belching.

Fats in the metabolism
Fats are broken down into triglyserides (glyserol + three fatty acids connected to it with esther bonds) by bile acid in the small intestine:

Picture from lecture material, original source unknown

Bile breaks the structure of the fats, and creates chylomicrons, which are then transformed to adipose tissues in the body. In the adipose tissue free fatty acids are attached to glycerols, formed from glucose in the same tissue. This creates a triglyseride, which then can be stored in the adipose tissue. Thus, fats are ingested as triglyserides, then broken down to chylomicrons for transfer, and finally stored again as triglyserides

Fatty acids can also be used in the liver, where triglyserides can be built and transformed further into lipoproteins. Lipoproteins may be transferred to the adipose tissue, and used as a material for triglyseride synthesis.

Deficiency symptoms
Deficiency of the three necessary fatty acids may lead to

• skin problems (the most common symptom)
• excessive drinking
• increased risk of bacterial infection
• kidney damange, bloody urine
• sterility
• eye problems, blindness
• heart muscle failure
• decrease of ATP synthesis in the liver and heart

Farm animal nutrition: carbohydrates

Carbohydrates may be frowned upon in some human diets, but for animals they are the main source of energy. Chemically carbohydrates consist of one or many saccharides (from Greek, sacchar: sugar), and mostly follow the formula (CH₂O)_n, where n >= 3. They can be classified according to the number of saccharide units in the carbohydrate:

• Sugars
• Monosaccharides
• Trioses, tetroses, pentoses, hexoses, heptoses (3-7 carbons, respectively)
• Oligosaccharides
• Disaccharides, trisaccharides, tetrasaccharides
• Non-sugars
• Polysaccharides
• Homo- and heteroglycans
• Complex carbohydrates
• Glycolipids, glycoprotein

Animals receive sugars from plants, of which 2/3 of dry weight is carbohydrates. Plants create carbohydrates via photosynthesis, and by adding minerals from the earth, they can create carbohydrates with sulphur, nitrogen or phosphorus. Carbohydrates important to farm animals consist of three saccharides, which can be thought of as building blocks: glucose, fructose and galactose. By joining these in chains, different carbohydrates of varied length can be created. In the digestive tract all carbohydrates are broken down into monosaccharides (the basic building blocks).

Cellulose and hemicellulose are both carbohydrates, which can be found from plants. Hemicellulose includes all the polysaccharides (except cellulose) found in the plant cell wall. It is a branched  heteropolysaccharide, while cellulose is a straight monosaccharide. Hemicellulose makes the plant cell wall flexible by creating bonds between cellulose and lignine. Cellulose is a supportive material, which gives plant cell walls strength. It's amount increases when the plant grows: young grass has very little cellulose, but straw has much. Ruminants have rumen microbes, which can break the structure of these molecules and use them as energy.

Starch is formed in the green parts of plants, and stored in roots, seeds and tubers. Starch consists of amylose or amylopectin, which is the most important carbohydrate in grains.  Starch and glycogen are reduced to maltose and glucose.

Glucose (also known as dextrose) occurs free in honey, fruits and plants. It is a component of many other carbohydrates, and very important for nervous tissue, energy and blood sugar. Glucose is the single energy source for the brain. Glucose is stored to the liver and muscles as glycogen (animal starch). Muscles use the glycogen when needed, but the liver can return it to blood circulation to maintain bloog sugar levels. All animals can generate glucose in the liver via gluconeogenesis, using propionate, lactate and glycerol as sources. For ruminants, this is the main source of glucose, since all ingested glucose is used by the rumen microbes. Glucose and fructose together form sucrose (also known as saccharose or table sugar).

Lactose is an oligosaccharide, which the mammary gland forms from glucose and galactose. Cow's milk has 43-48 g of lactose per kg; if the cow has glucose deficiency due to low-energy diet, it cannot produce milk well.


Fructans are reserve material in roots, stems, leaves and seeds of hays. They consist of fructose. In silage, lactic acid bacteria turns fructans quickly into acid, lowering the pH and thus ensuring the silage doesn't spoil. Ovedose of fructans may cause laminitis in horses.

Carbohydrates and ruminants
Ruminants, with their complex gastric system, are able to digest many complex carbohydrates.  Ruminating breaks the feed to fine mass. The surface area of the feed increases, which allows the rumen microbes to attach to the feed in great numbers, and to begin their enzymatic reactions. The microbes get ATP (energy) from reducing carbohydrates, and thus use the energy for their own actions. As a side product, the rumen microbes create volatile fatty acids (VFA). VFAs are absorbed into the ruminant through the rumen wall, and they in turn become the major source of energy for the animal. If pure glucose needs to be administered to a ruminant, it has to be given as an injection or infusion, not orally, since otherwise the rumen microbes would use up all the glucose, leaving none for the animal.

Last minute checks

Last quick checks before the exam on biotechnology...

Daughter design: One possible population structure when studying the QTLs of dairy cows. Genotype and markers are assessed on daughters of sires heterozygous for the markers. (Weller, Kashi, Soller 1990)

Epistasis: The function of one gene is affected by many other genes, also known as modifier genes.

Granddaughter design: One possible population structure when studying the QTLs of dairy cows.  Marker genotype is determined on sons of heterozygous sires and quantitative trait value measured on daughters of the sons. (Weller, Kashi, Soller 1990)

Interval: The chromosomal area or distance between two genetic markers. Can be measured by calculating recombination frequencies without interference in several cross- and backcross breeding. For a certain map location the function is
y_ij = m_j + e_ij
where y_ij is the value of the trait for the animal i, m_j is the mean effect of animals with genotype j, and e_ij is random error (Anderson, McRae, Visscher  2006).

Pleiotrophy:  One gene influences many phenotypic ("visible") traits. Examples of phenotypic traits are color and height.

QTL-mapping: Mapping of quantitative trait loci has four phases:

1. Measuring the quantitative traits to be researched
2. Analyzing the genotype of the animals to be researched
3. Building the connection maps
4. Finding statistically significant connections between desired traits and connection map

Mapping can be done either by studying a population or by cross-breeding two different lines of animals, and often inbred lines are used.

PS. Lastly, this is precisely my problem when studying:

Cramming for an exam on biotech

Although the lecturer said it'll be an exam with four essays, it can't hurt to clarify some of the key terms and themes concerning the basics of farm animal biotechnology. Ethical concerns and welfare issues are omitted - once I get started on that, there's no end to the rant.

Cloning: The practice of creating an animal from only one other animal of the same species. A cell sample, from skin or fur for example, is taken from the animal to be cloned. The nucleus is removed from one mature cell, and inserted into an egg cell, from which the nucleus has also been removed. The egg cell, now containing the genes of the animal to be cloned, is implanted on a female animal, which will eventually give birth to the cloned animal.

Genectic connection: For example, we might know that animals resistent to disease X have a mutation Y in their genome, while animals who suffer from X do not. Thus, even if it's not known which genes cause the resistance, the mutation Y can be used to  identify animals with X-resistance. Connections are deduced from the DNA of hundreds or preferably thousands of animals using statistical and genome analyzing tools.

Genetic marker: A piece of DNA, usually a microsatellite, which is connected to a specific trait. The marker can be either in a non-protein coding DNA or a part of the actual gene, in which case it is called the candidate gene. Markers are used to map genomes and to find genetic connections. Markers are not genes, and usually not active DNA at all. They can be thought of as genetic landmarks.

Marker assisted selection (MAS): The use of genetic markers linked to desired genes in breeding programmes. Animals can be selected to breeding based on traits which cannot be evaluated from the animal itself (like milk fat percentage from a bull) or while the animal is alive (such as pigs' carcass quality). When breeding choices are made from young animals and without genetic information, a male (like a popular dog) may pass on a serious disease to several offspring, before the male's sickness becomes known. MAS can be used to prevent this.

Microsatellite: A microsatellite is a short strand of DNA, which has a repetitive sequence of 2-4 bases, for example CACACACACACA. They are most often found in non-coding DNA. Microsatellites are found commonly on animal (including human) genome, and since they have a high polymorphism rate, they are often used in confirming descency and as genetic markers. Also known as STR or SSR for short tandem repeat or simple sequence repeat. Up to 30 % of a human genome consists of microsatellites, dinucleotine repeats being the most common.

Single-nucleotide polymorphism (SNP): SNP, pronounced snip, is a polymorphism of one nucleotide in DNA. A transition is when a purine is polymorphed to a purine or a pyriminide to a pyriminide (A to C, C to A, T to G, G to T). Transversion occurs when a purine is polymorphed to a pyriminide or vice versa. Both are explained clearly by Steven Carr.

Transgenesis: Inserting genes or other DNA material into a foreign cell. The original DNA can be taken from an animal of same or different species, and it may or may not be genetically modified. DNA can also be artificially created, and then inserted to the target cell. Transgenesis aims either at adding new properties, changing current properties or removing properties from the target.

Qualitative trait: A yes-or-no -trait, animal either has it or doesn't. Often an unwanted and monogenic trait, like a disease or bad meat quality. Whether a cow has horns or not is a qualitative, monogenic trait.

Quantitative trait: A trait, which is affected by several genes, possibly in several chromosomes. A polygenic trait, and often positive, such as milk yield in cows or large litter size in sows. A quantitative trait is described with a pluralistic variable like height, color, birth weight, milk yield or fat percentage. The color of a horse is defined by over 20 genes.


QTL/ETL: Quantitative trait locus / economic trait locus. Used to refer to a gene or a genetic marker related to a quantitative (polygenic) trait. Thus one gene solely responsible for a trait is not a QTL. QTLs for animals can be searched for example from Animalgenome.org.