Fur farming - breeding and welfare

When talking about animal breeding, it is important to understand what it is. Breeding aims at improving the genetics of an animal population with methological breeding systems and programs. Breeding has clear targets, traits to be measured, recorded and followed etc. Breeding is not about increasing the animal population by mating animals to one another, which is what some pet "breeders" do.

Colors of mink pelts (c) Fur Commission

Fur animal breeding has always aimed at producing pelts which fetch the highest price in the market. Three main qualities affect the price: the size, quality and color of the pelt. Size is measured as the length of the pelt. As a breeding target larger pelts require larger animals, so often the largest and the ones that grow fastest are selected as breeding animals. Large in this context means fat. This however has lead to severe problems with fertility: fat females give birth to small litters. Fur animals breeders must therefore balance between size and litter size to produce enough pelts of an adequate size.

Pelt quality consists of several traits. The most important quality factors are

• flaws (such as bite marks)
• the quality of the guard hairs
• the quality of the undercoat

The quality of the pelt is a combination of its mass and the coverage of the guard hairs. The ratio between guard hairs and undercoat contributes to the mass of the pelt. In a pelt of good mass the undercoat is thick, strong and elastic, and it supports the guard hairs. In a high quality pelt the guard hairs are longer than the undercoat, there are no color flaws and the length of the hairs is even.

The third important quality factor is the color of the pelt. The desirability of different colors varies yearly and depends on fashion trends. Color can be determined by several qualities, such as hue and darkness.

Breeding traits

The breeding objectives can be divided to three classes, all of which may or may not be used for all fur animal species. The targets are evaluated in a two-step process, first in grading and then as pelt quality factors.

Grading is a process where the quality and color of the fur of live animals is manually estimated. Four qualities are estimated: the size, color, purity and quality of the pelt. Grading is done at the fur farm, and may be done several times a year. The size of the pelt is either estimated or measured. Pelt size is measured from the tip of the nose to the beginning of the tail. The purity of the color is also evaluated. For blue foxes the pelt can have four hues ranging from blue to red. The darkness of the color is graded and the mass of the pelt is estimated.

Mink pelts at an auction (c) Searching for Style

The same traits are measured again after skinning in a process called evaluation of the pelt quality. The differences are that pelt quality evaluation is done post-mortem and usually automatically, while grading is done when the fur isn't yet fully developed and is a manual task. The number of classes to which pelts are classified also varies between grading and pelt quality evaluation. For example in grading the pelt quality gets a score from 1-5, while the pelt quality classes depend on the company selling the pelts.  There are six traits evaluated as pelt quality: grading qualities (the size, color, purity and quality of the pelt) plus mass and coverage of guard hair.


Fertility is probably the most important breeding target. There are two main fertility traits:

• Litter size = number of puppies alive at 3 weeks of age / number of dams with at least one 3wk old pup
• Litter result = number of puppies alive at 3 weeks of age / number of mated females

The litter size and result are counted after the pups are three weeks old, because the highest pup mortality is during the first weeks of life. Studies show that young blue fox dams produce larger litters, but the pups have higher mortality than the pups of older females. 2 year old blue fox vixens have the best litter results.

Heritabilities (h²) and genetic correlations in blue foxes

Heritabilities are a way of measuring how much genes impact a certain trait, i.e. how well can the trait be developed by animal breeding. Traits with high heritability are easier to develop than traits with very low heritability. Heritability ranges from 0 to 1, where 0 means that genes have nothing to do with the trait, and 1 means that the trait is affected by genes only and there's no environmental impact at all.

A Finnish doctor of animal science, Jussi Peura, has calculated heritabilities to several breeding traits for the blue foxes. He found that pelt traits have the highest heritabilities and fertility traits have the lowest. For example, color darkness has a heritability of 0.55 and pelt size 0.30. On the other hand, litter size at 1st parity (1st litter) had a heritability of 0,1, which is fairy low.

Litter of silver foxes (c) Bioacoustica

Peura also studies genetic correlations, i.e. how much traits depend on other traits. For example, in humans height often correlates with weight: the taller, the heavier. For blue foxes there were clear positive genetic correlations between size in grading and size in pelt quality (0,74), color in grading and pelt quality (0,84) and quality in pelt quality and mass in grading (0,75). When a correlation is positive, both traits increase simultaneously.

Negative correlations mean that increasing one trait decreases the other. Blue foxes had a significant negative correlation between size and litter size (-0,28). There were mild negative correlations also between size and color purity in grading (-0,25) and color in pelt quality and size in grading (-0,17).

What all these mean is that grading gives a reliable estimation of the actual size and quality of the pelt. However, the purity estimation in grading is a poor estimation of the actual purity. The correlations also clearly show that increasing the size of the animals result in poor litter results.

Welfare of fur animals

The issues and solutions presented in this text are based on WelFur, which is again based on WelfareQuality -protocol. Welfare issues here are classified under the four basic principles of WelfareQuality: good feeding, good housing, good health and appropriate behavior.

Animal welfare is a complicated concept with several different definitions and theories. Here animal welfare means the subjective experience the animal has about its own psychological and physiological state as the animal tries to adapt to its surroundings. Welfare cannot then be measured directly. Animal cannot have a welfare of "9.5" or "good" - we can merely measure its behavior and surroundings, and deduce the level of welfare from the findings.

Good feeding

Body condition score for blue foxes

As has been previously discussed, obesity is a severe problem for blue foxes. They naturally would eat a lot during fall, and show this behavior also in fur farms. In farms feed is easily available and high in energy, so the animals gain weight very fast, and the size of their pelt increases. Obesity causes their front paws to bend, which again makes mobility very difficult. Healthy paws are rare in any blue fox farm.

Fat animals cannot breed well, so the animals kept alive for breeding are nearly starved during the winter. While it would be natural for them to lose weight, in farms the difference between the Fall weight and Spring weight is much greater than in the wild. Normally a blue fox would weigh 3-5 kg - the average weight of farmed blue fox males is a staggering 19 kg, and 10 kg for the females.

In any farm where animals are kept in group cages there is no peace during feeding. The animals fight over the food, which causes stress, and fearful animals may be underfed while the more dominating animals are overfed.

Another problem common to all fur farms is the availability of fresh, clean water. During winter the water pipes may freeze, and during summer the water may heat and become unsanitary. Problems with availability of water are usually technical in nature: unlike with feeding, there is no reason to purposefully limit the animals' intake of water.

Good housing

Good housing is a wide concept, which consists of a comfortable place to lie, warmth and the easiness of mobility.

Foxes on a shelf (c) Dyrevern Alliansen

Small fur animals, like minks and ferrets, must have a nest box available all year round. Foxes have a nest only during whelping. The nest is the only part of the cage with solid floor and walls: otherwise the animals sleep, play and walk on a metal net ( = mesh). The nest box has been proven to increase fearfulness towards humans, because it gives a place for the animals to hide to. That, and the animals' tendency to defecate on solid surfaces, are the main reasons for keeping the nest box available only for a short while. 

Foxes must also have a shelf in their cage, unless they can lie on top of the nest.The shelf is actually very important for the foxes, who prefer high places from where they can scan their surroundings.

The main reason for using mesh flooring is that urine and feces pass through it. Fur animals have a tendency to defecate on a solid surface, which would then need to be cleaned daily to prevent the animals from soiling their fur. While a mesh floor sounds unpleasant, foxes actually prefer mesh over earth floor or solid floor such as wood at least as a resting place. This may be because the mesh allows their fur to stay "puffy" so the animal stays warm. There are no similar studies done on other fur animal species.

Good health

In order to have and to maintain good health, the animals must have good housing and good feeding. Good health means that the animals have no sicknesses, but also no internal or external injuries or disabilities. In fur farms mortality due to diseases is somewhat low, 3-4 % in foxes between April - October. Treatment of illnesses may be rare. Many animals are kept until skinning even if they are sick, or left to die.


Disease epidemics in fur farms are relatively rare. The only exception is plasmasytosis for minks, which occasionally causes significant losses due to sickness and exterminations. The most common diseases vary between animal species. For foxes and minks infections of the womb and gut are the most common illnesses. Eye and skin infections, urinary tract infections and diarrhea are sometimes seen in foxes. Diarrhea can also infect minks, but rarely raccoon dogs, who are capable of eating even partially rotten meat without trouble.

As has been noted before, bent front paws and obesity are extremely common health risks in blue foxes. They are not usually life-threatening or even painful in fur farm conditions, but most likely they do decrease the animal's welfare.

Compared to most farm animals (cows, pigs etc.) fur animals receive no painful treatments. For example, there are no surgical castrations, tooth cutting or cutting of the ears, which are all performed on piglets. Still, care must be taken to ensure that all fur animals are killed humanely and quickly before skinning. The killing and skinning must be done far away from the live animals to prevent fear and panic.

 Appropriate behavior

Expressing normal and appropriate behavior is mostly impossible in fur farms. Pups can be weaned at the "correct" age, but they cannot spread apart like they would do in the wild. Animals are not allowed a space for their own. They also do not need to hunt or forage, which in the wild would occupy most of their time.

Silver foxes would normally live in small groups, where only the dominant female would raise a litter, and the females of lower rank would kill their own pups if they have any. To keep thousands of females in adjacent cages, all with their own litter, may cause stress and increase situations where females kill their pups.

Group vs single housing is an important question for all fur animals, but many study results are contradictory. Group housed minks can fight more and therefore damage the pelts. Their stress levels may also be elevated if the group is not balanced. On the other hand, group housed minks have company, can play with one another, and in a balanced group are also less stressed than individually housed animals.

Fur farming - animal species and annual cycle

Fur animals are farmed to provide raw material for clothes designers and the fashion industry. The ethics of fur farming is an important topic and should always be considered, but it will not be covered here. This post is about the practices of fur farming, fur animal species and caring for fur animals.

Every year nearly 60 000 000 mink pelts and 4 000 000 fox pelts are produced, with Denmark as the leading producer of mink pelts (over 15 million annually) and Finland of fox pelts (nearly 2 million). When these numbers are considered, it is obvious that fur farming is important to the national economy to some countries. Still, major fur producing countries like the Netherlands have banned fur farming due to ethical concerns. Finland's house of parliament voted on the subject in 2012, and vetoed a bill demanding to end fur farming.

Fur animal species

Mink (Neovison vison)
Minks are the smallest of fur animals, weighing 1-4 kgs and ranging from black to brown to white in color. Minks, like all fur animal species, come to heat once in a year in the spring. Female minks are in heat during the beginning of March. Mating induced ovulation, so the mating time does not need to be carefully planned, and usually each female is mated 2-3 times. One male is allowed to mate with 4-5 females.

The gestation period for minks is 40-70 days. Most minks in one farm have their litter within 2 weeks from each other. Naturally minks would deliver 6-7 pups, but in captivity only 4-5 pups survive to adulthood. Minks are killed with gas (CO / CO₂) and skinned in November, apart from breeding animals which are kept over the winter and mated again in Spring.

Minks are raised either alone, or two or four animals in one cage. Studies show that group housing reduces stereotypical behavior, but only if the groups are kept steady and balanced. Usually groups consist of pups from the same litter, with one female and one male, or two of both. In Europe, four pups or 2 adult animals may be kept in a cage of 2550cm² in size. In the wild each mink would live alone in a territory covering several hectares.

(c) greengirlabroad

Blue fox (Vulpes lagopus)
The blue fox originates from the endangered arctic fox. Its weight ranges from 8-12 kg, but the largest males can be near 19 kgs. The largest animals are not muscular but obese: foxes are overfed to make them fat, which increases the size, and thus the price, of the pelt.

Obese animals suffer from major health issues, such as bent legs and difficulty to move. In recent studies in Finland, blue foxes with healthy legs are a rarity. Because fat animals breed poorly, the animals kept for breeding are kept on minimum food during the winter, so they lose weight and are able to breed in the Spring. While it mimics the natural habit of the animals (gathering body fat in the fall for the harsh winter), in farms it is taken into extremes and thus causes major stress for the animals.

Blue fox females, vixens, are in heat for 4-5 days during February and March. Most vixens are artificially inseminated using sperm collected from male foxes in the same farm. The gestation lasts 51-53 days, and each litter has 5-7 pups. This is a very poor result compared to the litter size of wild arctic foxes, which is 8-10 pups.

Blue foxes have a very thick fur to keep them warm. Because on solid surface the fur would flatten, the animals actually prefer net flooring to solid flooring. Still, overgrown claws and wounded paws may occur even if the net is covered with plastic.

(c) Wikimedia commons

Silver fox (Vulpes vulpes)
Silver foxes are descendants of the common red fox. They are smaller and leaner compared to the blue fox, and their fur is less thick. Silver foxes are not fattened and then starved like blue foxes, because due to their heritage they are more finicky eaters.

Silver foxes are in heat for 2-3 days during January-April, and deliver litters of 3 pups after 51-53 days of gestation. In the wild the litters have 4-5 pups. Artificial insemination is rarely used, and one male mates with 4-5 females. Breeding blue and silver females are kept in the farms for approximately 5 years, after which they too are killed and skinned.

In Europe silver foxes are raised in cages of two, or a female with her pups.The cages have a nest during whelping, and a shelf to provide a "solitary" place where the animal can watch its surroundings. Foxes want to see what happens around them, which is why they are often raised in a "shadow house" with free visibility to every direction.

(c) PeTA Asia-Pacific

Raccoon dog (Nyctereutes procuonoides)
Raccoon dogs weigh from 5-15 kgs, and come to heat for 3-4 weeks during February-April. Like with silver foxes, each raccoon dog male mates with 4-5 females. The gestation period is 60 days, after which a litter of approximately 6 pups is born. In the wild litters have 6-12 pups.

Raccoon dogs are monogamic: in the wild they form life-long partnerships, and both parents tend to the pups together. In fur farms this kind of behavior is entirely denied, and each female has to tend to her pups alone. On the other hand the farmed female doesn't need to hunt her food, and therefore doesn't have to leave the pups to go foraging. It is not known whether raccoon dogs should be farmed in pairs to improve their welfare.

(c) CBS Minnesota

Ferret (Mustela putorious)
Ferrets are possibly the least farmed species, even though they can have up to two litters of 6 pups in one summer. In the wild each litter would have 2-17 pups, so the ferret is the only farmed animal whose litter size in captivity is not markedly smalled than in the wild. Ferrets come to heat in April and gestate for 42 days. The second heat occurs two weeks after the first pups are weaned.

While these are the same animals than the ferrets kept as pets, farmed animals receive none of the caring of pets. They are raised in small cages, bred, weaned, killed and skinned like all other fur animals. The instructions and laws regarding pet ferrets do not apply for their farmed counterparts.

The annual cycle of fur farms

Each year in a fur farm can be divided into six phases, regardless of the farmed animal species. Each year follows the same pattern: mating in early Spring, whelping during Spring and early Summer, and raising of the whelps and separating them into their own cages during Fall. Selecting breeding animals and killing and skinning the rest takes place in early Winter, after which the breeding animals are "kept alive" until they can again be mated in Spring.

Human genetics, part II

This post continues to define certain key concepts and themes in human genetics. Basics of genetics are not discussed here. The focus is on identifying genes causing diseases, mechanisms of cancer and the impact of genetic diversity to drugs. The previous post can be found here.

Pharmacogenetics

Pharmacogenetics studies how genes influence the efficacy and side-effects of drugs. It explains why different people react differently to medicines. Other related terms are pharmacogenomics (the interactions between drug and the genome), pharmacokinetics (metabolism of drugs) and pharmacodynamics (the interactions between drugs and their molecular targets).

Stages of drug metabolism
(c) Elsevier

The response to a drug can be continuous or discontinuous. In continuous response, the responses are normally distributed, because the response is multifactorial (depends on genetics and the environment). In discontinuous response the genotype of the user defines the  response, and there are only a few possible response types. Consider the stages of metabolism in the picture to the right. For example, homozyous recessive users (genotype aa) might follow the route distribution - breakdown - excretion, while homozygous dominant (AA) might immediately excrete the drug. For both response types the drug is ineffective. Heterozygotes (Aa) might metabolize the drug correctly. In this case, there are three possible responses to the drug.

Drug metabolism occurs mainly in the liver, where glucuronide conjugation and acetylation are the most common mechanisms of metabolising drugs. Metabolism is usually two-phased: First a polar group is added to the drug molecule to make it water-soluble. This is usually due to P450 enzyme, and includes hydroxylation or oxidation.Then the drug is metabolised into an excretable product. This phase often uses N-acetyltransferase (NAT) or glutathione S-transferase (GST).

Isoniazid is a drug used to treat tuberculosis. It absorbs quickly from the gut, and the level of isoniazid in the blood rises fast. The speed of metabolization depends on the enzyme NAT2, which has two alleles: fast acetylation and slow acetylation. Users homozygous for the slow acetylation metabolize isoniazid very slowly. For them the drug may cause liver damage and neural inflammation, because the toxic metabolites accumulate to the body. Certain genotypes concerning CYP2E1 and GSTM1 enzymes are also connected to slow metabolization of isoniazid and therefore hepatotoxicity. 50 % of West Europeans are homozygous slow acetylators.

Some hemolytic anemias such as favism are caused by deficiency of the enzyme G6PD, glucose-6-phosphate dehydrogenase. It also causes sensitivity against primaquine, a malaria drug. G6PD deficiency is inherited as X-linked recessive trait. If G6PD deficient people use primaquine, they develop black urine, jaundice and low hemoglobine due to destruction of red cells. The condition is not lethal. The deficiency is very common in Africa where malaria is common, which may support the claim that the deficiency protects against malaria.

Coumarin and other anti-blood-clotting drugs mut be very carefully dosed to each patient. There is extiensive variation between individual reactions to the drug, and a relatively high risk of severe bleeding complications if the dose is incorrect. Genes, ethnicity, the intake of vitamin K, diet, health and other drugs all have an impact on coumarin. Genetically the most important factors are polymorphism is CYP2C9 and VKORC1. The enzyme CYP2C9 has over 29 variants, and accounts for 15 % of all drug metabolism in the liver. Its most common variants are 20-70 % less effective enzymatically, and therefore need smaller dosages than fast metabolizers. VKORC1 is a vitamin K reductase, which reduces a by-product of blood-clotting factors into vitamin K. Vitamin K is essential in blood clotting. Warfarin, a drug similar to coumarin, inhibits VKORC1.

More on dosing blood clotting drugs can be found from http://www.warfarindosing.org.

Ethical dilemmas associated with gene tests and prenatal screening

 Prenatal screening means the screening for inherited diseases in fetuses. It is a manner of genetic testing. Gene tests can also be done to humans of all ages to

• detect carriers of inherited disorders
• predict late-onset diseases, which cause symptoms only as the patient grows older
• detect of increased risk of multifactorial diseases
• detect of risk to adverse drug effects
• diagnose cancer and determine most effective medication.

(c) McGraw-Hill

Prenatal screening is mostly based on detecting non-DNA markers, which detect metabolic abnormalities. There are several methods for prenatal screening, such as chrionic villus samples,amniocentesis (sample of the fetal liquid), blood sample of the umpibical cord and endoscope visualization of the fetus. These are invasive techniques, and pose a small risk to the mother or the fetus. Non-invasive techniques include blood samples from the mother or ultrasonography. Ultrasonography, also known as ultrasound, can detect trisomies (Down synrdome, Patau syndrome, Edwards syndrome) or Turner syndrome, where a female has only one X chromosome.

Ethical dilemmas arise from several factors. One is the clinical validity: how trustworthy the test is? Ultrasonography images and test results may show unclear results, subtle anomalies of unknown significance or offer mild indications of a disease. In which case should these findings be concidered strong enough to decide whether to keep or abort the fetus? Laws may dictate that abortion is either illegal or legal only under certain conditions. Invasive tests also increase the risk of miscarriage. Lastly, how to estimate the risk of anxiety if the test results are inconclusive, or a sick child is born despite negative test results?

There is also a possibility that the result is erroneous, but it can be easily checked by taking another test.

Fundamental ethical principles are

• autonomy: the respect for privacy and absolute confidentiality. The patient is informed of the risks and validity of the offered test, and other options available.
• beneficence: the test is done for the best interest of the patient. 
• non-maleficence: the principle of not doing harm.
• justice: fairness, equity of access and opportunity. This is especially important when concerning countries without government-supported healthcare, where all mothers should have equal opportunities to participate to gene tests.

Gene therapy

Gene therapy is the deliberate introduction of genetic material into human somatic cells for therapeutic, prophylactic or diagnostic purposes. Currently gene therapy is still only experimental, and tried mostly on cancers. No major breakthroughs have been achieved.
 
Gene therapy can be either done on germline cells or autosomal cells. Germline mutations are permanent and inherited, due to which they are banned in many countries. No current trials use germline therapy. Autosomal cell therapies aim to modifying specific cells or tissues of the patient.

There are a variety of techniques used for gene therapy:
– Delivery of synthetic or recombinant nucleic acids into humans
– Genetically modified vectors (viruses or plasmids). This is the most used technique, covering over 60 % of all gene therapy trials. The usability of a given virus depends on the amount of foreign DNA it can carry, how it interacts with the host genome and how the transgene is expressed.
– Genetically modified stem cells
– Oncolytic viruses, which target only cancel cells, proliferate inside it and kill the cell after releasing new virusparticles to another cancer cells.
– Nucleic acids associated with delivery vehicles
– Naked nucleic acids
– Antisense techniques
– Genetic vaccines
– RNA interference
– Xenotransplantation of animal cells (but not solid organs)

For somatic cell therapy, the techniques can be divided into four methods. In gene supplementation a working copy of a gene is inserted to its target cells to treat loss-of-function conditions.Gene replacement replaces a mutant gene, and targeted inhibition silences certain genes. Lastly, gene therapy can be used for targeted killing of specific cells. In all cases the target gene can be inserted either directly to the patient cells (in vivo), or by growing and infection the patient's own cells with the target gene in a cell culture before injecting them to the patient (ex vivo).

All the previous techniques can be used to treat cancer. Supplementation can restore tumor suppressor gene function. Inactivation can silence an oncogene, and manipulation of tumor cells can lead to apoptosis. Cells can also be made more antigenic, and thus promote the immune system to target the cancer cells. Cell killing can be done by using oncolytic viruses, which targets certain cells. Another method is the suicide gene therapy. In suicide gene therapy the cells are modified to turn a safe substance into a toxic one. For example, a retrovirus is modified to infect cells with herpes virus kinase. The virus is injected directly to the tumor, where it infects only dividing cells. When the cells have been infected, they are treated with a drug, which the kinase metabolizes into a toxic substance. The infected and drug-treated cells die. 


Problems in gene therapy arise from several factors. Most serious problems are

• temporary effects: to be effective, some therapies need constant injections or "rounds" of gene therapy.
• immune response: patient's body may recognize the engineered cells and destroy them. Since the immune response is stronger in later infections, the patient may become immune to gene therapy.
• usage of viral vectors carries a risk of viral infections and mutated viruses in addition to possible toxicity and immune responses.
• multigene disorders cannot at the moment be treated with gene therapy at all. It is suitable only for monogenic diseases.

Ups and downs of gene therapy (c) Elsevier

RNA-therapy is a form of genetic therapy which uses RNA to affect genes and genetic expression. One example is the antisense nucleotide therapy used to treat Duchenne muscular dystrophy.

The principle of antisense oligonucleotide therapy for Duchenne muscular dystrophy

Dystrophin in a DMD patient and
patients treated with AON.
(c) Garland science

Duchenne muscular dystrophy, DMD, is a genetic disorder of muscle weakness and degeneration caused by lack of dystrophin in the muscle tissue. DMD occurs in 1 of 3500 boys, and first symptoms occur in early childhood. Most patients die as young adults due to degeneration of breating and cardiac muscles. Dystrophin can be seen in tissue samples as a strong border around muscle cells. In DMD patients the stains show very little or no dystrophin, and the muscle cells are without real form or support.
 
A milder version of DMD is the Becker syndrome, where the patients have a normal life expectancy. Becker syndrome patients have a partially functioning dystrophin, which can be smaller in size than normal, and/or have reduced abundance. The difference of DMD and Becker is caused by a genetic mutation. In DMD, the dystrophin protein has an out-of-frame deletion, which leads to an altered reading frame and eventually to a truncate and unstable protein. Becker patients have an in-frame deletion, which leads to a shorter but partly functional protein.

The antisense oligoribonucleotide (AON) therapy targets at fixing the broken reading frame. The deletion between exons 48 and 52 is severe, because the exons are not compatible. Therefore the spliceosome stops at the exon 48, unable to continue to 52. The gene therapy aims at bridging this cap. The antisense oligoribonucleotides are tailored to hybridize to exon 51 and hide it from the spliceosome. The exons 48 and 52 are compatible, so the spliceosome continues and runs to the end of the protein. The final product is a shortened protein, which is however party functional. Gene therapy does not cure DMD - it merely makes the disease milder and increases the lifespan of the patients.

Currently gene therapy has been tested on 150 antisense oligonucleotides. The deletion of exons 49-50 is just one possible mutation causing DMD, and other mutations need their own oligonucleotides. First clinical studies have been performed on three AON therapy methods to hide the exon 51. One of these requires weekly abdominal injections.

Examples of genetic diseases

Disease name	Cause	Inheritance	Symptoms
Hutchinson-Gilford Progreria Syndrome	de novo point mutations in LMNA gene in 1q22	-	Growth failure, loss of body fat and hair, aged-looking skin, stiffness of joints, hip dislocation, generalized atherosclerosis, cardiovascular (heart) disease and stroke
Huntington disease	CAG-repeat expansion in 4p16.3	AD	Movement abnormality, involuntary movements, memory impairment, dementia
Spinal and bulbar muscular atrophy	Expansion of a CAG-repeat in androgen receptor	X-linked	Muscle wasting, weakness, contractions, swallowing difficulties
Myotonic dystrophy	CTG-repeat expansion in 3'UTR or CCTG-repeat expansion in ZNF9 (leads to gain-of-function RNA)	AD	Progressive muscle weakness and myotonia. DM1 allele causes a more severe disease than DM2
Fragile-X	CGG-repeat in promoter region of FMR1 (suppresses transcription due to hypermethylation -> slow development of cerebral neurons)	X-linked	Learning difficulties, typical facial features (large ears, high forehead, long face)
Facioscapulohumeral muscular dystrophy (FSHD)	Shortened megasatellite repeat in 4q35 leading to hypomethylation and cascading effects (deregulation of several muscle genes)	AD	Striking asymmetry of muscle involment from side to side, unbalance between right and left side muscles
Achondroplasia	De novo mutations in FGFR3 gene in 4p16.3, usually a missense mutation Gly380Arg	AD	Short stature (120-130cm), characteristic facial features
Cartilage-hair hypoplasia (CHH)	Mutation in RMRP (insertion which prevents transcription or SNP), leads to lack of RNAse required for cell growth	-	Short-limbed dwarfism (100-140 cm), sparse hair, immunodeficencies
Diastrophic dysplasia (DTD)	SNP mutation in SLC26A2, leads to undersulphation of cartilage matrix	-	Short stature (100-160 cm), deformities of joints, hip dysplasia, hand deformities
Tibial muscular dystrophy	Heterozygous deletion-insertion in titin gene	AD	Mild weakness of tibial muscles (calves)
Down syndrome	Trisomy 21 (47, +21). Can be due to translocation (t14;21) or t(21;21) or mosaicism.	Extra chromosome often from mother	Hypotonia, mental retardation, characteristic facial features, adult height of ~150 cm. Lifetime expectancy of 50-60 years.
Patau syndrome	Trisomy 13 (47,+13). Can be due to translocation (t13;14)	-	Central nervous system malformations, heart defects, growth retardation, cleft lip and palate. Most die as newborns.
Edwards syndrome	Trisomy 18	-	Malformations in many organs, elfin features, mental deficiency. Most die within a week from birth.
Klinefelter syndrome (47, XXY)	Extra X chromosome(s) in males. Can also be (48, XXXY) or (49, XXXXY).	-	Taller than average, long lower limbs. All patients are infertile.
Turner syndrome (45, X	Lack of chromosome X in women	-	Short stature, infertility, no puberty.
XXX females	More severe symptoms if more than one extra X chromosome	-	Possible mild reduction in intellectual skills
Hermafroditism	Paternal X-chromosome has Y-chromosome sequences; Chimerism of XX and XY cell lines; androgen insensitivity in males; adrenal hypoplasia in females	-	Possibly taller stature

Human genetics, part I

Human genetics is the study of human genome and individual genes. It includes many different aspects and views, such as pharmacogenetics and -genomics (the study of interactions between genes and drugs), gene therapy and mapping out disease susceptibility genes. In this post I summarize some topics of human genetics.

The human genome

Humans have genetic material, DNA and RNA, in two places: in the nucleus and mitochondria of cells.

Mitochondrial genome is always inherited from the mother. It is 16,6 kb long, and consists of one circular (plasmid) DNA module. It can be divided to light and heavy strains as opposed to the leading and lagging strand of the nuclear genome. Mitochondrial genome therefore has no chromosomes. Each cell has several, even thousands, copies of the plasmid, but the copy number varies in cell types. The mitochondrial genome has only 13 genes, is mostly free of binding proteins and has very little repetitive sequences. It is thus very dense in genes: it has ~1 gene in 0,45 kb of DNA. It also has no introns, and over 66 % of the DNA codes a protein. There is no recombination in the mitochondrial genome.

Mitochondrial genome has even a small strand of triple strand DNA, called the 7S DNA. Like all plasmids, the mitochondrial genome has an ORI-segment (origin of replication), but also promoters for both the light and the heavy strand. Over 98 % of the mitochondrial genome is highly conserved. It also has a different amount of stop codons and amino acid coding codons than the nuclear genome.

Human mitochondrial genome and genes. (c) NCBI

The nuclear genome is what traditionally is understood by a "genome". It is located in the nucleus as chromosomes, of which humans have 23 (the haploid number). The nuclear genome is 3,1 Gb in size - that's 250000 times larger than the mitochondrial genome! The nuclear genome is packaged around histone proteins. It has plenty of repetitive sequences, untranslated regions and introns. Approximately half of the nuclear genome is repetitive sequences such as microsatellites. Recombinations are common in nuclear genome, and it is inherited chromosomally: Mendelian inheritance for X and autosomes, paternal inheritance for Y chromosome.

The nuclear genome has over 20 000 protein-coding genes at a density of 1 gene / 120 kb. Only 1 % of the genome codes proteins. Single genes vary in size, the smallest being few hundred basepairs and the longest 2,4 Mb. One gene is transcribed from one strand, unlike in mitochondrial genome where by swapping between light and heavy strands one sequence can be translated differently. Circa 6 % is highly conservated, ~45 % transposons and the rest is poorly conserved for other reasons.

Both genomes participate in some important parthways in the human body. Both code subunits for the oxidative phosphorylation system, with nuclear genome providing 80 and mitochondrial genome 13 subunits. They also both participate in building protein synthesis complexes: mitochondrial genome is solely responsible for producing the rRNA and tRNA, while nuclear genome produces only ribosomal proteins.

# of genes and sizes of human chromosomes.
(c) Wikipedia

Repetitive sequences and variation in the human genome

Repetitive sequences are common in the human genome, and nearly 50 % of the nuclear genome is repetitive. Microsatellites, minisatellites and the telomeres at the end of chromosomes are examples of repetitive sequences which are often used in genetic studies. There are also repetitive sequences within genes. The repetition number can cause illnesses and diseases due to a malformed protein or the gathering of long mRNA chains in the cell. Illnesses caused by insertion leading to the lengthening of a repetitive sequence are Huntington disease, fragile X and myotonic dystrophy.

There are several factors causing variation in the human genome: mutations, genetic drift, selection and migration. Mutations can be classified to substitutions, deletions and insertions.

• Substitutions are either synonymous (or silent), where the final amino acid chain of the protein does not change, or nonsynonymous, where the amino acid chain is changed. Non-synonymous mutations can alter the amino acid at the point of the mutation, cause a stop codon or lead to aberrant splicing or altered gene expression (mutations in promotor sequences).
• Deletions are either multiples of three or not. Multiples of three lead to deletions of whole amino acids. Other deletions disrupt the reading frame, causing premature termination or loss of function of the gene product.
• Insertions are like deletions: multiplies of three add amino acids, while non-multiples disrupt the reading frame. Insertions can also be insertions of entire genes or amplification, where the gene stability, function or expression is altered.

Cancer: inheritance and proto-oncogenes

Cancer is a genetic disease of somatic cells. Therefore all forms of cancer are genetic, some more than others. Environmental factors, such as lifestyle, are important factors in developing cancer. 37 % of cancers in the USA are estimated to be caused by diet high in fats, while ~30 % of cancers are caused by tobacco.

Cancer can never be inherited. Only genes which may or may not increase susceptibility to certain types of cancers, are hereditary. Cancer development depends on a few types of genes:

• proto-oncogenes: normal genes, which may develop into oncogenes if activated
• oncogenes: mutated forms of proto-oncogenes. Important in cell growth and differentiation. Can be classified to viral oncogenes and cellular oncogenes. Both types can be
• growth factors
• growth factor receptors
• intracellular signal transduction factors
• DNA-binding nuclear proteins
• Cell cycle factors
• Tumor suppressor genes: inhibit and control cell proliferation
• DNA repair genes: repair faulty and broken DNA, and can fix mutations. In cancer the gene repairs are not working for example due to mutation. Mutations in repair genes can be inherited, which may cause leukemia, solid tumors and other types of cancer.

Proto-oncogenes can be activated in many ways. Duplication is common, and many cancer genes have multiple copies of normal oncogenes. Point mutations can activate oncogenes of the RAS family, which mediate cell signaling. Translocations can create novel chimeric genes. Leukemia is most often caused by a chimera called the Philadelphia chromosome t(9;22).  Ph1 does not answer to common cell function controls. Chimeras are also common in hematologic (to do with liver) tumors and sarcomas.Oncogene can also be translocated to an transcriptionally active region, and the oncogene becomes overexpressed.

For example, colorectal cancer can be caused by hereditary conditions such as familial adenomatous polyposis (FAP) and hereditary non-popyposis colorectal cancer (HNPCC). FAP is an autosomal dominant disorder, where patients develop several polyps in their large intestine. In addition they have germline mutations in a tumor suppresson gene on chromosome 5, which causes the adenomas. HNPCC, also known as Lynch syndrome, is autosomal dominant disorder. It is caused by mutations in DNA repair genes.

Breast cancer can also be due to hereditary conditions. 15- 20 % of breast cancers in Western Europe are in women who have a family history of breast cancer. The susceptibility genes are BRCA1 and BRCA2, which are found in 30-50 % of all breast cancer families. Both are DNA repair genes. A heterozygous carrier can have 85 % chance of developing breast cancer. 

Methylation of DNA is a normal way of the body to increase or decrease the activity of a single gene or the whole genome. Methylation silences the gene, because a methylated gene cannot be transcribed. In hypomethylation the gene is inadequately methylated, and normally silent genes are expressed. Imprinting is also lost is the imprinted gene is hypomethylated. Reversely, hypermethylation silences a normally active gene. Cancel cell genomes are often hypomethylated. Genes can be silenced by methylation, mutation or both.

Chemical carcinogenesis

Chemical carcinogenesis is a system where chemicals cause cancer. It was discovered in 1770s, when chimey sweeps were often diagnosed with scrotal cancer. Some key terms in chemical carcinogenesis are

• Genotoxicity: toxicity to the genome (A substance can be genotoxic)
• Mutagen: chemical or physical agents inducing alterations in DNA
• Carcinogen: cancer-causing agent
• Co-carcinogen; chemicals that cause cancer only in specific combinations
• Genotoxic carcinogen: DNA reactive agents (mutagens) or agents acting on the chromosome level (causing aneuploidy)
• Non-genotoxic carcinogen: does not affect DNA but promotes growth in other ways (hormones, some organic compounds)

Chemical carcinogenesis is a multistep process involving initiation, promotion, malignant conversion, and progression. In initiation, a carcinogen causes an irreversible mutation. In promotion non-genotoxic agents cause the expansion of the initiated, mutated cells. This step requires many faulty mechanisms to be effective: cell to cell communication must be hindered, apoptosis must be blocked and other forms of cell proliferation inhibition must fail too. Promotion leads to conversion, where the cells become a malignant cell population. This step requires tumor suppresson genes to be inactivated and oncogenes to be amplified. Last step is the progression, where the cells continue to divide, eventually leading to metastasis.

Well known and unfortunately widely used chemical carcinogens are tobacco, alcohol, pesticides and certain types of fibers and dusts (e.g. asbestos and coal). Many substances become carcinogenic only after metabolization in human cells. For example, some smokers have overactive activator enzymes in their lungs, and most if not all precarcinogens in tobacco are metabolized to actual carcinogens. Smokers, whose activator is lazier, accumulate much less carcinogens from the same about of precarcinogens. Same kind of mechanism is in the kidneys, where a carcinogen eliminating enzyme can either be very effective or very passive. Examples of such enzymes are N-acetyltransferase (NAT) and glutathione S-transferases (GSTs).

Cytochrome P450 genes, also known was CYP, catalyze reactions where polycyclic aromatic hydrocarbons (PAH-compounds) are metabolized to carcinogens. Humans have 57 CYP-genes. Some are expressed in the lungs, some in the kidneys. Different CYP-genes have been scientifically proven to be connected with lung cancer.

Example: asbestos
- Asbestos is inhaled when working with asbestos without adequate protective gear
- Asbestos fibers penetrate lung epithelium, causing inflammation and tissue damage
- Free radicals are produced due to prolonged contact between asbestos and mesothelial cells, and due to prolonged exposure to inflammatory cells.
- Reactive oxygen causes DNA damage. Antioxidants can hinder this reaction, but cannot entirely prevent it.
- Asbestos fibres in the lung become covered in iron and calcium. Macrophages ingest asbestos fibres, whereupon growth factors are released, and fibroblasts coat the macrophages with collagen.  

Molecular genetics of Hutchinson-Gilford progeria syndrome

(c) Georgia Gwinnett College

Hutchinson-Gilford progeria syndrome or HGPS for short is a disease causing premature ageing in children. The children are born healthy, but begin to age rapidly when they reach 18-24 months of age. The disease causes growth failure, heart issues, loss of hair, loss of body fat, aged-looking skin and stiffness of joints. The childred die of atherosclerosis around 13 years of age. Progeria is very rare, 100 patients have been diagnozed within as many years.

The disease is caused by a mutation in lamin-forming gene LMNA. Most cases are new mutations, meaning that the parents are not carriers of the disease and the susceptibility cannot be estimated. 90 % of the patients carry the same single-point mutation, which leads to aberrant splicing and a lack of 50 amino acids in lamin A.

Due to the aberrant splicing the protein lamin A is not postprocessed correctly. A farnesyl group is added to end of lamin A in a cell. In a normal cell, this farnesyl group is soon removed, and the final protein, callen lamin A, is formed. In progeria-infected patients the farnesyl group remains, leading to instability of the protein (which is called progerin). The instability is what causes the premature aging, since lamin A is very important factor in maintaining cell integrity and structure.

Progeria is related to normal ageing. Each chromosome has long telomeres at the ends. Each division in normal cell shortens the telomeres, until they begin to "wear out". Shortened telomeres induce the production on progerin - the very same protein which in progeria-patients induces premature ageing, and for the same reason (aberrant splicing). In other words, progeria patients experience all of the symptoms and die of old age when ~13 years old.

Progeria cannot be cured. The progress of the disease has been hindered by farnesyltransferase inhibitors (FTIs). The current status of the research is available at http://www.progeriaresearch.org/.

Over 2000 pageviews

Over 2000 pageviews! Wow, thank you all who have stopped by, hopefully you've found useful information and sources here. It's been fun sharing the things I've learned with you.

As a new semester is about to begin, I'll cover some new topics this fall:

• Mathematics (matrices, integrals, derivative and a bunch of topics I've never heard of)
  (That'll be fun... no wait, no it won't)
• Statistics (linear models, computer software)
• Biotechnics (innovations, commercialization)
• Maintaining balance in an human body (hormones, enzymes, metabolism)

Poultry production: meat chickens and turkeys

Meat chickens

A layer and a broiler hen, both at 6 weeks of age
(c) Coop cam

Meat chickens (broiler chickens) are brought to European countries from Scotland (Ross-breed). The grandparent birds are brought to the country as eggs, and hatched there. The grandparents will produce the parent generation, which are raised until 18 weeks of age in another poultry house. The 18 week old broiler chickens are then transferred to a breeding facility, where the live until 60 weeks of age producing the progeny. A fourth poultry farmer incubates and hatches the production generation birds. Finally a fifth farmer buys the day old hatchlings, which arrive in crates and are simply poured on the floor. The birds are reared for 32-39 days, at which time they are slaughtered. Before another flock is brought in, the hall is disinfected and left to dry for 2-3 weeks. Flock sizes in Norther Europe are usually 20 000 - 80 000 birds.

Broiler chicken females used for breeding grow very fast. But since fast growth would cause severe injuries and deformations, the females receive only 1/3 of the feed they need. The nearly starving birds are constantly hungry and frustrated. Only because malnutrition their growth slows down, and the birds are able to mate with the roosters and lay fertile eggs.

Broiler chickens meant for meat production (instead of breeding) live only 5-6 weeks before slaughter.  During this time the currently used chicken hybrids grow from 40 g to 2,1 - 2,5 kg. In comparison, a layer-breed chicken of 6 weeks of age would weigh less than 800 grams. The temperature of the poultry hall is decreased from 34 C to 20 C as the birds mature. Injured and dead birds are removed from the flock and destroyed. During the rearing time mortality of 3-4 % is expected and accepted. In a flock of 54 000, ~1890 birds will die of various reasons before slaughtering. In Europe, broiler chickens are not medicated in any way. If the hall is disinfected properly between flocks and the rearing conditions are good, the birds stay free from any diseases or parasites, eliminating any need for treatments or preventive medication.

The rearing is mostly automatized. Ventilation, temperature and humidity control, feeding, watering and light programming are all automated. While it saves work, even relatively short power outages can kill the entire flock to suffocation due to rapidly raising levels of ammonia, H₂S and CO₂ in the air. Because the light/dark program is carefully designed and obeyed, broiler halls have no windows or any inlet for daylight (organic farms are an exception). Meat chickens are still manually inspected twice a day. The farmer ensures all the automated systems work, and that the litter is dry and clean.

Meat chickens are fed crumbled feed from the floor during the first two days. The chicks would survive from nutrients in their yolk sacs, but solid feed helps the development of  the digestive tract and production of gastric juices. Later the chicks eat granulated feed from feeding cups. Feed and water are freely available, and the height of water nips and feed cups are altered as the birds grow. Feeding is usually phased with four different feed mixes suitable for birds of different ages. Each successive phase has less amino acids, calcium and phosphorus than the previous phase, but the energy content stays at 12,4 MJ/kg ME. This is because the bones of the birds develop fast and need Ca, P and proteins to grow strong. The last phase has no coccidiostates to ensure drug-free meat at slaughter.

Australian broiler shed. (c) Animals Australia

The EU directive for meat chicken welfare sets strict requirements for animal density. Densities are measured as kg / square meter at the end of the rearing period. Density of < 33 kg / m² has no additional requirements. If each meat chicken weighs 2,5 kg, a density of 33 would mean 13,2 birds / m². Animal density of 33-39 kg/m2 requires the farmer to have a writter description of the rearing facilities and equipment available at all times. A secondary power source is required, and the indoor air must fulfill cleanness, humidity and temperature requirements.  The highest allowed animal density is 39-42 kg/m2, roughly 17 birds / m2. In addition to the previous requirements, a farmed using the highest density must have impeccable results from animal welfare auditions and daily bookkeeping on bird deaths and removals with reasons attached. The mortality per flock is limited, and exceeding the limit forces the farmer to drop the animal density to 39 until the conditions improve.

Turkey production

Wild Turkeys (c) Turkey Management

The turkey is the largest bird used in animal production. It's meat has more protein and less fat than that of chickens, geese, sheep or cows. The current production turkeys are white hybrids, descendants of the still-living wild turkey (Meleagris gallopavo).  Turkeys are classified by color (bronze, white or black) and by size (heavy, medium heavy and light). Heavy males weigh 15-16 kg, medium males 8-10 kg. Hens weigh only half of the males' size.

Turkeys are raised in flocks like meat chickens. During the long rearing time of 3-4 months (compared to the 5-6 weeks of broiler chickens) the turkeys grow to weigh 6-12 kg. Hens and roosters are reared separately because of the size difference. Otherwise they are reared much like meat chickens. Turkeys are, however, much more demanding. They must be given time to develop strong bones at first, so their feed cannot be too strong. Young turkeys must have 8-10 cm of warm, dry and clean litter.  The first few days they are kept under a heat lamp in 38 C degrees and in bright lightning. The behaviour of turkey chicks is closely monitored. If they are huddled together, the temperature is too low, or they are stressed. If they are scattered away from the lamps, the temperature is too high.

After the first few days all birds know where to find water and food, so the light intensity can be lowered. Light program is changed gradually to allow for a dark time of 8-10 hours. Humidity is kept at 60-75 %, and by the end of the rearing period the temperature has been decreased to 14-17 C . 

Turkeys are fed mostly with complete feeds consisting of wheat, soybeans and peeled oats. Feeding is phased. For example, the recommended phasing for Nicholas-breed turkeys is:

• prestarter (0-2 weeks)
• starter (2-6)
• Grower 1 (6.9)
• Grower 2 (9-12)
• Finisher 1 (12-16)
• Finisher 2 (week 16 onwards)

Commercial breed turkeys. (c) Zimbio

Prestarted feed has the most proteins, espcially lysine and methionine. Energy content grows slightly towards the finisher feeds, but otherwise the contents stay rather similar. The phasing is designed by weeks of age, but weight of the birds is a more accurate measurement since each flock is different. However, it is important to stay with the prestarter and starter feeds long enough for the bird to develop strong bones before the period of fast growth. 4-phased feeding can also be used with the same principle of gradually lowering the amino acid content.

Since turkeys are the largest of domesticated birds (not including ostriches or emu), their rearing densities are much lower than that of broilers. At the rearing phase, 3-4 hens or 1 rooster / m2 is used. In farms producing turkey eggs the density is 2 hens or 1 rooster / m2.

Healthcare of poultry

Vaccinating hens against H5N1. (c) Reuters

To understand healthcare of poultry, one must first understand the conditions in a poultry house. Apart from organic production, there are no limits to how many animals can be kept in one hall. Meat chickens and layers are reared in flocks of  10 000 - 40 000 or higher. Turkey and goose flocks are usually  smaller. It is easy to comprehend that medication and health checks are flock-based: it is impossible to monitor and care for each individual animal, even though their pains and problems are unique. Therefore a disease outbreak is often noticed as the production or growth of the entire flock are decreased.

Viruses and parasites spread nearly immediately to every bird in the flock. If there are several poultry farms in a small area, the disease can spread from one farm to another in car tires, boots, dirty hands, clothing, by wind etc. "Backyard hens" and wildlife are also a risk to commercial poultry producers. Disease control, preventive medication and quarantines are vital in animal import/export. As the bird influenza -epidemics have shown, international and even global disease outbreaks are possible, and carry heavy consequences to poultry and, in extreme causes, to humans as well.

Each poultry keeper should take and send samples to an official laboratory for disease screening. Easy and quick methods of taking samples are

• Shoe cover sample: Put on dispensable shoe covers, and walk amongst the floor-reared birds. Swap the covers between different sections of the hall. Send the individually-packed dirty covers for screening.
• Feces sample: Mix an adequate amount (100-200g) of feces from all feces collector mats or different parts of the poultry house.
• Incubation sample: Mix 100-200g of broken egg-shells and floor litter from the incubator
• Dust and swab samples: Take and store individual samples from all around the poultry house: floors, corners, feed trays etc.

(c) The Poultry Guide

All diseases are cheaper to prevent than to cure. Most diseases lower production, and may lead to eggs or carcasses being rejected entirely, which decreases profits and increases costs as decreased feed utilization rate and medical costs.  The steps for disease prevention are simple:

• Allow only necessary guests to the poultry house. 
• Ensure all visitors wear disposable shoe covers and other protective clothing provided by the farm.
• Ensure no one enters the poultry house if they've been abroad during the last 48 hours.
• Follow the official and recommended vaccination and medication programmes.
• Monitor the animals and production levels closely.
• Repel indects, flies, rats and other vermin. Ensure wild birds cannot enter the poultry house or feed storage through air ducts or ventilation shafts.
• Use barriers. Make sure all clothing and equipment used in the poultry house is kept there, and all "dirty" clothes and tools are left in the barrier area. 
• Follow the all-in, all-out method with thorough cleaning and disinfection between flocks.

Common diseases

Salmonellosis
Several bacterial strains can cause salmonellosis. Salmonella Enteritidis and S. Typhimurium can infect poultry and humans alike. Both bacteria are infectious if swallowed, and are common in eggshells and feces. Infection through infected feed is rare but possible. S. galliarum infects poultry only, and may cause 100% morbidity in birds of any age. It survives months in a normal climate, but is susceptible to disinfectants. S. pullorum infects only poultry aged three weeks or older. 

Symptoms of all types of salmonellosis on poultry are ruffled feathers, closed eyes, diarrhea, loss of appetite and thirst and stunted growth. Post-mortem lesions can occur. Morbidity is low to medium. Salmonella can be cured with antibiotics, which are added to the feed or drinking water. The meat of infected birds may be accepted for normal food processing after heat processing.

Infectious bronchitis, IB
Poultry can and should be vaccinated against IB. IB is caused by a Coronavirus, which evolves rapidly but infects only chickens. The symptoms depend on the age of the chicken. Chicks get flu-like symptoms. Their oviducts are damaged, preventing them from laying eggs later on. Young chickens show only mild symptoms. Adults have respiratory problems, their productivity decreases and their eggs have faulty shells. Some Corona-strains cause damage to kidneys. IB infection lasts 2-8 weeks. Post-mortem lesions can occur. Morbidity is 0-25 %.

IB can be treated with sodium salicylate. Antibiotics are often needed to treat secondary infections by E. coli.

Skin hemorrhage (c) CFSPH

Newcastle disease, ND
ND is caused by some strains of paramyxovirus. In the EU, ND-infections must be confirmed in a reference laboratory in England. The viruses are extremely resistant: it can live months in feces, weeks in carcasses and years in a freezer.  ND infects all birds. If an ND-infection is confirmed, a stamp-out may be ordered and all poultry within 3 kilometers must immediately be destroyed.

The symptoms of ND vary, but common ones are decrease of production, moulting, hemorrhage of the comb, skin and eyelids, respiratory problems, paralysis and sudden deaths. There is no cure for Newcastle Disease.

Typical posture for a hen with MD.
(c) Poultry Club SA

Marek disease (MD)
Marek is caused by a herpesvirus. It is transmitted as aerosols via respiration, and may infect all animals in a flock in a short time. The virus proliferates in the roots of the feathers, and is extremely resistant. Many healthy birds carry and spread the virus. Marek infects mostly hens, but the symptoms and susceptibility to infection depend on many factors. Most infected are aged 4 weeks or older, most commonly 9-24 weeks of age.

Symptoms include staggering walk, paralysis, dangling wings, enlarged crop, bent neck, respiratory problems, eye deformations and weight loss. Sick birds have normal appetite. There is no cure for MD, and even cured birds will get infected again later.

(c) The Poultry Site

Coccidiosis
Coccidiosis is caused by one-celled parasites of the Eimeria-family. There are nine known contagious Eimeria-species. The infection happens when chickens eat the eggs of the parasite, often brough to the poultry house in contaminated equipment or cargo boxes. The eggs proliferate in the chicken gut, and 4-7 days after the infection there are Eimeria-eggs in the chicken's droppings. The eggs need 1-3 days outside the chicken's body to become contagious. Eimeria infects mostly chickens of 3-6 weeks.

Symptoms are increased mortality, stunted growth, decreased immunity, diarrhea, bloody feces, dehydration and decrease in egg-laying. Coccidiosis can be prevented by adding coccidiostates to the feed, and by keeping the litter clean and dry. The only treatment is keeping the litter clean and treating the secondary infections with antibiotics.

(c) Cornell University

Avian Encephalomyelitis (AE)
AE is a viral disease of the central nervous system, affecting chickens, pheasants, turkeys, and quail. Grandparent, parent and production line birds can be vaccinated against AE. Developing fetuses can get infected by the parent, but oral infections may also occur. Mortality is high.

Symptoms of AE include sitting, paralysis, tremors, imbalance, muscle weakness and dull apprearance. There are no visible lesions in live animals. There is no treatment for AE. 

(c) Science Alert

Gumboro or Infectious bursal disease virus (IBDV)
IBDV attacks the immune system of chickens 14-28 days old, causing severe effects in young birds. It is caused by Birnavirus, and infects chickens, turkeys and ducks. White leghorns are more susceptible to Gumboro than brown breeds. The disease is highly contagious, with mortality of 0-20 %. Gumboro increases susceptibility to all other viral and bacterial diseases, including Newcastle Disease.

Symptoms of IBDV are depression, lack of appetite, diarrhea, hiding and unsteady gate. There is no treatment, but vitamins and water may help. Antibiotic medication may be indicated if secondary bacterial infection occurs. All laying chickens and parents to meat chickens must be vaccinated against Gumboro.

CAV virus (c) ICTV

Blue Wing Disease (BWD) / Chicken Anemia Virus (CAV)
CAV and BWD are different names for the same viral disease caused by Gyrovirus. Mortality is 5-10 %. The virus is very resistant to disinfectants, but is destroyed in 5 minutes in 80 C.

Symptoms of BWD/CAV include poor growth, paleness and a sudden rise in mortality. There is no cure for the disease. Good hygiene and management, and control of other diseases as appropriate, may be beneficial. All parent chickens should be vaccinated 6 weeks before their eggs are collected for incubation.

Evaluation of foot health

Leg deformations, broken bones and infections in the soles of the feet are common welfare problems for fast growing birds all over the world. The birds are bred to grow faster than their bones develop, and to a larger size than their feet can carry. Feet health can be improved by

• Enough dry and clean litter
• Allowing roosting
• Optimizing the ratio of calcium and phosphorus in the feed
• Optimizing the amount of minerals in the feed
• Keeping low animal density
• Allowing locomotion
• Using slow growing breeds  

Foot and leg health can be measured by gait scoring, latency to lie -test or post-mortem from carcasses. In gait scoring, a sample size of 100 birds is selected. Each bird is put in a small enclosure, when the animal is encouraged to walk. The gait is scored from 0-5, and the average of all results is calculated. A score of 0 means a normal gait, 3 is a gait problem affecting the animal's locomotion, and 5 means the animal is not able to walk. Gait scoring is a part of Welfare Quality assessment. In a  Latency to lie (LTL) -test, 2-4 birds are set in a cage with sawdust litter. After 15 minutes, when the birds are relaxed, 3 cm of lukewarm water is poured to the bottom of the cage. The birds will stand up and stay standing as long as possible before falling down to the water. The maximum measured time is 15 minutes. The longer the birds stay standing, the better their score. 100 birds are tested altogether.

Post-mortem examinations are done in slaughterhouses by evaluating the quality of foot soles. This can be done on live animals as well, but may cause unnecessary stress. Same visual evaluations can be done on hocks. Chemical and physical measurements such as tensile strength can also be done post-mortem. The dry matter content and ash composition can be measured from bones. Phosphorus and calcium concentrations in bones can be measured after cremation in a spectrofotometer.

Visual evaluation on foot health. (c) Welfare Quality

Breeding and growth of chickens

Egg-laying hens and meat chickens are sometimes infertile. They are hybrids, produced from two selective breeds or lines in a breeding facility. Meat chicken and egg producers do not raise their own animals, but buy them in large batches from the sellers.

In a breeding facility chickens are either inseminated or allowed to mate with a rooster. The sperm  cannot enter the ovaries immediately, because there are always developing eggs blocking the way. The sperm is deposited in the vagina, which has small membrane sacs for storing the sperm. When the oviduct is free after the oviposition (laying of the egg), the sperm can continue towards the ovaries. The funnel-like end of the oviduct, the infundibulum, has membrane sacs similar to the vagina. Here the sperm stay fertile for a long time: 8-10 days in chickens, less than a week in geese and 3 weeks in turkeys. Most fertilizations happen 2-3 days after the insemination. In poultry houses, best results ar achieved by inseminating non-pregrant hens once a week.

(c) Margaret Gunning

Roosters are sexually mature at the age of 16-20 weeks, but aren't selected for breeding until the age of 24-32 weeks when their sperm quality has increased. Most roosters cannot produce high-quality sperm for long. Roosters' testicles are located in the body cavity right behind the lungs. They have no penises, so the ductus deferens leads to the cloaca. Roosters and chickens mate by rubbing their cloacas together, during which the sperm enters the vagina. Breeding henhouses have one rooster for 10 hens, but using artificial insemination, the sperm from one rooster can be used for 48 hens weekly.

Two hormones affect the development of spermatozoa: FSH (follicle stimulating hormone) and LH (luteinizing hormone). FSH increases the development of spermatozoa, and LH increases the secretion of androgens from the testes.

Most production-line hens no longer sit on their eggs. This vital trait has been lost during the animal breeding, so the fertilized eggs must be incubated in an automated incubator. The incubation temperature is 37,6 - 38,6 C. Ventilation must allow constant supply of oxygen and removal of CO₂. The developing fetus "breathes" since day 1. Air humidity must be 60-70 %, and the eggs must be turned to avoid the fetus from touching the egg shells. Before incubation most eggs are treated with gas. The gas kills 96 % of the bacteria covering the egg shell (dirty eggs can have 50 000 - 200 000 bacteria). If needed, the eggs can also be medicated by dipping them into a liquid medicine.

The fetal cells start dividing within three hours after the internal temperature of the egg has risen above 22 C. The development of a chick proceeds as follows:

• Day 1: a yolk sac is formed, providing nutrients for the embryo. The Embryo weighs 0,0002 g.
• Day 2: The fetal membranes are developed. The heart starts to beat and ears are formed.
• Day 3: Nostrils, feet and wings can be seen.
• Day 4: Tongue starts to form. The fetus weighs 0,05 g.
• Day 5: Genitalia starts to form, the gender of the fetus is developed
• Day 6: The beak starts to develop
• Day 8: The feathers start to develop. The fetus weighs 1,15 g.
• Day 10: The beak hardens
• Day 14: The fetus turns around into a hatching position, head towards the blunt end where it can breathe from the air bubble. The weigh is 9,74 g.
• Day 19: The yolk sac starts to retreat to the chick's abdominal cavity during day 19, and is completely assimilated by day 20. 
• Day 21: The chick uses a sharp "tooth" on its beak to break the egg shell, and the bird hatches. The chick weighs over 30 grams.

The hatching times vary in different bird species. For chickens the development of the fetus lasts 21 days, 30-32 for geese, 28 for turkeys, 18 for doves and 42 for ostriches.  If the incubation temperature varies from the optimum (depends on species), the incubation time will also decrease (in colder temperatures) or increase a few days.

Growth of chicks and young chickens

(c) Unknown

Newly hatched chicks need water and warmth immediately. Their yolk sac has enough nutrition for 2-3 days, after which the chick will need to eat to survive. During the first days the chicks need a temperature of 31-32 C, and it can be decreased by 3 degrees weekly until the temperature is 16 C. For hygienic and safety reasons the chicks are raised separately from hens. The animal density is max 12 chicks / m² until they reach 12 weeks of age. Young chicks must be kept in a draftless area with good ventilation and 5-10 cm of litter.

The sex of the chick can be determined during the first three days after hatching. Male chicks are deemed useless and destroyed, usually by crushing . Chicken sexing is done manually, and can be very painful for the bird.

Egg and meat chicken producers byu their animals in batches (flocks). Therefore the breeders must make sure that each bird in a flock grows evenly: 90 % of the birds should weigh +- 10 % of the eaverage weight of the flock. Chicks are weighed 2 or 3 times between 5 and 15 weeks of age to assure even growth. In practice a selected sample will be taken and weighed, since each flock may have tens of thousands of birds. Young birds are also vaccinated. The light/dark program and light intensity are very important for young animals. If they will be raised in a poultry house with roosts, the chicks should be allowed to roost already at a young age.

The chick feeds depend on the breed of the bird. Chicken breeders have exact feeding programmes for the rearing poultry houses to use. Starter feed is usually fed for the first 3 weeks, or until the bird has reached a certain weight. The started feed includes all needed nutrients in pressed crumbs, preventing the chicks from selecting their feed. Grower feed has less energy, and is fed during weeks 1-8. Developer feed has as much energy as the grower feed, but less amino acids. Pre-laying feed accustoms the ~17 week old chickens for the feed they will be eating when they start laying eggs.