key: cord-0040102-zm07e5a2
authors: Clark, Michael Ian
title: Management of Breeding in Small Poultry Production Units
date: 2018-11-30
journal: Veterinary Reproduction and Obstetrics
DOI: 10.1016/b978-0-7020-7233-8.00030-6
sha: 46141fe1f1a5c0c8384870e437555f130f4a3181
doc_id: 40102
cord_uid: zm07e5a2

nan

publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

W ith the growing trend for keeping backyard/hobby poultry, it can be a daunting task for the new graduate to feel adequately equipped to deal with the veterinary requirement of owners. However, if new graduates draw together their anatomical, physiological, pathological, and medical knowledge of avian reproduction, then, subsequently, there is much that they can offer a client, whether there is a fertility or an egg production issue in a small flock.

This chapter will deal purely with the backyard chicken ( Fig.  30 .1), Gallus gallus domesticus. Though much that will be discussed will be pertinent to other kept poultry (turkey and waterfowl) and gamebirds (pheasant and partridge), there is some fundamental species variation.

Backyard poultry tend to be kept extensively, with the main purposes of companionship, egg production for human consumption, and occasionally breeding of replacement birds. Primarily, owners source their hens from pullet rearers or acquire former commercial laying hens. A female chicken is a 'pullet' once she is no longer a 'chick' (i.e., she has lost her feathery chick down and acquired adult feathering) but has not reached sexual maturity and laid an egg. Point-of-lay pullets are sold between 16 to 18 weeks of age, with the expectation that they will come into lay in the following month. The onset of lay is governed by three factors: the pullet being sufficiently old, being in adequate body condition, and subject to the correct light stimulation. There is a huge variation in the size of pullet rearing enterprises with many different breeds being reared, ranging from small silkies to the much larger Rhode Island Red. Former commercial hens will be acquired at the end of their commercial viability, which is typically 72 weeks of age. The four commercial systems used in the UK are: enriched cages, barn production, free range, and organic free range. Production can range from between 300 and 340 eggs per hen with the more intensive systems, resulting in the highest production figures. The commercial breeds commonly seen include Hyline, Lohmann, Bovan, and Novogen. The primary breed companies that produce these birds are a very good source of information on their husbandry and maximising their genetic reproductive potential (e.g., Hyline Website 2016 , Lohmann Website 2011 .

If there is no requirement for the backyard flock to produce progeny, then it is not necessary to have a cockerel. In fact, they are often perceived as a nuisance due to their early morning crowing and aggressive/protective behaviour. Many owners do put up with these inconveniences and have a cockerel in the flock, as there is a perception that this maintains a more natural flock dynamic. If fertilisation of eggs does occur but there is no incubation either naturally with broody hens or artificially with incubators, then there is no embryonic development, and the eggs are fit for human consumption. A few backyard flock keepers have birds that are intended to produce fertile eggs for incubation and chick production. For the amateur enthusiast, this can be frustrating because veterinary intervention is required to investigate any combination of low egg production, low fertility, low hatchability, and poor chick viability.

In the majority of avian species, only the left ovary is functional, and this holds true for chickens. Although the right one is present embryologically, it regresses during development and is vestigial in the adult bird. If the functional ovary is removed surgically or is destroyed by disease, the right rudiment enlarges and becomes functional. The age at which the removal of the functional ovary occurs determines the future development of the rudiment. If the ovary is removed from chickens younger than 20 days old, the rudiment hypertrophies into a structure resembling a testis and is capable of spermatogenesis. However, because the Wolffian duct system does not develop in genetic females, there is no duct connection between the testis and the copulatory organ in the cloaca. The structure of the normal poultry reproductive tract is shown in Fig. 30 .2.

Immature left ovaries are amorphous, granular, grey, triangular structures ventral to the cranial lobe of the left kidney. An active left ovary can take up a significant part of the mid coelom. Numerous developing follicles can be seen ranging from the smallest white pin head sized to the most mature follicles that are the size of egg yolks (as that is what they become) and are a rich yellowy/orange in colour. This is a single cell, and the yolk represents a very large lipid inclusion in its cytoplasm.

On hatching, a female chick has millions of oocytes, most of which become atretic. The remaining few follicles slowly grow for months or years. Neutral lipids are deposited as yolk in the oocytes, 8 to 9 weeks before onset of lay; then a small number oocytes start to enlarge, depositing more white, primordial yolk. They then enter the final rapid growth phase, with deposition of yellow yolk, which has lipids along with water, proteins, minerals, and vitamins. Follicles grow to larger than 35 mm in 7 to 11 days in the domestic hen. Developing follicles are an oocyte, surrounded by granulosa cells, and an outer layer of thecal cells. There is no fluid-filled cavity; the entire follicle is filled with yolk material. In the avian ovary, follicles do not mature synchronously; there is a hierarchy of maturation with the largest most orange coloured follicle being the next to ovulate. The next largest follicle will ovulate 25 hours later, and so on. Usually a hen's ovary has up to 10 follicles containing yolk, a larger number of small yellow follicles, and numerous small white follicles awaiting recruitment or atresia.

Anatomically, the oviduct is relatively complicated as it is not just involved in transporting the ovum. Spermatozoa enter the oviduct and are either stored or ushered up the oviduct to fertilise the ovum. The fertilised ovum is enveloped by the nutritious albumin and numerous membranes added before it being encapsulated by the protective shell as it journeys through the oviduct to the cloaca. The oviduct has several components: the infundibulum, magnum, isthmus, shell gland, and vagina. In immature or out of lay hens, the oviduct is a relatively small structure, but in a sexually active hen, it can be a 60 cm coil of glandular tissue of varying diameters traveling on a circuitous route from the left ovary through the left, dorsal, caudal body cavity to the cloaca.

As the follicle is released from the ovary, it has to be captured by the infundibulum. The infundibulum is attached to the body wall and closely associated with the left abdominal air sac. The fluted part to the infundibulum grasps the oocyte before its passing through the infundibulum in 15 minutes.

The magnum is highly coiled and the longest part of the oviduct. There are massive mucosal folds that add about half the egg's total albumin during its 3-hour passage through the magnum.

After a narrow aglandular zone, there is the isthmus that is thinner and has fewer mucosal folds than the magnum; further albumin is added and the two subshell membranes are applied to the egg during its 1-hour passage.

1. Synthesis of calcium ATPase in the shell gland; 2. Changes in bone composition -10 days before egg formation, calcify medullary spaces of long bones, especially tibia and femur; this will mobilise calcium for use in shell formation; 3. Production of very low density lipid protein (VLDL) by the liver, which is a major precursor of yellow yolk, and is transported to the ovary and deposited in yolk; 4. Increased size of the oviduct (important for egg formation); and 5. Together with male sex hormones causes changes to plumage, comb size, sexual receptivity to males As follicles mature, enzyme activity decreases in the theca cells but increases in the granulosa cells, resulting in a shift to increased progesterone synthesis near the time of ovulation. This can be seen in the rising blue line just before laying in Fig. 30 .4.

The ovulation positive feedback loop that occurs in poultry ( Fig. 30 .5), superficially, may look similar to that of mammals; however, there are differences:

• It is progesterone, not oestrogen that is involved in this positive feedback loop. • Ovulation of the dominant follicle (given the nomenclature F1) in birds is preceded by an increase in progesterone and LH. • LH stimulates secretion of more progesterone from the granulosa layer of the mature ovulatory follicle. • In experiments, administration of exogenous progesterone results in an LH surge and ovulation, so many believe it is progesterone that triggers the LH surge, not oestrogen as it does in mammals. In both mammalian and avian species, LH and oestradiol increase before ovulation. The big difference is that in mammals, progesterone only increases after ovulation, whereas in birds, progesterone

During the egg's 20-hour presence in the shell gland (uterus), further albumin is added from the flattened mucosal cells. There is deposition of the shell, its glaze, and the outer cuticle.

The egg passes through the vagina in a few seconds. The vagina ends at a slit-like opening in the lateral wall of the middle chamber of the cloaca (urodeum). When the egg is laid (air cell end first), the vaginal opening protrudes through the vent, minimising contact with faeces (Dyce et al. 2002) .

There are major endocrine differences in the reproductive cycle of avian species compared with mammals. For example, in birds, granulosa cells (cells surrounding the vesicular ovarian follicle) produce progesterone (rather than oestradiol as occurs in mammals). Most of this diffuses to thecal cells (cells making up the envelope of condensed connective tissue surrounding the ovarian follicle) and is converted to oestrogen. Fig. 30 .3 illustrates the hormonal changes (for luteinising hormone (LH), prolactin, oestradiol, and progesterone) encountered by a hen through the four phases:

• Preparatory period • Laying period • Brooding • Posthatching As with any endocrine cycle, it is difficult to conceptualise a starting point. However, it is sensible to focus initially on the rising oestradiol levels in preparation for the onset of lay: 

Chicken testes (left and right) can be seen during embryonic development at the cranial poles of the kidneys. Unlike mammals, there is no migration from this position during sexual maturation. Before sexual maturity the testes resemble grains of rice. In sexually active cockerels the testes are large white structures up to 5 cm long; in the quiescent period, they shrink to about half that size ( Fig. 30.7) . The seminiferous epithelium contains developing germ cells in distinct associations referred to as 'stages'. The stages are arranged sequentially in a helix that extends along the length of the seminiferous tubule (Scanes 2015) . There are no accessory sex glands in cockerels, resulting in a modest ejaculate of approximately 1 ml of semen.

There is an epididymis and ductus deferens, but there is no head, body, or tail to the epididymis, which appears as a slight bulge on the testis. The tightly packed efferent ductules join to form the deferent duct, which arises from the caudal end of the epididymis; the ductus deferens closely follows the ureter to the middle chamber of the cloaca (urodeum). In sexually active cockerels the ductus deferens is full of spermatozoa and thus is whitish in colour. The copulatory apparatus (phallus) of the chicken consists of two papillae and a rudimentary copulatory organ that is located in the vent (Scanes et al. 2004 ).

Each testis is surrounded by a layer of connective tissue containing the seminiferous tubules and Leydig cells, which are dispersed in the spaces between the tubules. The interstitial cells produce several androgens, but the major hormone is testosterone. As sexual maturity is attained, the production of testosterone is stimulated by the rising blood concentrations of LH. In the sexually mature cockerel, the blood concentration of LH is maintained by a negative feedback loop in which the elevated concentrations of testosterone inhibit increases before ovulation ( Fig. 30 .6) and is actually responsible for the LH surge which triggers ovulation.

There is an 'open period', which is a window of time each day when LH release can occur. It is usually 8 to 10 hours long and is from the onset of darkness to about 1 hour after the onset of light. Dusk signals the hypothalamus to set the circadian clock, which then sets the timing of the open period.

If the largest follicle (F1) produces and releases enough progesterone during the open period, then an LH surge and ovulation occur. After ovulation, unlike in mammals, no corpus luteum is formed in birds as there is no requirement to sustain a pregnancy. Synthesis of progesterone is restricted to the few mature follicles that are present because progesterone is responsible for the positive feedback cycle that triggers LH surge and ovulation. If it is too high, it will suppress GnRH and LH.

In domestic hens, ovulation occurs 6 to 8 hours after the LH surge, and then approximately 25 to 26 hours after ovulation, the egg is laid. Ovulation usually occurs 15 to 75 minutes after oviposition (time of lay is a practical guide to time of ovulation). Each ovulation occurs slightly later on subsequent days; as a consequence the hen eventually 'misses' the open period for that day's ovulation, resulting in a pause of 1 day in egg production. the secretion of GnRH, which in turn inhibits the secretion of LH.

As the secretion of LH declines, the concentration of androgens declines, and hence the secretion of GnRH and LH is enhanced. The Sertoli cells provide the microenvironment in which differentiation can take place and act as nurse cells to the developing sperm; the duration of spermatogenesis is approximately 14 days.

There are sperm storage tubules at the junction of the vagina and shell gland (uterus). Sperm are ejaculated into the cloaca or vagina and rely on their motility to reach the sperm storage tubules (SSTs). Some then enter the uterus and are carried passively to the infundibulum where fertilisation occurs; sperm storage tubules can store sperm for a long time (10 days) because bird sperm remains viable at body temperature (41°C) for up to 2 weeks in the female's genital tract, resulting in successful fertilisation. For comparison mammalian sperm remains viable in the female reproductive tract for a few days at most and then only under ideal conditions. After an egg is laid, some of these sperm may get 'squeezed out' of the tubules into the lumen of the tract, from where they may migrate further up to fertilise another egg.

is not removed from her. The daily removal of laid eggs and the reproductive physiology of an indeterminate layer can result in over 300 eggs per hen being laid over a 12-month period. Physiologically, she is striving to establish a clutch of eggs but is being thwarted on a daily basis by the stock keeper. After a clutch of eggs are laid, a hen's behaviour changes, and she becomes broody. This may be a desired quality if the owner wishes a hen to incubate her own fertilised eggs; it may be an undesirable trait if the purpose of the hen is to lay eggs for human consumption or to produce fertile eggs for artificial incubation. To prevent broodiness, eggs should be collected daily, and there should be few dimly lit hiding places for a hen in her enclosure. From an endocrinological perspective the following is occurring:

• In the ruptured follicle, granulosa cells synthesize progesterone, and, if sufficient, it inhibits further ovulation. • The ovary, oviduct, and comb regress. • LH levels decrease during incubation and hatching but increase if the hen lays a second clutch of eggs. • Gonadal steroids decrease, whereas prolactin increases. • Prolactin increases in males and females during egg laying, peaks during incubation, and declines when chicks hatch. The purpose of brooding is to keep the eggs warm. The hen develops a brood patch ( Fig. 30 .10) towards the end of the egg laying period, and the skin becomes oedematous and highly vascularised. Brood patches develop in response to ovarian steroid exposure. The tactile simulation of the defeathered, oedematous brood patch triggers transition from egg laying to brooding due to prolactin release. The blood flow to the brood patch is greatly increased, such that the heat from skin in this area incubates the eggs. Sensory fibres detect skin temperature where there is skin-toegg contact. If the hen's body temperature falls she will shiver to generate heat and increase her metabolism to ensure that eggs are at the optimal temperature for incubation. The brooding period ends when prolactin levels decline.

Moulting is a natural process in which the laying hen's reproductive function goes into abeyance and coincides with seasons of the year that are suboptimal for chick rearing. This is not a desirable trait for birds kept for egg production, but it may be of use to a small flock keeper who wishes to synchronise egg production. If that is the case, a flock moult can be induced by reducing the

Ovulation results in the release of an egg from a mature follicle on the surface of the ovary. At ovulation the ovum is captured by the infundibulum, which is covered with a ciliated simple columnar epithelium. The beating of the cilia is important in moving the egg into the funnel shaped/fluted upper end of the tube. After passive entry into the infundibulum by the egg, there is fertilisation when the sperm penetrates the ovum and there is fusion of the male and female pronuclei (syngamy). From here, the egg further develops during the 25-hour journey through the oviduct, with the end result being a fertile, shelled egg.

Because all male birds are ZZ (homogametic unlike the heterogametic mammalian male XY), all spermatozoa will carry the Z chromosome ( Fig. 30.8) , whereas at the end of the second meiotic division, the Z and W chromosomes of the heterogametic avian female will have segregated into 50% of the ova. At fertilisation any of the ova carrying the Z chromosome will develop into male chicks, whereas any ova carrying the W chromosome with develop into the female chicks.

The infundibulum also has a secretory function. It produces the first of the egg coats, the chalazae. These are the whitish string-like structures on either side of the yolk that keep the embryo in proper position during development (University of Illinois Extension). Around the yolk, there are four distinct layers of albumen ( Fig. 30.9 ):

1. The chalaziferous (inner thick) layer attached to the yolk (3% by weight) -produced in the infundibulum 2. The inner thin (liquid) layer (~17% by weight) -produced in the infundibulum 3. The outer thick layer (~55% by weight) -produced in the magnum 4. The outer thin (fluid) layer (~25% by weight) -produced in the magnum The inner and outer shell membranes are produced in the isthmus. There are three calcified layers to the eggshell.

The organic shell matrix is a series of layers of proteins and mucopolysaccharides in which calcification occurs. Just before oviposition (expulsion of the egg), the cuticle (a thin waxy layer) is applied to the shell.

A backyard hen that lays 5 or 6 eggs, whether they have been fertilised or not, is likely to become broody if the clutch of eggs The homogametic male avian chromosomes Z and Z. Fig. 30.9 The anatomy of a poultry egg.

are laid on their side, and the machine is a combined setter and hatcher. Such machines require a temperature of 38°C.

A single stage incubator has all eggs at the same stage of incubation. The advantage of this design is that, potentially, the incubator can provide the optimum environment for development and hatching for each day of incubation. There is also improved biosecurity, as the incubator will be empty periodically for thorough cleaning and disinfection. A disadvantage is cost, as these incubators are often large, and they need either to supply heat to the eggs or to remove heat or cool them.

A multistage incubator has eggs at various stages of incubation. This reduces the cost of the operation, as some eggs need to be supplied with heat, whereas others need to dissipate heat. However, the machine is providing 'average' conditions for the age range of eggs. There is also a biosecurity compromise, as the capacity of the machine is being maintained at its maximum with more recently laid eggs.

When monitoring a hatchery, the critical issue is embryo temperature; however the incubator air temperature may not necessarily reflect embryo temperature. It is known that egg shell temperatures correlate well with embryo temperatures if taken correctly with an infrared thermometer at the equator of the egg and therefore is better than a hatchery air temperature thermometer. The downside is that measuring the egg shell temperature may require opening of the machine, with a resultant dissipation of heat. From about halfway through incubation, an embryo changes from a net absorber of heat to a net producer of heat, though the optimal temperature for the embryo remains in the range 37.8°C to 38°C. This is a challenge for an operator of a small machine, as the focus changes from heat supply to heat dissipation. If the temperature is slightly suboptimal, then development is delayed, and if the temperature is slightly higher, target chick viability is compromised; if it goes even higher hatchability is also affected.

The optimal operating humidity for a hatchery is 55% to 60%. When incubated correctly, eggs will lose 11% to 12% of their • Fig. 30.10 The ventrum of a hen with a prominent red brood patch.

• Fig. 30 .11 A small incubator. day length to 8 hours and restricting (but not withholding) feed. After a rest period, production can be resumed by then increasing the day length to 14 hours over 4 weeks before raising it to 16 weeks, and increasing the ration. If hens in a flock appear to be losing feathering commencing at the neck followed by breast, body, wings, and tail, in that order, in conjunction with a drop in flock egg production, then a moult is occurring.

The aim of egg storage is to stop embryo development, and this requires a cool temperature: 17°C to 21°C (63°F-70°F), which should be ensured with careful monitoring using a minimum/ maximum thermometer. However, there are still potential problems, such as hot spots in the egg store. Temperature fluctuation during storage can cause a decline in hatchability of up to 3.5%, and eggs stored for longer than 10 days have a decreasing hatchability of 1% per additional day. However, judicious use of an egg store allows pooling of eggs before setting.

Fertilisation of the follicle is the first step in the production of a hatching egg.

The egg membranes and shell are then added over a period of approximately 24 hours, which is achieved in vivo at the hen's body temperature of 41°C. Therefore at the point of laying, the embryo is 24 hours old, and 1 day should be 'added' to the standard incubation periods for all species (i.e., 21 + 1 days for a hen egg). During this egg development period, the embryo progresses from one cell to 20,000 to 40,000 cells.

Incubation is divided into two processes: the 'setters' receive the eggs for the first 18 days, then for the final 3 days the eggs enter the 'hatchers'. For very small incubators (Fig. 30.11) , eggs

Candling is often carried out before transferring eggs from the incubator to the hatcher at day 18 of incubation. This should be done with great care to avoid damage to the developing fetus. Once in the hatcher, the eggs no longer need turning. The temperature requirement is now lower for the egg, but the humidity requirement is higher. With gas production and bacterial contamination, there is always a risk of what are described as 'bangers', namely exploding contaminated eggs with the consequential risk they pose to other eggs in the hatcher. With each batch of eggs being hatched, there should be an aim to have a short period of time when there are no eggs in the hatcher; this is referred to as a 'hatch window'. The longer the hatch window, the greater the welfare compromise and the disease risk to the first hatched chicks. A hatch window of 24 hours should be achievable. Excessive amounts of meconium present in a hatch basket would alert a veterinary surgeon to there being a long hatch window.

It is possible to harvest tissue from the young chicken for karyotyping. There are several laboratories in the UK that offer this testing service. Sampling techniques include:

1. Blood collection by venipuncture or clipping a toe nail so that a few drops of blood can be placed on a permacode card (Fig. 30.14) ; the card should be left to dry for approximately 20 minutes at room temperature. Once the card is dry, it should be placed in a small envelope with the submission form and sent to the appropriate laboratory. 2. Two or three feathers can be plucked from the bird (they cannot be naturally shed feathers, as they have only keratinised material with no DNA). Although any feather can be selected, as a general rule, they should be between 5 to 10 cm (2-4 inches) long. They are then placed into a sealed plastic bag to be sent to the laboratory. 3. After hatching, the shell remnant can be used for sexing the hatched chick. Allow the eggshell membrane to completely dry before submission. Shells may be left in the incubator or removed and allowed to air dry for 24 hours or until the egg membrane is no longer moist; removing the moisture will weight from the time of laying to day 18 of incubation. Small amounts of moisture loss occur during storage (approximately 0.5% per week), which need to be deducted from the incubation value. Egg weight monitoring is a valuable tool, but not commonly used (Aviagen Website). If the humidity is too high, then the egg's rate of moisture loss will be too low and the air cell too small; ultimately, the embryo cannot inflate its lungs. If the humidity is too low, then the rate of moisture loss will be too high, and thus there is a risk of embryo dehydration.

Egg turning is paramount for proper embryo development, as it prevents the embryo adhering to shell membranes. There is also better yolk sac and allantoic vascular development, better albumen protein utilisation, better hatch weight, and better embryo positioning before hatching. Turning in the first week is more important than in the second week and should be done at least 5 to 6 times per day. The eggs should not be turned in the last 3 days of incubation after transfer from the setter to the hatcher.

Air exchange is essential to prevent suffocation of the embryo. Removal of carbon dioxide (CO 2 ) is required as a concentration of 1% CO 2 has a marked detrimental effect on hatchability. However, in normal avian nests, CO 2 is 10 times higher than atmospheric CO 2 levels (0.4%-0.6% vs 0.04%). The operator's aim should be to ensure as much ventilation as possible can be provided while maintaining adequate temperatures. Ventilation is a major method of temperature control for the hatching egg; if it is too hot, this increases the rate of embryonic development, potentially affecting chick quality. If it is excessively too hot, there will be embryo mortality, resulting in reduced hatchability. Too cool a hatchery delays the rate of embryonic development. Temperature fluctuations cause embryo 'stress' -reduced hatchability, reduced chick viability. Hot and cool spots (e.g., due to egg size variability, air movement issues) will result in an increased hatch window (the duration of the interval from the first to the last egg to hatch), which influences chick viability (Engormix Website).

If eggs have a low total viable count of bacteria before incubation, then contamination should decline during the process (Fig.  30 .12). Highly contaminated eggs placed in dirty machines will result in bacterial proliferation, with detrimental consequences on hatchability and chick viability.

A bright light can be shone through the egg (Fig. 30.13 ) enabling the viewer not only to see if the egg is fertile and developing but also whether it has the correct amount of humidity. This is done by assessing the relative size of the air cell.

• Fig. 30.13 Candling of fertile egg. (Courtesy of Boehringer Ingelheim.)

• Fig. 30 .12 Low egg bacterial contamination will get lower during incubation whereas high levels of egg bacterial contamination will get higher during incubation.

technique. However, it needs much training to become proficient, as the anatomical differences in male and female vents are far subtler than other species such as ducks in which even at a day old the male phallus is quite obvious.

In some breeds of chickens, there are some easily observable sexlinked characteristics allowing identification of the sex of the chick on hatching.

1. Colour sexing. For example, the Barred Plymouth Rock breed carries a gene for barring, which produces a white bar on a black feather. Males have a large white head spot that is smaller and narrower in females. Furthermore, if a gold coloured male is mated to a silver female, the progeny will consist of silver males and gold females. 2. Feather sexing (Fig. 30.15 ). This is possible due to rapid or slow feathering and the subsequent differences in wing feathering. If rapid feathering males are mated with slow feathering females, the result is slow feathering males and rapid feathering females (i.e., males have shorter wing feathers).

There are numerous causes of reduced egg production, including infectious, nutritional, and environmental factors.

Egg binding is an unhelpful term, as many practitioners and producers have different views on its precise definition. Hens can suffer from dystocia in which an egg becomes trapped in the vagina. The trapped egg may be visible on examination and will certainly be palpable. Large eggs (especially those with two yolks) are a contributing factor, as are hypocalcaemia, obesity, and early onset of lay. It may be possible to assist the expulsion of the egg with adequate lubrication. Initially, intramuscular calcium supplementation can help in the form of calcium gluconate followed by calcium glubionate or calcium carbonate orally. Some veterinary surgeons advocate breaking the offending egg. However, though this may rectify the immediate problem, it does predispose the bird to developing salpingitis. If the flock is laying a high percentage of double yolked eggs, slow down the decay of the DNA required for testing. DNA is extracted from the vascular material lining the eggshell membrane. This testing method is very accurate.

It is possible to surgically sex birds, although not in very young birds, and it is not without risk. The patient requires general anaesthesia before the insertion of an endoscope through a surgical incision between the ribs at the level of the caudal thoracic air sac.

Fresh faecal samples can be assayed for testosterone and oestrogen concentrations in sexually mature birds. The chickens being tested must be healthy and the sampled faeces assigned to the correct individual; the test is safe and inexpensive.

Due to the slight anatomical difference in the male and female vent, it is possible to determine the sex of day old chicks with this • Fig. 30 .14 A permacard for submitting a blood sample for DNA sex determination testing. 

Infectious bronchitis (QX strain) is known to cause blind layer syndrome (Pattison et al. 2008) . For this to develop, the birds need to be infected when young chicks, before development of the oviduct. There may be partial, or almost complete, absence of the duct or vestiges that are nonpatent or cystic. Once sexually mature, the hen will ovulate, but the ovum is unable to pass normally through the oviduct and can be shed into the body cavity. The hen goes through the process of oviposition but fails to lay (hence blind layer syndrome). Affected hens have pendulous, fluid-filled body cavities and an obvious penguin-like gait. On postmortem examination, the ovary is normal but the affected oviduct is thin walled and cystic and can contain up to 1.5 litres of fluid.

Ectopic eggs can be an incidental finding but can also be a cause of mortality, particularly if associated with peritonitis. Causes of this condition include oviductal rupture and reverse oviductal peristalsis.

If the oocyte is not harvested by the infundibulum at ovulation, it may float freely in the body cavity. Rough handling of a hen may also dislodge other follicles from the ovary. It is possible that there is some reabsorption and no infection because free yolk is very irritating to the peritoneal lining of the coelom. This, or a progressively more severe salpingitis, can develop if egg material from the reproductive tract enters the coelom and becomes infected, leading to an egg peritonitis (Fig. 30.16 ). Affected hens are depressed and inappetant. If this condition becomes chronic, there may be involution of the ovary. Radiographs may show multiple radiopaque densities in the peritoneal cavity, though diagnosis is more frequently confirmed on postmortem examination. Coelomocentesis will yield fluid (unless the lesion is very consolidated) containing yolk material, inflammatory cells, and bacteria. If a flock is very hyperactive, husbandry measures should be taken to calm them; otherwise, egg peritonitis will occur at an unacceptably high level.

a review of the lighting schedule is required. A nutritional review should also be considered to ensure the hens are not overweight and the egg weight is not higher than breed recommendations.

Inflammation of the oviduct is often encountered due to ascending infections from the vent and cloaca. The incidence of this syndrome is increased in older hens, producing large eggs after a sustained period of production. Most commonly, E. coli are isolated from an infected oviduct. However, these may be opportunistic pathogens with a harder-to-isolate bacterium or virus being the primary pathogen.

An end point to dystocia or salpingitis can be oviductal impaction in which egg material (such as yolk, albumen, mucin) and purulent material occlude the oviduct and can ultimately lead to pressure necrosis of the oviduct wall. Birds that have oviductal impaction have been in lay before ceasing production and becoming progressively lethargic, depressed, and anorexic. It tends to be seen in older hens and may be regarded as a normal end point to production in the spent hen. Palpation or imaging of the caudal coelom can detect the caseous mass in the oviduct. Antibiotic treatment tends to be unrewarding and ovariohysterectomy a touch heroic.

Excessive positive pressure in the coelom, such as a discrete mass or excessive straining, can lead to an oviductal prolapse. If it does so, the individual is at risk of cannibalisation by other hens in the flock. Former commercial laying stock tends to have been beak trimmed, which can limit the severity of the cannibalism, but this procedure is rarely performed on pedigree/pet poultry. Even if this does not occur, the condition is a surgical emergency; however, euthanasia should be considered on welfare grounds. If this condition is prevalent in a flock, consideration should be made to providing more available nest boxes.

Uterine torsion occasionally occurs and normally proves fatal for the bird. There is often vascular compromise, and the oviduct will be oedematous, reddish black in colour, and friable.

Numerous cystic structures can occur; they may contain clear or cloudy fluid and are lined by proliferative mucosa of the particular portion of the oviduct involved. This is probably an endocrinopathy, but the exact cause is not known.

It is not uncommon to see oviductal cysts of the vestigial right oviduct, although two Müllerian ducts are present in the developing chick embryo. The left duct develops normally into the oviduct, and the right duct regresses; occasionally regression does not occur, and it becomes a dilated fluid filled cyst. It can be especially pronounced in the sexually immature pullet, although it is an incidental finding as they do not appear to inhibit subsequent sexual development or cause disease.

• Fig. 30 .16 Egg peritonitis with fibrin tags associated with a mature ovary.

large numbers of them should cast suspicion on the cockerel's fertility. Infertility can be due to lack, or poor numbers, of viable sperm or the inability to mate properly. In small flocks it is possible to identify hens that have been repeatedly mated; they will often have feather loss over their dorsum and neck, as well as damage to the integument. Conversely, it is also possible to identify those that have not been mated. A pullet that has not laid an egg will have a narrow gap between the points of the ischium. If a handler can position the width of two fingers or more between these points, the hen will have laid an egg. After the monitoring of embryonic death, a late peak (18-21 days) close to hatching will be identified. Normally, there is also an early peak in embryo mortality (0-4 days) when there is the period of cell differentiation and this is commonly associated with egg handling (possibly before placement in the incubator). Excessively high incubation temperatures and excessive movement of the eggs can also be implicated in these deaths. Midterm embryonic death is relatively uncommon.

Late embryonic death is likely to be associated with the physiological complication changes of switching to pulmonary respiration. For an egg to hatch, it is critical that it loses a certain amount of moisture, which, if not achieved, will result in embryonic death. Very late embryo mortality is a hatching issue and is manifested as pipped shells in which the chick has attempted hatching but failed. These eggs may have been incubated beyond the range of acceptable temperatures.

A few days before hatching, the shell membrane contracts around the chick making the air cell larger, and 24 to 48 hours before hatching, the chick positions itself with its head in the air cell, allowing it to breathe. Abnormal positioning is potentially life threatening and can result from improper turning of the egg during incubation.

Inflammation of the testes is rare. However, if there is an infertility issue in a flock, it should be considered as a differential diagnosis. On postmortem examination of an affected cockerel, the testis/ testes may be enlarged, reddened, and with multifocal lesions. Infectious causes of orchitis include fungal, bacterial (such as mycobacterium and chlamydia), and viral infections (e.g., infectious bronchitis).

Though various types of testicular neoplasia have been reported in birds, they are rare in backyard poultry (Schmidt et al. 2015) . In a small flock with one cockerel, it could explain a drop in fertility. Diagnosis would be on gross postmortem examination, when enlarged testes would be seen, followed by confirmation on histopathology.

Immature cock birds, reared separately from females, will subsequently have a low libido when introduced to a breeding flock. Submissive cockerels in a flock can be bullied by both dominant males and females, thus influencing their breeding capability. Not only are male to female ratios important in a breeding flock (~1 : 8) but also the establishment of a nonviolent pecking order.

Infection of the vent is called 'vent gleet'. A vicious cycle can be established in which there is initial trauma to the vent with subsequent infection, resulting in cannibalistic behaviour and further trauma; it can occur in both hens and cockerels.

Inflammation of the ovary can be secondary to infection of the peritoneal cavity or air sacs or associated with septicaemia. Viruses, bacteria, fungi, and mycobacteria are all possible causes. Ovarian lesions with intense blood vessel congestion and deformed shrunken ovules have also been associated with Salmonella enteritidis infection in laying hens (Pattison et al. 2008 ). If a salmonella species is isolated from infected birds, in the UK this must be reported to the Animal and Plant Health Agency (APHA), as part of the national control plan for salmonella; treatment with antibiotics is not permitted.

A drop or cessation in egg production could be attributed to ovarian neoplasia. Several different types of neoplasia have been reported, but they are rare. Some neoplasia can have a viral aetiology -for example Marek's disease. Confirmation of the diagnosis is made on histopathological examination of the affected ovary.

Increasing day length stimulates reproductive development and production, whereas decreasing day length has the opposite effect; thus artificial lighting regimens are used to mimic these changes and stimulate production. This can be difficult in small flocks in which the housing provided often allows for light pollution, and the producer can be unsure of the optimal light duration and intensity.

Affected hens show signs of paresis, and, although the hens may be in lay, they will have soft long bones. The flock will have a reduction in egg yields and poor shell quality. Supplementation with oyster shell can be beneficial.

If the husbandry of a small breeding flock is suboptimal, it is possible for some of the hens to develop the vice of egg eating. It can be difficult to identify the culprits and to ascertain the action needed to stop the vice.

Keepers of small breeding flocks should be aiming for fertility levels of over 90% and hatchability levels of over 75%. If there is a failure to hatch, the first question is whether the egg is fertile. Breakout work on unhatched eggs (Fig. 30.17) can be useful as it is possible to ascertain at which point in time embryonic development ceased. However, the aviculturist is often unaware of embryonic death; thus the egg is left in the incubator beyond the time of death, leading to severe autolysis.

An infertile yolk is virtually homogenous in appearance apart from a small white area that is the blastodisc. The presence of infected with MS remain asymptomatic. Others can show signs of lameness, mild lower respiratory signs, and a drop in egg production with some eggs showing signs of egg apex abnormality. Diagnosis is by similar methods to MG; live vaccines are available for control.

Although commercial hens are vaccinated against the adenovirus infection, egg drop syndrome (EDS-76), most small backyard flocks are not. Eight days postinfection, there is a massive growth in the pouch cell gland region of the oviduct, coincident with the occurrence of egg shell changes. Progeny from these infected eggs can hatch and appear clinically normal but latently infected. When a latently infected individual reaches peak lay, the virus is reactivated. The virus can be transmitted vertically and should an unprotected flock become infected during lay, the egg drop can be profound. Transmission is possible horizontally via the faecal/ oral route. Classically an infected flock will initially show a loss of shell pigmentation, followed by thin shelled, soft shelled, and shell-less eggs. There is an apparent drop in egg production, though overall production may be normal, but there will be fewer normal eggs. It has been calculated that the loss equates to about 10 to 16 eggs per hen when a naïve flock is infected (Pattison et al. 2008 ). Confirmation of a challenge is possible with rising antibody titres on paired serology or PCR testing (assuming isolation of the virus is not required). No treatment is available, but even in small flocks, vaccination should be considered. The only licenced EDS vaccines in the UK and internationally are polyvalent inactivated vaccines. Replacement pullets for an infected site should be injected with this vaccine intramuscularly between 14 and 16 weeks of age.

Both avian influenza and Newcastle disease are notifiable diseases of poultry, and both can produce a drop in egg production as a clinical sign. With highly pathogenical avian influenza (HPAI), there can be complete cessation of lay in a flock in conjunction with high levels of mortality and morbidity. It must be remembered that low pathogenical avian influenza (LPAI) (H5 or H7) is also notifiable. Clinical signs can be far subtler with much lower levels of mortality and drop in egg production rather than a cessation. Paradoxically this makes LPAI more difficult to diagnose than HPAI and a differential diagnosis for any flock with a drop in egg production. There are no pathognomic lesions for avian influenza on gross postmortem examination, with the carcass merely having lesions suggestive of an acute or peracute viraemia.

Clinical signs for a flock infected with Newcastle disease virus (NDV) are dependent on the pathotype of the NDV. The appearance of shell-less or soft shelled eggs, often laid outside the nest boxes, followed by complete cessation of lay, is a common presentation. With highly virulent forms, high levels of mortality will occur. There can be intestinal, neurological, and respiratory signs, depending on the strain. Like avian influenza, there are no pathognomic lesions. However, haemorrhagic lesions would arouse suspicion especially if the mucosal surface of the proventriculus was affected.

Early detection by veterinary surgeons of these diseases is important for national disease control but can be very difficult for the nonpoultry expert dealing with a small flock. If a suspicion of these diseases persists after an initial investigation, the veterinary surgeon must contact APHA. In cases of avian influenza in which the clinical signs are not profound and after discussions with APHA, the private veterinary surgeon may elect to test in order to exclude

A drop in egg production in a nonprotected flock caused by infectious bronchitis (IB) can be up to 50%. The pathogenicity is dependent on the strain of coronavirus causing the infection. Production can return 4 to 6 weeks after the initial challenge, though this often coincides with a rising number of pale, crinkled, weak shelled eggs; internally, the albumen will be watery. There can be concurrent respiratory signs (Fig. 30.18 ) and mortality. In immature flocks an early onset infection with IB QX strain is the cause of blind layer syndrome. On postmortem examination, birds from an infected flock may have lesions typical of egg peritonitis.

In situations in which it is not essential to isolate the virus, PCR is the test of choice for confirmation of diagnosis. Serological testing using either haemaglutination inhibition (HI) or ELISA can also be used. If a strain of IB is identified as the cause of a drop in egg production, there is no specific treatment. However, the flock keeper and veterinary surgeon should consider control by vaccination. Although commercial vaccines have 1000 doses as the smallest vial size, the live vaccines are relatively cheap and easy to use in small flocks.

Mycoplasma gallisepticum (MG) can be spread both horizontally and vertically. These bacteria survive well in the allantoic fluid and yolk. A laying flock infected with MG will show signs of upper respiratory tract disease (especially severe conjunctivitis and sinusitis) with a concurrent drop in egg production. Infected layers will have a caseous exudate in the oviduct. There are no pathognomic lesions, but there are three laboratory test approaches to diagnosis: antibody detection, isolation of MG, and detection of its DNA. With high levels of biosecurity and good screening programmes, eradication of MG has been possible in commercial primary breeding flocks. With a severely affected backyard flock, culling should be considered. If this is not viable, some level of control is possible with metaphylactic antibiosis and vaccination; both live and inactivated vaccines are available.

Like MG, mycoplasma synoviae (MS) has a short survival time outside the host and similar modes of transmission; some flocks which include infectious bronchitis, egg drop syndrome, and Mycoplasma gallisepticum. Nutrient imbalances in calcium, phosphorus, and vitamin D3 may also be responsible.

Nutrition plays a major part in yolk colour. Feed additives may enhance the richness of the yolk colour (e.g., carotene rich rations) or diminish the yolk colour (e.g., oxidisation of carotenoid feed additives). If blood spots are detected in yolks, it is assumed that the bird has been exposed to some acute stress, such as a thunderstorm or predation. Vitamin K deficiency may also be a factor.

Meat spots in the yolk are due to pieces of ovarian or oviduct tissue becoming embedded in the yolk. There appears to be a genetic component to this condition, as it is more prevalent in brown than white hens.

Watery albumen, revealed on cracking an egg, is often indicative of an active viral infection.

This condition is often associated with an infectious bronchitis challenge.

Inadequate vitamin A and D levels in feed may lead to thin egg shells. A sandpaper texture to eggs may be associated with inadequate levels of vitamin A and/or vitamin D.

Very occasionally, the intestinal nematode Ascaridia galli can migrate from the cloaca up the oviduct to become encapsulated in a shelled egg (Fig. 30.20) . avian influenza, rather than officially notify (Testing for Exclusion of Avian Notifiable Diseases).

Abnormal egg shells are often referred to as 'seconds' as they are downgrades from first class eggs. Numerous abnormalities are recognised (Fig. 30.19) , some of which have known aetiologies, whereas others are suggestive of particular conditions. Though egg shell abnormalities are often a result of nutritional or infectious disease in the hen, it should be borne in mind that poor egg handling and storage can lead to damage. Whatever the cause of the egg shell abnormality, invariably there will be a detrimental effect on hatchability.

Though this is can be regarded as a bonus in eggs for human consumption, in breeding programmes, they are an important issue, as no double yolked egg has been known to be fertile. Prevalence is higher in young flocks in which up to 20% of eggs can be affected. The condition is exacerbated by prolonged day length and light intensity; excessive intake of methionine can also induce this condition. This phenomenon does put the young hen under additional physical strain, as double yolked eggs are larger than single yolked eggs.

The causes are rough handling by the birds, the equipment, or the flock keeper; it is exacerbated in poorly mineralised, large eggs.

Some viruses can cause soft shelled eggs, notably adenovirus and infectious bronchitis virus. They can also be a manifestation of vitamin A, vitamin D or calcium deficiency.

In nest boxes, fully formed eggs minus the shell can be found. Infectious diseases known to damage the oviduct may be implicated, • Fig. 30.19 A tray of downgraded eggs infected with EDS. These changes range from the normal brown eggs (N), to the loss of shell pigment (1), thinning of the normal eggshell (2), cracks where the eggs are damaged in the nest box or handling to soft-shelled (4), and shell-less (5) eggs. (From Pattison M, Poultry diseases, 6th Ed, Philadelphia, 2008, Saunders.) as mushy chicks. The yolk sac can also be involved, being enlarged, discoloured, and oedematous; this is distinct from retained yolk sacs. In these cases, the chicks will not thrive, but the large yolk sac is a normal colour and not contaminated.

How to Measure Egg Water Loss

Breeder Management Supplement (Fast Feather Female

Avian anatomy

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Lohmann Brown Classic Free Range Management Guide

Poultry Diseases. 6th ed. Philadelphia: Saunders Elsevier

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New Jersey: Pearson Education

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Testing for Exclusion of Avian Notifiable Diseases

Avian Reproduction. Unpublished lecture notes

White hens tend to lay white eggs, and brown hens tend to lay brown eggs. The protoporhyrin-IX pigment that is secreted from the epithelial cells lining the uterus during the 90 minutes just before oviposition is responsible for the brown eggshell colour. Loss of pigment resulting in pale eggs can be seen with certain stressors, such as an infectious bronchitis challenge and the sudden exposure to high levels of UV light.

Flocks that are 'lit up' with a lighting programme that brings them into lay too early will be afflicted with the production of small eggs.

If blood stained eggs are noted, the veterinary surgeon has to ascertain whether the blood is from the distal intestinal, the reproductive tract, or the cloaca/vent.

As previously mentioned, egg apex abnormality (EAA) is highly suggestive of a Mycoplasma synoviae infection.

Late fetal deaths and neonatal deaths can be caused by a variety of nutritional, genetic, and infectious issues. Postmortem examination of such cases can reveal oedematous carcasses and is often a result of excessive hatchery humidity. Should the humidity be too low, then the carcasses are seen to be very dehydrated. Bacterial infections are often associated with poor husbandry and cleanliness, which can be traced back to the breeder flock, egg store, hatchery, or brooding hut. Pathogenical E. coli infections are the most common cause of lesions to the umbilicus and yolk sac. The umbilicus can be large, swollen, and reddened with the body wall becoming oedematous and discoloured; if this is extensive, the specimens are referred to