Managing health risks in free-range laying hens

Contents Introduction 2 Managing health risks in free-range laying hens Scope of this report HACCP and flock health plans

2 2 2

Mortality 4 Eggshell quality

8

Control of parasitic diseases

9

Introduction 9 Protozoa 9 Worms 10 Red mites 12 Other ectoparasites 12 Other diseases

13

Marek’s Disease Infectious Bronchitis virus QX strain Osteoporosis and fractures

13 13 14

Biosecurity and managing the range

16

Verandas 17 Inspection, isolation and culling 17 References 18

Managing health risks in free-range laying hens is a Morrisons Farming Programme publication.

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Introduction Managing health risks in freerange laying hens By Dr Claire A. Weeks, Dr Gerald C. Coles, Mrs Kathryn A. Stafford and Mr David G. Parsons, MRCVS

Public concern about the extreme space restriction and lack of opportunity to perform many instinctive behaviours in conventional (battery) cages has led, especially in the UK, to a switch back to free-range systems for laying hens. Ironically, health problems and the difficulties of maintaining a hygienic environment for hens on range were major drivers about fifty years ago for switching to keeping hens in cages. Despite the modern vaccines and pharmaceuticals which have been developed in the meantime, maintaining health and welfare in free-range commercial laying flocks is now even more challenging. The scale of the market requires many thousands of birds to be kept in permanent housing with minimal human attention, as labour is relatively expensive. Good stockmanship requires sufficient time to observe animals, to maintain housing and to pay attention to detail in order to ensure good hen welfare. Furthermore, compared with mobile housing, it becomes considerably more difficult in static housing to control pasture contamination by the traditional method of resting by rotation. The hen herself is also a totally different animal; in the last six decades intense genetic selection has developed a small, highly productive bird which lays almost an egg a day for the one year of her adult life. Modern genotypes have also been selected to live in small group sizes and either in warm climates or in warm, controlled-environment housing. There is some evidence – mostly anecdotal – that some strains cope with the challenges better than others. The few breeding companies are internationals selecting for a global market that continues to predominantly house laying hens in conventional cages. It could benefit hen health and welfare if genotypes better suited for free-range and colony cages were developed, but it is difficult to select from breeding birds that are housed in groups. The emerging change in selection emphasis, to persistence of lay rather than early onset of lay, by the main breeding companies might result in a slightly more robust bird, provided that feather cover can be maintained. This report outlines some of the challenges to the health of modern, commercial free-range laying flocks in the UK and indicates some future risks to health. We have found there is astonishingly little scientific or published evidence-based information; thus it is very difficult to obtain an accurate

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Hen Health Report

picture of current laying hen health. Furthermore, an analysis of hen carcases sent for post-mortem (PM) is only ever going to tell part of the story, as the great majority of hens which die are not sent for PM. We identify some of the many gaps in knowledge concerning the health status of the national flock and suggest a number of potential studies which could be of benefit to commercial egg producers.

Scope of this report The main aim of this report is to review the evidence, including scientific literature on common pathogens, parasites and other issues which are relevant to the risk of ill health in free-range laying hens in the UK. Thus the hazards for flock health will be identified in a generalised, ‘national flock’ picture. For an individual farm or flock the risks and strategies for controlling disease and improving flock health need to be identified and controlled with a specific, tailored plan. We will also identify some issues relevant to the prevention and control of disease. First we consider two quantifiable indices of health and welfare. Mortality in most instances is an indicator that can represent the ‘tip of the iceberg’ in terms of underlying problems that are likely to be affecting the rest of the flock. Even accidental death from being trapped in fixtures and fittings indicates underlying design problems. We also look at how eggshell quality can yield valuable information regarding flock health and welfare. We then consider parasites and a few emerging and poorly understood diseases affecting hens, plus the susceptibility of layers which develop osteoporosis to fractures of the keel in particular. We also consider management practices that could control and reduce these risks both specifically and in general. Gaps in current knowledge are indicated throughout and in the summary.

HACCP and flock health plans HACCP stands for Hazard Analysis and Critical Control Points and is a system widely adopted in food processing plants to identify potential physical, biological or chemical hazards and all the points (CCPs) during the process where these can be actively managed to ensure food safety. The basic principles are successfully applied in wider contexts and have merit for use on farms, They are the first link in the chain from “farm to fork”. Applying HACCP principles to flock health puts the producer in the driving seat and gives a proactive rather than a reactive approach. It is based around seven core principles: Principle 1: Conduct a hazard analysis. This could, for example, be a flock health plan which identifies the potential risks and identifies the preventive measures the plan can apply to control these risks. Principle 2: Identify critical control points. A Critical Control Point (CCP) is a point, step, or procedure at which control can

be applied and, as a result, a health hazard can be prevented, eliminated, or reduced to an acceptable level. Biosecurity is one example where potential points of contamination of birds, feed, housing or land are identified (so that measures are then taken to minimise the risks). Principle 3: Establish critical limits for each critical control point. A critical limit is the maximum or minimum value to which a health hazard must be controlled at a critical control point to prevent, eliminate, or reduce to an acceptable level. For example, it could relate to a worm egg count which triggers administration of anthelmintics. Principle 4: Establish critical control point monitoring requirements. Monitoring activities are necessary to ensure that the process is under control at each critical control point. Some monitoring procedures might be undertaken by a veterinary practice or assurance assessor. To use the worm example again, monitoring would require egg counts to be made after anthelmintics were administered to ensure they were effective and might even require checking that hens each received an effective dose. Principle 5: Establish corrective actions. These are actions to be taken when monitoring indicates a deviation from an established critical limit. To use just one example, you might decide you will call your vet in to determine the underlying causes when egg seconds reach a certain percentage.

Principle 6: Establish record keeping procedures. This would probably extend records required for assurance schemes, and include records of control and monitoring procedures. Principle 7: Establish procedures for ensuring the HACCP system is working as intended (i.e. validation and verification). For example, the routine veterinary visits to monitor flock health and welfare through clinical examination and examination of flock records. The Salmonella in eggs story is a good illustration of the limitations of relying on product quality control to identify problems. The industry as a whole has largely managed this particular issue by the widespread use of vaccination coupled with biosecurity, good hygiene, rodent and fly control etc. An approach based on HACCP principles might have prevented it happening (although HACCP relies on identifying and acting on known risks) and would also identify further methods of control as alternatives or supplementary measures. As indicated above, a good flock health plan uses essentially a HACCP approach to develop a farm-specific proactive health management strategy. Indeed just such an approach of applying effective measures at each stage of the chain of egg production was advocated to maximise control of Salmonella Enteritidis 1.

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Table 2. Poultry Health Centre Commercial Layer Diagnoses 1995 to 2010

Mortality

Number of post Percent of all mortems post mortems

Diagnosis

Whereas there are numerous published records of the proportion of hens which die during production, which is useful in defining the scale of the problem, establishing causes is less straightforward. Table 1 shows that there is a huge range of mortality rates, indicating a potential to reduce mortality to the low levels, which are more often associated with production in cages. A small survey of production and health problems including mortality in 16 Free Range flocks was reported on by Mr O. Swarbrick, MRCVS in 1986 2. In several cases poor husbandry including problems of birds accessing feed and water, was at the root of problems: in two flocks cannibalism was an issue and one flock had a severe red mite infestation. While the Egg Drop Syndrome 1976(EDS’76) was diagnosed as a cause of failures to peak or post peak drops in production, and egg peritonitis was the cause of excessive mortality, the causes of white or deformed eggs was usually undetermined. The top 20 causes of mortality determined for 1,200 free range commercial layers submitted for post-mortem examination at David Parsons’ specialist poultry practice are shown in Table 2. In addition, 31 normal and 22 culled birds were presented for PM.

Table 1. Mortality of free range hens in commercial flocks

Egg Peritonitis

362

30.2

Spotty Liver Syndrome

93

7.8

Undiagnosed

60

5.0

Vent Pecked

51

4.3

Salpingitis

43

3.6

Emaciated

33

2.8

Peck Injury

30

2.5

Pale Bird Syndrome

28

2.3

Cannibalised

37

3.1

Septicaemia

27

2.3

Anaemia

26

2.2

Kidney Failure

19

1.6

Enteritis

16

1.3

Hepatitis

16

1.3

Acute Septicaemia

15

1.3

Air Sacculitis

13

1.1

Gumboro Disease

12

1.0

Moult

12

1.0

Colisepticaemia

11

0.9

Tracheitis

11

0.9

* Flock sizes are given as reported but larger flocks must have been housed in smaller units Mortality (%) No. of flocks

Reference

Country

System

Lampkin, 1997

UK

organic

600 - 1,000

Berg, 2001

Sweden

organic

12 - 1,700

1 - 60

9

Sommer & Vasicek, 2000

Austria

free range

500 - 700

0 - 32

7

Emous, 2003

Netherlands

free range

16,000

8.0 - 28.5

14

Fiks et al, 2003

Netherlands

organic

80 - 5,400

0 - 21

11

Kreinbock et al, 2003

Germany

free range

Moberly et al, 2004

UK

free range

49

35 - 130,000

0 - 26.8

8

Hegelund et al, 2006

Denmark

organic

18

1,200 - 5,000

9 - 62

22

Whay et al, 2007

UK

free range

25

3,000 - 16,000

1.8 - 21.4

Croxall & Elson, 2007

UK, Germany, Netherlands free range

9

Unpublished MHS data, 2009

UK

free range

Stokholm et al, 2010

Denmark

Sherwin et al, 2010

UK

flock sizes*

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Hen Health Report

Mean 7

1,300 - 75,000

19

14

988

60 - 20,000

0.1 - 63

9.5

organic

11

2,428 - 4,500

1.6 - 91

21

free range

7

2,000 - 13,248

* flock sizes are given as reported but larger flocks must have been housed in smaller units

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Range

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Frequent causes of mortality in hens submitted for PM to this practice are infections causing inflammation and sepsis and pecking injuries from other hens (12%). One possible cause of the undiagnosed deaths is suffocation: obtaining an accurate case history is important to aid some diagnoses. A current study of transportation of end of lay hens at the University of Bristol has also found that sepsis is common in free range hens: recorded in about 10% of outwardly ‘normal’ birds and in a third of those which die during transport (CAW unpublished data).

Figure 1 compares the main causes of mortality between housing systems and graphically illustrates the ubiquitous problem of egg peritonitis. In addition, it indicates the opportunity for careful supervision of birds, especially pullets after placement, to ensure adequate feeding and drinking in order to improve their health and to reduce mortality.

Figure 1. A comparison between housing systems of principal causes of mortality in commercial laying hens (Poultry Health Centre data 1995 to 2010). Numbers shown are the total number of hens diagnosed with each condition

Cage Tracheitis

Vent Pecked

84 Infectious Laryngotracheitis

86

86

Salpingitis 102 Septicaemia

Egg Periontitis

115

592

Air Sacculitis 125

Non-Starter 254

Yolk Sac Infection

Starve-out

204

215

Barn Air Sacculitis

Acute Septicaemia

27 Septacemia

27

28

Non-starter 29 Yok Sac Infection

Egg Periontitis

41

213

Ascariasis 48

Starve-out

Coccidiosis

81 Vent Pecked

49

50

Free range Septicaemia 27 Peck Injury 30 Cannibalised 37 Salpingitis 44

Anaemia 26 Pale Bird Syndrome 28 Emaciated 33 Egg Peritonitis 363

Vent Pecked 51

Spotty Liver Syndrome 93

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Table 3. The top ten most common diagnoses compiled from the VLA data, 1999 to 2011 Commercial layers

Fancy Fowl

VIDA (1996-2009)

1

Marek’s Disease

Marek’s Disease

Coccidiosis

2

Red Mite

Infectious Laryngotracheitis

Colisepticaemia

3

Egg Peritonitis

Egg Peritonitis

Trauma/Fracture

4

Infectious Laryngotracheitis and Coccidiosis

Red Mite

Egg Peritonitis

5

Fowl Cholera

Adenocarcioma

Marek’s Disease

6

Colisepticaemia

Infectious Bronchitis, Caecal coccidiosis

Helminthiasis

7

Spotty Liver Syndrome

Mycoplasmosis, Impaction

Yolk sac infection/ omphalitis

8

Mortality and Avian TB

IBV QX strain, Avian TB

Mycotic pneumonia

9

Mycoplasmosis, Mg, Histomoniasis, Erysipelas, Caecal coccidiosis

Urolithiasis, Mg, Fowl Cholera, Coccidiosis, Candidiasis, Aspergilosis

Lead Poisoning

10

Impaction, Brachyspira infection, Aspergillosis

Visceral Gout, Undiagnosed, Tumour, Mycotic pneumonia, Mortality, Listeriosis, Capillariasis

Adverse environment not otherwise specified

The avian part of the Monthly VLA (Veterinary Laboratories Agency) Newsletter (previously VIC) has been compiled (by DGP) into a database dating from 1999. This information has been categorised as chicken (commercial layers) or fancy fowl (small numbers of commercial breeds or pure breeds). These results of PMs from birds mainly from southern England are shown in Table 3 (excluding broilers). The last column in Table 3 summarises all diagnoses made within the VLA for the whole of the UK on all categories of birds (i.e. not specific to commercial layers and including broilers).

These three summaries of post-mortem findings all indicate egg peritonitis (Figures 2) to be a principal cause of death in laying hens. We speculate that there may be a link with the very high productivity of modern genotypes, which lay continuously, rather than in clutches as unselected birds do. The oviduct thus never has a rest and may be susceptible to infective agents such as E. coli tracking up and causing peritonitis 3. It should be noted that milder cases of egg peritonitis are not necessarily fatal and we have observed it in end of lay hens at slaughter. Indeed, it is a common cause of rejection for human consumption of the carcase.

Figure 2. Photographs of hens with egg peritonitis at post-mortem and a normal hen for comparison

Egg Peritonitis with parchment-like pus

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Egg Peritonitis with fibrinous pus

2 1

Left Lateral View of the abdomen of a normal laying hen 1. Ovary 2. Oviduct The causes of mortality throughout lay in 15 organic freerange laying flocks, placed between 2001 and 2003 in Denmark, have recently been published 3. The main cause at PM was infection with E. coli and this was prevalent (mean 40.5%, range 16.3 - 61.8%) in all flocks, often as local infections of airsacculitis, chronic productive forms of peritonitis and salpingitis. Outbreaks of fowl cholera and erysipelas caused high mortality in a few flocks. Blackhead (Histomonas melagridis) was reported as a problem in these flocks and as an emerging issue for free-range flocks in Denmark.

The majority of hens which die on farm are not submitted for PM examination. This tends to be reserved for large outbreaks, early losses and instances when the farmer is unsure of the likely cause of death. Thus there are few reports which indicate the actual prevalence and causes of losses during production. It is not merely a case of multiplying the findings at PM by overall mortality to arrive at the answer. The Danish study 3 augmented the PM findings with farmer records and thereby found cannibalism, suffocation and losses from predation to be frequent causes of loss. Another systematic study of hen welfare during lay 4 comparing 6-7 flocks in each of 4 systems in the UK, recruited producers to frequently record mortality, prevalence of red-mites, injurious pecking behaviour, egg shell quality and possible causes of mortality. These results are given in slightly more detail in the funder’s report 5. For a third of deaths producers could not determine a possible cause but ‘illness’ accounted for almost half the birds found dead. Across all systems injurious pecking (12%) and trauma (4%) were common causes of death during production. Furthermore, there were small increases with age in the proportion of hens culled, found dead, found dead due to injurious pecking, and, found dead for unclear reasons. The researchers therefore suggested that, alongside other evidence, the health and welfare of most layer hens progressively decreases throughout their lives 5. Estimates of losses from predation are seldom published; a survey of 53 farms published in 2004 6 indicated losses to range from 0-11.6% with an average of almost 2%. Apart from using electric fencing, llamas and alpacas are reported to reduce predation – this needs to be formally examined along with other methods of predator control. A current study at the University of Bristol will shortly be reporting possible strategies for reducing the risk of injurious pecking, following a trial of 40 potential interventions on more than 50 commercial farms (contact CAW for more details).

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Eggshell quality There is growing evidence, but scope for considerably more research, that eggshell quality can indicate underlying problems in the individual hen and the flock as a whole. Under conditions of stress, hens will delay laying eggs which results in additional calcium carbonate being deposited on the eggshell 7. Sherwin and others 4, 5 used calcification spots to monitor and compare stress levels between housing systems and found lower proportions in their 7 monitored free-range (1.7%) and 6 furnished cage (1.2%) flocks than in 6 conventional cage (3.5%) or 7 barn (4.1%) flocks. Blood might be found on eggs for a number of reasons including vent pecking, prolapse or the eggs being too large for the cloaca, all of which indicate both a direct reduction in welfare and an increased potential for disease or infection. The industry has linked white eggshells from brown hens to exposure of poorlyfeathered flocks to sunlight. The reasons for this are as yet unknown, but could be linked with excess vitamin D production. Figure 3 illustrates some eggshell quality defects – in most cases the cause of these is unknown. Routine recording of egg quality on farm (for example of a few trays once a week) and linking these to the health status of the flock would, we believe, yield valuable information for comparatively little effort. Figure 3. Eggshell defects associated with stress and health problems in laying hens

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a) Calcium splash

b) Calcium lumps

c) Ridging

d) Pale egg ridging

f) Faeces urate

e) thickened middle ridging

Hen Health Report

Photos © DG Parsons

Control of parasitic diseases Keeping hens under free range systems increases exposure of the birds to their faeces which enhances the risk of infection with both bacteria and parasites 8. Hens Parasites fall into three main categories: 1. Single celled parasites or protozoa of which the best known example are the coccidia (Eimeria sp), 2. Worms which include round worms (nematodes) and tape worms (cestodes) and 3. Ectoparasites of which the most troublesome is the red mite. All can cause varying degrees of disease or even death, depending on parasite burden, age and health status of the birds. Young birds are usually more susceptible to infections as they have not yet developed some natural immunity.

Protozoa Coccidia Seven species can infect chickens and disease ranges from mild to very serious. The disease they cause depends on the species involved but all basically live and reproduce within the cells of the hen’s body. They damage the intestines (caeca) primarily by killing these cells when the parasites emerge. The multiplication factor is huge – just one oocyst (egg) ingested by a hen can lead to hundreds of thousands shed in the faeces. Usually only one or at most three species infect a bird at one time. In deep litter housing huge numbers of oocysts can build up and pose a very serious threat to young birds. With replacement laying birds on wire, no treatment should be required. If birds are on deep litter, vaccination with attenuated (precocious strains) should be used. The coccidia used for vaccination cause minimal damage to the gut of the bird but allow the birds to build up a natural immunity. This needs to be reinforced by letting the birds encounter more oocysts in their environment. Coccidia usually cause morbidity but a number of species can cause mortality. Eimeria acervulina is usually chronic resulting in poor weight gains but can cause diarrhoea, ruffled feathers and drooping wings. Similar effects can be caused by Eimeria brunetti, Eimeria necatrix, and Eimeria tenella, although this last species often produces bloody faeces. A large intake of oocysts can result in disease before oocysts are shed and appear in the faeces. E. brunetti can be more serious than E. acervulina with blood tinged mucus in the faeces and heavy infections can kill as can E. tenella. If an outbreak of coccidiosis occurs, then treatment with chemical agents is required. First the species involved needs to be determined. This will be undertaken by a specialist veterinary surgeon following post mortem of some birds. How

the outbreak develops will be determined by a range of features including the age of the birds, the breed of the birds, whether the population of birds are of mixed age, the stocking density, the humidity of the litter (moist litter is a problem) and the presence of other diseases. Just detecting oocysts in the faeces may be too late as the cysts are only present after the damage has been done to the bird’s intestine. Presumptive diagnosis will be made from the symptoms and history of the birds. The choice of drug for treatment will depend on the susceptibility of the species present to the available drugs, so this should be left to the vet. Possibilities for control include maduramycin, monensin, narasin, robenidine and toltrazuril. It is because there is such a wide range of drugs, and resistance may occur in some coccidial species but not others to some drugs, as well as the need to observe withdrawal periods, that professional advice from a specialist in chicken health is required for management of coccidiosis outbreaks. Of course prevention by good hygiene and use of vaccination is the best way forward. Black head disease This is caused by Histomonas meleagridis, and affects primarily the caeca and liver in young turkey poults where it usually causes 100% mortality. It is a common cause of death in layers (Table 3) and it can be a significant problem for a few flocks on free range. First signs may be death from egg peritonitis; look harder and caecal lesions can be found. Liver lesions are not always a feature of black head disease. A big problem for poultry producers is that the only available drugs have been withdrawn on the grounds of their toxicity, so there is a desperate need for a vaccine or a new safe treatment. There have been recent reports 3, 9 of Histomonas causing disease in hens (Table 3 also) but often in hens it will go unobserved. Hens may be transmitting the parasite where there are or will be turkeys on the ground, thus different classes of poultry should not share housing or pasture (even in rotations). What is most interesting, scientifically speaking about Histomonas is that is uses the eggs of the worm Heterakis gallinarum as a method of transferring from bird to bird and Heterakis is very common in free range hens, hence the value of routine worming. Trichomonas gallinae This causes canker in the oesophagus, crop and pharynx of chickens. If severely infected, birds may stand in huddled groups and if forced to move may fall over. Diagnosis is by seeing motile swimming parasites collected from the lesions. Infection comes from drinking water that has been contaminated by pigeons. Therefore drinking water must be protected from these birds. There is no approved treatment for infections in hens.

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Cryptosporidium meleagridis This is a tiny coccidial type of protozoan that causes diarrhoea in birds and is infective to humans. Diagnosis is by microscopy and specialised staining of faecal samples and by immunological or DNA based methods. Infection is by ingestion of oocysts shed in the faeces so good hygiene is essential and droppings must not be allowed to contaminate drinking water or feeding trays. Wet litter will encourage the infection of birds. There is no reported treatment for the infection.

Worms The main problem comes from round worms (nematodes) although tapeworms do occur. Fluke are usually rare and need a wet area with snails to act as intermediate hosts for the life cycle to be completed. It is thought that young birds are likely to mount stronger immune responses to worms than laying adults which are diverting protein into egg production rather than the immune system. How this affects worm burdens in laying hens is not clear. Ascaridia galli is the largest worm of chickens and lives in the small intestine. Females can reach 12 cm in length. Eggs are deposited in the faeces where they take 10 days or longer to develop before they become infective. In moist conditions eggs may survive for up to 3 months. Birds are infected by ingestion of the eggs but can also become infected by eating earth worms that have swallowed Ascaridia eggs. Adults do not usually show symptoms but are carriers of the infection. In young birds heavy infections may occur resulting in enteritis or haemorrhagic enteritis and even blocking of the small intestine. This will show as anaemia, intermittent diarrhoea leading to emaciation and, in egg laying birds, loss of production. Diagnosis is usually by seeing the eggs in faecal samples but it must be remembered that the prepatent period, the time from ingestion of worm eggs to eggs in the faeces, is 4-5 weeks in young birds but may be longer in adults. Figure 4. Photo showing roundworm infestation in the intestines at post mortem

In laying birds the only licensed treatment is flubendazole which is incorporated in the diet or as a suspension in drinking water. In younger birds, worms can be treated with piperazine, where efficacy of at least 95% should be obtained, or levamisole. These latter two are not licensed for use in chickens so can only be given if flubendazole does not work. They require a prescription from your veterinary surgeon. Heterakis gallinarum is a very common worm found in most flocks that on its own will not usually cause significant problems. As already discussed, its importance is aiding in the transmission of Black head. The worm primarily inhabits the caeca of the bird but also can be found in the intestines. Flubendazole should be effective (but see below). Capillaria annulata the hairworm or thread worm, causes nonspecific symptoms. Eggs passed out in the faeces are ingested by earth worms where they become infective around 2-3 weeks later making this a worm of free range hens. The worms are found in the oesophagus plus crop and heavy infections can kill. The infection is likely to be worse in young birds with adults acting as carriers. Diagnosis is usually at post mortem as symptoms may occur before eggs are found in the faeces. Treatment is by administration of anthelmintics, e.g. flubendazole or levamisole in drinking water but, to break the life cycle, birds should be moved after treatment to clean ground. The related Capillaria obsignata has a direct life cycle and can be very pathogenic leading to death of birds. Capillaria anatis also has a direct life history and can produce enteritis and bloody diarrhoea. Strongyloides avium (thread worm) like other Strongyloides species can reproduce both in animals and as free living worms in faeces on the ground. Interestingly the worms in the bird are solely female. Although infection may occur through ingestion of larvae, they can also penetrate through the skin. The infection can be a serious problem in floor reared birds. Flubendazole should control the infection. Trichostrongylus tenuis The infective stage of this small hair like worm is the L3 larvae that are ingested by the birds. T.tenuis is best known for its potentially serious effect on the health of grouse. In non-egg laying chickens it can be controlled by flubendazole in the diet and also levamisole in the water. Use of levamisole will require veterinary prescription which would only be given if flubendazole was shown to be ineffective. Syngamus trachea (gapeworm) lives in the lungs. Eggs are coughed up and swallowed being passed out in the faeces. It is primarily a problem in young birds, particularly game birds where the infection result in pneumonia and death. Birds can show head shaking and coughing and gasping for breath. Confirmation of infection is the finding of eggs in faeces or worms in the trachea at post mortem. Infection can be avoided by keeping young birds and adults apart, keeping runs dry and not allowing access by wild birds. It can be controlled with benzimidazoles in the diet or levamisole in the drinking water.

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Prophylactic worming is sometimes used to control worms in flocks. Infection with a single species of worms will usually be rare and symptoms are therefore generalised. The only treatment approved for laying birds is flubendazole given either as a suspension in drinking water or as a food additive. The problem with all self administered drugs is that not all the animals involved may be taking an adequate dose and it has been well established with experiments in sheep that underdosing encourages the development of resistant worms. There is circumstantial evidence that in some cases Heterakis may not be fully responding to therapy. Whilst this may not be very significant in the less pathogenic species, if serious pathogens cannot be controlled the health and productivity of the birds may be seriously compromised. Results from recent studies at the University of Bristol, of 44 flocks of free-range hens in which egg counts from fresh faecal samples were made using the FLOTAC method, and some birds were post mortemed, indicate that most (93%) of flocks were infected with one or more species of nematodes. Ascaridia galli was present in 76% of flocks and Heterakis gallinarum in 56%. The prevalence of Syngamus trachea was 16% and was more common in faecal samples collected outside, whilst Trichostrongylus tenuis was present in 25% of flocks, and was more common in indoor samples. The welfare implications and effects on egg production remain to be determined. Chicken guts three weeks after treatment with flubendazole still contained mature H. gallinarum while

six weeks after treatment they also had A. galli and T. tenuis present. The finding of mature H.gallinarum worms three weeks after therapy with in-diet flubendazole, emphasises the need for further investigations as it could not be determined if this was due to inadequate self medication or the development of anthelmintic resistance. Since flubendazole is the only anthelmintic licensed for use in laying hens, resistance could present a major problem for flock health. Tapeworms all need an intermediate host and thus are not usually found in indoor birds. The most pathogenic is the small tapeworm Davainea proglottina that has gastropod molluscs (slugs and snails) as the intermediate host. Although it is only a very small worm, 3-4 mm long with only 4-9 segments, heavy infections can cause haemorrhagic enteritis whilst light infections can result in retarded growth. Raillientina cesticillus is a much larger tapeworm, 10-14 cm in length, that can cause reduction in growth rates and emaciation. Its intermediate hosts are certain species of beetles. Raillietina echinobothrida, that grows up to 25 cm, has ants as its intermediate host and can cause lesions in the intestine. Raillietina tetrogona is a long tape worm, up to 25 cm also with ants as the intermediate host. The best way of diagnosis is by observation of the tapeworms at post mortem and in the case of Davainea by examining intestinal scrapings. In all cases the best drug is praziquantel given at 10 mg/kg orally but this will require a veterinary prescription 10.

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Figure 5. Red mite magnified (L) and red mite on a hen at PM (R)

Ectoparasites Red mites Dermanyssus gallinae are the major ectoparasite of chickens and particularly laying hens and infestation is common (Figure 5). Guy and others reported in the north of England red mites were present on 25 out of 29 farms 11. Whilst in another survey, 50% of free range units reported infestation 12. Mites live in cracks in the chicken house or cages by day and come out at night to feed on the birds’ blood. Infestations can reduce egg production and increase egg downgrading. Heavy infestations can kill birds and the mites can also bite humans. The life cycle can be a short as 7 – 10 days meaning that very large populations of mites can build up rapidly. An estimate of what is going on can be made using mite traps (Figure 6) that can be purchased (from ADAS or Animal Aids) or be homemade by using small tubes of corrugated cardboard. The ‘hot spots’ should be identified and control concentrated in these areas. Mites can be introduced into a property with new birds and on clothing. The mites are also found in wild birds’ nests, so it is important that wild birds cannot nest in or on chicken houses. One non-chemical method of control is the use of diatomaceous earth i.e. very fine particles of silica. These act by scratching the surface of the mites, disrupting the wax coating which means the mites lose water and die from desiccation. The silica can be dusted into the relevant places (e.g. dust-baths) or sprayed as a suspension. A new spray comes as a white suspension of a synthetic hydrophobic silicon dioxide (Decimite, Sorex and BASF). Chemical control is difficult because several of the insecticides/ acaricides have been withdrawn. Pyrethroids are still available as fog fumers or sprays but there is resistance and in 2005 Fiddes and others 12 reported that 60% of farmers thought cypermethrin was not effective. Mites were tested from 8 farms and all showed resistance to cypermethrin in laboratory tests. It would be worth having mite susceptibility determined before using pyrethroids.

Control of red mites can be summarised: 1. If you don’t have red mites at present only buy certified mite free birds and use good biosecurity measures to prevent spread via humans. 2. Clean houses thoroughly between flocks with steam cleaning especially of cracks. 3. Use cardboard traps to monitor populations. 4. Try silica based products if treatment is required. 5. Don’t use pyrethroids without first testing whether they work with lab based tests. 6. Explore the possibility of the new product MiteStop. Ornithonyssus sylvarium, the nearest fowl mite, is the other mite that can infest chickens is the northern fowl mite. Unlike the red mite the northern fowl mite spends its life on the fowl, so treatments must be given to the birds. The mites suck blood and can transmit a number of infections including fowl pox and Newcastle disease. White mite eggs can be seen around the vent of the feathers, and feathers may become matted with scabbing. Weight gain is reduced in infested birds. A study in China 15 showed that oil solution of lambda-cyhalothrin was more effective than wettable powders due to the hydrophobic nature of chickens’ feathers. There is no recent information indicating how common the infestation is in the UK and whether resistance has developed to the pyrethroids. However in a study 16 in southern California, resistance was present to some acaricides. Other ectoparasites such as Lice are of concern. There are a number of different lice that can infest chickens: Cuclotogaster hetergraphus (head louse), Goniocotes gallina (fluff louse), Goniodea dissimilis (brown chicken louse), Goniodes gigas (large chicken louse), Lipeurus caponis (wing louse), Menacanthus stramineus (chicken body louse) and Menopon gallinae (shaft louse). Heavy infestations with lice can kill chicks and affect egg production. Skin can become inflamed and covered in scab and blood clots. Lice only survive off the birds for 5-6 days so cleaning between flocks should eliminate any problems. The main treatments now offered is either diatomaceous earth or Poultry Louse Powder, which is based on plant oils, but the effectiveness of these products has not been independently assessed. Traditionally pyrethroid powders or Malathion were used and it has been suggested that eprinomectin in drinking water will work. These are off licence use and require veterinary prescriptions which will only be given if other treatments have failed. Figure 6. An example of a red mite trap and numbers of mites captured

Treatment of the birds, usually with ivermectin, may help a little but the prime attention must be focused on the buildings and particularly to the nesting area. Cracks should be filled in where possible and before new birds are introduced likely hiding places should be steam cleaned. There is now a product based on the natural product, neem oil, MiteStop ([email protected]) which has been reported to be very effective 13. There is also published research 14 suggesting that spinosad may be effective. Red mite trap

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Low infestation

High infestation

Other diseases

Figure 7. Classical Marek’s Disease – (a) tumour filled liver and proventriculus and (b) abnormal spleen (L) compared with normal

This report is not a handbook of poultry health and disease, (of which several are available) but we highlight three conditions of interest because they are cyclical, poorly understood and possibly of emerging significance. We also include information about osteoporosis and keel fractures, which have a high prevalence. Marek’s Disease is an example of a disease that has been recognised for over a century. First described in 1907, as a disease affecting the peripheral nervous system, it was not until 1926 that it was realised that it also caused tumours in various organs in the abdomen (see Figure 7). It was another 40 years before proved that some of these tumours were caused by the tumour-forming herpes virus that causes Marek’s disease, and others, by the tumour-forming retroviruses. In the early 1970’s, the first vaccine for Marek’s disease became available. The chicken vaccine was the first vaccine to be produced that protects against cancer. Marek’s disease vaccines have transformed the fortunes of the poultry industry. However, they have not eradicated the disease. Figure 8 taken from the VIDA reports shows the variation in Marek’s disease diagnoses over time (1996 to 2010). Marek’s disease had previously been a problem for the industry around the early 1990s (D.G. Parsons, Nuffield Farming Scholarship Study Tour report). The VIDA reports can potentially give early warning of upsurges in the disease. With the burgeoning interest in keeping fancy and backyard fowl, these are potential reservoirs of infection for commercial

a) Tumour filled liver

b) Abnormal spleen

Figure 8. Annual number of diagnosed cases of Marek’s disease in the UK (source: VIDA) 200 180 160 140 120 100 80 60 40 20 0

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Figure 9. Photographs of hens at post-mortem with erysipelas (a) and spotty liver syndrome (b)

a) Erysipelas

b) Spotty liver syndrome

flocks. In unvaccinated birds the disease may peak in the summer and autumn, but as yet there are no indications of seasonal changes in national figures. Among possible reasons for the cycling of prevalence of Marek’s include:

Infectious Bronchitis (IB) Virus QX strain is a well known cause of egg production problems that include failure of a flock to reach peak production, drops in egg production, shell abnormalities, internal egg quality abnormalities, oviduct development abnormalities, respiratory disease and kidney disease. There are many serotypes of IB and this number is constantly increasing. Prior to the introduction of vaccines, infection could result in severe respiratory disease and drops in production to levels of 20% or less. Damage to the oviduct was permanent. Consequently, the flock would not return to expected production. The introduction of effective vaccines controls this very severe disease, but new IB serotypes which are not fully controlled by vaccination can appear and cause small drops in egg production and reduced egg quality. Routine monitoring to assess the efficacy of a vaccination programme should be the norm, but DGP would suggest that this is not so.

1. Vaccination will tend to select for strains of infectious disease that can develop in the immune birds 2. Personal knowledge of flock can be lost when staff change with practices that seem irrelevant to newcomers actually being those that keep disease at bay. 3. Absence of a problem will always tend to encourage the relaxation of protocols. Spotty Liver Syndrome is a condition that predominantly affects free range flocks although it has been seen on occasion in caged layers. It is characterised by a sudden increase in mortality as the flock is coming up to peak lay. This is accompanied by a significant drop in production. Post mortem examination reveals lesions associated with an acute septicaemia and focal hepatitis. The hens will be in good condition, in lay and often have food in the crop and intestines. Possible differential diagnoses would include acute Fowl Cholera, Erysipelas, Vibrionic Hepatitis and Salmonella gallinarum infection. The distinguishing feature of SLS is the inability to isolate either the causative bacteria of the infections above or any other bacteria. Campylobacters have been recovered occasionally. There is a likelihood that bacteria of some kind are strongly associated with the condition, as clinical treatment with antibiotic (e.g. chlortetracycline medication in the feed) can halt mortality and aid the return to normal egg production. Further investigations are required to establish the causative organism(s) and investigations are ongoing at the AHVLA. Although DGP recorded incidences from 1993, nothing was in the public domain until a paper in 2003 17. This illustrates the very important point that emerging health problems may remain ‘unknown’ until they are officially reported or recorded. There may be a number of conditions ‘out there’ of which individual farmers and vets might be aware but there is no national recognition or recording of prevalence.

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In 1996, a new strain of IB was identified in China that has become known as the QX strain. Infection with this strain results in false layers, a cystic oviduct and hens with a penguinlike stance as a result of the excessive quantity of fluid in the oviduct. The infection has gradually spread around the world being first recognised in the UK in backyard fowl in 2007. It has now spread into broilers where it is associated with kidney and stomach (proventriculitis) disease, and may cause classic disease, in commercial layers. Fortunately, the vaccines available can offer good protection against the disease. Osteoporosis is prevalent among all laying flocks and increases with age. The progressive loss of structural bone throughout lay results in the bones becoming more fragile and susceptible to fracture. The Farm Animal Welfare Council (FAWC) has recently published an Opinion which reviews these issues 18. Osteoporosis develops in part from lack of weight-bearing exercise, which is another reason for introducing furnished or colony cages that allow wing flapping, more exercise and the hens to jump up and down from perches. However at least one in four birds in any type of cage sustains a fracture during production 19, 20. The very high productivity of modern genotypes (egg output has more

than doubled in the last 70 years) means that the hen’s need for calcium exceeds her body reserves by about 30 times and it may not be possible for all her needs to be supplied in the diet. The incidence and severity of osteoporosis may be reduced by improved nutrition and genetic selection – furthermore the benefits are additive 21. Despite the benefits of exercise, free-range hens are especially susceptible to bone fractures, with a study of 18 flocks in 2006 recording 44% sustaining one or more during production and 14% at depopulation 19. A more recent survey 20 of 48 freerange and organic flocks showed that the majority of hens had fractures of the keel bone with means of about 65% in typical free range units, rising to 87% in 6 units with suspended perches. Here the severity of fracture was also greater. As well as diet, house design and possibly flock size may affect the number and severity of fractures within a flock. Both organic mobile (maximum 2,000 birds) and colony cage flocks had about a third of birds with keel fractures, but those in cages had the weakest tibia (leg bones) whereas those in organic systems the strongest 20. Keel fractures are apparent from peak lay onwards, so bone structural fragility develops early.

of fracture 25 but further commercial trials are needed to determine exact proportions and benefits in addition to those that are currently underway. Human studies have shown the value of calcium in the diets of young people in preventing subsequent osteoporosis and similarly it is important to maximise the deposition of calcium and other minerals into the skeleton of pullets during rearing. Algal Boost has been shown to improve shell strength and quality in end of lay hens by improving calcium uptake. The FAWC Opinion noted that more needs to be done to reduce the prevalence of bone fractures in laying hens and suggested an interim target of fewer than 20% during lay and 5% at depopulation. There clearly needs to be a large survey of both prevalence and risk factors for fractures during production as these will be affected by breed, housing design, lighting patterns and diet among other factors. In the meantime free-range producers should: • buy pullets reared on high quality mineral rich diets (preferably including particles of calcium) and with experience of using perches and accessing different levels • make sure pullets are well-grown before onset of lay • Ensure comparable equipment between rear and laying sites – colour, type etc. • use high quality mineral rich diets appropriate for the stage of lay • use well-designed housing and modifications such as ramps from the litter to the slatted areas to minimise collisions • observe birds moving within the house and adjust layout to facilitate easy traffic: in particular swinging perches should be avoided • provide particulate calcium (e.g. limestone, oyster shell) • take measures* to ensure the flock is calm • cull (or separately nurse) hens with leg or wing fractures • supervise depopulation

Several studies are currently underway looking at the effects of fractures, which are thought to be both painful and to restrict the hen’s ability to freely access all resources. Results from one study indicate a significant reluctance to jump or fly down from a perch (level) that increases with the severity of keel fracture 22. It is clearly important to handle birds very carefully during depopulation. Previous research of a high incidence of fractures during depopulation from cages 23 led to two-leg catching and the use of breast slides which effectively reduced the levels.

[footnote: * These may include walking the house using different routes & clothing, encouraging birds to use the range and providing good range cover including near the house]

There is scope for dietary inclusions to reduce osteoporosis or susceptibility to bone fractures in laying hens. Feeding calcium as particles rather than finely ground in with the mash has been proven to improve bone strength 24. Inclusion of specific levels and types of fatty acid in the diet (omega-3) may enhance bone strength and substantially reduce rates

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Biosecurity and managing the range There are many routes by which free-range hens can become infected with organisms that have the potential to cause disease. Whether infection actually develops into disease depends on several factors. The immune status of the bird is one.

up bothering with important hygiene measures which can in fact make a real difference by reducing exposure and levels of infection. Three key principles should be followed:

Healthy adult birds which are not stressed are likely to tolerate low levels of infection without becoming ill. However pullets have less resistance to disease and take time to develop immunity to parasites in particular. The typical scenario for pullets is to be caught, vaccinated, transported and then exposed to a raft of organisms on the laying farm, many of which they will not have encountered before. The vaccinations alone will challenge their immune system to cope, never mind the multitude of other stressors (such as new housing, lighting, food, water an humans).

2. Preventing cross-contamination between flocks.

Figure 10. Puddles may be a source of contamination from parasites and faecal organisms, as well as leading to wet litter and soiled eggs

1. Minimising exposure of hens to their own droppings.

3. Good hygiene of humans, house and range. There are few scientific publications relevant to the modern commercial free-range situation but we have seen healthy, well-feathered flocks resulting from tried and tested methods of good husbandry and management. There is a clear need for epidemiological surveys to determine the best methods of reducing disease risk. In addition, optimum ways of managing the range, reducing contamination close to the house and disinfection during turnaround between flocks need to be determined. Pending the availability of further science-based advice we suggest the following as some of the possible measures to adopt to limit disease. Note that disinfectant solutions lose efficacy when they become dirty or diluted with rain. The Defra Code of Practice for the Prevention and Control of Salmonella in Commercial Egg Laying Flocks 26 forms a sound basis for the prevention and control of other diseases as well. • Disinfection of all vehicles which come near any hens such as delivery lorries, vet, assurance scheme and other visitors (e.g. wheel washes, disinfectant sprays, mats). • Boot dips, overalls, masks, hair covers and gloves for humans entering each house (NB overalls should be frequently laundered, boots regularly disinfected and kept specifically for each house for routine stockpeople). • A minimum 2-day gap since the previous visit to a poultry farm is advisable for visitors – where this is impossible, then plan visits from youngest to oldest, one company per day. Same type of stock each day – do not mix parents, commercials, different species.

Thus it may help to get the pullets in well before the point of lay so that they can recover and adjust before experiencing the extra demands of egg laying. Alternatively, as is common in Austria, pullets could be vaccinated at 16 weeks but not moved until 17-18 weeks of age. Rearing your own pullets is another way of reducing health risks and stressors on the birds. Another main factor in disease risk is the magnitude of exposure: how many different ‘bugs’ do the hens encounter and how many of each? Recognising and controlling both how hens can become infected, and with what, is key to managing their health. In our experience many free-range farmers take the view that their hens are bound to be exposed to numerous things which are outside their control. So they give

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Hen Health Report

• The house must have adequate minimum ventilation particularly in winter when hens may range less – this is to dilute viruses, bacteria, dust and noxious gases such as ammonia (the latter will irritate hens’ lungs and eyes; increasing susceptibility to airborne infections). • Maintaining good friable litter will help compost and dilute droppings and any organisms they contain – but beware of controlling dust levels • Keep airborne dust levels low (Salmonella persists in house dust 27)

• Maintain clean drinking water both inside and outside the house using nipple or quill drinkers. Ensure that header tanks are covered. Ideally use recirculating systems to avoid water stagnation in the line. Regular water sanitisation should be encouraged. Puddles and ponds can become contaminated with pathogenic parasites, viruses and bacteria from the laying flock and also wild animals and birds. These can be important reservoirs of infection. Wet areas can also harbour snails that are intermediate hosts for some parasites. • Pasture rotation is the tried and tested method for reducing range contamination. • Maintain cover throughout the range to encourage hens to both use the range and to spread out further, thus limiting the degree of contamination close to and inside the house and reducing stocking density within the house during the day. • Ensure birds cannot perch above drinkers and contaminate them – also flush through water lines after soluble medication is used. • Maintain gutters, downpipes and use soakaways (or extend the down pipes right into the range). • The area near popholes must be kept clean. Use of stones, concrete aprons, wire grids and ramps and bark are all possible methods. • Lime has traditionally been used to keep pasture clean and ‘sweet’. Its value needs to be scientifically investigated but it may be of particular benefit on clay and acidic soils and it is recommended by Dr. Katie Thear, who was an experienced poultry keeper 28. Multi-tier housing is increasingly adopted. Two benefits from a health perspective are the removal of droppings via belts and the fact that they tend to be warmer thus enabling more ventilation and reducing condensation in winter. A possible downside is the difficulty of inspecting all hens on all levels. It remains to be determined whether multi-tiers reduce social stress by enabling subordinate hens to escape to other levels and whether accessing multiple tiers increases the risk of fractures. Verandas We are not aware of any formal studies which have compared the health of hens in houses with and without verandas (or as they are known in Europe, winter gardens). However, numerous authorities suggest many benefits for hen welfare and management. For example, the Lohmann management recommendations for laying hens states: ‘A winter garden attached to the poultry house has proved highly beneficial. Winter gardens in front of the laying house have a positive effect on both litter quality and house climate. When the popholes are opened, cold air does not flow straight into the building and the indoor temperature is less affected than without a winter garden. This beneficial effect of a winter garden can be improved further by staggering the position of the popholes in the building and the winter garden.’ Verandas are a halfway house without the extremes of climate (including light levels) and higher levels of infectious agents (e.g. parasites) potentially found on the range. They may offer pullets, in particular, many of the benefits such as

reduced stocking density, cleaner air, sunlight and exercise with a reduced risk from exposure to wild birds, predators and infection. Verandas reduce the amount of moisture and mud entering the main house with the birds and are easier to maintain than the littered areas of the house. Inspection, Isolation and culling It is a legal requirement to inspect every bird at least once per day. The Codes of Recommendation 29 state (12-15) that this should be a thorough inspection of the health and behaviour of every hen. Furthermore paragraph 10 includes the statement that, ‘It is essential to ensure that enough time is available within the flock-keepers daily work routine for birds to be properly inspected and for any remedial action to be taken.’ Given current economic pressures it may be tempting to reduce the time spent on routine husbandry, whereas preventive measures are more likely to be cost-effective. As well as treatment (medication) Remedial action for sick birds can include isolation in ‘hospital pens’ or culling. In our experience many carers of free-range hens are reluctant to cull as they do not like performing neck dislocation and other methods can be expensive. Among the organisations able to provide advice and training is the Humane Slaughter Association (HSA) 30. It is part of the responsibility of those in charge of livestock to prevent unnecessary suffering and this may require humane and effective culling. In particular we have noted that producers may not cull hens towards the end of lay and this may give rise to welfare issues at depopulation.

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References 1. Anon (1998) Salmonella enteritidis risk assessment: shell eggs and egg products. Final report: US Food Safety and Inspection Service 2. Swarbrick, O, (1986) Clinical problems in ‘free range’ layers. Veterinary Record, 118(13): 363 3. N. M. Stokholm, A.A. Permin, B.M. Bisgaard, A and J. . Christensen, (2010) Causes of Mortality in Commercial Organic Layers in Denmark. Avian Diseases, 54: 1241–1250. 4. Sherwin, C. M. , Richards, G. J. and Nicol, C. J. (2010) ‘Comparison of the welfare of layer hens in 4 housing systems in the UK’, British Poultry Science, 51 (4): 488-499 5. http://randd.defra.gov.uk/Document. aspx?Document=AW1132_8834_FRP.pdf (accessed 6.6.11) 6. Moberly, R.L., White, P.C.L. and Harris, S. (2004) Mortality due to fox predation in free-range poultry flocks in Britain. Veterinary Record, 155: 48-52.

16. Mullens, B.A., Velten, R.K., Hinkle, N.C., Kuney, D.R. and Szijj, C.E. (2004) Acaricide resistance in northern fowl mite (Ornithonyssus sylvarium) populations on caged layer operations in southern California. Poultry Science, 83: 365-374. 17. Crawshaw, T. and Young, S. (2003) Increasing mortality on a free range layer site. Veterinary Record 153(21): 664 18. FAWC (2010) Opinion on osteoporosis and bone fractures in laying hens. Farm Animal Welfare Council. www.fawc.org.uk 19. SAC (2006) The welfare effects of different methods of depopulation on laying hens. Scottish Agricultural College, Defra Project AW0231. Search at http://randd.defra.gov.uk 20.University of Bristol (2008) Detection, causation and potential alleviation of bone damage in laying hens housed in non-cage systems. Defra Project AW0234. Search at http://randd.defra.gov.uk 21. Fleming, R.H., McCormack, H.A., Mcteir, L. and Whitehead, C.C. (2006) Relationships between genetic, environmental and nutritional factors influencing osteoporosis in laying hens. British Poultry Science, 47: 742-755.

7. Reynard, M. & Savory, C.J. (1999). Stress-induced oviposition delays in laying hens: duration and consequences for eggshell quality. British Poultry Science, 40: 585-591

22. Nasr, M.A.F. Nasr, Murrell, J., Wilkins, L.J. and Nicol, C.J. (in press) The effect of keel fractures on egg production parameters, mobility and behaviour in individual laying hens. Animal Welfare

8. Fossum, O, Jansson, D.S., Etterlinm, P.E. and Vågsholm, I. (2009) Cause of mortality in laying hens in different housing systems in 2001 to 2004. Acta Veterinaria Scandinavica 51: 9 pages.

23. Gregory, N.G., Wilkins, L.J., Alvey, D.M. & Tucker, S.A. (1993) Broken bones in domestic fowls: effect of husbandry system and stunning method in end of lay hens. British Poultry Science, 31: 59-69.

9. Esquenet, C., De Herdt, P., De Bosschere, H., Ronsmans, S.Ducatelle, R. and Van Erum, J. (2003) An outbreak of histomoniasis in free range layer hens. Avian Pathology, 32, 305-308.

24. Fleming, R.H., McCormack, H.A. and Whitehead, C.C. (1998) Bone structure and strength at different ages in laying hens and effects of dietary particulate limestone, vitamin K and ascorbic acid. British Poultry Science, 39: 434-440.

10. Rajendran and Nadakal (1988) The efficacy of praziquantel (Droncit R) against Raillientina tetragona (Molin, 1985) in domestic fowl. Veterinary Parasitology, 26: 253-60.

25. J. F. Tarlton, N. C. Avery, L. J. Wilkins, L Knott (2011). Omega-3 (n3) fatty acid supplemented diets reduces bone breakage and increases bone strength in free range laying hens. Proceedings of the World’s Poultry Science Association UK branch Spring Meeting, Nottingham, 70.

11. Guy, J.H., Khajavi, M., Hlalel, M.M., and Sparango, O. (2004) Red mite (Dermanyssus gallinae) prevalence in laying units in Northern England. British Poultry Science 45: Suppl 1: S15-16. 12. Fiddes, M.D., Le Gresley, S., Coles, G.C., Stafford, K.A., Parson, D.G. and Epe, C. (2005) Prevalence of the poultry red mite (Dermanyssus gallinae) in England. Veterinary Record 157: 233-235. 13. Locher, N., Al-Rasheid, K.A., Abdel-Ghaffar, F., Mehlhorn, H. (2010) In vitro and field studies on the contact and fumigant toxicity of a new-product (Mite-Stop) against the developmental stages of the poultry red mite Dermanyssus gallinae. Parasitology Research 107: 417-423. 14. George, D.R., Shiel, R.S., Appleby, W.G. Knox, A. and Guy J.H. (2010) In vitro and in vivo activity and residual toxicity of spinosad to the poultry red mite, Dermanyssus gallinae. Veterinary Parasitology 173: 307-316. 15. Pan, B., Liang, D., Zhang, Y., Wang, H. and Wang, M. (2009) Comparative efficacy of oil solution and wettable powder of lambda-cyhalothrin to naturally occurring Ornithnyssus

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sylvarium infestation in chickens. Veterinary Parasitology 164: 353-356.

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26. Defra (2007) Code of Practice for the Prevention and Control of Salmonella in Commercial Egg Laying Flocks. Defra Publications, Admail 6000, London SW1A 2XX http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/ atoz/zoonoses/documents/reports/sallay.pdf 27. Davies, R.H. and Wray, C. (1996) Persistence of Salmonella enteritidis in poultry units and poultry food. British Poultry Science, 37: 589–596. 28. Thear, K. (2002) Free Range Poultry. Whittet Books Ltd; 3rd Revised edition. ISBN-13: 978-1873580592 29. Defra (2002) Code of recommendations for the welfare of livestock: Laying hens. Defra Publications, Admail 6000, London SW1A 2XX http://archive.defra.gov.uk/foodfarm/ farmanimal/welfare/onfarm/documents/layerscode.pdf 30. The Humane Slaughter Association: The Practical Slaughter of Poultry – A Guide for the Small Producer. ISBN 1 871561 167. The HSA also runs courses on small-scale humane slaughter of poultry. www.hsa.org.uk

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