Poultry Health: A Guide for Professionals

Poultry Health

A Guide for Professionals

Poultry Health

A Guide for Professionals

Edited by

Paul Barrow

University of Surrey

Venugopal Nair

Pirbright Institute

Susan Baigent

Pirbright Institute

Robert Atterbury

University of Nottingham

and

Michael Clark

University of Nottingham

CABI is a trading name of CAB International

© CAB International 2021. All rights reserved. No part of this publication may be reproduced in any form or by any means, electronically, mechanically, by photocopying, recording or otherwise, without the prior permission of the copyright owners.

References to Internet websites (URLs) were accurate at the time of writing.

A catalogue record for this book is available from the British Library, London, UK.

Library of Congress Cataloging-in-Publication Data

Names: Barrow, P. A., editor.

Title: Poultry health : a guide for professionals / editors, Paul Barrow, University of Surrey, Venugopal Nair, Pirbright Institute, Susan Baigent, Pirbright Institute, Robert Atterbury, University of Nottingham, Michael Clark, University of Nottingham.

Description: Wallingford, Oxfordshire ; Boston, MA : CAB International, [2021] | Includes bibliographical references and index. | Summary: Providing a comprehensive overview for small animal veterinarians with poultry clients, this book covers the poultry industry, avian biology, diseases and their agents, infection control, and disease investigation and legislation. Written by international experts, it includes full colour images to aid identification and diagnosis-- Provided by publisher.

Identifiers: LCCN 2021018814 (print) | LCCN 2021018815 (ebook) | ISBN 9781789245042 (paperback) | ISBN 9781789245059 (ebook) | ISBN 9781789245066 (epub)

Subjects: LCSH: Poultry--Diseases. | Poultry--Physiology. | Poultry--Health.

Classification: LCC SF995.P683 2021 (print) | LCC SF995 (ebook) | DDC 636.5/0896--dc23

LC record available at https://lccn.loc.gov/2021018814

LC ebook record available at https://lccn.loc.gov/2021018815

ISBN-13: 9781789245042 (paperback)

9781789245059 (ePDF)

9781789245066 (ePub)

DOI: 10.1079/9781789245042.0000

Commissioning Editor: Alexandra Lainsbury

Editorial Assistant: Emma McCann

Production Editor: Tim Kapp

Typeset by SPi, Pondicherry, India

Printed and bound in the UK by Severn, Gloucester

Contents

List of Contributors

Preface

Section 1: Poultry and the Poultry Industry

1Basic Anatomy and Physiology

David Parsons

2The Immune System of the Chicken

Paul Wigley

3The Genetics of Disease Resistance in Poultry

Androniki Psifidi

4The Poultry Industry

Barry Thorp

5The Broiler Industry and Management of Broilers and Broiler Parents

Paul McMullin

6The Commercial Layer Industry, Management and Disease

Peter Cargill

7Backyard (Pet) Poultry

Grant Hayes

8The Turkey Industry and Diseases

Richard Jennison

9The Duck Industry and Diseases

Michael Clark

10 Diseases of Gamebirds

Michael Clark

11 Hatchery Practice

Richard Jennison

12 Feeding Poultry and Potential Problems Associated with Diet

Patrick Garland

13 Skeletal Problems

Barry Thorp

Section 2: Infectious Diseases of Poultry

14i–ix: Bacterial Diseases

14i Mycobacterium and Avian Tuberculosis

Paul Barrow

14ii Avian Pathogenic Escherichia coli

Rikke Heidemann Olsen

14iii Campylobacter

Michael Jones and Paul Barrow

14iv Salmonella

Paul Barrow

14v Clostridium and Necrotic Enteritis

Evelien Dierick, Evy Goossens, Richard Ducatelle and Filip Van Immerseel

14vi Pasteurella and Related Organisms

Jens Peter Christensen

14vii Brachyspira – Avian Intestinal Spirochaetosis

Roberto La Ragione and Jade Passey

14viii Mycoplasmas

Janet M. Bradbury and Chris Morrow

14ix Miscellaneous Bacterial Infections

Paul Barrow and Robert Atterbury

15i–xiv: Viral Diseases

15i Avian Reoviruses – Viral Arthritis

Richard C. Jones

15ii Infectious Avian Encephalomyelitis

Richard C. Jones

15iii Adenoviruses

Joan A. Smyth

15iv Infectious Laryngotracheitis

Richard C. Jones

15v Infectious Bursal Disease

Andrew J. Broadbent

15vi Avian Astroviruses

Victoria J. Smyth

15vii Avian Influenza

Ian H. Brown

15viii Newcastle Disease

Ian H. Brown

15ix Avian Metapneumovirus Infection

Kannan Ganapathy

15x Infectious Bronchitis

Jane K.A. Cook

15xi Chicken Anaemia Virus and Circoviruses

Joan A. Smyth

15xii Avian Leukosis and Reticuloendotheliosis

Venugopal Nair

15xiii Marek’s Disease

Venugopal Nair

15xiv Fowlpox

Richard C. Jones

16i–iii: Parasite Diseases

16i Coccidiosis

Damer Blake

16ii Histomoniasis (Blackhead Disease)

Hafez Mohamed Hafez and Rüdiger Hauck

16iii Other Important Parasites

Fiona Tomley

Section 3: Control of Poultry Diseases

17 The Chicken Microbiota and How to Modulate It

Fien De Meyer, Annatachja De Grande, Richard Ducatelle and Filip Van Immerseel

18 Biosecurity

Richard Jennison

19 Poultry Chemotherapy and Antimicrobials

Michael Clark

20 Vaccination Strategies and Application of Vaccines

Peter Cargill

21 How to Carry Out a Field Investigation

Paul McMullin

22 Laboratory Diagnosis of Poultry Diseases

Susan Baigent, Vivien Coward, Scott Reid, Rowena Hansen, Vanessa Ceeraz and Paul Barrow

23 Legislation

Richard Jennison and Paul Barrow

Index

List of Contributors

Robert Atterbury School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire, UK. E-mail: [email protected]

Susan Baigent Viral Oncogenesis Group, The Pirbright Institute, Woking, Surrey, UK. E-mail: [email protected]

Paul Barrow School of Veterinary Medicine, University of Surrey, Daphne Jackson Road, Guildford, Surrey, UK. E-mail: [email protected]

Damer Blake Royal Veterinary College, Hawkshead Lane, North Mymms, Hertfordshire, UK. E-mail: [email protected]

Janet M. Bradbury Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Leahurst Campus, Neston, UK. E-mail: [email protected]

Andrew J. Broadbent Department of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA. E-mail: [email protected]

Ian H. Brown Animal and Plant Health Agency-Weybridge, Addlestone, Surrey, UK. E-mail: [email protected]

Peter Cargill Wyatt Poultry Services, part of CVS (UK) Ltd., Mortimer Business Park, Hereford, UK. E-mail: [email protected]

Vanessa Ceeraz Avian Virology Investigation Unit, Animal and Plant Health Agency-Weybridge, Addlestone, Surrey, UK. E-mail: [email protected]

Jens Peter Christensen University of Copenhagen, Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, Frederiksberg, Denmark. E-mail: [email protected]

Michael Clark School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington Campus, Loughborough, Leicestershire, UK. E-mail: [email protected]

Jane K.A. Cook Independent Consultant, Huntingdon, Cambridgeshire, UK. E-mail: [email protected]

Vivien Coward Avian Virology Investigation Unit, Animal and Plant Health Agency-Weybridge, Addlestone, Surrey, UK. E-mail: [email protected]

Annatachja De Grande Flanders Research Institute for Agriculture, Fisheries and Food, Animal Sciences Unit – Poultry and Rabbit Husbandry, Melle, Belgium. E-mail: [email protected]

Fien De Meyer Livestock Gut Health Team (LiGHT), Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.

Evelien Dierick Livestock Gut Health Team (LiGHT), Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium. E-mail: [email protected]

Richard Ducatelle Livestock Gut Health Team (LiGHT), Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium. E-mail: [email protected]

Kannan Ganapathy Institute of Infection, Veterinary and Ecology Sciences, University of Liverpool, Leahurst Campus, Neston, Cheshire. E-mail: [email protected]

Patrick Garland Premier Nutrition, Brereton Business Park, Rugeley, Staffordshire, UK. E-mail: [email protected]

Evy Goossens Livestock Gut Health Team (LiGHT), Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium. E-mail: [email protected]

Hafez Mohamed Hafez Institute of Poultry Diseases, Free University Berlin, Berlin, Germany. E-mail: [email protected]

Rowena Hansen Avian Virology Investigation Unit, Animal and Plant Health Agency-Weybridge, Addlestone, Surrey, UK. E-mail: [email protected]

Rüdiger Hauck Department of Pathobiology and Department of Poultry Science, Auburn University, Auburn, Alabama, USA. E-mail: [email protected]

Grant Hayes Hayes VS Ltd, Little Downham, Ely, Cambridgeshire, UK. E-mail: [email protected]

Rikke Heidemann Olsen Department of Veterinary and Animal Science, University of Copenhagen, Frederiksberg, Denmark. E-mail: [email protected]

Richard Jennison Poultry Health Services, Leominster Enterprise Park, Leominster, Herefordshire, UK. E-mail: [email protected]

Michael Jones School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, Loughborough, Leicestershire, UK. E-mail: [email protected]

Richard C. Jones Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool, Leahurst Campus, Neston, Cheshire, UK. E-mail: [email protected]

Roberto La Ragione Department of Pathology and Infectious Diseases, School of Veterinary Medicine, University of Surrey, Guildford, UK. E-mail: [email protected]

Paul McMullin Poultry Health International, Thirsk, North Yorkshire, UK. E-mail: [email protected]

Chris Morrow Bioproperties, Ringwood, Victoria, Australia and University of Melbourne, School of Veterinary Science, Victoria, Australia. E-mail: [email protected]

Venugopal Nair The Pirbright Institute, Woking, Surrey, UK. E-mail: [email protected]

David Parsons Poultry Health Centre, Trowbridge, Wiltshire, UK. E-mail: [email protected]

Jade Passey Department of Pathology and Infectious Diseases, School of Veterinary Medicine, University of Surrey, Guildford, UK. E-mail: [email protected]

Androniki Psifidi The Royal Veterinary College, University of London, Hatfield, Hertfordshire, UK. E-mail: [email protected]

Scott Reid Avian Virology Investigation Unit, Animal and Plant Health Agency-Weybridge, Addlestone, Surrey, UK. E-mail: [email protected]

Joan A. Smyth Department of Pathobiology and Veterinary Science, College of Agriculture, Health and Natural Resources, University of Connecticut, Storrs, Connecticut, USA. E-mail: [email protected]

Victoria J. Smyth Avian Virology Unit, Agri-Food and Biosciences Institute (AFBI), Stormont, Belfast, UK. E-mail: [email protected]

Barry Thorp St Davids Poultry, Easter Bush Veterinary Centre Roslin, Midlothian, UK. E-mail: [email protected]

Fiona Tomley Department of Pathobiology and Population Sciences, The Royal Veterinary College, University of London, North Mymms, Hatfield, Hertfordshire, UK. E-mail: [email protected]

Filip Van Immerseel Livestock Gut Health Team (LiGHT), Department of Pathology, Bacteriology and Avian Diseases, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium. E-mail: [email protected]

Paul Wigley Department of Infection and Microbiome, IVES, University of Liverpool, Leahurst Campus, Neston, UK. E-mail: [email protected]

Preface

Poultry are one of the most important sources of high-quality meat worldwide for several reasons, including their acceptability to a wide range of cultures and religions, small size and comparative cheapness allowing mass accessibility.

The last few decades have seen great changes in the global poultry industry both economically and geographically and with increasing emphasis on public health in addition to animal health. Production and productivity of the broiler and layer sectors continue to rise, not only in domestic fowl, but increasingly in ducks, turkey, geese and quail.

The centre of gravity of poultry production is inexorably moving east, as standards of living in China and many other regional countries increase, with higher disposable incomes and demand for meat, and also to Brazil and South American countries which are emerging as major exporters. Clearly, these changes bring many advantages in terms of overall human nutrition but may also accompany turbulent changes in local, national and international systems of production and marketing, which can lead to undesirable consequences on the road to progress. Thus, continued production of local birds combined with their sale and slaughter in wet markets, which have been common in the Far East, together with the international movement in humans and animals, has resulted in a number of localized disease outbreaks and the global spread of avian influenza, exacerbated by wild bird migration.

In Asia, intensification and integration of production is increasing and the small producer is fast disappearing, while in Europe and North America intensive production runs in parallel with increased free-range production, as a result of public pressure, combined with increases in backyard hobby/pet birds. These changes increase the risk associated with wild bird contact, frequently exacerbated by – in the case of hobby/pet birds – poor levels of vaccination.

Infection is both a pathological and an evolutionary process which are staple topics for study by poultry veterinarians and researchers, but these processes also ensure that infectious disease problems continue to evolve. This may take the form of natural microbial evolution as occurs with RNA viruses, leading to the appearance of new infectious bronchitis virus strains and avian influenza virus types, or may be expressed as increasing virulence as seen with Marek’s disease virus in response to vaccinated hosts. Similarly, widespread use of chemotherapeutic agents to control parasitic and bacterial infections has resulted in extensive resistance, such as that observed in coccidiosis, resulting in the need to manipulate treatment programmes.

The transmissibility of antibiotic resistance in enteric bacteria has been known for more than five decades with huge global concerns for animal welfare and public health as a result of infections becoming increasingly intractable to chemotherapy. This remains an evolving global issue with recent demonstration of transmissible colistin resistance in China followed rapidly by its identification in many other parts of the world. This pressure is leading to some companies rearing birds completely free of antibiotics.

Large outbreaks of food poisoning associated with poultry consumption and increased public pressure in relation to animal welfare have also resulted in increasing national and international legislation to improve these situations. Food-borne pathogens per se are a One Health problem, and several countries and the EU have targeted them with some success in the case of Salmonella.

The global nature of the industry inevitably has led over the years, via a ripple effect, to changes in one country necessarily being adopted by others.

Working in the poultry industry remains an attractive career decision and it is well known that the emphasis in most veterinary schools on companion animal medicine leaves little room in the curriculum for the extensive training needed for poultry vets to become competent. This deficit affects those entering the intensive poultry world but also veterinarians in private practice who see an increasing number of pet poultry of which they have little experience.

Because of this, the editors realized the need for a readily accessible up-to-date and well-illustrated handbook, rather than a standard text covering all aspects of poultry health. This book will fill a much-needed gap in the market.

There was also a desire amongst the editors to produce a book for the Poultry Health Course, the renowned postgraduate course originally designed for those entering the UK poultry industry, organized first at Houghton Poultry Research Station (Huntingdon), transferred to the Institute for Animal Health (Compton), and most recently run jointly by the Pirbright Institute (Surrey) and the University of Nottingham, School of Veterinary Medicine and Science.

The authors of this book are largely those who have taught on this course, in some cases for almost 40 years, and therefore bring a wealth of expertise in both clinical poultry medicine and research covering the host biology, immune response and genetics, the microbiology, infection biology, epidemiology and control of the pathogens involved, and all relevant aspects of poultry health management.

Paul Barrow

Venugopal Nair

Susan Baigent

Robert Atterbury

Michael Clark

December 2020

1Basic Anatomy and Physiology

DAVID PARSONS*

Poultry Health Centre, Trowbridge, Wiltshire, UK

*[email protected]

1.1 Introduction

There are important differences between avian and mammalian anatomy as well as between different avian species. Comparison should be made between the external anatomy of the domestic fowl with that of the domestic turkey, domestic duck and domestic goose. The anatomical differences are matched by adaptations in avian physiology.

Diseases of the alimentary, reproductive and respiratory systems are common. An understanding of the anatomy and physiology of domestic poultry underpins the understanding of the spread of infection within a flock and the pathogenesis of the disease in the individual bird.

The anatomy and physiology of these systems are discussed based on Gallus gallus domesticus, the domestic fowl.

1.2 The Respiratory System

The respiratory tract consists of the upper airways: the nostrils, nasal cavity, sinuses and larynx, and lower structures (trachea, lungs and air sacs) (Fig. 1.1).

Fig. 1.1. The respiratory tract and other organs visible during initial dissection of the thorax and removal of the rib cage. Tr – trachea; Br – bronchus; L1 – left lung; Pr – proventriculus; Ov – ovary; Lk – left kidney. Small arrow = syrinx. Dotted arrow = primary bronchus. (Author’s own image.)

The nostrils, with the keratinized operculum and cartilaginous lamella, open into the nasal cavity, containing the rostral, middle and caudal conchae. The nasal cavity is separated into two halves by the nasal septum. The choanal cleft is a fissure in the midline of the palate which connects the nasal cavity with the oropharynx. The infraorbital sinus lies laterally and rostroventrally to the eye in the upper jaw. It connects with the nasal cavity ventral to the caudal concha. The nasolacrimal duct opens rostral to the choana and ventral to the middle concha and drains lacrimal secretions from the eye. As in mammals the nasal cavity has important olfaction, air filtration and thermoregulation functions.

Air passes through the choana to the larynx or through the oropharynx in open mouthed breathing to the larynx. The glottis closes reflexly when swallowing to prevent feed entering the trachea. The trachea is made up of about 120 complete signet ring shaped interlocking cartilages that link the larynx to the syrinx which is the voice box and junction with the primary bronchi that connect to the lungs. Branches from the primary bronchi give rise to smaller diameter secondary bronchi, then parabronchi which connects with the atria. The atria are small diverticula that lead to the air capillaries which are the site for gas exchange.

The paired, wedge shaped lungs lie dorsal to the heart. There is no diaphragm. Consequently, the air in the airways of the thoraco-abdomen approximates atmospheric pressure. The lungs are small and non-distensible. The lung can be divided into two parts called the paleopulmo and the neopulmo. In the former, the airflow is unidirectional whilst in the latter it can flow in either direction according to the stage of the respiratory cycle.

The primary bronchus extends to the caudal edge of the lung linking to the ostia from which the abdominal air sac arises. There are nine air sacs in the fowl: a single clavicular and paired cervical, cranial and caudal thoracic and abdominal air sacs (Table 1.1). Their function is ventilation and reducing body weight for flight. The sacs are lined by a single epithelial layer surrounded by connective tissue and are very poorly vascularized. The air sacs arise from secondary bronchi. The exception is the abdominal air sac which has connections with the primary and secondary bronchi.

Table 1.1. Air sac volumes in domestic fowl. (Adapted from Sturkie, 1986.)

The cervical air sac lies between the lungs and dorsal to the oesophagus. Diverticula extend into the cervical vertebrae along the neural canal and outside to the level of the axis. The clavicular air sac comprises both intra- (around the heart and along the sternum) and extra-thoracic (between bones and muscles of the thoracic girdle and shoulder joints) diverticula. Oesophagus, syrinx, trachea, associated muscles, nerves and blood vessels are suspended in the clavicular or between the clavicular and cervical air sacs. The cranial and caudal thoracic air sacs have no diverticula. The abdominal air sacs have perirenal diverticula to the kidney, pelvis, synsacrum, free thoracic vertebrae and femoral diverticula to bones and muscles of the pelvic limb.

The poor vascularization and absence of cilia make removal of purulent material and treatment of this area difficult. This also facilitates spread of infection throughout the body via the diverticula or directly across the membrane. Thus, airsacculitis detected at slaughter means rejection of the whole carcass.

The cranial group of air sacs (cervical, clavicular and cranial thoracic) contains almost as much air as the caudal group (caudal thoracic and abdominal). Most respiratory movement occurs caudally. Therefore, on inspiration most air enters the caudal air sacs.

In the domestic fowl, the following are pneumatized: subcutaneous facial planes and between skeletal muscle, humerus, coracoid, sternum, ribs, synsacrum, pelvis, cervical and thoracic vertebrae.

Circulation of air through the respiratory tract requires two breathing cycles. Inspiration draws fresh air into the posterior air sacs (caudal thoracic and abdominal air sacs) and oxygen depleted air into the anterior air sacs (the cervical, clavicular and cranial thoracic air sacs). Expiration pushes fresh air from caudal thoracic and abdominal air sacs into the lungs and oxygen depleted air from the cervical, clavicular and cranial thoracic air sacs into the bronchi and trachea to be breathed out.

It is important to remember that holding a bird upside down or holding a bird too tightly will cause respiratory distress and possibly death.

Breathing (Table 1.2) is controlled by the central nervous system (CNS) with sensory inputs from (i) central chemoreceptors – identified in mammals and probably present in birds; (ii) arterial chemoreceptors; (iii) intrapulmonary chemoreceptors and others including: (iv) air sac mechanoreceptors; (v) thermal receptors in the spinal cord; (vi) upper airway receptors sensitive to irritants, cold and possibly (vii) arterial baroreceptors.

Table 1.2. Respiratory parameters in domestic fowl. (Adapted from Sturkie, 1986.)

Increasing ambient CO2 will increase ventilation. However, ventilation is also influenced by exercise, hot or cold temperatures and altitude. There is a balance between the stimulatory and inhibitory drive to ventilate. Hence, in hot weather gular fluttering is important because heat is lost with minimum active ventilation.

1.3 The Alimentary System

In addition to its role in nutrition, the alimentary system is also the largest immunological organ (see Chapter 2 this volume) as well as being host to a vast microbiome (see Chapter 17 this volume). The alimentary tract is short and antiperistalsis is an important compensation in digestion. Many growth and developmental changes occur soon after the chick hatches. Managing the development of the alimentary tract to maturity is vital in promoting and maintaining good bird health and welfare. (See Fig. 1.2 for general structure.)

Fig. 1.2. The alimentary tact exposed. Pr – proventriculus; V – ventriculus (gizzard); Sp – spleen; Li – liver; H – heart; D – duodenum; J – jejunum; MD – Meckel’s diverticulum; I – ileum; C – caeca; I-C – ileo-caecal junction; R – rectum; Cl – cloaca; BoF – Bursa of Fabricius; V – vent. The crop is not shown but is located immediately caudal to the proventriculus. (Author’s own image.)

The beak consists of a hard, keratinized epidermal covering which, at its edges, is continually worn away and replaced, and is supplied with extensive sensory innervation, particularly at the tip. The egg tooth is a pointed protuberance on the upper beak which drops off after hatching.

The mouth and pharynx are known as oropharynx. There is no soft palate or pharyngeal isthmus. The choana in the roof of the mouth links oral and nasal cavities. The infundibular cleft behind this is the common opening of the auditory tubes. The salivary glands are located in the roof, cheeks and floor of the mouth. The fowl has about 300 taste buds on the epithelium of the upper beak, and the base and ventrolateral surface on the tongue, with broiler breeds having approximately twice as many as layer breeds.

Food passes along the oesophagus to the crop which is thin walled and distensible. It is a storage organ where bacterial fermentation takes place, reducing the pH to about 4–5.

The proventriculus immediately cranial to the gizzard, produces hydrochloric acid and pepsinogen which is converted to pepsin in the low pH (pH 1–4 depending on food content).

The gizzard (ventriculus) has thick and muscular walls, with a thick yellow to green cuticle on the mucosal surface to protect it from acid and mechanical damage. Finely ground feed – low in fibre – results in poor muscular development while whole grain and high fibre promote good muscular development. Insoluble grit will lodge in the gizzard to facilitate grinding.

The U-shaped duodenum is the first section of the small intestine, enclosing the pancreas in the loop and with a pH of 5.7–7.2. The remains of the yolk sac presents as a small stub, Meckel’s diverticulum, which is used as a marker to separate the jejunum from the ileum. Digestion and absorption of carbohydrates, fats, proteins and also water absorption take place in the small intestine.

The large, paired caeca are attached to the intestine via a sphincter at the ileo-rectal junction. A small enlargement in the neck of the caecum is the caecal tonsil which is a lymphoid organ sampling the microorganisms that enter and leave the caeca. The caeca are filled by the convergence of peristaltic contractions from the small intestine and antiperistaltic contractions from the cloaca and rectum. Liquid only enters the caeca, and the pH varies from 5.7 to 9. The caeca evacuate between one and twelve times daily. Its function is unclear since birds thrive after its removal but some hind-gut fermentation and water reabsorption are thought to take place.

The short rectum has a role in water conservation and carries urine to the caeca by antiperistalsis.

The cloaca is relatively complex for its size with the coprodeum separated from the urodeum which is the smallest chamber into which the urinary and reproductive tracts empty. This is separated by the uroproctodeal fold from the proctodeum which has an external opening through the vent. In the juvenile there is an opening dorsally to the Bursa of Fabricus, the important immunological organ where B cells mature (see Chapter 2 this volume).

Two important additional organs involved in nutrition are the liver and pancreas. The liver is a key organ manufacturing carbohydrates, proteins and fats and is important in detoxification. It also generates heat, raising normal body temperature to 41.5°C for chickens. The body temperatures of turkeys and ducks are similar.

The gall bladder produces bile, aiding lipid uptake, and contains amylase from 4 to 8 weeks of age.

Sick birds that are not eating often have enlarged gall bladders and may excrete green droppings. The green colour in droppings is due to biliverdin. Fowl have very little or no biliverdin reductase for conversion to bilirubin. Brown caecal droppings are possibly due to bacterial breakdown of biliverdin to bilirubin.

The pancreas secretes a number of digestive enzymes and sodium bicarbonate. In the fowl, three pancreatic ducts open into the distal end of the ascending loop of the duodenum on a papilla with the bile ducts.

Transit time depends on whether soluble or insoluble markers are used. Larger insoluble particles are retained longer in the digestive tract. First feed through the digestive tract can be detected in 1.6–2.6 hours but normally the mean retention time is between 5 and 9 hours (Scanes, 2015). Retention time increases with age, amount of fat or protein in the diet and high temperature, whilst cold decreases retention time. Intestinal motility also shows diurnal variation, increasing during the day.

Once hatched, the chick changes from a fat to a carbohydrate-based diet. Early feeding after hatching encourages increased length, weight and enzyme activity when compared to unfed chicks. Villus growth in the duodenum is maximal by 7 days of age and 14 days, at the earliest, for the jejunum and ileum. Enterocyte proliferation occurs along the length of the villus. Migration of enterocytes to the tip of the villus takes about 3 days in four-day-old chicks and 4 days in older chicks.

Absorption of nutrients is not dissimilar to mammals. Volatile fatty acids and uric acid are fermentation products from the caeca.

1.4 Reproductive System

Broilers and layers are genetically different with layers producing high egg numbers on minimal feed consumption and broilers showing rapid growth and good egg production by the parents. Both require different husbandry and management. Parent flocks comprise between 7 and 12% males depending on flock age.

The development and control of the normal functioning of the reproductive tract of the laying hen is affected by a complex combination of factors including temperature, day length, feed and water supply, and the neuroendocrine functions of the hypothalamic–pituitary–gonadal axis.

Unlike mammals, the sex can be reversed prior to gonad differentiation by inhibiting oestrogen production in genetic females resulting in testes development. Temperature during incubation does not determine sex.

Primordial germ cells can be found in the right and left gonads by 2.5 days of egg incubation. Differentiation of the gonads occurs between 6.5 and 7 days. In the male and female, the left gonad is larger. The left ovary and oviduct develop and right ovary regresses. The oviduct consists of the infundibulum, magnum, isthmus, shell gland and vagina. Because there is no connection between the ovary and the oviduct, ova can miss the infundibulum, but these are usually absorbed in the following 48–72 hours, or may be caught by the infundibulum at the next ovulation resulting in double-yolked eggs. But they may also become infected giving rise to egg peritonitis.

1.4.1 Control of sexual maturity and egg laying

The development of sexual maturity and persistence of egg laying is the result of complex interactions between circannual and circadian rhythms, environmental entrainment factors (predominantly photoperiod but also temperature, feed and water availability) and physiological age.

Day length increases at the onset of spring which stimulates reproductive behaviour until the saturation day length is reached. For fowl, the critical and saturation day lengths are about 10 and 15 hours. Chicks are insensitive to day lengths (photorefractory) and modern commercial layers and broiler breeders show significant deviations from these patterns. Selection for egg numbers and the lack of broodiness in commercial layers has resulted in almost complete loss of photorefractoriness. Broiler breeders require restricting feed which delays the dissipation of juvenile photorefractoriness. Commercial husbandry and lighting practices are optimized for the different types of poultry to ensure appropriate physiological development, the best welfare and good production for flocks derived from chicks hatched at any time of the year.

1.4.2 Perception of light

The avian skull is translucent and allows light to penetrate the brain. Photoreceptors are found in the retinae, pineal gland and encephalic photoreceptors situated in the lateral septal organ (LSO), preoptic area and tuberal and mediobasal hypothalamus (MBH). The relative importance of these areas in controlling the reproductive circadian clock is probably species specific. The pineal photoreceptors are sensitive to short and long wavelength light whilst the LSO and MBH on the base of the brain are more sensitive to the long wavelengths. Thus, using orange or red lights to control cannibalism has minimal effect on egg production.

1.4.3 Circadian rhythms

The production of melatonin does not seem to entrain the reproductive photoperiodic response. In fowl, there is a specific period during the circadian rhythm which in fowl occurs about 11.5 hours after dawn, the photoinducible phase. Photo-stimulation during this phase triggers gonadotrophin releasing hormone (GnRH) resulting in gonad development.

1.4.4 The egg laying cycle

When photostimulated between 16 and 18 weeks of age, all birds in the flock respond and mature sexually together. The increased day length allows the photostimulation during the photoinducible phase of the circadian clock triggering release of GnRH from neurons in the MBH. GnRH triggers release of luteinizing hormone (LH) and follicle stimulating hormone (FSH), produced in the pituitary, that promotes maturation of the testes and ovary. Oestrogens and androgens stimulate the development of the secondary sexual characteristics, both physical and behavioural.

About 2 weeks later the first eggs are laid. Hens are indeterminate layers; if the egg laid one day is removed then she will lay another to replace it. The presence of a cockerel is not needed to stimulate hens to lay. The number of eggs laid in a sequence reflects the time taken to form a shelled egg. The closer to 24 hours, the shorter the time from ovulation to oviposition and the longer the sequence will be. The term sequence is preferred to clutch, the latter being reserved for non-domesticated species, because of the large numbers of eggs laid on consecutive days and the absence of incubation and brooding.

It takes time for the circadian clocks within the brain, ovary and oviduct to become entrained. Thus, for the first two weeks or so after commencement of lay, thin shelled eggs, membrane eggs and double or triple-yolked eggs may be laid.

Ovulation is preceded by an increase in LH, 4 to 6 hours earlier. The LH surge is promoted by an increase in progesterone. There is only one LH surge a day and hence only one egg is laid a day.

The first egg of a sequence is usually laid early in the photophase. Ovulation of the next ovum occurs 15–75 minutes after oviposition. Thus, the egg tends to be laid about an hour later each day associated with an LH surge occurring later during the LH sensitive period known as the ‘open period’. Eventually, the next ovulation would be associated with an LH surge that is outside the ‘open period’. In this situation, the LH surge does not occur and the hen does not lay the next day but resumes the day after with the LH surge being associated with the beginning of the ‘open period’ and the sequence repeats.

Egg formation takes 24 to 28 hours. After ovulation, the ovum (Fig. 1.4) is engulfed by the infundibulum (Fig. 1.3) where the egg will be fertilized, if mating has occurred.

Fig. 1.3. Cartoon of reproductive tract. (Produced by and with permission of A. Parsons.)

Fig. 1.4. Ovary from laying hen showing follicles F1–F4 in reverse order of maturity. Arrows = small white follicles. (Author’s own image.)

The first albumen is deposited here before the egg passes into the magnum to be coated with more albumen. In the isthmus the egg membranes are formed. On entering the shell gland water is added to the albumen, a process known as plumping, which stretches the egg membranes allowing them to act as a template for the deposition of the eggshell.

Approximately 2–2.5 g of calcium is transported by the shell gland to calcify each egg. Most calcification occurs over night when the hen is not feeding. Whilst most calcium comes from the feed. A proportion (30–40%) of the eggshell calcium is supplied by medullary bone.

Finally, the egg enters the vagina, and under the influence of arginine vasotocin (AVT), oviposition occurs.

Following mating in a breeding flock, spermatozoa become motile and are stored in specialized storage tubules at the uterovaginal junction. Viability is maintained for 7–14 days. Following oviposition, the sperm migrate to storage glands in the infundibulum or directly fertilize the ovum.

Flock egg numbers decrease towards the end of the laying cycle. As the hen ages, fewer follicles are selected into the preovulatory hierarchy and there is an increase in follicle atresia. Fewer follicles receive more yolk and are therefore bigger. The maturation of each follicle also takes longer. This means that the number of eggs in a sequence decreases, and relatively, the number of non-laying days increases coupled with more first sequence eggs that generally have poor shells. As the amount of calcium deposited on each egg remains relatively constant through the laying period, larger eggs will have thinner shells. Consequently, both egg numbers and shell quality decrease with age.

1.5 References

Scanes, C.G. (2015) Sturkie’s Avian Physiology, 6th edn. Elsevier, London.Sturkie, P.D. (1986) Avian Physiology, 4th edn. Springer-Verlag, New York.

1.6 Further Reading

Bar, A. (2008) Calcium homeostasis and vitamin D metabolism and expression in strongly calcifying laying birds. Comparative Biochemistry and Physiology Part A 151, 477–490.

King, A.S. and McLelland, J. (1984) Birds: Their Structure and Function,2nd edn. Baillier Tindall, London.

Lewis, P. and Morris, T. (2006) Poultry Lighting: The Theory and Practice.Cambridge University Press, Cambridge, UK.

Nakane, Y. and Takashi, Y. (2018) Seasonal reproduction: photoperiodism, birds. In: Swanson, P and Skinner, M.K. (eds) Encyclopedia of Reproduction, 2nd edn, vol. 6. Elsevier, Oxfore, UK, pp. 409–414.

Piper, H. (1887) Piper’s Poultry: A Practical Guide to the Choice, Breeding, Rearing, and Management of All Descriptions of Fowls, Turkeys, Guinea Fowls, Ducks and Geese for Profit and Exhibition,5th edn. Groombridge and Sons, London.

Rose, S.P. (1997) Principles of Poultry Science. CAB International, Wallingford, UK.

Scanes, C.G. (2015) Sturkie’s Avian Physiology, 6th edn. Elsevier, London.

2The Immune System of the Chicken

PAUL WIGLEY*

Department of Infection and Microbiome, IVES, University of Liverpool, Leahurst Campus, Neston, UK

*[email protected]

2.1 Introduction

Avian species, of which the chicken is by far the most studied, have a complex immune system that protects against a range of pathogen challenges and which we can exploit to protect against infection through vaccination. Modern mammals and birds are separated by more than 200 million years of evolutionary divergence, so it is perhaps not surprising that although the structure and function of the avian immune system are largely similar to that of humans and mice there are differences that reflect their evolutionary separation. Our knowledge of avian immunology has largely been driven by the development of vaccines to protect the billions of birds reared each year for meat and eggs. As such, our understanding of immune responses is somewhat biased towards commercially important viral and parasitic infections and to foodborne bacteria such as Salmonella that may be carried in the chicken’s intestinal tract. In recent years there have been more studies on other domesticated species including turkeys and ducks, though our knowledge of other bird species immune systems is limited.

2.2 Overview of the Chicken Immune Response

As in other species, the chicken has broad non-specific intrinsic defences against infection that do not require prior exposure to an infectious agent that we term innate immunity. These can range from simple physical barriers, to secreted antimicrobials through to cells that act to kill invaders. The immune system also has the ability to produce specific cell and antibody responses that have memory that we term adaptive immunity. In general terms innate immunity is rapid and non-specific and does not offer improved protection against the same agent following re-infection, whereas adaptive responses are slower to initiate but offer a much more specific response that is often effective in preventing re-infection. It is this memory or anamnestic response that is the basis of vaccination.

Whilst the overall nature of the mammalian and avian immune response is the same, there are some fundamental differences. In general, the avian immune system is more compact, with less polymorphism in major receptors and fewer classes of antibody. This may seem an unusual strategy in potentially leaving the host more open to infection, but equally it can be argued that the chicken immune system is well-suited to the host, avoiding some of the functional redundancy of the mammalian immune system with a lower physiological cost to the host by reducing some of the complexity.

2.3 Structure of the Avian Immune System

The structure of the avian immune system (Olah et al., 2014) differs somewhat from mammals. The two key differences are the specific primary lymphoid organ the bursa of Fabricius which is the site of B lymphocyte development and the absence of distinct encapsulated peripheral lymph nodes, though in some species such as ducks there are rudimentary structures.

Haematopoesis takes place in bone marrow and foetal liver, with development of T lymphocytes taking place in the thymus and B lymphocyte development taking place in the bursa of Fabricius. The bursa is located at the end of the gut near to the cloaca, the common opening for the avian gastrointestinal and urogenitary systems. It is a highly folded structure containing multiple follicles of B lymphocyte development. Haematopoetic stem cells migrate to the bursa from the foetal liver to differentiate and develop into B lymphocytes. The bursa is an active lymphoid organ in ovo and in chicks, but atrophies within the first 6 months of life.

The avian secondary lymphoid system differs considerably from mammals, with birds lacking distinct encapsulated peripheral lymph nodes. The avian spleen and liver perform broadly similar functions to mammals as major secondary lymphoid tissues. The structure of the avian spleen is similar to that of mammals though the areas of red pulp, white pulp and the marginal zones are less well defined. The avian spleen also possesses a closed circulatory system. It is the largest lymphoid tissue associated with the generation of systemic immune responses. Germinal centres are follicular structures of B cell development and maturation. In the red pulp, along with the erythrocyte population, are scattered lymphocytes and macrophages. Specialist macrophages called Kupfer cells in the liver are important in phagocytosis of dead cells, cellular fragments and pathogens.

The chicken possesses a number of distinct lymphoid organs in the Harderian gland and the caecal tonsils, the latter of which are small lymphoid structures found at the ileal–caecal junction. Although there are no lymph nodes in the sense found in mammals, for example no distinct Peyer’s patch structures in the gut, birds do appear to form looser lymphoid aggregates in the gut and reproductive tract. There is a suggestion that this looser structure allows for a more flexible response to mucosal infection. The Harderian gland is located within the orbit behind the eye and with conjunctiva-associated lymphoid tissue in the lower eyelid forms a distinct eye-associated lymphoid structure. This eye-associated tissue is exploited through the use of eye-drop vaccination. The immune system within the respiratory tract is poorly understood, whilst there are clear lymphoid structures associated with the nasal cavity and bronchus, lung structures are ill defined. In common with mammals are the presence of alveolar macrophages and secreted IgA antibodies in the lungs.

2.4 Cells and Effectors of the Chicken Immune System

2.4.1 Myeloid cells

Heterophils

Heterophils are the most common circulating leukocyte in the chicken. This polymorphonuclear (PMN) cell is the broad equivalent of the mammalian neutrophil and is the main professional phagocytic cell of the avian immune system. Heterophils are a key first line of defense to infection and are efficient phagocytes that are capable of killing pathogens effectively. They survive a short time in circulation.

Monocytes and macrophages

Circulating monocytes and resident macrophages survive much longer than heterophils, up to 80 days following release from bone marrow. They are phagocytic cells that kill pathogens and also act as important antigen-presenting cells with Class II major histocompatibility complex (MHC) expressed on their surface and play a key role in the directing and activating the adaptive immune response through their repertoire of cytokines.

Dendritic cells

Dendritic cells (DCs) are derived from the same myeloid lineage as macrophages. DCs act as professional antigen-presenting cells and also function as accessory cells in adaptive and innate immune responses. Mature DCs primarily reside in lymphoid tissue with several subsets described. Follicular DCs are found primarily around germinal centres and play a key role in presentation to B cells. Interdigitating DCs are found in areas such as the peri-arteriolar lymphoid sheath (PALS) in the spleen and are mostly associated with presentation to T cells. The related Langerhan’s cells are antigen-presenting cells (APCs) located in the squamous epithelial layer of the skin. Bursal secreted DCs are found in the bursa and are key to B lymphocyte maturation (Nagy et al., 2016), thymic DCs are also found, but their role is not clear.

Thrombocytes

Thrombocytes, like platelets, have a primary function in haemostasis or blood clotting. Avian thrombocytes are cellular and phagocytic, expressing MHC Class II on their surface. They appear to share basic functions of macrophages both as APCs and in response to infection (Ferdous et al., 2016).

2.4.2 Lymphoid cells

T lymphocytes

T lymphocytes (Smith and Gobel, 2014) are named as they maturate in the thymus. The main T cell receptor is the T cell receptor (TCR). In the chicken there are three TCR variants, αβ1 and αβ2 and γδ. αβ T lymphocytes are those associated with classical adaptive antigen-specific responses, whereas γδ T cells play a bridging role between innate and adaptive immunity.

T lymphocytes play a key role in the development of both humoral (antibody) and cellular adaptive immunity. Broadly all T cells express the CD3 receptor whilst T cells with the CD8 receptor primarily act as cytolytic T cells (CTL) killing infected cells and bind to MHC Class I (MHC Class I restricted). CD4+ cells are associated with acting as T helper (Th) cells directing the immune response into cellular (Th1) and humoral responses (Th2). Regulatory T cells control inflammatory responses and Th17 T cells are key sentinels in protecting mucosal surfaces, wound repair and may be associated with some inflammatory conditions in mammals.

B lymphocytes

B lymphocytes are named from their primary lymphoid organ, the bursa of Fabricius. The main role of B lymphocytes is the production of antibodies, although they may play other regulatory roles and act as antigen presenting cells. The B cell receptor is surface-bound immunoglobulin. B cells mature to form antibody-secreting plasma cells. Like αβ T cells, B cells are antigen specific.

NK cells

Natural killer (NK) cells are large granular lymphocytes that are not antigen specific, and primarily act to kill cells with altered MHC Class I expression.

2.5 Cytokines

Cytokines are small proteins that signal between cells and tissues of the immune system. They are produced by a range of cells and act via receptors on the cell surface to turn cellular functions on and off, to signal for recruitment of cells and the release of inflammatory mediators. Cytokines include interferons, interleukins and small cytokines such as chemokines which are sometimes classified separately. The simplest way to classify cytokines is by their main function, whether pro-inflammatory, regulatory, Th1, Th2 or Th17 as summarized in Table 2.1.

Table 2.1. Major functional groups of cytokines in the chicken.

In general, the cytokine repertoire function of the chicken is similar to that of mammals (Kaiser et al., 2005) but several of the key cytokine families have fewer members in the chicken.

2.6 Antibodies

Antibodies are made up of glycoproteins called immunoglobulins. The basic structure is a ‘Y’ shaped molecule made up of Fc (crystalline fragment) of heavy chains and a Fab (antigen binding fragment) made up of heavy and light chains that branch from the hinge regions. The Fc region possesses a receptor (FcR) that allows phagocytic cells to bind to the antibody. Chickens produce three classes of immunoglobulin. IgM is first produced around 3–4 days after challenge (Ratcliffe and Hartle, 2014). It has relatively low affinity but has a pentameric form with the monomers joined by a ‘J’ chain and the base of the Fc region which means it is highly efficient at opsonization and fixing complement proteins. IgY is the main class of antibody which is analogous in function to IgG and sometimes labelled as such. IgY has greater affinity and avidity than IgG being highly antigen specific and starts to be produced in increasing amounts around 7 days after challenge. High levels of IgY may also be found in egg yolk and as maternally transferred antibodies in newly hatched chicks. Unlike mammalian IgG, there are no subclasses of IgY. The final immunoglobulin, IgA, which can be found as a monomer but more usually as a secreted dimeric form, is strongly associated with protection at mucosal surfaces.

Antibodies act as the surface receptor of B cells but are also secreted by B cells that have differentiated into plasma cells. Each B cell clone is specific for an individual amino acid epitope. During infection, clonal expansion of antigen-specific B cells occurs that leads to a polyclonal response recognizing multiple antigens of a pathogen. Antibodies protect in a number of ways. They can fix complement via the classical pathway, they may opsonize a pathogen to improve phagocytosis, they may bind phagocytic cells via the FcR which in turn kill the pathogen in a process known as antibody-dependent cell-mediated cytotoxicity, or they may bind to the pathogen surface that prevents it interacting with host cells or binding to cell receptors. This last form of protection is known as a neutralizing antibody and is of particular importance during the response to viral infection.

2.7 Complement

The complement system is a protein cascade system that acts to complement adaptive immunity via the classical pathway or act directly as part of the innate immune system through the alternative pathway. Complement proteins act to bind to pathogens through a mechanism called opsonization that assists in phagocytosis, it can enhance inflammation and acts to kill pathogens through the development of a membrane attack complex (MAC) that disrupts their outer membrane.

The classical pathway is triggered through binding and crosslinking of antibodies with components of the complement system. The alternative pathway is triggered directly through binding to the surface of a pathogen.

2.8 The Immune Response

2.8.1 Innate immunity

Innate immunity is formed of natural barriers, secreted antimicrobials and cells that form the first line of defence to infection. In general, innate immunity lacks ‘memory’,