Veterinary · Para-clinical · also MSVE VPP-321, Poultry Diseases
The diseases of commercial and backyard poultry: viral, bacterial, parasitic, nutritional and toxic.
In the exams: ICAR AICE-JRF Medicine and Pathology units; China comprehensive paper poultry 20; SAVC poultry 15
Avian pathology is the study of the diseases of poultry: chickens above all, but also turkeys, ducks, geese, quail and backyard and village birds. It deals with how each disease is caused, how it spreads, what the flock looks like, what you find when you open the birds, how the laboratory confirms it, which other diseases look the same, and how it is prevented. Poultry are the world's largest source of animal protein, kept in flocks of tens of thousands, so one mistake in diagnosis or vaccination can cost a farm its whole flock, and two diseases in this subject, Newcastle disease and highly pathogenic avian influenza, can close a country's export trade and, in the case of influenza, threaten human health.
This manual follows the curriculum units: the viral diseases (Newcastle disease, avian influenza, infectious bronchitis, infectious laryngotracheitis, infectious bursal disease, Marek's disease, avian leucosis and hydropericardium syndrome), the mycoplasmal and bacterial diseases (mycoplasmosis, pullorum disease and fowl typhoid, necrotic enteritis), the parasitic disease that costs the industry most (coccidiosis), and toxic, fungal, nutritional and metabolic conditions (mycotoxicosis, aspergillosis, vitamin and mineral deficiencies, ascites and gout). For each, it gives the signs, the post-mortem lesions, the differential diagnosis and the principles of control and vaccination. It opens with a chapter on how to investigate a flock problem and perform a poultry post-mortem, because that is how the subject is used in practice and examined in practicals.
The subject is examined worldwide. In India it is the MSVE course VPP-321 and appears in the pathology and medicine units of the ICAR PhD entrance, in the ICAR Master's entrance and in state veterinary officer papers. China's practising veterinarian examination reportedly gives about 20 of its 100 comprehensive-paper marks to poultry, South Africa's registration examination about 15 marks of a paper, and NAVLE and the Australasian Veterinary Examination test poultry as flock problems. Examiners ask for the characteristic lesion, the age of the bird, the key differential and the right vaccine or control step. Learn each disease as that set of facts, and then practise applying them to a flock case.
In poultry medicine the patient is the flock. A broiler house may hold tens of thousands of birds of one age, line and feed, so the questions are how many birds are affected, from what age, how fast it is spreading and what it costs. Start with records: daily mortality and culls, feed and water intake, body weight against the breed standard, egg numbers and egg quality, vaccination history (product, route, date, who gave it), medication, ventilation and temperature, and chick origin. A fall in water intake often comes a day or two before deaths rise. The mortality pattern is itself a clue. A sharp spike that peaks in two or three days and settles within a week suggests infectious bursal disease or hydropericardium syndrome; a steady loss over weeks suggests Marek's disease, leucosis, chronic respiratory disease or a nutritional fault; very high mortality at all ages with a collapse in egg production suggests virulent Newcastle disease or highly pathogenic avian influenza, which must be reported to the veterinary authority in almost every country. Walk the house before handling birds: note where sick birds are, respiratory noise, droppings (green, white, bloody, watery, urate-rich), posture (paralysis, twisted neck, 'splits') and the state of the litter.
Open five to ten representative birds, freshly dead or sick birds humanely killed; autolysed carcasses mislead. Record weight and condition, then external signs: comb and wattle colour, head swelling, discharges, vent pasting, skin, shanks, joints and footpads. Reflect the skin and look at the breast and thigh muscles for haemorrhage. Open the body and examine the air sacs (cloudy or caseous in mycoplasmosis and colibacillosis), pericardium, liver, spleen and kidneys. Open the larynx and trachea along their length. Examine the proventriculus and gizzard, then the whole intestine including both caeca, noting which segment is affected, since coccidia are identified largely by site. Examine the bursa of Fabricius, thymus, both sciatic and brachial nerves (compare left with right), gonads and, when needed, the brain. Take sterile samples for culture before opening the gut. For PCR or RT-PCR, take tracheal or oropharyngeal and cloacal swabs, or tissues, kept cool. Newcastle disease and avian influenza viruses are isolated in the allantoic cavity of 9 to 11-day-old specific-pathogen-free (SPF) embryonated eggs and detected by haemagglutination (HA); infectious laryngotracheitis virus forms pocks on the chorioallantoic membrane (CAM). Fix thin tissue slices in ten volumes of 10 per cent buffered formalin. Serology (haemagglutination inhibition, HI; ELISA; plate agglutination) is read at flock level from about 20 sera, against the titres expected from vaccination, so paired samples and titre uniformity matter more than one value.
Control has three pillars. Biosecurity: all-in all-out placement, cleaning and disinfection with downtime between flocks, one age per site, controlled entry of people, vehicles and equipment, rodent and wild-bird exclusion, and safe disposal of dead birds. Vaccination: live vaccines are given by mass routes (drinking water, spray, in ovo injection at the hatchery) or individually (eye drop, nasal drop, wing web, injection); inactivated oil-emulsion vaccines are injected before lay for long immunity and to pass maternal antibody to chicks. Maternal antibody protects the chick but neutralises live vaccine given too early, so timing matters. Water vaccination needs chlorine-free water, often stabilised with skimmed milk powder, slightly thirsty birds and enough drinker space for all birds to drink within about one to two hours. Schedules vary by country, disease pressure and product; follow the label. Treatment is possible only for bacterial, parasitic and nutritional conditions. Antimicrobials given in water or feed carry withdrawal periods before meat or eggs are sold, several are banned in food birds in some countries, and none helps a viral disease. Any dose must be checked — confirm against the product label and your national formulary.
Newcastle disease (ND; Ranikhet disease in India) is caused by virulent strains of avian paramyxovirus type 1 (APMV-1), species Avian orthoavulavirus 1, family Paramyxoviridae: an enveloped virus with non-segmented, negative-sense single-stranded RNA. Its haemagglutinin-neuraminidase (HN) protein agglutinates chicken red cells; its fusion (F) protein decides virulence. Virulent strains have several basic amino acids (arginine or lysine) at the C-terminus of F2 and phenylalanine at residue 117, so F0 is cleaved by furin-like proteases present in many tissues and the virus spreads systemically. Low-virulence strains need trypsin-like enzymes of the respiratory and intestinal tracts and stay local. Pathotypes are viscerotropic velogenic (haemorrhagic intestinal lesions, high mortality), neurotropic velogenic (respiratory and nervous signs, high mortality), mesogenic (respiratory signs, low mortality), lentogenic (mild respiratory) and asymptomatic enteric. Virulence is measured by the intracerebral pathogenicity index (ICPI) in day-old SPF chicks, scored 0 (normal), 1 (sick) or 2 (dead) daily for 8 days, range 0.0 to 2.0; by the mean death time (MDT) of embryos, under 60 hours for velogenic, 60 to 90 hours for mesogenic and over 90 hours for lentogenic strains; and by the intravenous pathogenicity index (IVPI). The World Organisation for Animal Health (WOAH) defines ND as infection with APMV-1 that has an ICPI of 0.7 or more, or the multiple-basic-amino-acid motif at the F cleavage site. Pigeon paramyxovirus type 1 is an antigenic variant causing nervous signs and polyuria in pigeons.
Chickens are most susceptible; ducks and geese usually show few signs but can carry virus. Incubation is 2 to 15 days, commonly 5 to 6. Velogenic virus in unvaccinated chickens causes sudden death, depression, gasping, swelling of the head in some birds, greenish watery diarrhoea and, in survivors, tremors, torticollis, circling and paralysis; mortality can approach 100 per cent. Layers stop laying, and eggs are pale, thin-shelled, soft or misshapen with watery albumen. In vaccinated flocks there may be only an egg drop, a small rise in deaths and a few nervous birds, so ND is easily missed. Classic lesions of viscerotropic velogenic ND are haemorrhages on the tips of the proventricular glands, haemorrhagic or necrotic ulcers over intestinal lymphoid aggregates, haemorrhagic caecal tonsils and tracheal haemorrhage, with egg yolk in the abdomen in layers. Neurotropic strains may leave no gross lesion; histology shows non-suppurative encephalomyelitis. No lesion is pathognomonic, so laboratory confirmation is required.
Swabs or tissues (brain, lung, spleen, intestine, caecal tonsil) are tested by RT-PCR, and the F cleavage site is sequenced to decide virulence. Virus isolation is in the allantoic cavity of 9 to 11-day SPF eggs; the allantoic fluid is tested by HA, and the agent identified by HI with APMV-1 antiserum, then pathotyped. HI and ELISA serology show exposure or vaccination; in vaccinated flocks a rise or unusually variable titres support, but do not prove, field infection. Differentials: highly pathogenic avian influenza (adds cyanotic comb and wattles and shank haemorrhages), infectious bronchitis and infectious laryngotracheitis (no nervous or intestinal lesions), fowl cholera (culture of Pasteurella multocida, hepatic necrotic foci), infectious bursal disease (proventricular-gizzard junction haemorrhage with bursal lesions), and for nervous signs Marek's disease, avian encephalomyelitis, vitamin E and thiamine deficiency and botulism.
Virulent ND is WOAH-listed and notifiable almost everywhere. Free countries stamp out; endemic countries vaccinate and must add biosecurity. Live lentogenic vaccines (Hitchner B1, LaSota, F strain and cloned lentogenic strains) are given by eye or nasal drop, spray or water; LaSota is more immunogenic but more reactive than B1. Live mesogenic strains (such as R2B or Mukteswar) are still used in some countries as boosters in older birds by wing web or injection, never in young chicks. Inactivated oil-emulsion vaccines before lay, after live priming, give high uniform titres through lay. Turkey herpesvirus (HVT) vectors carrying the F gene are given in ovo or at hatch without respiratory reaction. Vaccination prevents disease and production loss but not all infection and shedding, so vaccinated flocks can spread ND silently. The enveloped virus is killed by most disinfectants but survives weeks in cool faeces and litter. It can cause transient conjunctivitis in vaccinators and laboratory staff.
Avian influenza (AI) is caused by influenza A viruses (species Alphainfluenzavirus influenzae, family Orthomyxoviridae): enveloped, with eight segments of negative-sense RNA and haemagglutinin (H) and neuraminidase (N) spikes. Birds carry H1 to H16 and N1 to N9. A segmented genome allows reassortment (antigenic shift); point mutations cause antigenic drift. Wild waterfowl and shorebirds are the reservoir and usually carry low pathogenicity (LPAI) viruses without disease. WOAH defines a highly pathogenic (HPAI) virus as one with an IVPI greater than 1.2 in six-week-old chickens, or that kills at least 75 per cent of four to eight-week-old chickens inoculated intravenously; H5 and H7 viruses that do not meet this but have multiple basic amino acids at the HA0 cleavage site are also treated as HPAI. Natural HPAI viruses have all been H5 or H7, arising when an H5 or H7 LPAI virus circulating in poultry acquires a polybasic cleavage site. That is why LPAI H5 and H7 in poultry are notifiable too. The goose/Guangdong H5N1 lineage, first found in 1996, gave rise to clade 2.3.4.4b, which since 2020 has caused a panzootic in wild birds and poultry on several continents and infected many mammal species.
LPAI causes mild respiratory signs, sinusitis in turkeys, depression and an egg drop, made worse by secondary bacteria. HPAI in chickens and turkeys is peracute: sudden death of many birds, mortality that may approach 100 per cent within days, collapse of feed and water intake and egg production, and in birds that survive longer, oedema of the head, face and neck, cyanosis and necrosis of the comb and wattles, haemorrhages on the shanks and feet, green diarrhoea and sometimes nervous signs. Peracute deaths may show few lesions. Others show subcutaneous oedema of the head and neck, shank haemorrhage, petechiae on epicardial fat, serosae, keel and proventricular mucosa, necrotic foci in pancreas, liver, spleen, kidney and heart, and haemorrhagic tracheitis. Ducks and geese may carry H5 HPAI with few signs, though some clade 2.3.4.4 strains kill waterfowl and cause nervous signs and corneal opacity.
Suspicion must be reported at once, and samples are taken under official direction. Oropharyngeal and cloacal swabs are tested by real-time RT-PCR for the matrix gene (all influenza A), then H5 and H7 assays and sequencing of the HA cleavage site. Isolation in 9 to 11-day SPF eggs by the allantoic route is done only in laboratories of suitable biosafety; the isolate is subtyped by HI and neuraminidase inhibition, and pathogenicity is set by IVPI or sequencing. Agar gel immunodiffusion (AGID) and ELISA detect antibody to the conserved nucleoprotein and matrix proteins, so they detect any influenza A infection; HI with H5 or H7 antigen identifies subtype. Differentials: virulent ND, acute fowl cholera, infectious laryngotracheitis (slower, no head oedema), heat stress and acute poisoning.
Most countries control HPAI by stamping out: humane killing of infected and in-contact flocks, safe disposal, disinfection, protection and surveillance zones, movement controls, then surveillance to regain freedom as defined in the WOAH Terrestrial Code. Prevention means keeping wild birds and their droppings away: closed houses, covered feed and water, controlled access, and housing orders in high-risk seasons in some countries. Some countries (for example China, Egypt, Indonesia and Mexico) have vaccinated routinely, and others now use targeted vaccination; policy differs and changes, so check national rules. Vaccines are inactivated H5 or H7 oil-emulsion vaccines and HVT- or fowlpox-vectored H5 vaccines. Vaccination reduces disease and shedding but not always infection, so it needs surveillance with a DIVA strategy (differentiating infected from vaccinated animals), such as a vaccine with a different N subtype from the field virus or a vectored vaccine that induces no nucleoprotein antibody. AI is zoonotic: H5N1, H7N9 and other subtypes have infected people after close contact with poultry, with high case fatality for some lineages, so handlers need personal protective equipment. The enveloped virus is killed by heat, drying and disinfectants but survives long in cold water and faeces.
Infectious bronchitis (IB) is an acute, highly contagious disease of chickens caused by infectious bronchitis virus (IBV), a gammacoronavirus (species Avian coronavirus): enveloped, positive-sense single-stranded RNA. The S1 subunit of the spike protein carries the neutralising epitopes and determines serotype. Error-prone replication and recombination produce many serotypes and genotypes with poor cross-protection; examples are Massachusetts (basis of the H120 and H52 vaccines), 793/B (4/91) and QX-like strains. IBV replicates first in ciliated respiratory epithelium and then, depending on strain, in kidney, oviduct and intestine. Loss of cilia lets Escherichia coli invade, turning mild disease into airsacculitis, pericarditis and perihepatitis. In chicks, IB causes gasping, coughing, tracheal rales, nasal discharge and huddling; morbidity approaches 100 per cent and mortality is low unless complicated. Lesions are catarrhal to caseous exudate in trachea and sinuses, cloudy air sacs, and sometimes a caseous plug at the tracheal bifurcation. Nephropathogenic strains cause swollen pale kidneys with urate-distended tubules and ureters, sometimes visceral gout. In layers, egg numbers drop and may not fully recover; shells are thin, soft, wrinkled or misshapen, brown eggs lose colour, and the albumen is watery. Infection in the first two weeks of life can permanently damage the developing oviduct, producing 'false layers' with a cystic oviduct that never lay; QX-like strains are notorious for this.
RT-PCR on tracheal, cloacal, kidney or caecal tonsil samples detects IBV, and sequencing of the S1 gene identifies the genotype and whether it matches the vaccine; live vaccine virus persists for weeks, so read results against the vaccination record. Isolation is by serial allantoic passage in 9 to 11-day SPF eggs; field strains then cause dwarfing and curling of the embryo, with feet deformed over the head, clubbed down and urates in the mesonephros. Tracheal organ cultures show ciliostasis. Paired sera by ELISA (group-specific) or HI and virus neutralisation (more type-specific) show seroconversion. Respiratory differentials: ND, infectious laryngotracheitis, avian metapneumovirus, mycoplasmosis and infectious coryza. Egg-drop differentials: ND, egg drop syndrome (a duck adenovirus that causes thin-shelled and shell-less eggs without the watery albumen), Mycoplasma synoviae and nutrition. Renal differentials: ochratoxin, excess calcium in growers and water deprivation.
Biosecurity, good ventilation and control of E. coli and Mycoplasma limit losses. Live attenuated vaccines, mostly Massachusetts type plus locally relevant variant types, are given to day-old chicks by coarse spray, eye drop or water, and repeated as needed. The mild, highly passaged H120 strain is used for priming, and the less attenuated H52 only for boosting older birds. Giving two different serotypes together, often Massachusetts plus a 793/B type, broadens cross-protection; this is the protectotype principle. Breeders and layers receive inactivated oil-emulsion vaccine before lay, after live priming, to protect production and supply maternal antibody. Live IB vaccine can cause a respiratory reaction, worse with poor ventilation or Mycoplasma, and should not be given together with live ND vaccine unless licensed as a combination, because the viruses interfere. Because variants keep emerging, RT-PCR surveillance and S1 sequencing guide vaccine choice in each region.
Infectious laryngotracheitis (ILT) is caused by Gallid alphaherpesvirus 1 (genus Iltovirus, subfamily Alphaherpesvirinae). Chickens are the main host; pheasants and peafowl can be infected. The virus enters by the upper respiratory tract and conjunctiva and replicates in laryngeal and tracheal epithelium. Like other alphaherpesviruses it becomes latent, mainly in the trigeminal ganglion, and carriers shed again under stress such as onset of lay or moving. Carriers, fomites and poorly controlled live vaccines spread it, especially where multi-age, backyard and commercial flocks are close together; spread within a house is slower than with IB or ND. The severe form shows marked dyspnoea with the neck extended and open-beak gasping, rattling, coughing and head shaking with expectoration of blood-stained mucus, so blood is found on walls, cages and other birds' faces. Mortality in severe outbreaks can reach 50 to 70 per cent but is usually far lower. The mild form causes conjunctivitis, watery eyes, sinus swelling, mild tracheitis and low mortality. Lesions are haemorrhagic tracheitis with blood clots and mucus, or, later, a yellow caseous membrane or plug that can block the larynx and kill by asphyxiation. Histology shows loss of cilia, syncytia and eosinophilic intranuclear inclusion bodies in tracheal epithelial cells, best found in the first days.
Blood-stained tracheal exudate in adult birds is strongly suggestive, and syncytia with intranuclear inclusions confirm it. PCR on tracheal swabs is the usual test, and sequencing can separate field strains from chicken embryo origin (CEO) vaccine strains. Isolation on the chorioallantoic membrane of 9 to 12-day SPF eggs produces opaque plaques (pocks). Serology shows exposure but cannot separate vaccination from infection. The chief differential is the diphtheritic (wet) form of fowl pox, which also produces yellow caseous plaques in the larynx and trachea but has large eosinophilic intracytoplasmic inclusion bodies (Bollinger bodies) rather than intranuclear ones. Others are ND and highly pathogenic avian influenza (haemorrhagic tracheitis with systemic lesions), IB, infectious coryza, mycoplasmosis, vitamin A deficiency and aspergillosis.
Because vaccinated and recovered birds can carry latent virus, biosecurity comes first. CEO live vaccines are highly protective and given by eye drop (sometimes water or spray), but they spread bird to bird, can regain virulence on passage and have caused 'vaccinal laryngotracheitis', so many countries restrict them to areas already infected. Tissue culture origin (TCO) live vaccines are safer and spread less but protect less and must be given by eye drop. Recombinant HVT- or fowlpox-vectored vaccines are given in ovo or at hatch, are safe and do not become latent, but immunity develops more slowly and is less complete against heavy challenge. Vaccinating unaffected birds during an outbreak can shorten it. Cleaning, disinfection, downtime and control of movement complete the programme.
Infectious bursal disease (IBD, Gumboro disease, after Gumboro in Delaware, USA) is caused by IBD virus, genus Avibirnavirus, family Birnaviridae: non-enveloped, with two segments of double-stranded RNA. Segment A encodes a polyprotein giving the capsid proteins VP2 and VP3 and protease VP4, plus VP5; segment B encodes the polymerase VP1. VP2 carries the neutralising epitopes and a hypervariable region that defines antigenic type and, with VP1, affects virulence. Serotype 1 causes disease; serotype 2 is not pathogenic. Serotype 1 includes classical strains, antigenic variants (United States, mid-1980s: escape classical vaccine immunity and cause rapid bursal atrophy with little inflammation) and very virulent strains (vvIBDV, Europe from the late 1980s: high mortality). The virus resists heat, pH change and many disinfectants and persists in houses for months. It destroys actively dividing IgM-bearing B lymphocytes, above all in the bursa of Fabricius, causing acute disease and, in young birds, lasting immunosuppression.
Clinical disease is seen mainly at 3 to 6 weeks, when the bursa is largest; infection before about 3 weeks is usually subclinical but most immunosuppressive. After 2 to 3 days' incubation, birds become depressed and ruffled, with whitish watery diarrhoea, soiled vents and vent pecking. Mortality rises sharply, peaks within 3 to 4 days and returns to normal in 5 to 7 days (spiking mortality). Classical strains usually kill under 10 to 20 per cent; vvIBDV kills many more, especially in layer-type birds. In the first days the bursa is enlarged, often about twice normal, oedematous and yellowish, with a gelatinous yellow transudate and longitudinal striations, and sometimes haemorrhagic throughout, like a dark cherry. From about day 5 it shrinks, and by about day 8 it is small, grey and firm. Other lesions are haemorrhages in thigh and breast muscles and at the proventriculus-gizzard junction, swollen kidneys with urates from dehydration, and dark dehydrated carcasses. Variant strains cause atrophy without the oedematous phase. Histology shows lymphocyte necrosis and depletion in bursal follicles, then cysts and fibrosis.
Birds that lose B cells early respond poorly to ND, IB and Marek's vaccines and suffer more inclusion body hepatitis, hydropericardium syndrome, chicken infectious anaemia, gangrenous dermatitis, colibacillosis and necrotic enteritis, so unexplained vaccine failures should raise the question of IBD. Acute diagnosis rests on age, spiking mortality and bursal lesions. The bursa-to-body-weight ratio of affected birds divided by that of healthy controls (bursa-body weight index) below about 0.7 indicates atrophy. RT-PCR of bursa with VP2 sequencing identifies classical, variant, very virulent or vaccine strains; antigen-capture ELISA and immunohistochemistry detect antigen; ELISA serology shows exposure and maternal antibody. Differentials: ND (proventricular haemorrhage without bursal oedema), coccidiosis, nephropathogenic IB, sulphonamide or mycotoxin haemorrhagic syndromes, and chicken infectious anaemia (thymic and bursal atrophy with pale marrow).
Breeders receive live vaccine in rearing and inactivated oil-emulsion vaccine before lay, so they pass high, uniform maternal antibody to chicks. Maternal antibody declines predictably; the half-lives commonly used in planning are about 3 days in broilers and about 5 to 5.5 days in layer-type chicks. Live vaccine given while antibody is high is neutralised. The best vaccination age is estimated from ELISA titres of day-old chicks with the Deventer formula, which uses the flock titre, the titre each vaccine can break through and the half-life. Live vaccines are graded mild, intermediate and intermediate-plus ('hot'); hotter strains break through more antibody but can damage the bursa. Immune-complex vaccines (live virus bound to specific antibody, given in ovo or at hatch) and HVT vaccines expressing VP2 avoid the timing problem. Cleaning with disinfectants active against non-enveloped viruses and a long downtime reduce the virus load.
Marek's disease (MD) is a lymphoproliferative disease of chickens caused by Gallid alphaherpesvirus 2 (genus Mardivirus), MD virus serotype 1. Two non-oncogenic relatives serve as vaccines: serotype 2 (Gallid alphaherpesvirus 3) and serotype 3, turkey herpesvirus (HVT, Meleagridid alphaherpesvirus 1). In most tissues the virus is strictly cell-associated, but feather-follicle epithelium releases fully infectious virus in dander, which stays infectious in house dust for months; chicks inhale it, so exposure is almost universal. The virus first lyses B cells, then infects activated CD4+ T cells and becomes latent; in some birds these T cells are transformed, largely through the viral oncogene Meq, and form lymphomas. MD also causes immunosuppression. Host genetics (the B21 MHC haplotype is linked with resistance), age at exposure, maternal antibody and virus pathotype affect the outcome. Field strains have become more virulent (vMDV, vvMDV, vv+MDV), a trend widely attributed to vaccines that stop tumours but not infection and shedding.
Disease usually appears from about 6 weeks, often at 12 to 30 weeks, earlier with very virulent strains. The classical neural form causes asymmetric paralysis: one leg forward and one back ('splits'), drooping wings, and a dilated crop when the vagus is involved. Affected peripheral nerves (sciatic, brachial, coeliac plexus, vagus) are enlarged, often two or three times normal, grey or yellow and oedematous, with loss of cross-striations; compare both sides because lesions are often unilateral. The visceral form produces diffuse enlargement or grey-white lymphomas in ovary, liver, spleen, kidney, heart, lung, proventriculus, muscle and skin. The ocular form ('grey eye') shows depigmented iris and an irregular pinpoint pupil. The cutaneous form shows enlarged feather follicles, found at processing. Transient paralysis causes flaccid paralysis resolving in 1 to 2 days. The bursa is usually atrophic or diffusely infiltrated. Lymphomas are pleomorphic: small, medium and large lymphocytes and lymphoblasts, mainly CD4+ T cells, with plasma cells and macrophages.
MD was the first cancer controlled by a vaccine. Vaccination prevents tumours, not infection, so it must precede exposure: injection of day-old chicks at the hatchery or in ovo injection at about 18 days of incubation. Vaccines are HVT (serotype 3), SB-1 or 301B/1 (serotype 2) and attenuated serotype 1 strains, above all CVI988 (Rispens), which protects best against very virulent strains; bivalent combinations act synergistically. Cell-associated vaccines are stored in liquid nitrogen, thawed rapidly, diluted gently and used within the label time, because the living cells die quickly. Failures follow poor handling at the hatchery, heavy early challenge before immunity forms (about 1 to 2 weeks), immunosuppression by IBD or chicken infectious anaemia, and very virulent field strains. Hatchery hygiene, separating chicks from older birds, all-in all-out and genetic resistance support vaccination. Vaccinated birds still become infected and shed field virus, so hygiene in the hatchery and brooding house sets the challenge dose the vaccine has to cope with, and condemnations for skin tumours at processing are a useful check on how well the programme works.
Avian leucosis viruses are alpharetroviruses (Retroviridae) whose RNA is reverse-transcribed into DNA that integrates in the host genome. Chicken subgroups are A to E and J; E is endogenous and of low pathogenicity, A and B cause lymphoid leukosis (LL), and J, first isolated from meat-type breeders in the United Kingdom in the late 1980s, causes myeloid leukosis. Transmission is vertical through egg albumen and horizontal by contact; chicks infected congenitally become tolerant, viraemic without antibody, and shed virus. LL usually affects birds from about 16 weeks, commonly around sexual maturity; the tumour cells are B lymphocytes originating in the bursa. Signs are non-specific wasting and a large abdomen; the liver may be hugely enlarged ('big liver disease'), with diffuse or nodular tumours in liver, spleen and bursa, and peripheral nerves are normal. Myeloid leukosis produces chalky myelocytomas on the sternum, ribs, pelvis and skull. Osteopetrosis ('thick leg') evenly thickens long bones. There is no vaccine; primary breeders eradicate infection by ELISA testing of egg albumen and vent swabs for p27 group-specific antigen, removing shedders, and hatching in isolation. MD and LL are separated by age (MD often younger), nerves (enlarged only in MD), bursa (atrophic in MD, nodular tumour in LL), cells (pleomorphic T cells in MD, uniform IgM+ B lymphoblasts in LL) and control (vaccination versus eradication). Reticuloendotheliosis virus, a gammaretrovirus, causes similar lymphomas and runting.
Hydropericardium syndrome (HPS), or hydropericardium-hepatitis syndrome, was first recognised in 1987 in broilers near Karachi, Pakistan, where it was called Angara disease after the Angara Goth area; it has since been reported across Asia, the Middle East, the Americas and elsewhere. The cause is fowl adenovirus serotype 4 (FAdV-4), species Fowl aviadenovirus C (genus Aviadenovirus, family Adenoviridae): a non-enveloped double-stranded DNA virus resistant to heat and many disinfectants. Fowl adenoviruses form five species (A to E) and twelve serotypes; species D and E serotypes cause inclusion body hepatitis (IBH) without marked hydropericardium, and FAdV-1 is linked with gizzard erosion. Spread is vertical through the egg and horizontal through faeces. Broilers of about 3 to 6 weeks are mainly affected, and immunosuppression by IBD or chicken infectious anaemia makes outbreaks worse, although the highly pathogenic FAdV-4 strains that emerged in China from 2015 cause disease without it. Birds that were growing well become lethargic and die suddenly; mortality rises over several days and declines over one to two weeks, commonly 20 to 30 per cent and sometimes much more. The defining lesion is clear or straw-coloured watery or jelly-like fluid distending the pericardial sac, with a flabby heart. The liver is swollen, friable, pale to yellow and mottled with petechiae or necrotic foci; kidneys are swollen and lungs oedematous. Hepatocytes contain large basophilic intranuclear inclusion bodies.
Sudden mortality in 3 to 6-week broilers with pericardial fluid and a swollen pale liver is highly suggestive; confirmation is by hepatic histology and by PCR of liver with hexon gene sequencing to identify species and serotype. The virus grows in chicken embryo liver cells. Serology has limited value because many flocks carry antibody to harmless adenoviruses. The main differential is ascites (pulmonary hypertension) syndrome: fluid mainly in the abdomen, a dilated, thickened right ventricle and a congested or shrunken liver rather than a swollen pale one. Others are vitamin E and selenium deficiency (exudative diathesis with greenish subcutaneous oedema), sodium and ionophore toxicity, IBH, aflatoxicosis and bacterial hepatitis. Pericardial fluid alone occurs after many deaths, so read it together with the liver and histology.
Control rests on biosecurity, clean chick sources, prevention of immunosuppression, disinfectants active against non-enveloped viruses and adequate downtime. Where HPS is common, FAdV-4 vaccines are used: first locally made formalin-inactivated liver-homogenate vaccines, now mostly inactivated cell-culture and, in some countries, live or subunit vaccines; vaccinating breeders protects progeny. Chicken infectious anaemia (CIA) often precedes adenoviral disease. Chicken anaemia virus (genus Gyrovirus, family Anelloviridae) is a tiny non-enveloped circular single-stranded DNA virus, very resistant, spread vertically by breeders infected in lay and horizontally. Chicks infected vertically without maternal antibody fall ill at 2 to 4 weeks with pallor, haematocrit commonly below about 27 per cent, thymic atrophy, pale yellow fatty bone marrow, haemorrhages and gangrenous dermatitis. The virus destroys marrow precursors and thymic T-cell precursors. Control is by making breeders immune before lay, by exposure or live vaccination during rearing.
Mycoplasmas are the smallest free-living bacteria. They lack a cell wall, so they are pleomorphic and naturally resistant to penicillins and cephalosporins. Mycoplasma gallisepticum (MG) causes chronic respiratory disease (CRD) in chickens and infectious sinusitis in turkeys. Mycoplasma synoviae (MS) causes infectious synovitis, subclinical respiratory infection, and with some strains eggshell apex abnormalities: a band of thin, rough, translucent shell at the pointed end that cracks easily. M. meleagridis and M. iowae affect turkeys. Transmission is vertical through the egg and horizontal by aerosol and contact; infected birds stay carriers, and stress triggers disease. MG alone causes rales, coughing, nasal discharge, lower egg output and poorer feed conversion. Combined with respiratory viruses or live vaccines and Escherichia coli, it produces complicated CRD: thickened air sacs with yellow caseous exudate, fibrinous pericarditis and perihepatitis, rising mortality and carcass condemnations, running slowly over weeks. Turkeys show swollen infraorbital sinuses and foamy eyes. MS synovitis causes lameness with swollen hocks, footpads and keel bursae containing creamy to caseous exudate, pale combs and green droppings.
Culture needs enriched serum-containing media such as Frey's medium and takes about 3 to 10 days; colonies are tiny with a 'fried-egg' look. PCR on tracheal or choanal swabs is therefore the usual test, and sequencing separates vaccine from field strains. The rapid serum plate agglutination test is cheap and sensitive but gives false positives, for example after oil-emulsion vaccines, so positives are confirmed by HI or ELISA; breeder monitoring schemes test set numbers of birds at set intervals. Differentials: IB, ND, ILT, avian metapneumovirus, infectious coryza (Avibacterium paragallinarum: acute facial swelling and foul nasal discharge), colibacillosis and aspergillosis; for lameness, staphylococcal and E. coli arthritis and reovirus tenosynovitis with gastrocnemius tendon rupture.
Best practice is to buy chicks from breeder flocks certified free of MG and MS and keep them free with single-age sites and biosecurity. Primary breeders eradicated infection by serological testing and removal of positive flocks and by heat treatment or antibiotic dipping of hatching eggs. Where infection is endemic, treatment reduces signs, losses and egg transmission but does not clear a flock. Active drug classes include macrolides (tylosin, tilmicosin), pleuromutilins (tiamulin, valnemulin), tetracyclines, lincosamides and, where permitted, fluoroquinolones, which some countries have withdrawn for poultry; any dose must be checked — confirm against the product label and your national formulary. Tiamulin given with monensin, narasin or salinomycin causes toxicity. MG vaccines include live attenuated strains (F strain, ts-11, 6/85), inactivated bacterins and fowlpox-vectored vaccines; live MS vaccines exist. Vaccination is used mainly in layers on multi-age sites and reduces losses without always preventing infection.
Pullorum disease and fowl typhoid are caused by two biovars, Pullorum and Gallinarum, of the host-adapted Salmonella enterica serovar Gallinarum. Both are Gram-negative, non-motile rods (most salmonellae are motile), belong to serogroup D (O antigens 1, 9, 12), and are separated by biochemical tests such as ornithine decarboxylation and dulcitol fermentation. They cause systemic disease in chickens and turkeys and rarely infect people, unlike the paratyphoid salmonellae such as Salmonella Enteritidis and Typhimurium, which colonise poultry silently and cause human food poisoning. Both diseases are WOAH-listed, eradicated from commercial flocks in many developed countries, and still common in parts of Asia, Africa, Latin America and backyard flocks. Pullorum disease (bacillary white diarrhoea) affects chicks and poults in the first two to three weeks. Carrier hens have ovarian infection, so eggs hatch infected chicks or die in shell, and chicks infect hatch-mates. Chicks huddle with drooping wings, breathe hard and have white chalky diarrhoea pasted around the vent; mortality is high and survivors are stunted. Lesions are unabsorbed yolk, congested liver with small necrotic foci and, in chicks that survive longer, grey-white nodules in myocardium, lung, gizzard and caecal wall, and caseous caecal cores. Adult carriers look normal but have misshapen, discoloured, cystic or pedunculated ova.
Fowl typhoid is an acute or chronic septicaemia mainly of growing and adult birds, though young birds can be affected and vertical transmission occurs. Spread is mostly horizontal, through faeces, contaminated feed and water, fomites and carriers. Birds show depression, ruffled feathers, pale anaemic combs and wattles, thirst, loss of appetite and yellow-green diarrhoea, and flock mortality can be high. The liver is swollen and, after exposure to air, turns a characteristic bronze or greenish-brown, often with small grey necrotic foci; the spleen is enlarged and mottled, the blood thin and watery, and hens may have misshapen ova, pericarditis and peritonitis. The bronze liver is the classic examination point, and anaemia in adult birds helps separate typhoid from pullorum, which is mainly a chick disease.
Isolation from liver, spleen, heart, ovary, yolk or caecal tonsil on enrichment and selective media, with biochemical identification and serotyping, is definitive. Flocks are screened with the rapid whole-blood or serum plate agglutination test using crystal violet-stained antigen; because the biovars share O antigens, one test detects both. Reactors are confirmed by tube agglutination, ELISA or culture. Breeders are controlled by repeated testing and removal of reactors until negative, hatching only eggs from clean flocks, and hatchery hygiene. Antimicrobials may reduce deaths but do not remove carriers and should not be used to rescue breeding stock. A live rough strain, 9R, is used against fowl typhoid in some countries; it can interfere with serology. Bacterial differentials include colibacillosis (omphalitis, colisepticaemia with fibrinous polyserositis, salpingitis, cellulitis), fowl cholera (Pasteurella multocida: acute septicaemia in adults, pinpoint hepatic necrosis, coronary fat petechiae, swollen wattles when chronic), infectious coryza and omphalitis from poor hatchery hygiene.
Chicken coccidiosis is caused by Eimeria protozoa multiplying in intestinal epithelium. Seven species are recognised: E. acervulina, E. brunetti, E. maxima, E. mitis, E. necatrix, E. praecox and E. tenella. Each is host-specific and site-specific, and immunity is species-specific. The life cycle is direct: oocysts in faeces sporulate in warm, moist, oxygenated litter within one to two days, each sporulated oocyst holding four sporocysts of two sporozoites. After ingestion, a fixed number of asexual generations (merogony) is followed by sexual reproduction and new oocysts, so infection is self-limiting and severity depends on the dose swallowed. Oocysts resist common disinfectants and survive months in litter. Disease is commonest in broilers of 3 to 6 weeks and pullets on litter, from subclinical poor growth (the costliest form) to bloody diarrhoea and death. E. tenella: caeca distended with blood, later firm cores of clot and debris, anaemia and high mortality. E. necatrix: mid small intestine ballooned with bloody mucus, white spots and petechiae on the serosa ('salt and pepper'); oocysts are produced in the caeca; it affects older birds, such as pullets of 8 to 18 weeks. E. acervulina: white transverse ladder-like plaques in the duodenum. E. maxima: mid-intestine thickened with orange mucus and petechiae, largest oocysts, strongly predisposes to necrotic enteritis. E. brunetti: lower intestine and rectum, coagulation necrosis. E. mitis and E. praecox: few lesions, lost performance. Lesions are scored 0 to 4 on the Johnson and Reid scale. Mucosal scrapings show oocysts and schizonts; litter oocyst counts by the McMaster method and PCR help monitoring.
Broilers are usually protected by anticoccidials in feed, withdrawn before slaughter. Polyether ionophores (monensin, salinomycin, narasin, lasalocid, maduramicin, semduramicin) disrupt ion transport across the parasite membrane and allow some parasite leakage, so birds become immune and resistance develops slowly. Synthetic drugs (amprolium, clopidol, decoquinate, diclazuril, halofuginone, nicarbazin, robenidine, zoalene) act on specific pathways and select resistance faster. Shuttle programmes change drugs between starter and grower feed within a flock; rotation programmes change them between flocks. Ionophores are toxic to horses and other non-target species and interact with tiamulin. Amprolium is a thiamine analogue. Live vaccines of several species, non-attenuated or attenuated precocious lines, are given at the hatchery by spray or in the first days, and are standard for breeders and layers; birds must recycle vaccine oocysts in the litter, and drugs active against vaccine strains must not be fed at the same time. Outbreaks are treated in water with drugs such as amprolium, toltrazuril or sulphonamides where permitted — confirm against the product label and your national formulary. Dry litter and sound drinkers reduce sporulation.
Necrotic enteritis (NE) affects mainly broilers of 2 to 6 weeks. It is caused by Clostridium perfringens, a Gram-positive anaerobic spore-forming rod normally present in the gut; disease follows overgrowth of strains producing the pore-forming NetB toxin, called type G under the toxin-typing scheme revised in 2018 (formerly type A). Predisposing factors are mucosal damage from coccidiosis, especially E. maxima; wheat, barley or rye diets whose non-starch polysaccharides raise gut viscosity; fishmeal and high animal protein; sudden feed change; immunosuppression such as IBD; and withdrawal of antibiotic growth promoters. Acute NE causes sudden death, depression and dark diarrhoea, with mortality rising over several days. The jejunum and ileum are distended with gas and foul fluid, thin-walled and friable, and lined by a yellow-brown or green pseudomembrane with a 'Turkish towel' appearance. Subclinical NE reduces growth and feed conversion and shows at processing as cholangiohepatitis. Diagnosis is by lesions, Gram-stained mucosal smears full of large Gram-positive rods, and anaerobic culture with toxin-gene PCR. Differentials are ulcerative enteritis (Clostridium colinum, 'quail disease', with button ulcers in the lower intestine and caeca and liver necrosis) and coccidiosis. Treatment is in water with antibiotics active against clostridia, such as penicillins, where legal — confirm against the product label and your national formulary. Prevention depends on coccidiosis control, diet (viscosity-reducing enzymes, controlled protein), litter management and alternatives such as probiotics and organic acids.
Mycotoxins are toxic fungal metabolites formed on grains and oilseed meals in the field or in store. Mycotoxicosis is poisoning, not infection: disease follows a feed batch and stops when feed is changed. Aflatoxins, from Aspergillus flavus and A. parasiticus on maize, groundnut cake and cottonseed in warm humid conditions, matter most. Aflatoxin B1, activated in the liver, is hepatotoxic, carcinogenic and immunosuppressive. Turkey X disease, which killed many turkey poults in England in 1960, was traced to imported groundnut meal and led to the discovery of aflatoxin. Ducklings are the most sensitive poultry, then turkey poults; chickens are more tolerant. Signs are poor growth and pigmentation, lower egg production and egg size, bruising and poor vaccine response; the liver is enlarged, pale yellow, fatty and friable, later small and nodular with bile duct hyperplasia. Ochratoxin A (Aspergillus ochraceus, Penicillium verrucosum) is nephrotoxic: swollen pale kidneys, urate retention, sometimes visceral gout, and wet litter. Trichothecenes such as T-2 toxin (Fusarium) cause necrotic crusty lesions in the mouth, beak commissures, tongue and crop and poor feathering. Poultry tolerate zearalenone and fumonisins relatively well. Ergot (Claviceps purpurea) causes gangrene of comb, wattles and toes. Diagnosis combines history, lesions and feed analysis, remembering toxin is patchy and the batch may be eaten. Control is drying grain before storage, dry storage, testing, rejecting or diluting bad batches, and binders such as hydrated sodium calcium aluminosilicate, which adsorb aflatoxin well and other toxins less well. Legal feed limits differ by country and species.
Aspergillosis is infection by inhaled Aspergillus fumigatus spores from mouldy litter, feed or hatchers. In chicks and poults it causes 'brooder pneumonia': gasping, drowsiness and deaths in the first weeks, with yellow-white caseous nodules in lungs and air sacs, sometimes grey-green mould on air-sac surfaces, and occasionally eye or brain lesions. Wet mounts show septate branching hyphae; culture is on Sabouraud agar. The source must be removed; flock treatment is impractical. Candidiasis (Candida albicans) thickens the crop mucosa with whitish pseudomembranes. Nutritional diseases mimic infections. Vitamin E and selenium deficiency causes encephalomalacia ('crazy chick disease', ataxia with cerebellar softening and haemorrhage, commonly at 2 to 4 weeks), exudative diathesis (blue-green subcutaneous oedema of breast and abdomen) and muscular dystrophy. Riboflavin deficiency causes curled-toe paralysis with markedly enlarged sciatic and brachial nerves, a key differential for Marek's disease. Thiamine deficiency causes polyneuritis with head retraction ('star-gazing'). Vitamin A deficiency causes white keratinised pustules in the oesophagus and renal urates. Vitamin D3, calcium or phosphorus deficiency causes rickets (rubbery beak, beaded ribs) and, in layers, cage layer fatigue. Manganese and choline deficiency cause perosis (slipped gastrocnemius tendon). Biotin deficiency causes footpad and facial dermatitis.
Ascites (pulmonary hypertension) syndrome affects fast-growing broilers whose oxygen demand exceeds lung capacity, especially at altitude, in cold weather and with poor ventilation. Hypoxia causes pulmonary vasoconstriction, right ventricular hypertrophy and dilatation, and right heart failure, with abdominal fluid and fibrin clots. The right-to-total ventricle weight ratio measures the hypertrophy; published cut-offs are around 0.25 to 0.28 depending on the source. Sudden death syndrome kills well-grown male broilers, found on their backs, apparently from arrhythmia. Visceral gout, chalky urates on pericardium, liver capsule and kidneys, follows renal damage or dehydration (nephropathogenic IB, ochratoxin, excess calcium in growers, water deprivation); articular gout in the foot joints is linked with genetics and high-protein diets. Fatty liver haemorrhagic syndrome kills over-conditioned caged layers on high-energy diets through bleeding from an enlarged, yellow, greasy, friable liver. Tibial dyschondroplasia, a plug of cartilage below the proximal tibiotarsal growth plate, lames fast-growing broilers. These are controlled by growth rate, lighting, ventilation, diet and genetics, not by drugs.
Learn each disease as a grid: agent and family, age affected, main signs, the one lesion that points to it, the confirmatory test, the key differential and the control measure. Practise the poultry post-mortem in a fixed order until it is automatic, and learn to recognise bursal oedema and atrophy, enlarged sciatic nerves, proventricular haemorrhage, caecal cores and the Eimeria lesion sites on real specimens. In the laboratory, learn to read an HA and HI plate and to inoculate eggs by the allantoic and chorioallantoic routes. Revise the WOAH definitions of Newcastle disease and highly pathogenic avian influenza word for word, because they are asked repeatedly and matter in practice.
A poultry vet with five years of practice is called to flock problems: a mortality spike in broilers, a drop in egg production, respiratory noise, lameness. The work is reading records, walking the house, opening enough birds and choosing samples that answer the question. Typical decisions are whether a spike is IBD, hydropericardium syndrome or necrotic enteritis; whether an egg drop is IB, egg drop syndrome, Mycoplasma synoviae or feed; when to vaccinate against IBD from maternal-antibody ELISA results; whether water vaccination is being done well; how to shuttle or rotate anticoccidials; and when to report a suspicion of ND or avian influenza to the authorities and stop movement from the farm at once.
After twenty-five years a poultry veterinarian usually runs health programmes for an integration, a breeder company or a government region. The questions become strategic: which vaccine types and schedules suit the regional strains of IBV, IBDV and fowl adenovirus; how to monitor breeder flocks for Mycoplasma, Salmonella and leucosis; how to cut antimicrobial use without losing flocks to necrotic enteritis; how to design biosecurity and emergency plans for highly pathogenic avian influenza; and how to use slaughterhouse condemnations, serology and production data to find problems before they show clinically. They also train staff, audit hatcheries and work with regulators on notifiable disease response.
A researcher with long field experience asks why diseases change. Examples are the evolution of Marek's disease virus to greater virulence under imperfect vaccines; the emergence of very virulent and variant IBDV and reassortants; recombination and new genotypes of IBV; the global spread of H5 clade 2.3.4.4b and its entry into mammals; the rise of virulent fowl adenovirus 4; and the ecology of Clostridium perfringens after antibiotic growth promoters were withdrawn. Their work designs DIVA vaccines, vectored and immune-complex vaccines, genomic surveillance, host-genetic resistance studies and field trials, and turns them into policy advice on vaccination, trade and One Health.
This manual covers the thirteen curriculum units and adds short accounts of aspergillosis, candidiasis, chicken infectious anaemia and the main nutritional and metabolic diseases because they are constant differentials. It does not give full accounts of fowl pox, fowl cholera, colibacillosis, infectious coryza, egg drop syndrome, avian metapneumovirus, avian encephalomyelitis, reovirus arthritis, duck and goose diseases (duck plague, duck viral hepatitis), turkey diseases (haemorrhagic enteritis, histomoniasis), helminths, lice and mites, or pet-bird diseases such as psittacosis; these appear only as differentials. Vaccination schedules are described in principle only, because they differ by country, disease pressure and product; always follow the label and national guidance. Drug doses and withdrawal periods are deliberately not given. Numerical cut-offs such as the maternal-antibody half-lives used in IBD vaccine timing, and the right-to-total ventricle ratio for ascites, are given as commonly taught approximations, not fixed standards. Country disease status, vaccination policy for avian influenza and legal mycotoxin limits change quickly and should be checked against WOAH WAHIS and the national authority. Prepatent periods of individual Eimeria species were left out because the writer could not confirm them precisely enough.
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