poultry disease manual

7/23/2019 Poultry Disease Manual

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Poultry Disease Manual

Pro/. Antonio Zanella


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Contents4 1 PREFACE

IMMUNITY IN BIRDS: GENERAL CONCEPTS

NEWCASTLE DISEASE

4 AVIAN PNEUMOVIRUSES

AVIAN INFLUENZA

INFECTIOUS BRONCHITIS

INFECTIOUS LARYNGOTRACHEITIS

26 FOWL POX

13 INFECTIOUS BURSAL DISEASE

Neopl asti c Diseases - MAREK'S DISEASE- LEUKOSIS/SARCOMA GROUP- RETICULOENDOTHELIOSIS

CHICKEN INFECTIOUS ANAEMIA

4-2 REOVIRUS INFECTIONS

44 rn ADENOVIRUS INFECTIONS

M AVIAN ENCEPHALOMYELITIS

PARATYPHOID INFECTIONS

54 m PULLORUM DISEASE AND FOWL TYPHOID

COLIBACILLOSIS

INFECTIOUS CORYZA

FOWL CHOLERA

62 NECROTIC ENTERITIS

m RiEMERELLA ANATIPESTIFER

Mycoplasmosis 65 - MYCOPLASMA GALL1SEPTICUM INFECTION

- MYCOPLASMA SYNOVIAE INFECTION69 - MYCOPLASMA MELEAGRIDIS INFECTION

70 COCCI DIOSIS

. VACCINE ADMINISTRATION SYSTEM

79 FACTORS INFLUENCING VACCINATION

81 M DIAGNOSIS OF DISEASE

5 si- DIAGNOSIS OF SOME MOST IMPORTANT POULTRY DISEASE


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Preface

I am honoured tha t FATRO requested me to wri te this (shor t)

man ual o n infectious diseases, mostly of intensively-reared dom estic

poultry.

This review is not completely original, but is obviously a mixture

o f da ta r epor ted by many eminent C ol leagues , Resea rche rs o r

Practitioners, with the addition of my own personal observations,

derived from m ore than 50 years o f intensive experience in poultry

pathology. M y only merit, I repeat, has been to collect and update

the know ledge on the various diseases regarding their epidemiology,

clinical signs, lesions, diagnostics and, obviously, their control

through biosecurity measures, treatments and vaccinations.

1 dedicate this b oo k to m y beloved wife, children and grandchildren,

wh o bore with me th roughou t this long period o f my professional life.

I wish to par t icular ly thank m y C olleag ue s D r. F. Mc liota ,

Dr. C . Tassi, D r. A. Vo lorio, Mr. P. Milani and M rs. D ebora Bcrtozzi

for their valuable help.

I


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Immunity in birds: general concepts

Th e imm une system o f the b i rd s Iconsis ts o f two pr im ary lymph oidorgans, the thymus and the bursa ofFab r ic iu s (BF) , bu t a l so o f manys e c o n d a r y l y m p h o i d o r g a n s o rstructures, which include bone-marrow,spleen, Harderian gland, Peyers patches,Meckel diverticulum, caecal tonsils an dother lymphoid aggregates distributedin the body (birds lack the equivalentof mammalian lymph nodes).In the primary organs, which developduring the embryo stage, a differenttiation of the germinal immune cellsinto two types of lymphocytes takesplace, T-cells in the thymus and B-cells

in the BF. These cells produce a specificimmune response agains t an t igenswhich are extraneous to the organism.In the secondary structures , besides

lymphocyte storage areas, there are the differentiation sites for otherimm une cells, such as mo nocytes and macro phag es, granulocytes, |

Diagram of the Immune System of birds j k ('j]er (JC) natural killer (NK) cells, which are pro duc ed in the Jbone-marrow and generally play a non-specific role in immunity.B'lyrnphocytes, after transformation into plasmocytes, are responsible

| for imm unoglobulin or antibody production, in response to antigenstimulation.

T'bmpfioQtes are responsible for cell-mediated immunity and forregulation of the imm une system reactions, in cluding the activationo f B-cells.Macrophages (derived from circulating monocytes), granulocytes, NK and K cells are involved non-specifically in immune reactionsby phagocytosis or by cytotoxicity. Macrophages are also importantin antigen processin g and p resenting cell to T and B lymphocytes.Immunoglobulins (Ig) or antibodies are glycoprotein molecules, ableto react specifically, both in vivo and in with the antigens whichoriginally induced their production.

Harderian gland

Payer's patches

thymus

spleen

bursaof Fabricius

cecal tonsils

Meckel diverticulum

bone marrow


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Small lymphocyte

Plosmo-cell

Large lymphocyte

In birds, three main classes of Ig have been reported :IgM, which appear very soon, 2-4 days after the ini t ial immune

stimu lation, reaching their peak conc entration at the 9'1' day; they

represent the first imm un e barrier to infection; IgG (or, better, IgY, showing som e structural differences to m amm alian IgG), which arethe main Ig in the serum (70-80%) and the main effec tors of

hu m oral imm unity; they are the only antibod ies able to transfer to

the yolk-sac and provide systemic imm unity to the new born chick; /gAS, which are the Ig p re sent in m uco sa l sec re tion s an d in biologica l

fluids, as bile and responsible for mucosal imm unity; the existenceo f IgD and IgE, a s in m am m als, is very likely, bu t little is know n o n

this matter.

HUMORAL IMMUNITYHu m oral im mu nity is subdivided into act ive and passive.

Active im m un ity is triggered by contact with the antigen, pathogenor vaccine and i s charac ter ized, a f te r a var iable la tent per iod(3 to 10 days), by an initial rapid sh or t increase in IgM , followed

by a slower increase in IgG and IgA, which persists longer (primary

response). Sub seque nt contact with the sam e pathogen o r antigeninduc es a higher, more rapid and long-lasting produc tion o f specific

IgG an d IgA (secondary response). Th e rapidity o f the secondaryresponse is due to the presence o f mem ory lymphocytes", produceddu ring the prim ary response; for this reason i t is also named the

an amn estic response. Repeated vaccinations (hyperimmunizationor booste r effect) enable the attainm ent o f high specific antibody levels.

Passive immunity is provided almost exclusively by IgG, transferredfrom the blood stream to the ovary and then transmitted to the

chicks via the yolk-sac; th e level of an tibo dies in th e yolk sac generallycorrelates with the m othe r s antibody level.

Du ring passage o f the egg through the oviduct, the albumen acquiresrather low levels o f IgM an d IgA, which pass through the amniotic

fluid to the gut , providing temporary protection to the mucosa.Th e level of m aternal antibod ies in the progeny normally decreasesin about 15-20 days; the rate of decrease is partly linked to the

degree o f growth o f the chick.The protection provided by passive antibodies varies, depending

on the disease: for example, it is strong against infectious anaem ia,encephalomyelitis, infectious bursal disease, fairly effective against

Newcas t l e d i sease and poor aga ins t mucosa l d i seases , such a sinfec tious bronch i t is and la ryngotrachei ti s and against M areks

disease.

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Monocyte

CELL-MEDIATED !MMl)NITYCell-mediated immunity (CMI) is controlled by T-lymphocytes,

which do no t produce antibo dies, bu t operate destroying the target

directly or indirectly, in ducin g oth er accesso ry cells to destroy it byinterm ediation o f solu ble factors, the interleukines. T-lymphocytes

are divided into three sub po pu lation s: T-helper, T-suppressor andT-cytotoxic cells, beside s m em ory cclls:T-helper cells have regulatory activity, modulating the immunerespon se and intervening in the coopera tion between cell-mediatedand humoral immunity;T-suppressor cells have regulatory activity, l imiting the antibodyresponse, when this tend s to becom e excessive;

T-cytotoxic cclls have effector activity, attacking and destroyinginfected or altered target cells. CM1 is of primary importance inimm une d efences aga in s t m ic roo rgan isms wi th in t race llu la rparasitism (viruses, some bacteria, protozoans, etc.). In general,while humoral immunity can be measured quite easily by checkingin vitro the level of antibo dies in the serum , it is more difficult or

complex, in a routine check, to evaluate die degree of mucosal and CM1.Moreover, the degree of protection provided by a vaccine cannotbe always strictly correlated to the level o f antibo dies in the serum.

Basophil Granulocyte

Heterophil Granulocyte

VACCINESLive a ttenuated vaccines are prepared with:1) naturally apatho genic m icroorganisms (turkey herpesvirus, Newcastle disease virus st ra ins NDV 6/1 0 or H itchner Bl) ;

2) m icroorga nism s, wh ose pathogenicity- has been artificially reducedor removed by serial passages through an appropriate substratum,such a s emb ryon ated egg or tissue-cultures(infectious bronchitis virus, infectious bursal disease virus an d many other vaccinal viruses);

3) other techniques, for the m om ent m ainly experimen tal (deletion,expression o f antigen in live apathog enic vectors).Th e artificial attenuation of m icroorganisms is som etimes unstablean d, after som e back-passages in the natural host, it may be reduced

(laiyngotracheitis, infectious bursal disease, infectious bronchitis viruses, etc.).Attenuated vaccines are normally administered to birds by the

natural route, like the pathogenic microorganisms, but they inducevery low or no sym ptom s o f disease.Th e com m on route o f adm inistration in the f ield is by drinkingwater or spray or, individually, by eye or n asal-drop adm inistrationor wing-web injection. Protection due to the vaccination is often

provided q uite quickly after adm inistration (local im mun ity system),


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Eosinophil granulocyte

although antibodies appear in the serum only after 10-15 days.For som e diseases, just one vaccination at a variable age, depen ding

on the vaccine , i s suff ic ien t to protec t b i rd s for a lon g r ime(Mareks disease, fowl pox, laryngotracheitis, encephalomyelitis, infectious

anaemia) o r for the period w hen they are susceptible (infectious bursal disease).

For other diseases, revaccina t ions or boosters a re requi red to

strengthen the protection (Newcastle disease, infectious bronchitis, etc.).

For som e path ogen s, the birds are susceptible only up to 2-3 weekso f age and i t is sufficient to vaccinate p arent m ens before going

into lay (infectious anae mia, encephalomyelitis) to protect the youngprogeny. Live vaccines may present some risk of contamination

wi th fore ign agents present in the subst ra te (leukosis, infectious anaemia, e tc .) , or accidental ly introduced dur ing their processing(or manu facturing). In any event, the use o f eggs from well-controlled

SP I- flocks and the ad option of severe puri ty controls, f i rst ly o f

m aster seeds, but a lso o f each ba tch o f vaccine , a rc essent ia l .Some l ive vaccines are also prepared with at tenuated bacteria orprotozoans (for instance, safmonedas, mycoplasmas and coccidia).

Inactivated vaccines are prepared with microorganisms, or part of

them, which have lost their virulence and abil i ty to replicateand spread through the organism. However, their tmmunogenicityremains in tac t . Such vaccines are administered by individual

injection, intramuscularly or subcutaneously.They are o f ten associa ted wi th adjuvants , which s t rengthen the

immune reac t ion. The adjuvants mainly used are minera l o i l

(emulsion) or alum inium hydroxide. Th e strengthe ning o f antibody

pro du ction an d, p artially, of cell-mediated reactivity, is due to agrad ual release of antigen (dep ot effect) and local irritation, with

aspeci f ic ac t iva t ion o f lymphocytes . The imm uni ty provided byinactivated vaccines is completely established in 3-4 weeks and, forsome diseases, lasts longer then that produced by l ive vaccines.

Inactivated vaccines are often administered, with a better booster

effect, after a priming with live vaccines.

Macrophage


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Poultry diseases


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Newcastle DiseaseNewcastle disease (ND) is regarded as the most important disease

to be controlled in poultry. The importance is not only due to the

rapid spread and devastating effects on the infected birds, with

flock mortality rates Lip to 100%, but also to the economic impact

that might ensue, due to trading restrictions and embargoes placedon countries, where outbreaks have occurred. Because of the severe

nature o f the disease, N D is included in the list o f diseases reported

by Office In ternat ional des Epizoot ies (OIE), which contains

transmissible diseases with a potential for very serious and rapid

spread. M ost m emb er countries enforce statutory control m easuresin the event of outbreaks o f disease. N D is caused by a paramyxovirus

serogroup 1 (APMVT) belonging to the familyParamyxoviridae ,

genus Avulavirus] only one serotype is known, b ut different pathotypes

exist: very virulent (velogenic), medium virulent (mesogenic), mildlyvirulent (lentogenic), or apathogenic strains. These latter two types

o f strains are com m only used in the p reparation o f live vaccines.

EpizootiologyOver 250 species of birds have been reported to be susceptible.

ND virus is highly contagious, horizontally transmitted through

infected respiratory discharge and droppings, by either inhalation

or ingestion. The spread among farms, even at a long distance,

occurs by movement of l ive birds (game and exotic birds, feralpigeons, commercial market poultry), movement of contaminated

poultry- products, people, equipment, feed and water and by airbornespread. Ve rtical transm ission is very controversial, probably occ urring

only very rarely in newly hatched chicks.

Clinical signs and lesionsDepending on the signs, lesions and tissue tropism, ND virus strainshave been divided into five groups or pathotypes: 1)viscerotropic

velogenic: highly virulent disease with high mortality and typicalhaem orrhagic and n ecrotic gastrointe stinal lesions; 2) neurotropic ivelogenic: respiratory and nervous signs with very high mortality;

3) pneumotropic mesogenic: respiratory and, in some cases, nervous signs

with considerable mortal i ty in young b irds but low in adul ts ;

NEWCASTLE DISEASE


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DiagnosisA presumptive diagnosis is based on the characteristic signs andlesions and is conf irm ed by virus isola t ion an d identif ica t ion(inoculation o f specimens, taken from tracheal and intestinal swabsor tissues, in 9-11 day-old emb ryonared eggs, H A an d HI tests with

allantoic f luids). More recently molecular diagnostic techniqueshave been developed, such as RT-PCR and nucleotide sequencing.Th e laboratory assessm ent o f virus pathogenicity is determined bythe m ean death time (M DT ) in cmbryonatcd eggs, the intracerebralpathogenic index (ICPI) tor one-day-old chicks and the intravenous

patho genic index (IVPf) fo r six-week-old SP F chick ens (see table).These and other molecular properties allow distinct viral profilesto be developed, distinguishing between avirulent and virulentisolates. An tibodies are dem onstrated using the h aemagglutination

inhibition (HI) or E U SA tests.

Control of diseaseTh e objectives are both ro prevent susceptible birds from becominginfected an d to reduce the num ber o f susceptible birds by vaccination.Control policies are applied at international, national and farmlevel and consist of the application of all biosecuritv measures

directed at preventing the intro duction an d sp read o f virus within

coun tries and areas. Th e establishm ent o f restrictive m easures onthe m ovement o f birds and their products, quarantine proceduresfor im portation o f all kind o f dom estic or wild birds, the stamping-ou t of outbreaks of disease, national and international surveys and

reports o f disease o utbre aks - everything is organized a nd controlledby the H ealth A uthorities u nder O IE . Except for a few countries

ND nervous sign: twisted neck or torticollis

4) ptieumocropic lentogenic mild or un apparen t infection o f the respiratoiy

tract, with no mortality' (used as vaccines); 5) naturally apachogenic,mostly therm oresistant, used more recently as non-stressing vaccines.In the field, respiratory (laboured breathing, rales and sneezing),enteric (greenish diarrhoea) and nervous signs ( twisted neck or

torticollis, leg weakness o r paralysis, etc.) and respective lesions canall be present at the sam e time, but are not strictly pathogn om onic.The drop in egg production is very rapid, sometimes to zero; eggsmay have thin and discoloured shel ls or no shel l ; the ovarydegenerates and egg yolk is present in the abdominal cavity, with

consequent per i toni t is . Morbidi ty may reach 100%; morta l i tyvaries, depen ding on virus virulence and the residua! imm une state

o f birds, som etim es reaching over 80%.


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NEWCASTLE DISEASE

ND haemorrhagic lesions in proventriculus

ND necrotic lesion or ulcer in intestinal mucosa

(Scandin avia, New Zealand and Sw itzerland), vaccination is adopted

universally, most recently even in Australia, particularly in intensive

rear ing a reas . Vacc ina t ion usua l ly p ro tec t s b i rds f rom theconseq uenc es o f the disease, interfering with the sprea d o f virulent

virus, althou gh virulent virus replication and she ddin g may sti lloccur, albe it at reduced levels. In any event, it well applied , vaccination

represents an effective barrier to the spread o f infection. Tw o types

o f vaccines are u sed, live and inactivated.Live vaccines: These are prepared with the infected allantoicfluid o f em bryona ted eggs kept freeze-dried. T he strains o f virusused for vaccine prod uct ion are d iv ided in to 3 gro up s , fu lly

apathogenic, lentogenic and mesogenic (sec table).

Mesogenic strains are often used only in countries or areas where

N D is endem ic, with widespread presence of backyard birds andnot very intensive rearing. T hey cause very severe post-vaccinal

react ions , somet im es with som e s igns o f d isease; therefore theyare used , where i t i s permit ted , most ly for revaccinat ion and

intramuscularly, after a priming with apathogenic or lentogenic

vaccine. Lentogenicstrains genotype II , such as Hi tchn er B1 and L a

Sofa (1CPI 0.2-0.4L which replicate particularly in the mucosa ofthe respiratory tract and can induc e post-vaccinal reaction s and

respiratory s igns , part icu lar ly in young chicks and in primary

vaccination, d epe ndin g on the health status, intercurrent bacterialinfections (Mycoplasma, E.coli) o f the b irds and environmental

conditions (ammonia, dust, etc.); the La Sota strain is the moststressing and no t recom me nded for use by spray as a first vaccination.Apathogenic strains genotype I (virus multiplies well in enteric andrespiratory tracts), such as N D V 6/1 0, U lster 2C, Q uee nsland V4,

isolated from waterfowl an d chickens, are fully asymp tomatic withan 1CP1


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Th e m ass app lication o f live vaccines by spray or aerosol is also verywidespread, b ecause a large num ber o f birds can be treated in avery sh ort rime. Spra y vaccination can be perform ed in the hatchery

or o n the farm. T o achieve the correct droplet size is very impo rtant.A coarse spray of relatively large particles (> 100 m icrons) doe s notpenetrate deeply into the respiratory tract o f birds and producesless o f a reactio n; this is less conditioning with apathogenic strainshaving an ICPI = 0.0. Th e spra y m etho d at one-day-old m ay result

in the es tab l ishment of in fect ion with vaccinal v irus , desp i tem aternally-d e rived i m mu n i ty.Inactivated vaccines: Th ese are produ ced with allantoic fluidsfrom embryo nated eggs, infected with different lentogenic strains,such as L a Sota or Ulster 2C , rarely with m esogenic strains (Roakinstrain), generally no lon ger with velogen ic strains, inactivated w ith

fi-propiolactone or formalin and mixed with mineral oil to forma stable emulsion. O n e or mo re additional viral or bacterial antigensmay be incorporated into the same em ulsion a s polyvalent vaccines.Th e vaccinc is adm inistered by in tram uscular or subcutaneousinjection. The se vaccines are usually used in pu llets, on ce o r twice,

before going into lay, giving long-lasting immunity. They have

som etim es been used in broilers, at one-day-old, togethe r with livevaccine, particularly in endem ic areas o f disease o r in case of verysevere epidem ics.

Characteristics o f some NDV strains

13

VIRUS STRAIN PATHOTYPE GENOTYPE ICPI TEMPERATURERESISTANCE ORIGIN

6/10, Ulster 2C, V4 Apathogenic 1


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Avian Pneumoviruses

Avian pn eum oviruses are members o f the familyParamyxoviridae, gen us Metapnewmovirus. Infectio ns, affec ting prim arily turkeys and

chickens, and have been termed turkey rhinotracheitis (TRT) andchicken swollen head syndrome (SHS) respectively. The disease inchickens was first reported in South Africa in the late 1970s.It later spread to Euro pe, particularly to turkeys and chickens, first

to Italy an d the U .K ., then elsewhere); afterwards an d to a limitedextent , to the USA, Japan, Brazi l and probably to a number ofother countr ies. Studies using m onoclonal ant ibodies have madeit possible to distinguish four subtypes of the virus, referred to asA, B, C and D.

EpizootiologyC ou ntries reporting isolations o f the virus are relatively few, andthese particularly in turkeys; presence o f infection ha s frequentlybeen b ased on serological evidence. C ur ren t evidence suggests that

the virus is only likely to be shed for a few days after infection andthat no carrier state exists. Sp read o f the infection occu rs by contactand is a i rborne ; movem ent o f equ ipm ent and peop le may a lsobe implicated, although resistance of the virus is nor high.Spr ead over greater distanc es is apparen tly slight.

Clinical signs and lesionsT R T , particularly in you ng po ults, is characterized by more o r lessevident sneezing, coughing , nasal discharge, swollen infraorbitalsinuses, conjun ctivitis and head shaking. In laying birds, there maybe a d rop in egg product ion o f up to 70%, wi th an increasedincidence o f po or egg shel l quali ty. M orbidi ty is can be 100%,mortality varies greatly, from less than 1% to as high as 30 % , mostlydep end ing on the severity o f bacterial co-infections, which complicatethe viral infection.

In the pure form, the only lesion is the presence of exudate intu rb ina tes and in f raorb i ta l s inuses ; in mature females , some

abnormali t ies are observed in the ovary and oviduct , such asregression, folded shell m em brane s in the oviduct, m isshapen eggs,peritonitis.


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Poult affected by TRT: sinusitis and conjunctivitis

W hen secondary bacterial co-infcctions oc cur (mostly - coii), avariety of gross lesions have been observed, including pn eum onia,

per icardi t i s , a i rsaccul i t i s and m eningi t i s. SH S in chicken s ischaracterized by the same respiratory symptoms and swell ing ofperiorbital sinuses, ear an d eye discharge, opisth oton us and torticollis.

Usu ally less than 3% o f the flock is so affected, although respiratorysigns may be widespread. In heavy breeders a reduction in egg

production, of the order of less than .5%, may occur. Mortal i tyrarely excee ds 1-2%. Th e only significan t lesion is an extensiveyellow, gelat inous to puru lent subc utane ous oed em a o f the head

and , som etim e, the wattles.

DiagnosisClinic al diag nosis, particularly in turkeys, can only be presum ptive,

because many othe r condit ions, such as m ycoplasmosis, influenzaand New castle disease, can show similar symptoms.Therefore, other investigations, such as virus isolation at the firstsigns of disease, molecular identificat ion (RT -PCR ) and serology(ELI SA, im mu nofluorescence) are required tor a definitive diagnosis.Virus isolat ion, not so easy to do, is performed in embryonated

eggs, via the yolk-sac, and in embryo tracheal organ cultures (T O C).

ControlLive attenuated vaccines are used both in turkeys and chickens.W hen adm inistered correctly, by coarse spray, these vaccines provide

good protection, stimulating both systemic and local immunity inthe respiratory tract . Good cross protection among the subtypesoccurs. Usually, turkey broilers are vaccinated at 1, 10 and 45 dayso f age; chickens are vaccinated only once, between 1 and 10 dayso f age. In bre eders, live vaccines are often follow ed by an injectionot inactivated vaccine in oily em ulsion, two weeks before the startof laying.


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Avian Influenza

Avian influenza (AI) is caused by a virus belonging to the familyOrthomixoviridae, genus Influenza vines, serotype A. Al viruses havea worldwide distribution. Infection can occ ur in m any form s, fromasymptomatic ro respiratory disease and a drop in egg production,to systemic disease, with a mortality rate o f up to 100%. Therefore,viral isolates are subdivided into low (LP) and high pathogenic

(HP); som etime s, strains o f som e subtypes (to date, H5 and H7)

can mutate from LP to HP. Highly Pathogenic Avian Influenza

(HPA1) is included in the list of diseases rep orted by the OfficeInternational de s E pizooties (OIE ), similarly ro Newcastle D isease.Influenza A virus is classif ied in sa b types, based on serologica l

reac t ions of sur face g lycopro te ins , h aem agglu t in in ( I f ) andneuraminidase (N). Sixteen H and 9 N antigens have so far been

recognized; many com binations o f H and N antigen in virus subtypes

have been reported in dom estic and wild birds. Antigenic variations,

more (shift) or less (drift) wide, have been reported in poultry,though fewer than in mam m als.

EpizootiologyThe m ost f requen t source of A I virus are waterfowl, especia l lyduck s, geese, gulls and other wild birds, which are considered asthe natural reservoirs; in these latter species, AI virus infectionusually cause s sporad ic or n o disease. AI virus has, in the past been,

sporadically isolated from dom estic integrated com m ercial poultry,m ost frequently turkeys and , slightly less often, chickens an d otherdom estic birds. Anim als from the live poultry market (LPM) system

an d backyard flocks have som e o f the high est infection rates.However, outb reaks or actual epizootics in com me rcial poultry havebecom e m ore and m ore frequent in the last 20 years, particularlyrecently, worldwide. W hen A I infections d o occur, they, sometimes,spread rapidly through the integrated poultry system, from farm tofarm, resulting in epizootics of LP or HP A I. In som e developing

countries or in some areas where the LPM system is widespread,AI ha s often become endem ic.AI virus is excreted by the respiratory and enteric routes, so it istransm itted by direct contac t between infected and susceptible birds

16

Chickens affected by HPAI before death


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Turkeys affected by HPAI

or by indirect contact through aerosol drop lets or exposure to viruscontaminated fom ites, equipmen t and people. Sources o f infection

lor initial intro duction o f AI virus into com mercial poultry flocks

include other do m estic and confined poultry, m igratory waterfowl,

pet b ird s or, in som e cases , even dom est ic p igs. In traspeciestransm ission is frequent and easy; interspecies transm ission may

occur, being ever less f requent as the d ifferences between the

phylogenetic classes of the anim als increase; bu t som e exceptionshave occurred, although at present ro a relatively limited extent:

H IN 1 from swine to turkey in the US A and , move recently, H5N1and H 7N 7 f rom poultry to hum ans, respect ively in A sia and in

T he Netherlands. Although the transmission of infection commonly

occu rs horizontally, evidence o f vertical transm ission is lacking;however the virus has been isolated from the internal contents o f

the eggs during natural outbreaks of disease.

Clinical signs and lesionsClin ical s igns are ex tremely var iab le , depending on the v irus

pathotype and other factors, including host species, age, concurrent

inlections and environmental conditions.LPA1 virus infection in wild birds usually produces no signs.

How ever, in dom estic poultry it normally prod uces mild to severe

respiratory symptoms, such as coughing, sneezing, rales, together

with variable m alaise, ano rexia and d iarrhoea ; in breeders andlayers, a decrease in egg pro duc tion (varying from 10 to 80% ) is

a l so poss ib le . Somet imes h igh morb id i ty, bu t low mor ta l i ty(less than 3-5%), is the rule, unless complicated by secondaryinfections o r it the disease occurs in very youn g birds.

The most frequent lesions in the respiratory tract are: catarrhal-

fibrinous to purulent sinusitis, tracheitis, bronchopneumonia, more

or less severe airsacculitis , also d epen ding on secondary bactcrialinfections; catarrhal to fibrinou s enteritis and oviduc titis may alsobe observed.

HPAI virus infection in wild birds and domestic ducks usuallyproduces few or no clinical signs; however, a few cases have been

reported with moderate to high mortality. In domestic poultry,

such as turkeys, chickens, guinea fowl and quail, the clinical signs

vary, depen ding o n the degree o f dam age induced by viral replicationinto the specif ic organ s and cardiovascular and nervous systems.

In m ost cases, the disease is fulminating, in the absen ce o f any clear

sym ptom ; if birds survive for a few days, some o f them may exhibitresp ira tory and nervous d isorders . Respira tory s igns are less


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Chickens broile r affected by HPAI

DiagnosisA presumpt ive d iagnosis o f AI i s based on ep idem iological and

clinical data, which, however, are no t pathog no m onic. A de finitivediagnosis is established by direct detection o f antigens or D N A o f

the virus in various specimens (tracheal and cloaca! swabs, tissues,etc.), and by isolation and identification of the virus in embryo nated

eggs or by R T-PCR , fo llowed by detection o f ant ibodies (EL ISA,HI , AGP, VN) .

prom inent than with LPA1. A precipitous drop in egg productionis the rule. Morbidity and mortality is very' high (50-90 to 100%).

Edem atous, haem orrhagic and necrotic lesions in visceral organs,

often including the pancreas and non-feathered skin, are observed,haemorrhages are prominent in the epicardium, proventr iculus

an d Payers patches. In sudd en d eath, n o gross lesions bu t only ageneral severe congestion may be observed.

ControlM ethod s for the control o f AI virus infection arc mainly based on

knowledge of how the virus is introduced into a farm or an area

an d how it can sp read. T h e reservoir o f the virus in wild birdsshou ld be cons idered a m ajo r source o f p rimary in fec t ion fo rcom me rcial birds, p articularly free-range birds. The strict application

of biosecurity- m easures is the first line o f defence, preven ting notonly direct , bu t also indirect contact of contam inated equ ipme nt,footwear, clothing, vehicles or people with infectious materials

(excreta).

Co ntam inated poul t ry m anure appears to be a m ost likely sourceo f virus spread betw een flocks or farms, even at long distances.Co nsidera ble difficulties are som etime s encountered w ith application

o f al l biosecuri ty m easures, p art icularly in area s with very high

concen trat ions o f farms. W hen infection by subtype H5 and H7(the only subtypes wh ich have so far show n a capacity to convert

from L PAI ro HP AI) is detected, the response m ust be prom pt and

complete , even resort ing to immediate cul l ing or depopulat ion.A s regards prevention by vaccination, inactivated vaccines in oilyemulsion have been used, part icularly in chickens and turkeys.

Th eir effectiveness in preven ting sym ptom s and mortality has beenwell doc um ented . However, difficult ies in prep aring a vaccine inadvance arise, because there are 16 different H sub types o f AI virus.

W hen an outbreak o f AI occurs an d the virus subtype is identified,vaccination may be a useful tool , part icularly in areas with high

8


19/93

poultry pop ulation densities, bu t the preparation o f a vaccine has

to be quite rapid. Vaccination should be considered a valid optionto control the spread of infect ion, remarkably reducing thesusceptibili ty of birds to the infection and the amount of viralshed din g in the environm ent. T he con trolled use o f vaccines, ever

in cases of LPAI H 5 and H7 outbreaks m ight reduce the possibilityof HPAI viral emergencies; their use cont inues to be debated,particularly in Euro pe and North A merica.

He terologous vaccine has also been u sed for the N antigen , applyingthe DIVA (differentiating infected from vaccinated animals) strategy,based on serological tests to highlight different specefic anti-Nantibodies. The trend seems to be in this direction, also consideringthe recent exam ples o f results obtain ed in certain countries.

The jud ic iou s use of vaccine , m aking i t poss ib le to reducetransmission and spread o f infection, and the susceptibility of birdsto the virus, w ould favour eradication o f the disease, also preventingit from becom ing endemic.

Layinq curve in an outbreak of LPAI (subtype H7N1) in a farm of 4 houses with layers o f different ages


20/93

Infectious Bronchitis

Trachea:a) normalb) affected by IB

Infectious bro nch itis (IB) is an acute, highly conta gious viral diseaseof poultry, caused by a virus classified in the fam ilyCoronaviridae, ge nu s CoroncR'irus, wh ich particu larly affe cts th e respiratory tract,but a lso the k idneys and reproduct ive t ract . The occurrence ofm ultiple serotypes (to date over 60 different serotypes have been

reported all over the world) seem s to com plicate the p revention ofthe disease by vaccination.

EpizootiologyIB (1BV) causes considerable damage to the poul t ry indust ry

worldwide. Chickens and, ro a lesser extent , pheasants are theprimary natural hosts. All ages are susceptible, bur the disease ism ore severe in young chicks.IB virus (IBV) spreads rapidly in a flock or in a farm, within 24-48hou rs; the virus is excreted by cough ing and sneezing for ab ou t 10

days, but rhe infection can persist tor weeks or even months in the

kidneys and gut, being shed by droppings.W ith rhe exception o f the Massachusetts serotype, p resen t all overthe world, other serotypes are more located in different areas,

countries or continents (Connecticut, Gray, AZ-23 /74 , Arkansas DPI, UK -4/91, A Z 27 /98 or h-02, A Z-40/05 or QXlike etc.).

0

Clinical signs and lesionsTh e ch aracterist ic respiratory signs in young chicks are gasping,coughing, sneezing, nasal discharge, tracheal rales, occasionally

swollen sinuses, together with more or less severe depression andreduc ed weight gain. In birds olde r than 6 weeks an d in adult birds,the signs are similar, but less severe.Infection in chicks, a few days old, is reported to produce somepermanen t damage to the ov iduc t , w i th reduced fu tu re eggproduction and appearance of false layers: in the field, this isnorm ally prevented by the presen ce o f goo d levels o f maternally-derived antibodies.In laying flocks, a decline in egg pro duc tion a nd quality is observe d,in addition to more or less evident respiratory symptoms.T he severity o f the d rop in egg prod uctio n varies greatly, from slight

Kidney lesions caused by nephropathogenk IBV


21/93

to over 50%, varying with the period of lay, causative virus strainand incomplete vaccinal immunity. Four to eight weeks may elapse

before egg production returns to the pre-infection level, but in mostcases this is never attained. Disco loured , rough- or soft-shelled a ndmisshapen eggs are produced, hatchability is reduced.

Chickens, particularly broilers, affected by nephropathogenic strainsof IBV, in addition to the more or less severe typical respiratory

symptoms, show signs of severe depression, wet droppings with

urates, increased water intake, dehydratation.Morbidity1may be very high, mortality is variable, depending onvirulence of the virus strain, immunity status, cold stress andsecondary bacterial infections (tmcopl/ismfls, Escherichia coli, etc.),

which complicate the course of illness, particularly in broilers(chronic respiratory disease).At necropsy, infected chickens show serous-catarrhal or fibrinous

exudates in nasal passages and sinuses, but mostly in the tracheaand air-sacs. A caseous plug may be found in the tracheal bifurcationand bronchi in young chicks. In neph ropathic infections, swollen

and pale kidneys, due to interstitial nephritis and distend ed ureterswith urates are present; in layers, after the acute phase, urolithiasismay occur.

Characteristics of eggs laid from hens affected by IB:a) normalb) different degree o f alteration

Embryo lesion in SPF eggs inoculated vsith IBV: dwarfing, curling, persistence of mesonephros

DiagnosisA presumptive diagn osis of IB is based on the rapid on set o f clinical

signs and on the lesions, which, however, are not very specific.Lt is confirmed by the detection o f IBV antigen (imm uno fluorescen ce

assay), isolation and eventual typing of the virus (inoculation in

embryonated eggs or tracheal organ cultures) and RT-PCR fromaffected tissues or embryo fluids. Later, serological tests are appliedto detect group-specific antibodies (AGD and ELISA tests) or type-

specific antibodies (HI, VN).

The wide ant igenic var ia t ions of IBV add complexi ty to thecond uction of tests an d the analysis of results. Cross-reactions are

more evident when sera are collected after field infection in broilers,but mainly in layers , which may have received one or more

vaccinations or infections.

ControlBiosecurity measures against IB are very' difficult to apply, due tothe high density' of farms in certain areas and when multiple ages

are present in the same farm. A logical consequence is the need toresort to vaccination to prevent losses of production.

21


22/93

Both l ive a t tenuated and inact iva ted vaccines are used in IB

immunization. In broilers, one or two vaccinations are performed

with a live vaccine , m ostly at 1 and 12-20 days of age. In bree ders

and layers, a combination of live vaccines, administered during the

pullet (2-3 times) and laying periods (every 3 months) and one or

two injections of inactivated vaccine (preferably prepared with

2 or 3 different serotypes) before entering the laying period, are

recommended.

IBV strains used for live vaccine preparation have been attenuated

by serial passages in embryon ated eggs, avoiding excessive n um ber

of passages to prevent reduction o f immun ogenicity.Vaccine prepared with Massachusetts serotype continues to be the

most commonly used vaccine in the world, also because viruses

isola ted in most countr ies be long to this serotype . The most

widespread vaccinal s t ra in is named H120; i t be longs to theMassachusetts serotype, but other strains are also present on the

market. This serotype provides fairly good cross-protection, which,

however, does not cover com pletely all other serotypes or variants

o f the virus. Oth er serotypes are used in live attenuated or inactivated

vaccines worldwide. Unlike ND and IBD, maternal antibodies do

not interfere greatly with vaccination p erform ed at one day of age.


23/93



24/93

INFECTIOUS LARYNGOTRACHE1TI5

Infectious LaryngotracheitisInfectious Laryngotracheitis (ILT) is caused by a virus classified inthe family Herpesviridae, genus Ct-herpesi'irus, which replicates in the

respiratory tract.

EpizootiologyChickens are the primary natural host., particularly adult birds.

Numerous cases of ILT have also been reported in pheasants; other

birds appear to be refractory. The natural route of entry for the

vims is through the upp er respiratory and ocular tract. Tran sm ission

of the disease occurs by direct contact with infected birds, by theI ai rborne route or by contaminated equipm ent and people .

) Clinical signs and lesions

ILT is usually characterized by acute respiratory symptoms-, nasalI discharge, coughing, gasping, tracheal rales, expectoration of bloody

mucus to casts, due to fibrinous-haemorrhagic tracheitis. Mild forms

of disease have often been observed, characterized by conjunctivitis,

I swelling of infraorbital sinuses and nasal discharge.

; Th e course of infection varies with the severity of the lesions: the! most characterist ic in acute forms is the hem orrhagic-diphtheric

exudate, which can extend to the entire length of trachea.

! ILT i n d u c e s a mo re o r le ss s ev e re d ro p in e gg p ro d u c t i o n

(10 to 60%), depending on the severity of disease, for a period of3-5 weeks.

i In acute forms, m orbid ity is very high; mortality, however, is veryvariable, from 5 to 60% , but usually within the 10-1.5% range.

In mild enzootic forms, mortality is rather low, less than 2%.

I DiagnosisIn cases of severe signs and lesions, with expec toration o f blood y

mucus and high mortality, the diagnosis is reliable. Otherwise,

laboratory diagnosis procedures are advisable, including the presence

of intranuclear inclusion bodies in tissues stained with Giemsa,

isolation o f virus in em bryonated eggs and PC R.


25/93

Poultry Disease Manua l

Control

Besides the application of appropriate biosecurity measures, thecontrol of the disease in geographic areas, where it is endemic orfrequent, is based o n the use o f attenuated vaccines. Attenuation

has been obtained by ser ia l passages on t issue cul tures or inembryonated eggs. The most efficacious route of administration isby eyc-drop. W he n the nu m ber o f birds to vaccinate is very high,ir can b e advisable to a dm inister the vaccine via the drinking water,

preferably at two successive times and ar 1f - 2 doses per bird, sothat a ll ch ickens can consum e an adequate am oun t of the v irus .

A ddition o f skim m ed milk 1% to fresh water is advisable. Som etimesadverse post-vaccinal reactions may occur, wh en the environm entalcond itions are subo ptim al (dust, am m onia, cold) or administration

o f the vaccine is incorrect. If a considerable num ber o f chickensdo not receive the vaccination, bird-to-bird passage might result inreversion o f the virus to greater virulence.

Usually, only pullets destined ro become layers or breeders arevaccinated against ILT, with a single administration at 5-8 weekso r twice, at 3 4 a nd 16-18 weeks of age, in high risk farms. Som etim es,

mostly in ende m ic areas, the vaccination of broilers may also berequired, particularly when flocks are close to outbrea ks o f disease

or the b irds are growing over. In such cases, broilers are vaccinatedat 14-16 days o f age by eye-drop or, mo re often , via the drinkingwater, ensuring th e vaccine is correctly administered.

Characteristic attitude o f chicken affected by ILT,

during breathing


26/93

FOWL POX

Fowl PoxFowl pox (FP) is a com m on disease o f poultry (chickens, turkeys,pheasan ts, etc.), as well as of pets and wild birds, caused by num erousspecies o f the genusAvipox virus, family Poxviridae. Different species

are m ore o r less distingu ishable from each other, blit with varying

degrees o f cross-relationship.

Pox lesion on eyelids o f a layer

EpizootiologyPoxvirus infects bird s at any age, b ut mostly after 8-10 weeks o f age.

It survives for a long time in the scabs a nd dried p ustules a nd it istransmitted by direct or indirect contact or by biting m osquitoes

or mites; in the latter case, it can also affect nearby flocks. In som e

areas, the disease is seasonal (wet-hot weather and presence of

insects).

Clinical signs and lesionsFP may occur in two forms, cutaneous or diphther ic , or both.

The cutaneous form is characterized by the appearance of nodularor wart-like lesions on the comb, wattles, eyelids, legs and other

non-feathered areas o f the skin, yellow to brown in colour.Th e diphth er ic form , or wet pox, occurs in the m ucosa o f them outh and oesoph agus an d, m ainly, o f the larynx and trachea ,

with the appearan ce o f nodules or patches, which increase in sizeand often coalesce to form yellow, cheesy, necrotic, diphtheric

m em brane s or plugs; in such cases, the bird can even choke. If rhesc a b s o r d iph the r i c me mbr a ne s a r e r e move d , a g r a nu la t i ng

hemorrhagic tissue, with erosions, is observed.M orbidity and course o f the disease are variable, a lso depen dingon virus virulence, hygiene and climate. Th e cffects of pox usually

involve em aciation, p oor weight gain and m ore or less reduced eggprod uc tion. T h e cou rse is 3-4 or m ore weeks. Mortality- also varies,

from 1-2%, when mild cutan eou s lesions are present, to over 30%when diph theric form s are prevalent.

DiagnosisWart-like lesions o f the com b, wattles and eyelids and diphthericlesions in rhe mouth, larynx and tracheal mucosa strongly suggest

Pox lesion on legs o f chicken


27/93


Pox lesion on the beak of a pigeon

the presence o f this disease. A definitive diagno sis can be m ade bya histological exam ination.Differential diagno sis is som etim es necessary with laryngotracheitis;

a histological exam ination can be definitive.

ControlSom etim es the removal o f warts and d iphtheric m embranes andthe treatment of local lesions with disinfectants are performed.However, the control of FP is based on imm unization o f birds with

attenuated vaccines before the season, when the disease is likely to

occur; in m ultiaged farms and in tropical climates, the vaccinationmay be performed at any time o f the year. Even when an outbreakis at an early stage, it is advisable to vaccinate the flock immediately,which very often prevents the disease from spreading any further.Tw o types of vaccines can he used, mainly, using FP virus attenuated

by numerous passages in embryonated eggs or on tissue cultures,or non-attenuated pigeon pox-virus. Bo th vaccinal viruses are grownin em bryona ted eggs o r on tissue-cultures and freeze-dried.Th e vaccine is applied by the wing-web m ethod, u sing a stick withtwo grooved needles dipped in vaccine solution. In breeders andlayers, a single vaccin ation is given benv een 4 an d 14 week s of age;

normally broilers arc not vaccinated, but in som e seaso ns or areas

it can be necessary to preserve the integrity o f the skin.Turke ys m ay be vaccinated by the wing-web metho d, bu t it is moreadvisable ro do so in the m iddle o f the thigh, by scarification at8-12 weeks o f age; breeders sho uld be revac cinated before laying.Th e presence o f local swelling at the injection site, 8 days aftervaccination, show s that birds have been correctly imm unized.

27


28/93

INFECTIOUS BURSAL DISEASE

Infectious Bursal Disease

Bursa o f Fabricius in IBD: diffuse mucosal haemorrhages

Bursa o f Fabricius in IBD:ml! oedema and catarrhal-haemorrhagic lesions in mucosa

Infectious bursal d isease (IBD), a lso known as Gu m bo ro d isease,

is an acute, highly contagious viral infection o f you ng ( 3 /6 - week-old)

chickens, caused by a member of the family Birnaviridae genusAvybirnovirus, serotype 1. It primarily affects the lymphoid tissues:

the most affected organ is the bursa of Fabric ius (BF), but the

rhynuts, spleen and othe r lym pho id tissues are also involved.B-lymphocytes are the prim ary target cells. T he virus (IBD V ) is very

s t a b l e i n t h e e n v i ro n me n t a n d c a n s u rv i v e fo r mo n t h s i ncontaminated farms.

Until 1987, the strains of IBD V were o f moderate virulence, usuallycausin g less than 5-10% specific m ortality, bu t well controlled by

mild vaccines. In rhe late 1980s, vaccination failures began to bereported in different parts of the world. In Norrh-America it was

demonstrated that the new isolates had been affected by antigenicdr i f t /sh if t (variants), w hereas in Eu rope a nd , la ter, on o therCo ntinen ts, the occurrence and spread o f very virulent strains of

virus (wIB D V ) were reported. Th ese latter strains, even if antigenicallyclosely related to rhe classic viruses (only p untiform m utations),

produce more severe symptoms and lesions in lymphoid t issues,particularly in the thymus, with very high m ortali ty, som etim es

over 3 0% , occurrin g over a period o f 2-6 days. Mild vaccines were

showed to be almost ineffective against these w IB D V , therefore

less attenuated an d m ore invasive vaccinal strains became essential.

EpizootiologyTh e ch icken is considered rhe only species in which natural infection

occurs, but antibodies have been also detected in other specics.All breeds are affected, with more or less severe reactions andmo rtality (genetic influence). T h e ag e o f greatest suscep tibility to

the d isease is between 3 and 6 weeks . IBDV' is t ransmit tedhorizontally directly or indirectly, but, appa rently, no t vertically.

Clinical signs and lesionsTh e incubation period o f the disease is very short and the clinicalsign s occ ur wirhin 2-3 days o f exp osure . C hic ks, p icking initially

ar their own vents, show anorexia, depression, ruffled feathers,

28


29/93


Bursa o f Fabricius in IBD: different appearance o f more or less severe lesions

whitish an d watery diarrhoea, trem bling and severe prostration;

dea th oc curs in a few hours. M orbidity is very high, even close to

80-10 0% . M ortality is very variable, but it can be as h igh as 10 to70% , depe ndin g on the degree of pathogenicity of the virus involvedand on environmental conditions.In birds which succu m b to infection, dehydratation, haemorrhagesin the pectoral and thigh musclcs and , often, in the muco sa of the

proventriculus, can be detected. The BP is swollen, gelatinous tohaemorrhagic; in cases o f w lB D V , a greater decrease in thymussi;e and m ore severe lesions in other lymphoid organs arc found.A fter recovery, in acute form s, in sub-clinical infection a nd when

var ian t s a re p resen t , the BF becomes more o r l es s a t roph ic .That resul ts in a variable immunosuppress ion , wi th enhancedsusceptibility to other viral an d bacterial infections an d conseq uen t

poor performance, wi th lower weight gain and a h igher feedconversion ratio.

Haemorrhagic lesions on proventriculus mucosa in IBD

DiagnosisAcute outbreaks of IBD are easily recognized and a presumptive

diagnosis can be readily made (see gross lesions); in subclinical

cases, histological lesions may give indications, together withimmunofluorescence or v i rus iso lat ion on the chorioal lanto icme mbrane (CAM ) o f 9-11 day-old embryos, on BF cultures or onBG M- 70 cell-1 ines. M ore recently, RT -PC R an d mo lecular sequenc inghave been introduced in the diagnosis. Th e m ost com m on serological

method for antibody evolution is the ELISA test.

ControlHygiene and disinfection are essential m eansto redu ce the infection

rate, hu t generally they are n ot sufficient, also be cause the virus isvery resistant to disinfectants. How ever, imm unization o f chickens,broilers and pullets with live vaccines at 2-3 weeks of age is themain method to contro l the d isease. Booster immunizat ion ofbreeder f locks with inact ivated vaccines in o i ly emuls ion hassometimes proved to be important, in order to extend the maternalimmunity of the progeny to 3-4 weeks. However, the protection inbroilers do es not extend till slaughter, so they need to be vaccinatedwhen maternal an tibodie s are reduced (2-3 weeks).

Mild live vaccines were satisfactorily used until the em ergency o fvirus variants in N orth America and w lB D V on other Continents,when the classic prophylactic m easures were called into question.To contro l IBDV variants , i t became necessary ro use specif ic

29


30/93

INFECTIOUS BURSAL DISEASE

attenuated strains, together with the classic on es. Less at tenuated

and more invas ive vaccines were in t roduced in the control ofw IB D V . D epen ding on thei r abil ity to induce imm uni ty in thepresence o f maternal antibo dies and their residual pathogenicity,these vaccines have been classified as interm ediate , intermediate-plus or hot types. Ar the moment, the first two types are them ost used al! over the world, whereas the last is currently ban nedin many countries, due to the severe lesions it causes to lymphoid

tissues. It has been found that marketed vaccines, particularly thosedefined as intermediate-plus, present very' variable degrees of

res idual pathogenici ty or invas iveness ; for th is reason, widerinvestigations and standardisation sh ould be recom me ndable, sincerhe use o f som e o f them is som etim es associated with clear injury

to, and atrophy o f the BF a nd , probably, o f other lymphoid tissues,together with imm unodep ression.Th e main problem encoun tered in the choice of the proper t imefor vaccination is that m aternal antibod ies interfere with replicationo f vaccin al virus in lym phoid t issues. Alth oug h rhe paren ts areboosted with inactivated vaccine, the maternal antibodies provide

a good level of protect ion only for the f i rs t 3 or, somet imes ,4 weeks, then the birds become fully susceptible.T h e key for efficaciou s protection ag ainst IBD is to vaccinate earlyenou gh to prevent the establishm ent o f wild virus infection, but

late enough to allow the maternal antibodies to decline sufficiently,so a s no t to interfere with the vaccinal virus. However, a universal

vaccinat ion program m e cannot be offered. Th e bes t mo m ent forvaccination depe nds o n the rate o f decrease of m aternal antibodies,which, in its turn, is linked to the growth rare o f the birds, morerapid in broilers than in light pullets. D ifferent meth ods to de terminethe prop er age of vaccinat ion have been developed (Daven ter sform ula, central vaccination d ate, etc.) , based on antibo dy levelsar 1-3 days o f age, b ut it is no t always possible to exactly determ inethe pro pe r time, either because a ntibod y tirres in a flock o f chicksare heterogen eous o r when facilities for serological controls are notava i l ab le . However, var ious exper i ences ( fa rm pas t h i s to ry,epidem iological data) can help to improve the control o f the disease.

In many areas , the use o f on e vaccinat ion at 18 days or twovaccinations at 15 and 22 days with intermediate vaccine resultedin goo d control o f the disease. In other areas, such a s the tropicsand in som e p eriods of the year, or in the presence o f very virulent

wild strains, the m ore or less temp orary use o f interme diate plus"vaccine at 12 to 16 days o f age can at least be temp orarily suggested.

Haemorrhages on the leg muscles in IBD


31/93


A c t iv e IB D V a n t i b o d y d e v e l o p m e n t a f t e r o n e a d m i n i s t r a t i o n o f

i n t e r m e d i a t e o r i n t e r m e d i a t e - p l u s v a c c in e a t 1 8 d a y s o f a g e :

w i th l es s a t te n u a t e d v a c c in e a n t ib o d y p r o d u c t io n b e g in s a w e e k

e a r l i e r


32/93

NEOPLASTIC DISEASES - MAREK'S DISEASE

Neoplastic diseases

Avian neoplastic disease includes a variety of conditions with one

common feature: their tumoral nature. The economically most

important diseases are Mareks disease, caused by a herpesvirus,

Leukosis-sarcoma and Reticuloendotheliosis, caused by retroviruses.


33/93

Marek's disease


Great sciatic nerve enlargement, which is normally monolateral, in MD

Mareks disease (MD) is a common lymphoproliferative disease of

chickens, caused by a cell-associatedHerpesvirus, with lymphottopic

properties similar to 7 -Herpesvims, but a molecular structure similar

to a -Herpesvirus, where it is actually classified.

Th ree serotypes of M D virus have been dem onstrated ; only serotype1 (MDV-1) is patho gen ic, causing tum ours; the other two serotypes

(MDV-2 and HVT-3) are non-oncogenic and ate used as vaccines.

Since its discovery, MDV-1 has increasingly enhanced its virulence,

From mild (m) to very virulent plus (w+); at the moment, virulenceseems to be fairly stable or progressing slowly.

bpizootioiogYM D is widespread throu ghou t the world. The prevalence of infection

is much higher than the prevalence of the disease. Chickens are by

far the most important natural host, with wide differences in genetic

suscept ibi l i ty among the breeds. Natura l outbreaks of MD arerelatively com m on also relatively comm on in Japan ese quail. Tum our shave occasionally been reported in turkeys, but, more recently,

severe outbreaks have been reported in these birds in France and

Israel. M D has also been reported in pheasants.

Transmission of infection occurs only horizontally, by direct or

indirect contact between birds, apparently by the airborne route.

The sources of environmental contamination are the epithelial cellsof feather follicles, where the complete virus replicates.

The keratinized dander and feathers, which preserve the virus evenfor several months at Z5C and for some years at 4C, are the main

virus shedder. Under field conditions, particularly it houses are not

cleaned and disinfected carefully, young chicks are usually exposedto infection very rapidly, which spreads quickly from bird to bird.The virus persists in infected animals for a long t ime, often

indefinitely, also in the form of latent infection in T-lymphocytes.

Factors affecting the de velopm ent o f the disease are; virus virulence,breed genetic susceptibility, environ me ntal hygiene, stress, imm une

state, environm ental tem perature (tropics), interaction with otherimm unod epressive viruses, toxins, etc. However, to control M D the

hygien ic cond i t ions o f t he pou l t ry house a re o f pa ramount

33

Lymphoid proliferation and en largement of tne peripheral nerve (neck) in MD:a) normalb) affected


34/93

importance, with careful removal of litter and dust, washing and

disinfection , all in-all o ut bree ding systems, particularly for the firstfew weeks o f life, u ntil the chicks are well protected by the vaccine.

Spleen and liver tumoral infiltration due to MD infection

Breeder with tumoral lesions due to MD in a) muscles and b) spleen

MD is sometimes characterized by progressive paresis and, at a later

stage, by spastic paralysis, associated with lymphoid infiltration of

peripheral nerves, mainly visible in the sciatic and vagus nerves,

mostly on one side. However, more frequently the birds show

depression, weight loss, palour, anorexia and, at necropsy, the

presence of more or less widespread neoplastic lesions in variousorga ns, mainly in the liver, spleen, pro ven trie ulus, kidneys, gon ad sand skin.

A transient paralysis syndrome has been reported in the field, but

with lower frequencies since vaccination yet became widespread.

However the pathogenesis of this syndrome has not yet became

clear. Very virulent MDV strains can induce sudden death in a fewdays in young chicks with or without macroscopic tumoral lesions

(mostly in chicks experimentally inoculated when they are one-day-old).Morbidity and mortality are rather variable. The usual occurrence

of disease, under field conditions, is when the birds are between

10 and 30 weeks old; the p ercentage o f birds simultane ously affected

does not exceed 2-3%. The incidence, before the use of vaccines,

was very variable: losses in flocks of breeders or layers were estimatedto range from a few birds to 40%, occasionally as high as 70%, also

depending on the breeds. In broilers, in addition to relatively low

mortal i ty, condemnat ion at the s laughter house could be from

0.5 to 10%, as a result of cutaneous and visceral tumoral lesions.Presently, in most coun tries or areas, nearly all bree de rs and layers

are vaccinated against MD; for this reason, losses have dropped to

less than 2 to 4% , o ften practically zero. Broilers, which are vaccinatedin many co untries, may experience very low specific m ortality and

condemnation (0.1-0.5%).

DiagnosisDiagnosis o f M D has long been part icularly based on macro- andmicroscopic lesions in tissues. After the discovery that feather follicle

epithelium (FFE) is the m ain site of active M DV replication, the

agar-gel diffusion (AG D) test was also applied, using a hom ogena te

of FFE or feather t ips (FT) as ant igen, agains t a hyperimmuneantiserum as reference antibody. The test also makes it possible to

differentiate between pathogenic and non pathogenic (or vaccinal)


35/93


strains or serotypes o f the virus, because FFE , infected with thelatter types o f virus, rarely induc es any positive reaction; this is due,

in all likelihood, to a low virus replication and concentration in

FFE. T he reac t ion u sual ly persis t s unt i l the dea th o f the bi rd .It has also been dem onstrated that there is a significant relationship

between the percentage o f positivity to the A G D test, mainly whenperformed a t 12-16 weeks of age, and the estimated c umu lative M Dmortal i ty during the production cycle. Therefore, the use of the

AGD test with FT deserves part icular at tention for a simple andaccurate diagnosis, feasible in all laboratories, bu t also for its reliable

prognostic value on future M D incidence in a flock of long-livedbirds. S o it cou ld be o f value , at least indicatively, if not legally, in

the sale ot pullets, a frequen t practice in several countries.

Recently a P CR test has been used to d ifferentiate the serotypes.

ControlVaccination represents, now and for the foreseeable future, themain strategy for the prevention and control o f M D. Selection for

genetic resistance and biosecurity m easures were used as the soletool available before, the discovery and application o f the vaccines,

and subsequently as adjun cts to vaccination. O bviously, the efficacy

ot the vaccine is higher in genetically more resistan t breeds; therefore,

a recon sideration o f genetic selection is in progress, particularly invery sensitive lines o f chickens.Vaccination is performed when chicks are one-day-old, mostly at

the hatchery, becau se early im m unity is essential. R evaccination at

one day or at 7 days is sometimes recommended, part icularly tovaccinate birds which m ight have been skipped (their percentage

could be as high as 5% or even more) or to reinforce immunity.Vaccines are administered by means o f intramuscular or subcutaneousinjection. In b ig hatcheries, particularly in bro ilers, the vaccine is

o f ten adm in i st e red in-ovo on th e 18th day o f incub ation, th us

postponing exposure to wi ld vi ruses for a t least 3 days af te rvaccination. At least 7 days are required to establish a solid immun ity

after vaccination.As regards the choice of vaccines, H V T a lone provides adequateprotection to broilers under normal epidemiological condit ions,

bu t a bivalent vaccine is often requ ired, com binin g serotype 3 with

serotype 1 or 2, particularly against w M D V. In breeders and layers,

the use o f the original CVI-988 or Rispens strain o f MDV-1, aloneor in associat ion with H V T, is recom m ended nearly everywhere.H V T vacc ine is available as cel l-associated (frozen) or cel l-free

Breeder chicken with cutaneous tumoral lesions in MD

35

Lymphomatous lesions in the proventriculus in MD


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NEOPLASTIC DISEASES -MAREK'S DISEASE

AGD test with leather tips: precipitation line versus positive serum

(freeze-dried) types; M D V serotypes 1 an d 2 are available only incell-associated form, preserved in liquid nitrogen. In this case,prop er ha ndling o f the vaccine during thawing, reconstitution and

injection is very important, in order to preserve cell integrity,

viability, and, consequently, the vaccinal titre.M D outbreaks in vaccinated flocks may occu r for various reasons:improper storage, han dling and injection o f vaccine, also a shorter

interval between vacc ination a nd exposure to wild viruses, weakvaccines such as H V T against wM DV , higher genetic susceptibility

o f som e breeds to the disease, imm unosup pressive stress, particularly

d u r i n g t h e o n s e t o f e g g la y i n g , i n t e r a c t i o n w i t h o t h e rimm unosu ppressive viruses (1BDV, CAV , R EV, etc.) and, finally,certain unknown vagaries.

AGD test with leather tips: precipitation line versus positive serum


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NEOPLASTIC DISEASES - LEUKOSIS/SARCOMA GROUP Poultry Disease Manual

Leukosis/Sarcoma groupThe leukosis /sarcoma (L/S) d isease group includes a var iety ofbenign and mal ignant neoplasms of poul t ry caused by cer tain

members of the family Retroviridae, genus Oncovirus. Th e mo s tcom m on o f them arc lymph oid and, m ore recently, myeloid leukosis.

They posses the enzyme reverse transcriptase, which directs thesynthesis of the proviral DN A form from viral RN A in the cclls ,where it integrates into the genome.

On ly certain diseases o f this group have any significant econom icimportance, part icularly those du e to avian leukosis virus (ALV),with some mortality, less than 2%, occasionally over 20%, or sub-clinical infections with a dep ressive effect on v arious pe rforman ce

factors, including egg production and quality. Their public healthsignificance h as n ot b een clearly determ ined, al thoug h evidencessuggests that ALV' apparent ly docs not const i tu te a danger for

humans.

EpizootiologySubgroups A and J o f AL V are the m os t comm on v i ruses caus inglymphoid and myeloid leukosis (LL or ML) respect ively; o thersubgroups (B, C, D) have been isolated , most ly sporadical ly.

A ntibod ies to som e of them have also been observed in wild birds.

Exo gen ous AL V s are transmitted vertically by the egg to the progenyor horizontally by direct or indirect contact from bird to bird.Al though vert ical t ransmiss ion is not f requent , th is method oft ransmiss ion is very important , becom ing a mean s to m aintaininfection, generation after generation. ALV is present in albumen

and transmission to the embryo is due ro the el im ination o f virusby the glands o f the oviduct. Four different classes o f ALV infectionare recognized, wi th or wi thout v i remia and wi th or wi thouts imu l taneous presence of v irus and ant ibodies . The incubat ion

period of the disease depen ds on the strain and quanti ty o f virus,the route o f infection, the age at exposure and the genetics o f the host.

Clinical signs and lesionsThese include inappetence, weakness, diarrhea, emaciation andthickening o f the long bo nes of the l im bs (os teopetros is), e tc .


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NEOPLASTIC DISEASES - LEUKOSIS/SARCOMA GROUP

Lesions depe nd on the cells involved and include neoplasm s in the

liver, spleen, bursa of Fabricius, kidney, lung, mesentery, etc.( L L , e r y t h r o b l a s t o s is , m y e l o c y to m a t o si s, n e p h r o b l a st o m a ,fibrosarcoma or osteopetrosis, etc.); tumours in the bursa o f Fabriciusare pathognomon ic o f ALV.

DiagnosisVirus isolation and dem onstration o f the antigen or antibody are

signs o f infection, bu t nor o f disease. M any laboratory tests areavailable for the detection o f virus antigen or antibodies. Sam ples

to control include albumen, blood, serum, mecornium, cloacalswabs, embryos, tumours etc; the most important tes ts are the

C O FA L, ELISA, RIF and P C R tes ts, etc .

ControlC on trol is obtained by eradicat ion , part icularly from primarybreeding stocks. C om pan ies prod ucing birds o f this type have madesignificant progresses, in reducing or eradicating A LV su bgro ups

A, B an d J; in commercial stocks, the application o f these programmesis more complicated and too expensive. Eradication is based mainly

on the test for the antigen in albumen and for the antibodies in

serum.Selection for genetic resistance is in progress, but is very difficultto apply.No commercial vaccines are available for infection with ALV; theidea has been extremely at tract ive, even i f the dam age du e to

infection is normally quite low and occasional.

Characteristic tum oral lesions in inner sternum and costochondral junction of ribs in J Leucosis


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NEOPLASTIC DISEASES - RETICULOENDOTHELIOSIS Poultry Disease Manual

ReticuloendotheliosisReticuloendothel iosis (RE) is a group of pa thologica l syndrom es

caused by a m embe r of the familyRetroviridae in several avian species:these include ranting disease , chronic neoplasia and acute reticulum cell neoplasia. There is li t t le or no evidence for human involvement.

EpizootiologyREV infec t ion is common, but not ubiquitous. In contrast , the

incidence of RE V-assoc iated clinical disease in com me rcial poultry

varies from sp oradic to negligible. H orizontal transm ission occurs

by contact, direct or indirect (also through insects); novel viralreservoirs , such as fowl poxvirus and M D V, which m ay conta in

infec t ious c lones of REV. could a l so be cons ide red . Ver t ica ltransm ission from anim als with persistent viremia may occur, but

usually at low frequency.

Clinical sign and lesionsBirds may be stunted a nd pale and som e o f them may have abnormal

fea ther ing (nakanuke) ; morta l i ty is rare . Var ious pathologica l

situations may be observed: 1)mnting disease: atrophy o f the thymus

and BF, runting, proventriculitis, etc. 2) bursal lymphoma: typicalbursal tum our: 3) no n bursal lym phom a in various organs; 4)turkey lymphoma: inf i l t ra t ion of the l iver, spleen and other organs;

5) multiple syndromes.

DiagnosisDiagno sis is especially based on the demon stration o f RE V by PC R

or ant ibodies by ELISA. Th e pathology o f REV-induced tumours

can be confused with M arek's disease and lymphoid leukosis.

Control

N o proced ures have, until now, been app lied in farms, partly dueto the sporadic n ature o f the disease.


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INFECTIOUS CHICKENS ANAEMIA

Chicken Infectious AnaemiaCh icken infectious anaemia (CIA ) is caused by a Gjiownts, a m emberof the family Circoviridae; apparently no antigenic differences havebeen recognized between the various isolates, although one hasrecently been hypothesized in the U SA . Th e virus, isolated for thefirst time in Japan in 1979, was soon reported worldwide.

EpizootiologyC hicke ns are the only known host of the virus. Although birds of

all ages are susceptible to infection, the d isease only occurs in chicksup to 2-3 weeks o f age. W hen breeders becom e infected d uring rhelaying period, they transm it the virus vertically for 2 to 4 w eeks orlonger to their progeny, which show severe anaemia and high

mortality (10-20% or more). H orizontal transmission o f infectionoccurs at any age, bu t birds fall ill on ly up to a few weeks o f age.

Appearance o f normal 7 day-old chick (right) and affected by CIA virus (left)

Thimus in norm al chick, 3 week-old

Clinical signs and lesionsClin ical signs generally develop 10-14 days after infection. Th e onlyspecific signs o f disease are depression and anaem ia, with peaks at

14-21 days; haematocrir values range from 8 to 28% (in healthybirds it is normally over 30%).G ross lesions are characterized by atrophy o f rhe thymus, som etimes

with com plete destruction, d iscoloure d aplastic bone marrow, wellevaluable in the femur, reduced bursa, swollen and mottled liver.Hemorrhages and necrosis are often present, particularly in thewings, m ost likely du e to second ary bacterial infections (septicemia,blue-wing).

C IA virus, inducing d am age to imm une tissues, is obviously extremelyimm unosuppressive, also interacting with other imm unosuppressiveviruses, such as M D V , IBDV, REV.

DiagnosisPresumptive diagnosis of C IA is based on epidemiological data andlesions (thymus atrophy and anaemia). Confirmation is given byisolation of the virus on M S B ! cell-culture lines for ab out 10 passages,until cell death is observed, o r by inocu lation into susceptible one-day-old SPF chicks, to reproduce the disease. The ELISA and VNtests are those m ost com m only used fo r antibody detection


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ControlThe contro l o f CIA is based o n the p revent ion o f ver tical v irus

transmission by imm unization o f breeder f locks. Com m ercial l ive

vaccines, more or less attenuated, arc available in several countries.

Vaccine should be adminis tered v ia rhe dr ink ing water or by

injection at ab ou t 12-15 weeks o f age, bur n ever later than 3-4 weeks

before the first collection of hatchin g eggs. A single adm inistration

is sufficient to cover the entire laying period.

Atrophy of the thymus in 3 week-old chick affected b y CIA

41


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REOVIRUS INFECTIONS

Reovirus InfectionsAvian reovirus, a m em ber o f family Rcoviriclae, is often ubiquitousin commercial poultry; i t is com m only foun d in the digestive andrespirator^' tract. Th e va rious strain s can be differe ntiated by theirrelative pathogenicity and antigenic characteristics, being isolatedfrom birds affected by assorted disease condit ions. T he diseases aregroupe d into two m ain categories:a) arthritis/tenosynovitis;b) stunting or m alabsorption syndrome, which includes pale birds,abn orm al feathering syndrome (helicopter disease), etc.

EpizootiologyViral arthritis or tenosynovitis is an economically important disease,mostly in chickens for m eat produc tion (breeders and broilers), butit has also been observed in layers and in turkeys. The disease iscaused by different serotypes and p athotype s o f reovirus; however,the best know n and m ost widely studied isolate has been the strainS I 133 o f van d er Heyde. Horizontal t ransmission o f reovirus hasbeen extensively documented, but a vertical transmission has beenclearly dem onstrated.Malabsorption syndrome is considered a multi factorial disease, wheredifferent serotypes o f reovirus and other viruses have been isolated.Th is syndrome is hardly reproduced, in laboratory conditions, whenreovirus only is inocu lated.

Clinical signs and lesionsIn arthritis - tenosynovitis, the incubation period varies, dependingon the v i rus pathotype, h os t age, route o f exposure a nd type o fbreed; sometimes infection is unapparent and demonstrable onlyby serology or virus isolat ion. The affected birds show lamenesswith swelling, oede m a and inflam m ation o f the tibio-tarsal-metatarsaltendon sheaths , h ighl ighted by palpat ion jus t above the hock;rup tu re o f the gas trocnem ius tend on is som et imes observed .M orbidity an d m ortali ty are very variable; the latter is generally2-3%, sometimes even reaching 10%, particularly in males; loss ofgrowth a nd infertility are also evident.Malabsorption syndrome is characterized by reduced and unevengrowth rates and other disorders, mainly indicating the varyingcffects on gastrointestinal tract function. Morbidity, mortality anddelayed growth vary greatly.

Lesion in the synovial sheath

Tenosynovitis in the tibio-tarsal join t after infection


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ControlTh e co nt rol o f v i ra l a r thr i t is , besides the appl ica t ion o f good

breed ing t echn iques and hyg ien ic measures , i s ob ta ined byvaccination o f breeders with live attenu ated virus (strain S 1133) at:abo ut 7 days o f age, followed by a booste r with live or inactivatedvaccine in oily em ulsion, when birds are abo ut 18 weeks old.Th e chicks batch ed from these breeders are protected by maternalantibo dies for 2-3 weeks, an d sh ould only be vaccinated in case ofhigh viral pressure.At tempts to cont rol malabsorpt ion syndrome have been made,with very variable results, using d ifferent serotypes o f virus, oftenin polyvalent inactivated vaccines in oily emulsion.

DiagnosisA presum pt ive diagnosis of d ifferent syndrom es may be madeaccord ing to signs and lesions. D em onstration o f the viral antigenin tendon sheaths by PCR, immunofluorescence, virus isolat ionin embryonated eggs or t issue cultures and inoculat ion into thefoot-pad of suscep tible I -day-old chicks (swelling) p rovide furtherevidence of arthrosynovit is due to reovirus. Antibodies can bedetected by the A G P an d ELIS A rests.

Swelling (tenosynovitis) oftarsal-metatarsal tendon sheaths in pullets:a) normalb) with lesions

Tenosynovitis in tibio-tarsal tendon sheaths in heavy breeder, tendon rupture



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ADENOVIRUS INFECTIONS

Adenovirus InfectionsAdenoviruses, mem bers o f the familyAdenoviridae, genus Aviadeiuwirus are common infectious agents in poultry worldwide. Most of theseviruses are present in healthy birds with no signs o f infection, orcan behave as opportunistic pathogens, when additional factors,either infectious or not, are involved. How ever, som e adenovirusesare pr imary pathogens, such as those causing turkey hemorrhagic enteritis, pheasant marble spleen disease, chicken egg-drop syndrome andquail bronchitis virus.

SUB-GROUP I ADENOVIRUST h e role o f these viruses as patho gens is n ot well defined, with rheexception o f qu ail bronch it is , hydropericardium syndrom e and

inclusion body hepatitis.Inclusion body hepatitis (IBH) is normally observed in meat-typechickens at 3-7 weeks o f age and is characterized by a sud den on setof mortality for 3-5 days, which may reach a threshold of 10% oreven higher. Many serotypes have been associated with naturaloutbreaks o f disease. Th e m ain lesions are pale, friable and swollenliver, with pinpoint haemorrhagic and necrotic spots.Hydropericardium syndrome (H IS), or An gara disease, was recognizedas a devastat ing disorde r in broi lers in Pakistan in 1987 and

sub seque ntly in othe r countries. It affects birds 3-4 weeks-old andis characterized by an accumulation of clear, straw-coloured fluidin the pericardial sac, pulm ona ry oed em a, swollen liver an d kidney.Experim ents with vaccination, apparently successful, with inactivatedliver hom ogenare ob tained from infected birds, have been reportedin Pakistan.Quail bronchitis (Q B) is a disease o f econ om ic significance worldwide,characterized b y rapid o nse t, with high morbidity' an d mortality' inbirds of less than 3 weeks of age. Sick birds show ruffled feathers,difficulties in breathing, nasal-ocular discharge. The main grosslesion s arc localized in rhe respiratory tract. Prevention is based onthe usual sanitation proce dures an d biosecurity' m easures; to date,no v accines are available.

SUB-GROUP II ADENOVIRUS


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ADENOVIRUS INFECTIONS - 4, .

Histological lesions with intranuclear inclusions

in epithelial cells of the oviduct plica in EDS

or more. N o ocher signs, except for a possible transient diarrhoea,

or mortality, are d etected.EDS can be effec t ive ly control led by injec t ing pulle ts with an

inactivated vaccine in oily emulsion, p erform ed only once, at theage o f 14-18 weeks.

DiagnosisDiagnos is o f Ad enovi rus in fec tions is based on symptom s andlesions, bu t isolation o f the virus from excreta or tissue hom ogcnates

is often necessary on chicken embryo liver or kidney cell tissue-

cultures. Group-specific-antibodies can be detected by the AGDor EL ISA tests; in case of ED S, the H I test is also used.

Laying curve in vaccinated and control layers, chal lenged wi th a virule nt strain o f FDS virus


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AVIAN ENCEPHALOMYELITIS

Avian EncephalomyelitisAvian encephalomyelitis (AE) is caused by an enterovirus, a m em bero f the family Picornaviridae. It usually affects very you ng ch icks, less

than 2 weeks old, and hens in lay.

EpizootiologyAE occurs virtually all over the world. Chicks, turkeys, quail,

pheasants and guinea-fowl are known to be susceptible . Under

natura l condit ions, AE being an enter ic infec t ion, the virus isexcreted with the faeces for 1-2 weeks or more in young birds.H or izonta l t r ansm iss ion occurs by inges t ion o f feed or wa ter

contam inated by faeces. Vertical transm ission is the main and most

dam aging route o f infection. Breeders, infected du ring the layingperiod, tran sm it the virus to their progeny for at least 4-5 weeks ormore.

Clinical signs and lesionsIn yo un g chicks, 1-3 weeks old, the d isease is characterized by flaccidparalysis; weakness may also be o bserved a t h atching. A progressive

ataxia occurs until the chicks are totally paralysed, prostrated anddie; head an d neck trem or may often be present.

Th e usual m orbidity rate is to 60 % , m ortality is over 10% an d mayexceed 40 % , depen ding on the per iod o f lay when the infec tionoccurs in parents.

In breeders, infected dur ing the laying period, A E is only characterizedby a variable drop in egg produ ction (without any change s in shell

quality), reduced hatchability an d transmission o f the virus to theprogeny. In laying hens, a variable (20 to 40 % ) d rop in egg production

occurs, which rapidly returns to normal production in 2-3 weeks.Th ere are only m icroscopic lesions to the central nervous system:non-puru lent inflam m ation with a striking perivascular lymphocytic

infiltration.

DiagnosisAtaxia and rapid tremors of the head in young chicks and a sud den

drop in egg production in laying hens, with no changes in shellquality, is indicative o f AE . Histological exam ination o f the brain

Eighteen day-old embryos, normal or affected byAEV

Twelve day-old chicks vertically infected byAEV


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Legs o f embryos affected or n ot b y AEV

and pancreas reveals the typical lesions o f disease. R eproduction

o f the disease in SPF chicks, ino culated by the inrracerebral route

at one-day-old, is a co nfirm ation. T o dem onstrate a ntibodies, theELISA or VN tests are the metho ds o f choice.

ControlThe contro l o f A E is ach ieved by vaccinat ion o f breeder flocks

(sometime also layers) during the growing period, at 12-15 weeks

o f age, to ensure that they becom e infected and develop antibodiesbefore go ing into lay, thereby preventing virus sh ed din g by rhe egg-

born e route. Maternal a ntibod ies protect the progeny from co ntact

with AE virus during the critical first two weeks of life.Th e m ost comm only used comm ercial vaccines are prepared mainlywith the strain C aln ek 1143, only partially attenu ated in em bryona ted

eggs; obviously, the virus must maintain the spreading ability and

enterotropism of wild virus, so it mu st not becom e too adap ted to

the embryo. Th e adm inistration may be individual into the beak

or by eye-drop or by drin king water. To ensu re tha t birds have been

well immunized, a serological check can be carried our 3-4 weeks

after vaccination .

Laying curve in vaccinated an d co ntrol hens, infecte d with virulen t AEV

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Paratyphoid InfectionsThe species o f genusSalmonella, (S) o f the family Enterobacteriaceae which arc most important in animal and human pathology areS. enteritidis and S. cyphimurium; nevertheless, man

poultry disease manual

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