Important poultry disease handbook intervet


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Important poultry disease handbook intervet

  1. 1. Important Poultry Diseases
  2. 2. IMPORTANT POULTRY DISEASESContentsForeword 3Infectious respiratory Diseases Chronic Respiratory Disease 7Coryza 10Aspergillosis 12Newcastle Disease 14Infectious Bronchitis 16Infectious Laryngotracheitis 18Avian Influenza 20Pneumovirus 22Neoplastic DiseasesLymphoid Leucosis 27Marek’s Disease 29Avian Adenoviral DiseasesInclusion Body Hepatitis 35Egg Drop Syndrome ’76 38Miscellaneous viral DiseasesFowl Pox 43Avian Encephalomyelitis 45Infectious Bursal Disease 47Reovirus infection 49Malabsorption Syndrome 51Infectious Anaemia 53Miscellaneous Bacterial DiseasesInfectious Synovitis 57Fowl Cholera 59Pullorum Disease/Fowl Typhoid 61Ornithobacterium Rhinotracheale infection 63
  3. 3. Infectious Viral Diseases of ducksDuck Virus Hepatitis 67Duck Plague 69Parasitic DiseasesCoccidiosis 73Endoparasites 78Blackhead 80Deficiency DiseasesRiboflavin 85Vitamin E 86Vitamin D3 87
  4. 4. ForewordWe first published the “Important Poultry Diseases ”in 1972 and, ever since, it has remained the mostsought after of all our publications.However, in the intervening years new causes of disease suchas chicken anemia virus and pneumovirus were identified.Therefore, Intervet Research teams developed new vaccinesto combat the changed pattern of diseases. Many of theseare inactivated vaccines, in either single or combined form,resulting in new vaccination programmes. We have, therefore,produced this fourth edition of the handbook to cover thesedevelopments. It is intended as a pocket reference book forpeople working with poultry.It is not highly academic as it is written from a practical angleto assist with every day problems in the field.Intervet Research continues to co-operate with the poultryindustry, worldwide, to stay ahead of disease problems.The farmer who uses an Intervet vaccine can do so knowingthat it is the best product available.For detailed information on any of our products contact thelocal Intervet representative orIntervet International BVBoxmeer- HollandP.O. Box 315830 AA Boxmeer, The NetherlandsPhone +31 485 58 76 00Fax +31 485 57 73 33Telex 37306 inte nlE-mail
  5. 5. Infectious RespiratoryDiseases • Chronic Respiratory Disease (CRD) • Coryza • Aspergillosis • Newcastle Disease (ND) • Infectious Bronchitis (IB) • Infectious Laryngotracheitis (ILT) • Avian Influenza • Turkey Rhinotracheitis/Swollen Head Syndrome
  6. 6. Chronic respiratory Disease(CR­­D) (Airsacculitis)CauseThe underlying cause of CRD is Mycoplasma gallisepticum(Mg). The condition is frequently triggered by respiratoryviruses such as ND and IB and subsequently complicated bybacterial invasion. The main agents involved in the infectionare Mycoplasma gallisepticum and E. coli. Stress caused bymoving the birds, by debeaking or other operations or otherunfavorable conditions e.g. cold or bad ventilation, make thebirds more susceptible.TransmissionThe main problem is that parent birds infected withMycoplasma gallisepticum can transmit the organismthrough the egg to their offspring. In addition, infectioncan occur by contact or by airborne dust or droplets. Theincubation period varies from 4 days to 3 weeks.Species affectedChickens and turkeys.Airsacculitis
  7. 7. Clinical signsYoung chickens (broiler chicks or layer pullets) will showrespiratory distress. The birds frequently show a lackof appetite, decreased weight gain and increased feedconversion ratios.In adult birds the most common symptoms are sneezing,coughing and general signs of respiratory congestion. Inlaying birds a drop of egg production between 20-30 % canoccur.CRD does not normally cause an alarming number of deaths.The effect is more of a chronic nature causing reduced weightgain and feed conversion ratios in broilers and lower eggproduction in breeders and layers. In this way the overalleconomic loss can be very great in broilers but less dramaticin breeders and layers.Internal lesionsA reddish inflamed trachea and/or cheesy exudate in airsacs,especially in complicated cases (e.g. with secondary E. coliinfections) are observed. In mild Mg infections the only lesionmight be slight mucus in trachea and a cloudy or light frothin the airsacs.Turkeys with Mg infection usually have swollen sinuses underthe eyes.DiagnosisDiagnosis of Mg infection can be made by blood testingof chickens, post-mortem examination and ultimately byisolating the causative Mg organism from tracheas or airsacsof affected birds.
  8. 8. Differential diagnosisRespiratory virus infection (Newcastle disease or infectiousbronchitis) with secondary infection (E. coli, etc.) can givesimilar lesions.TreatmentTreatment of Mg-infected chickens or turkeys with suitableantibiotics or chemotherapeutics has been found to beof economic value. However, control by medication orvaccination and eradication of Mg infections has been by farthe most effective method of combating the disease. Fertileeggs from infected birds can be treated with antibioticssuch as tylosin to eliminate the Mycoplasma gallisepticumorganisms.Methods used are the injection of fertile eggs or egg dipping.Blood serum testing of breeder chickens for Mg antibodieshas become a routine to test flocks for a Mg infection.Pericarditis, peritonitis andperihepatitis is frequently observedin birds with CRD
  9. 9. Infectious CoryzaCauseThe bacterium causing this disease is Hemophilusparagallinarum.TransmissionThe disease spreads from bird to bird and flock to flockby contact and airborne infected dust particles and via thedrinking water.Spread by equipment and personnel has also been reported.The incubation period varies from 1 to 3 days.Species affectedChickens appear to be the only natural hosts ofH. paragallinarum.Clinical signsThe main signs of the disease are inflammation of eyes andnose with foul-smelling discharges, conjunctivitis, sneezingand facial swellings. Feed and water intake is reduced,leading to loss of weight. Egg production in laying birds willdrop.Mortality will vary with the virulence of the infection but isgenerally low.10
  10. 10. 11DiagnosisA field infection produces similar symptoms to chronicrespiratory disease, a diagnosis is difficult to establish.The most certain diagnosis may be obtained by the isolationof the organism from the sinus or airsac exudate fromaffected birds. This procedure must be carried out in thelaboratory.Treatment and controlTreatment with antibiotics can be given to subdue clinicalinfection, but eradication and prevention are the mostdesirable means of control of coryza. Vaccines have beendeveloped, but are only used in areas where the disease isendemic and cannot be eradicated.Typical facial edema
  11. 11. Aspergillosis (Fungal Pneumonia)CauseThe disease is caused by a fungus, Aspergillus fumigatus.TransmissionTransmission is by inhalation of fungus spores fromontaminated litter (e.g. wood shavings) or contaminated feed.Hatcheries may also contribute to infection of chicks.Species affectedYoung chicks are very susceptible, older chickens are moreresistant to infection. Turkey poults, pheasant chicks, quailchicks, ducklings, and goslings may also become infected.Clinical signsInfected chicks are depressed and thirsty. Gasping and rapidbreathing (“pump handle breathing”) can be observed.Mortality is variable, from 5 to 50 %.Gross lesions involve the lungs and airsacs primarily. Yellow-white pinpoint lesions can be found. Sometimes all bodycavities are filled with small yellow-green granular fungusgrowth.12
  12. 12. DiagnosisThe presence of Aspergillus fumigatus can be identifiedmicroscopically or sometimes even with the naked eye in theair passages of the lungs, in the airsacs or in lesions of theabdominal cavity.Treatment and controlThere is no treatment for aspergillosis. Affected chicks shouldbe removed and destroyed. Strict hygiene in breeder andhatchery management is necessary. Choice of litter material isimportant so that no spore-bearing wood shavings are used.13Gross lesionsof the lungs
  13. 13. Newcastle Disease (ND)CauseNewcastle disease is caused by a paramyxovirus. Onlyone serotype of ND is known. ND virus has mild strains(lentogenic), medium strength strains (mesogenic), andvirulent strains (velogenic).The strains used for live vaccines are mainly lentogenic.TransmissionNewcastle disease virus is highly contagious through infecteddroppings and respiratory discharge between birds. Spreadbetween farms is by infected equipment, trucks, personnel,wild birds or air. The incubation period is variable but usuallyabout 3 to 6 days.Species affectedChickens and turkeys.Clinical signsNewcastle disease causes high mortality with depression anddeath in 3 to 5 days as major signs. Affected chickens do notalways exhibit respiratory or nervous signs.Mesogenic strains cause typical signs of respiratory distress.Labored breathing with wheezing and gurgling, accompaniedby nervous signs, such as paralysis or twisted necks(torticollis) are the main signs. Egg production will decrease30 to 50 % or more, returning to normal levels in about 2weeks. Eggs may have thin shells and eggs without shellsmay also be found. In well-vaccinated chicken flocks clinicalsigns may be difficult to find.14
  14. 14. Internal lesionsInflamed tracheas, pneumonia, and/or froth in the airsacs arethe main lesions. Haemorrhagic lesions are observed in theproventriculus and the intestines.DiagnosisIs made by virus isolation from tracheal or cloacal swabstogether with blood testing to demonstrate high antibodylevels. Infectious bronchitis or infectious laryngotracheitis cangive similar clinical signs, but lesions, blood tests, and virusisolation tests are decisive.Treatment and controlThere is no treatment for Newcastle disease. Vaccinationagainst ND with live and/or inactivated (killed) adjuvantvaccines is the only reliable control method.15Neurotropic form of ND Haemorrhagic proventriculus
  15. 15. Infectious Bronchitis (IB)CauseCorona-virus is the causal agent. Several different serotypesof IB virus are known to exist.TransmissionThe virus is transmitted from bird to bird through theairborne route. The virus can also be transmitted via the airbetween chicken houses and even from farm to farm.Species affectedOnly chickens are susceptible to IB virus.Clinical signsIn young chicks IB virus infection causes a cheesy exudatein the bifurcation of the bronchi, thereby causing asphyxia,preceded by severe respiratory distress (“pump handle”breathing). In older birds IB does not cause mortality. Eggproduction will decrease dramatically, deformed eggs withwrinkled shells will often be laid.16Respiratorysymptoms of IB inchickens
  16. 16. Internal lesionsMucus and redness in tracheas, froth in airsacs in olderchickens. In young chicks a yellow cheesy plug at the trachealbifurcation is indicative of IB infection.DiagnosisThere are three main factors to be considered in order toarrive at a diagnosis.a. The clinical picture including post-mortem findings in the flock.b. Isolation of the virus in the laboratory.c. A rising antibody titre when the serum is tested against a known strain of bronchitis virus.Treatment and controlThere is no treatment for infectious bronchitis.Secondary bacterial infections may be prevented by, ortreated with antibiotics.Prevention by vaccination is the best method to control IB.17Misshapen, shellless andnormal eggs
  17. 17. Infectious Laryngotracheitis(ILT)CauseILT is caused by a virus belonging to the herpes group. Onlyone serotype is known.TransmissionField infection occurs from bird to bird by the respiratoryroute. Most outbreaks of ILT on farms are traced back totransmission by contaminated people or equipment (visitors,shoes, clothing, egg boxes, used feeders, waterers, cages,crates etc.). The incubation period varies from 4 to 12 days.Species affectedChickens and pheasants are natural hosts for ILT.Clinical signsRespiratory distress is usually quite pronounced due to buildup of blood, sloughed tracheal lining and even caseousexudate in larynx and trachea. When a caseous plug occludesthe larynx or trachea, the affected chickens will have extremedifficulty breathing (“pump handle” breathing) and willfrequently die from suffocation. Mortality is approximately1 % per day in a typical ILT outbreak. Milder forms of ILToutbreaks occur where less virulent strains of ILT virus areinvolved. Conjunctivitis and respiratory sounds (wheezing)can be observed, with little or no mortality in such cases.18Haemorrhagic lesi-ons in trachea
  18. 18. The disease spreads through a chicken house more slowlythan either IB or ND. Egg production in laying flocks willusually decrease 10 to 50 %, but will return to normal after3 to 4 weeks.DiagnosisIn a chicken flock, spreading of respiratory distress, withpossible coughing up of blood and mortality is indicative ofILT.Bloody mucus and cheesy exudate can be found in larynx andtrachea. In the laboratory a definite diagnosis can be made byhistological examination of tracheal tissues or virus isolationfrom tracheal mucus in embryonated chicken eggs.Treatment and controlPrevention of ILT by vaccination with mild eye-drop vaccineis by far the best control method. Sometimes such vaccinesare applied by drinking water or spray methods with variablesuccess. Even when an outbreak of ILT has been detected in achicken flock, immediate vaccination is advisable to stop thespread of infection.19Some birds showsymptoms of gaspingwith the head extendedand the beak open
  19. 19. Avian InfluenzaCauseAvian influenza is caused by a myxovirus. There are severalserotypes.TransmissionAirborne virus particles from the respiratory tract, droppings,and people-carrying virus on their clothing and equipment arethe main routes of transmission.Species affectedTurkeys and ducks are mainly affected but chickens, geese,and wild birds can also be infected.Clinical signsClinical signs may vary, depending on the type of influenzavirus. Respiratory disease with mortality in turkeys has beenobserved, but a drop in egg production without clinical signshas also been seen in chickens. Swelling of the head andneck, swollen sinuses with nasal discharge can be seen withrespiratory involvement.Mortality is usually low. Fowl plague, also an avian influenza,is an exception to the rule in that it causes high mortality inturkeys and chickens.20Influenza in turkeys
  20. 20. DiagnosisA laboratory diagnosis is necessary by serological (agar gelprecipitation AGP) or virological methods (virus isolation).Avian influenza can be confused with Newcastle disease,fowl pox, Mycoplasma infection, Staphylococcus, or otherrespiratory or systemic infections.Treatment and controlThere is no treatment for avian influenza. Antibiotics will helpprevent secondary bacterial infections.21AI infected heartand proventriculus
  21. 21. Pneumovirus Infections(Turkey Rhinotracheitis/Swollen HeadSyndrome)CauseThe disease is caused by a pneumovirus.TransmissionThe virus may be transmitted horizontally by contaminatedwater, personnel and equipment as well as from bird to bird.Species affectedTurkeys and chickens.Clinical signs and lesionsIn young turkeys sneezing. Rales and nasal discharge,conjunctivitis, swelling of the infraorbital and submandibularsinuses can be seen.In laying flocks a drop in production may occur along withrespiratory distress. Morbidity is high whereas mortalitymay vary being usually higher in young poults. In chickensthe pneumovirus may be involved in the so called “swollenhead syndrome” (SHS). In such cases affected chickens mayshow swelling of the periorbital and infraorbital sinuses,torticollis, cerebral disorientation and depression. Marked eggproduction losses can be associated with SHS.At necropsy the lesions seen may vary due to othermicroorganisms that may complicate the original picture. Incases of SHS apart from oedema in the head also purulentor caseous subcutaneous exudate can be found. Rhinitis,tracheitis and sinusitis are frequently noted in both chickenand turkeys, hence also the name turkey rhinotracheitis (TRT).Poliserositis affecting the air sacs and pericardium may bedue to secondary infections (E. coli). The kidneys may beswollen and congested as well as the lungs which may show afibrinous exudate in the pleural cavity.22
  22. 22. DiagnosisThe diagnosis based only on clinical signs is difficult toestablish since other agents may be involved. The mostcertain diagnosis may be obtained by the isolation of theorganism from nasal secretions or tissue scraped from thesinus of affected birds. Antibodies can be detected by severalserological methods such as the VN test, IFT and ELISA.Treatment and controlTreatment with antibiotics can be given to control secondarybacterial infections. The use of vaccines should be the bestapproach to control the disease.23Swollen headsyndromeYoung turkeywith conjunctivitisand sinusitis
  23. 23. 24
  24. 24. Neoplastic Diseases • Lympoid Leucosis • Marek’s Disease25
  25. 25. 26
  26. 26. Lymphoid Leucosis(LL, Big Liver Disease, Visceral Leucosis)CauseLymphoid leucosis (LL) is caused by a retro (leuco) virus.TransmissionThe lymphoid leucosis virus appears to be transmittedthrough eggs. However, horizontal transmission at a youngage may occur. Infected breeders can be detected by testinghatching eggs and cloacal swabs for the presence of thevirus. In this manner eradication of lymphoid leucosis willbe possible.Clinical signsVisceral tumors are the main feature of lymphoid leucosis.They can be found in liver, spleen, kidneys, and bursa ofbirds that are in general older than 25 weeks. In affectedlayer flocks a lower egg production can be observed.Osteopetrosis is lymphoid leucosis of the bones of legs andwings which become enlarged, but is quite rare. Affectedbirds have bowed, thickened legs. Lymphoid leucosis canalso occur as blood leucosis. Such erythroid and/or myeloidleucemias are also quite rare.27Lymphoid Leucosis(big liver)Right: normalLeft: affected
  27. 27. Affected birds are listless, pale, and are wasting away.Because of the tumours, LL may be confused with Marek’sdisease, but in LL the nervous system is never involved (noparalysis). LL generally causes birds to weaken, lose weightand eventually die. Histopathological examination is essentialfor a proper diagnosis.“J” VirusRecently, within the known subgroup of exogenous LLviruses (A, B, C and D), a new subgroup denominated “J” hasemerged. The new “J” virus shows tropism for cells of themyelomonocytic series, causing tumors, which are identifiedby histopathology as being myelocytomas. The virus hastropism for meat –type birds. The tumors caused by thisvirus are normally seen from sexual maturity onward andare frequently located on the surface of bones such as thejunction of the ribs, sternum, pelvis, mandible and skull andmay be also found in visceral organs.Treatment and controlNo treatment is known. The best control method is thelaboratory detection of infected breeders. Breeding leucosis-free offspring from leucosis-free breeders can eventually leadto eradication of the disease.28
  28. 28. Marek’s Disease(MD, Neurolymphomatosis)CauseMarek’s disease is caused by a herpes virus.TransmissionMain transmission is by infected premises, where day-oldchicks will become infected by the oral and respiratoryroutes. Dander from feather follicles of MD-infected chickenscan remain infectious for more than a year. Young chicksare particularly susceptible to horizontal transmission.Susceptibility decreases rapidly after the first few days of age.Species affectedThe domestic fowl.Clinical signsInfected birds show weight loss, or may exhibit someform of paralysis. Mortality varies from 5 to 50 % inunvaccinated birds. The classical form (paralysis) with legnerve involvement causes a bird to lie on its side with one legstretched forward and the other backward.When the gizzard nerve is involved, the birds will have a verysmall gizzard and intestines and will waste away.Mortality usually occurs between 10 and 20 weeks of age.29MD leg paralysis
  29. 29. DiagnosisThe presence of tumours in liver, spleen, kidneys, lungs,ovary, muscles, or other tissues is indicative of MD, but theycan also be indicative of lymphoid leucosis. However, nerveinvolvement, either grossly (swelling of leg, wing or othernerves) or microscopically, is typical of MD.Eye involvement can be visible as an irregular constriction ofthe iris (ocular lymphomatosis).Skin involvement (skin leucosis) often consists of tumoursof feather follicles or in between follicles. Skin leucosis is areason for broiler condemnation in certain parts of the world.A proper diagnosis to differentiate MD from LL requireshistological examination.30The paralysis iscaused by lesionsand enlargements ofthe affected nerves.The picture showsan enlargement of asciatic nerve
  30. 30. Treatment and controlVaccination of day-old chicks is an effective mean of control.It has been demonstrated that MD vaccine only prevents theappearance of Marek’s disease tumours and paralysis. It doesnot prevent the birds from becoming infected with MD-virus.It is therefore of major importance to maintain high hygienicand sanitary measures by good management to avoid earlyexposure of young chickens.31Tumors may beobserved in the ovaries.In the acute formvisceral tumours aremost common
  31. 31. 32
  32. 32. Avian Adenoviral Diseases • Inclusion Body Hepatitis (Hydropericardium-Hepatitis Syndrome) • Egg Drop Syndrome 1976 (EDS ’76)33
  33. 33. 34
  34. 34. Inclusion Body Hepatitis(Hydropericardium-Hepatitis Syndrome)CauseThe disease is caused by an avian adenovirus (for examplethe Tipton strain) and is usually simultaneously accompaniedby other immunosuppressive diseases such as infectiousbursal disease or infectious anaemia. There are 12 knownserotypes of avian adenoviruses that may be involved in thedevelopment of this disease.TransmissionEgg transmission is an important factor.Horizontal transmission from bird to bird by contact withdroppings.Once the bird becomes immune, the virus can no longer beisolated from the droppings.Species affectedChickens, turkeys and pheasants and possibly other birds canbe affected by avian adenovirus.Clinical signsChickens with inclusion body hepatitis are affected at usually5 to 7 weeks of age. The birds are listless, with ruffledfeathers. Mortality is usually quite severe, up to 25 % in thefirst 10 days of the disease.Internal lesionsAffected chickens have mottled livers, many with pinpointnecrotic and haemorrhagic spots. Pale bone marrow and, insome cases in presence of infectious anemia, gangrenousdermatitis can be seen. Kidneys are pale and swollen. Thespleen is usually quite small (atrophy).35
  35. 35. If Gumboro disease (infectious bursal disease) has beenpresent in the birds, even if subclinical, the bursa of Fabriciuswill be very small (atrophic). Such chickens are immune-suppressed and usually have more severe cases of inclusionbody hepatitis and/or infectious anaemia.Mature birds do not have clinical signs of adenovirusinfection, they only start showing antibodies in their blood.Hydropericardium-Hepatitis SyndromeHHS was reported for the first time in 1987 in Pakistanand was referred to as “Angara disease”. The disease hasmeanwhile been reported from several other countries,including India and countries in the Middle East and LatinAmerica. Hydropericardium-hepatitis syndrome is causedby a virus belonging to the family of the fowl adenoviruses(FAV). Despite of the diversity in the geographical distributionof the disease, in all areas the infection is caused by a virusbelonging to FAV serotype 4. There are three features whichunderline that this condition is a new disease, differentfrom the known IBH. IBH and hydropericardium accompanythis syndrome. Once outbreaks of HHS occur, it remains aproblem for the poultry industry. And while IBH is shown tobe caused by strains belonging to various FAV serotypes, HHSis, contrary to this, caused by FAV serotype 4. The infectedflocks show high mortality rates and beside the lesionstypical for IBH, a marked hydropericarditis is found in theaffected birds.36
  36. 36. DiagnosisTypical mottled livers with pinpoint lesions, pale bone marrowand kidneys, small spleen and bursa are good indicationsof the disease. In the case of HHS the typical lesion(hydropericardium) is also found. Histological examination(intranuclear inclusion bodies) of liver and/or virus isolationare helpful means of diagnosis.Treatment and controlNo treatment exists. Antibiotics can be used to preventsecondary bacterial infection and possible gangrenousdermatitis.The best method of control is to ensure adequate immunityagainst other immune suppressive diseases (e.g. infectiousbursal disease). Chickens may be vaccinated s.c. duringthe first two weeks of life with an inactivated oil-emulsionvaccine.37Affected chickenshave mottled livers,pale bone marrowand sometimes gang-renous dermatitiscan be seen
  37. 37. Egg Drop Syndrome 1976(EDS ’76)CauseThe disease is caused by an avian adenovirus (strain BC14,virus 127), the EDS virus does not belong to any of the 12fowl adenoviruses.TransmissionThe virus is transmitted through the egg to a few birds in aflock, these birds carry the virus until the flock comes into layat which time they begin to excrete virus and infect birds keptin the same house.Horizontal spread through infected litter can and does occuronce a flock shows the disease but it seems that the virus isnot very infectious or the level of virus excretion is low.Species affectedOnly chickens are susceptible to clinical disease due to EDSvirus; however, the virus is widespread in ducks but does notcause any problems.38Non-peaking effect ofearly EDS ’76 infectionEgg drop byinfection during lay
  38. 38. Clinical signsEDS ’76 affects only layers and breeders at the start of orduring their egg production.Affected flocks show a failure to reach peak egg productionor a drop in egg production accompanied by an inferioreggshell quality and in the case of brown eggs, a loss of shellcolor.Affected birds may also appear to be anaemic, may showa transient diarrhoea and sometimes the food intake maybe reduced. No increased mortality or other symptoms areobserved.Internal lesionsNo specific internal lesions have been observed.DiagnosisClinical signs provide the diagnosis for EDS ’76. Virusisolation and antibody tests can confirm this.39Misformed andsoft shelled eggs
  39. 39. Differential diagnosisInfectious bronchitis and to a lesser extent Newcastle diseaseand infectious laryngotracheitis will have to be considered.Proper diagnostic tests such as the antibody tests willeliminate doubt.Treatment and controlThere is no treatment against egg drop syndrome 1976.Vaccination with an inactivated vaccine before point of lay isthe only available, effective method for the control of EDS ’76.40
  40. 40. Miscellaneous viraldiseases • Fowl Pox • Avian Encephalomyelitis • Infectious Bursal Disease • Reovirus Infectious • Malabsorption Syndrome • Infectious Anaemia41
  41. 41. 42
  42. 42. Fowl Pox(Avian Pox, Avian Diphtheria)CauseFowl pox is caused by a pox virus.TransmissionIntroduction of infected or “carrier” birds in a susceptibleflock will cause an outbreak by direct contact and water orfeed transmission.Mosquitoes and other flying insects can also transmit thevirus from bird to bird and also transmit the disease tonearby flocks. The incubation period varies from 4 to 20days.Species, affectedChickens, turkeys, pheasants and pigeons can be affected bydifferent fowl pox virus strains.Clinical signsThe lesions of fowl pox can be external (mainly on the head)or internal (“wet pox”) in the mouth, oesophagus and/ortrachea, they can also be found on other parts of the body(skin of legs, cloaca etc.). The lesions on the head, combs,and wattles are usually wart-like in appearance, yellow to darkbrown in color. The internal lesions in the mouth, oesophagusand/or trachea are yellow-white and cheesy in appearance.Affected birds will be depressed, lack appetite and when“wet pox” is present they breath laboriously.MortalityMortality is variable, from a low 1 to 2%, when slight headlesions are present, to over 40% when the diphtheritic form(“wet pox”) is more prevalent.Reduced egg production can be observed in laying birds,this will return to normal in a few weeks.43
  43. 43. DiagnosisWart like lesions of the head particularly of the comb andaround the eyes or yellow cheesy lesions of the mucousmembranes of the nasal and buccal cavities are suggestive offowl pox. A definitive diagnosis can be made in a diagnosticallaboratory by histological examination (inclusion bodies) orvirus isolation in embryonated chicken eggs.Treatment and controlIt is difficult to treat affected birds. Treatment of locallesions with disinfectant and/or removal of the diphtheriticmembranes from the throat to improve respiration has beenpractised.Preventive vaccination using a live vaccine is by far the mostsuccesful control method. Even when an outbreak of fowlpox has been diagnosed, it is advisable to vaccinate the flockimmediately to stop further spread of the infection.44Fowl pox lesions on the headand appendages
  44. 44. Avian Encephalomyelitis (AE)or Epedemic TremorCauseAvian encephalomyelitis (AE) is caused by an enterovirusbelonging to the picornavirus group.TransmissionEgg transmission is the major route of transmission of AEvirus. Infected breeders will transmit the AE virus for severalweeks and cause a decrease in egg hatchability. Infectedchicks that hatch will show clinical signs of the disease andspread the infection in the incubator to other newly hatchedsusceptible chicks. Young chicks can also be infected onthe farm. The incubation period varies from 5 to 14 daysdepending on the route of infection.Species affectedPrimarily chickens are susceptible to AE, but turkeys andpheasants have been reported as natural hosts.Clinical signsThe disease is mainly seen in young chicks, between 1and 3 weeks of age. Affected chicks sit on their hocks, donot move well, and many fall on their sides. A fine, rapidtrembling of the head and neck can be seen, but especiallyfelt when affected chicks are held in the hand. In laying andbreeding flocks, AE virus infection causes a marked drop inegg production which returns to normal in about 2 weeks.Mortality in naturally infected chicks varies and can be ashigh as 75%.45
  45. 45. DiagnosisClinical tremors in chicks, together with a drop in productionand hatchability in the parent breeders, is indicative of AEinfection. Chicks will not have gross lesions, but histologicalexamination of brain, proventriculus and pancreas revealstypical lesions of AE. This will also differentiate the diagnosisof AE from encephalomalacia (Vitamin A deficiency, crazychick disease). Laboratory testing of blood serum frombreeder flocks, or their hatching eggs, can determine if aninfection occurred.Treatment and controlPreventive vaccination of breeder pullets with live AEvaccine before egg production is the only effective meansof AE control. If a breeder flock has not been, or has beeninadequately, vaccinated against AE and an outbreak occurs,it is advisable to stop hatching eggs from the flock for severalweeks until the breeders have acquired immunity and nolonger transmit AE virus through their eggs.46AE infected young chickens Effect of AE on egg production
  46. 46. Infectious Bursal Disease(IBD, Gumboro Disease)CauseThe disease is caused by a birna virus of serotype 1. Virusstrains can be divided in classical and variant strains. Thevirus is very stable and is difficult to eradicate from an infectedfarm.TransmissionIBD virus is very infectious and spreads easily from bird tobird by way of droppings. Infected clothing and equipmentare means of transmission between farms.Species affectedChickens and turkeys appear to be natural hosts.Clinical signsClinical IBD occurs usually between 4 and 8 weeks of age.Affected birds are listless and depressed, pale and huddling.Mortality varies. Usually new cases of IBD have a mortalityrate of about 5 to10% but can be as high as 60% dependingon the pathogenicity of the strain involved. In subsequentinfection on the same farm, mortality is lower and eventually,with successive attacks, there is no mortality noted.The subclinical form caused by the immunosuppressiveeffect of the IBD virus is now of more economic importancein that the immune system of the bird is damaged. Gumborodisease related diseases such as inclusion body hepatitis aremore frequent in these birds. Inbroilers this form of the diseaseresults in bad performance withlower weight gains and higherfeed conversion ratios.47Normal (right) and affectedbursa three days post infection
  47. 47. DiagnosisIn acute cases the bursa of Fabricius is enlarged andgelatinous, sometimes even bloody. Muscle haemorrhagesand pale kidneys can be seen. Infection by variant strains isusually accompanied by a fast bursal atrophy (in 24-48 hours)without the typical signs of Gumboro disease. Also in chroniccases the bursa is smaller than normal (atrophy). The bursadestruction is apparent on histologic examination. The lackof white blood cells (lymphocytes) results in a reduction inthe development of immunity and decreased resistance ofthe birds to other infections. Typical signs and lesions arediagnostic of IBD. Histopathological examination, serologyand/or virus isolation are helpful tools. IBD can be confusedwith sulfonamide poisoning, aflatoxicosis, and pale birdsyndrome (Vitamin E deficiency).Treatment and controlNo treatment is available for IBD. Vaccination of parentbreeders and/or young chicks is the best means of control.The induction of a high maternal immunity in the progenyof vaccinated breeders, together with the vaccination of theoffspring is the most effective approach to successful IBDcontrol.48IBD infected chicken(right)
  48. 48. Reovirus InfectionsCauseReovirus infections, also know as viral arthritis/tenosynovitisis caused by an avian reovirus.TransmissionThe virus may be transmitted by droppings from bird to bird.Egg transmission is also a factor when breeder flocks becomeinfected during egg production.Reovirus is a common inhabitant of the intestines of birdsand not all strains are pathogenic.Species affectedChickens, turkeys and possibly pheasants are natural hosts.Clinical signsThe first signs of reovirus infection are usually observed inbroiler breeder chickens between 6 and 10 weeks of age.The birds are reluctant to walk and when forced up have apainful, trembling gait. A distinct swelling of the tendons ofthe shanks and also above the hock joint can be observed.Affected birds have malpositioned feathers, especially on thewings.Internal lesionsThe hock joint may be somewhat swollen, but usually notas severely as with Mycoplasma synoviae or Staphylococcusinfections. Upon opening the legs the tendons usually appeardiscolored, brown or blood-tinged, with straw coloured fluidbetween them.Ruptured tendons may occur and, in older broiler breeders(29-30 weeks old), one may feel a hard scarry knot inthe tendon above the hock joint. When the infection iscomplicated by Ms or Staphylococcus the fluid may appearyellow and creamy. In commercial egg-laying breeds ofchickens, the disease is not as common as in broiler breedersand broilers.49
  49. 49. DiagnosisLeg problems in broilers or broiler breeders associated withswelling of shank tendons or tendons above the hock jointsometimes accompanied by ruptured tendons, are indicativeof reovirus infections.A positive blood test with the agar gel precipitation (AGP) testis of some value as an indication of exposure to reovirus,but does not constitute proof of diagnosis. Histopathologicalexamination of affected tissues and isolation of virus fromsuch tissues are needed for a definite diagnosis.Treatment and controlReovirus infection cannot be treated successfully, butantibodies are of help in preventing secondary bacterialinfections, particularly Staphylococcal infections.Vaccination of broiler breeders with certain live andinactivated vaccines to ensure maternal immunity in theiroffspring appears to be of benefit to the birds themselves.50VA infected birds havemalpositioned feathers Swollen tendons
  50. 50. Malabsorption SyndromeThis complex disease has been reported under various namessuch as helicopter disease, femoral head necrosis, brittlebone disease, infectious proventriculitis, pale bird syndrome,running disease and stunting disease.CauseThe malabsorption syndrome appears to be a diseasecomplex involving avian Reoviruses and other viral andbacterial agents which may affect the digestive systemresulting in nutritional and deficiency signs and lesions.TransmissionOnly circumstantial evidence is present at the momentto indicate that the causal organism(s) may be verticallytransmitted. Horizontal transmission also seems to play a roleon infected sites.Species affectedChickens and possibly turkeys.Clinical signsThe disease is mainly observed in broiler flocks. Manyaffected broiler flocks have a history of diarrhoea, beginningas early as a few days of age and lasting until 10-14 days ofage. Light or dark brown, foamy droppings can be found withundigested food particles. Several affected broilers in a flockmay exhibit malpositioned feathers, especially on the wings.Early rickets with extreme paleness of legs and heads can beobserved.Encephalomalacia is also regularly found. At a later age (5-6weeks) osteoporosis becomes clinically evident, frequentlyunilateral causing the birds to limp. Later an important effectis the delayed growth of the affected birds. Mortality isvariable and in general as low as 4 %.51
  51. 51. DiagnosisThe clinical disease is characterized by one or more of thefollowing lesions: enteritis with watery brown and foamingcontents and the presence of undigested food in theintestine. Mucosal and submucosal proventricular lesions.Pancreatic inflammatory infiltration with degenerativechanges have been found. Osteoporosis and osteomyelitis,femoral head necrosis whereby the bone of the epiphysis ofthe femur is unusually soft.Since the causal agent may differ it is difficult to base adiagnose on virus isolation or serology.Treatment and controlTreatment is impossible, vaccination against reovirus in thebreeders helps to reduce problems in the progency.Strict hygienic and sanitary measures will reduce theincidence of the disease.52
  52. 52. Infectious AnaemiaCauseInfectious anaemia is caused by a very resistant small virusknown as CAV (Chicken Anaemia Virus).TransmissionThe major mode of transmission of infectious anemia isvertical transmission from infected breeder hens. Horizontaltransmission from bird to bird or by infected equipment,clothing, etc. is also possible.Clinical signs and lesionsCAV causes a syndrome in young chicks up to approximately3 weeks of age. Adult birds may get infected but will notdevelop clinical signs. The disease is characterized byincreased mortality and anaemia associated with atrophy ofthe haematopoietic tissues in the bone marrow. Subcutaneousand intramuscular haemorrhages can be found accompaniedwith atrophy of the lymphoid system. Affected birds mayshow focal skin lesions (also known as blue wing disease).Mortality rates vary from 20 % to 70 %.Affected flocks will show poor growth reflected in economiclosses.53A marked difference in size and growth retardation is observedbetween healthy (left) and infected (right) birds.
  53. 53. DiagnosisThe diagnosis can be based on the clinical signs andpathological findings in affected birds. Blood serum testingfor specific CAV antibodies can be carried out (IFT, VN, ELISA).Virus isolation is also possible but it is time-consuming andexpensive.Treatment and controlNo treatment is available for infectious anaemia. Maternallyderived antibodies can offer protection. The induction of highmaternal immunity in the progency by vaccinating breeders isthe best approach to succesful CAV control.54
  54. 54. MiscellaneousBacterial Diseases • Infectious Synovitis • Fowl Cholera • Salmonella Pullorum Disease/ Fowl Typhoid55
  55. 55. 56
  56. 56. Infectious SynovitisCauseThis disease is caused by Mycoplasma synoviae (Ms).TransmissionThe major mode of transmission of Ms is vertical (egg)transmission from Ms-infected breeder hens. Horizontaltransmission from bird to bird and by infected equipment,clothing, shoes, egg boxes and other fomites.Clinical signs and gross lesionsVary from asymptomatic infection to mild respiratory signs,airsacculitis and synovitis, an inflammatory swelling of thejoints of legs and wings and inflammation of the sternalbursa (“breast blisters”).Creamy exudate in joints extending into tendon tissues isindicative.Airsacculitis with frothy to cheesy exudates in the airsacs canbe found, especially if secondary infection with E. coli ispresent.57Swollen hock-joint
  57. 57. DiagnosisBlood serum testing for specific Ms antibodies with Msantigen and the findings of specific lesions are indicativeof Ms infections. Isolation of the causative Ms organisms isdecisive for diagnosis.Differential diagnosisStaphylococcus arthritis can also cause swollen joints witha creamy exudate sometimes extending into the tendonsheaths. Reovirus infection can also cause swelling of jointsand tendon sheaths, but the exudate is more watery or blood-tinged, unless secondary Staphylococcus infections occur.Treatment and controlMs infections can be treated with antibiotics with variabledegrees or success (tetracycline, erythromycin, tylosin,tiamulin). However, control of Ms has been largely successfulby blood testing of breeder chickens and elimination ofpositive Ms reactors.58
  58. 58. Fowl Cholera (Pasteurellosis)CauseFowl cholera is caused by a bacterium: Pasteurella multocida(several serotypes).TransmissionTransmission of fowl cholera is mainly from bird to bird bywater or feed contamination. Rodents (rats and mice) alsoappear to play a role in contamination of water and feed withPasteurella multocida.Species affectedChickens, turkeys, game birds and other bird species aresusceptible.Clinical signsAffected birds are depressed and have decreased appetite.Egg production will drop 5-15 % and mortality will be highin acute fowl cholera. Birds that die from acute fowl cholerafrequently have bluish combs and wattles.Chronic fowl cholera will not cause high mortality, althoughthere will be an increase in deaths. Swollen wattles is afeature of chronic fowl cholera.59Fowl cholera
  59. 59. Internal lesionsGross lesions in acute cases are mainly internal haemorrhageand congestion of liver, spleen and kidneys. In chronic fowlcholera cheesy exudates can be found between the intestines,and on liver and heart.Treatment and controlTreatment with appropriate antibiotics or chemotherapeuticscan be successful in halting mortality and restoringegg production. However chronic carrier birds have beenfound in flocks of chickens after treatment. If clinical fowlcholera with mortality reappears in such flocks, one musttreat again. Rodent control is also very important to preventreintroduction of the infection. Vaccines, both inactivatedbacterins as well as live vaccines are available.60
  60. 60. Pullorum Disease and FowlTyphoidCausePullorum disease is caused by a bacterium, Salmonellapullorum. Fowl typhoid is caused by Salmonella gallinarum,which is related to, but not identical to, S. pullorum.TransmissionPullorum can be transmitted by infected (carrier) breeder hensthrough their eggs. Chicks that hatch from such infectedeggs will have typical pullorum disease (white diarrhoea) andhigh mortality. Infected chicks can also infect other chicks viadroppings.Fowl typhoid is more a disease of adult chickens, with highmortality and morbidity. Horizontal transmission is importantwith fowl typhoid through infected droppings, dead birdcarcasses, and infected clothing, shoes, utensils and otherfomites.Species affectedChickens, pheasants, ducks, geese and guinea fowl cancontract both pullorum and fowl typhoid.Clinical signsPullorum in chicks causes typical white bacillary diarrhoea,with pasted cloacas and high mortality. Infected adultbreeders do not have clinical signs of the disease but haveinternal lesions in the ovary (miss-shaped, dark colouredfollicles).Fowl typhoid in adult chickens causes listlessness andsulfurcoloured diarrhoea. The birds have generalized infectionwith swollen livers, spleens, and kidneys and haemorrhagesin such tissues. Mortality is usually high: 25 to 60 %.61
  61. 61. Treatment and controlTreatment of pullorum disease will not bring about a cure andis undesirable from a standpoint of eradication. It is far morepractical to control the disease by elimination of infectedcarrier breeder hens.Blood testing of breeder chickens by the serum plate ortube agglutination test with suitable S. pullorum antigen willdetect infected carrier birds which can then be culled. Suchcontrol measures will stop the incidence of egg-transmittedpullorum disease. If hatching eggs from tested pullorum-freebreeders are kept free from contamination through infectedeggs from infected breeders or through contaminatedequipment, chickens can remain after treatment. The bestcontrol method is eradication of infected birds. Breeder flocksshould be blood tested with antigen for typhoid. The typhoidcarriers can then be eliminated.Vaccination for fowl typhoid with a special S. gallinarum (9Rstrain) has been practiced in several countries, but it shouldbe discouraged in breeders when an eradication programmeis in operation.62S. pullorum infected internal organs
  62. 62. Ornithobacteriumrhinotracheale (OR) InfectionCauseOrnithobacterium rhinotracheale is a gram-negative rodresponsible for causing infections in chickens and turkeys ofall ages.TransmissionHorizontal transmission from bird to bird and by infectedfomites. Infected breeder hens may transmit the diseaseagent vertically to their offspring.Clinical signs and gross lesions:OR may cause a respiratory disease in turkeys, usuallybetween 2-6 and 12-20 weeks of age. The birds may showrespiratory disease with watery eyes and swelling of thesinus infraorbitalis. Broilers may also show respiratory signsafter infection at around 4 weeks of age. A severe purulentpneumonia, accompanied by airsacculitis and pericarditis maybe found in broilers as well as in turkeys. Affected birds alsoshow growth retardation. Concomitant viral infections mayintensify the severity of the lesions.63Pneumonic lungscaused by OR infection
  63. 63. DiagnosisBlood serum testing using a commercially available ELISAfor the detection of specific antibodies against OR and thefinding of specific lesions are indicative of OR infection.Isolation of the organism and its biochemical determinationmay be attempted but care should be taken that these arecarried out using appropriate methods in order to avoidunreliable results. Differential diagnose with bacteria causingsimilar disease patterns is recommended (E. coli, P. multocida,MG).Treatment and controlOR infections may be treated with broad -spectrum antibioticswith variable degrees of success. An inactivated vaccine forbroiler breeders and turkey poults is available.64
  64. 64. Infectious viral diseasesof ducks • Duck Hepatitis • Duck Plague65
  65. 65. 66
  66. 66. Duck Virus HepatitisCauseDuck virus hepatitis is caused by a picornavirus. It is possiblethat there are more serotypes.TransmissionThe disease can spread rapidly to all susceptible ducklings inthe flock via faeces. The incubation period varies from around24 hours to a few days.Species affectedDucklings under 6 weeks of age are susceptible.Clinical signsThe disease has a very short course, with all affected birdsdying within a few days.Signs, if seen at all, may include somnolence and convulsions,followed by quick death. Mortality up to 95 %.Internal lesionsPrincipal lesions found in the liver, showing fattydegeneration, yellowish and with many small or biggerhaemorrhages.67Signs may includesomnolence andconvusions, followedby quick death
  67. 67. DiagnosisSudden death in small ducklings is highly suggestive. Virusisolation can confirm this diagnosis.Treatment and controlSerum therapy is possible.Strict isolation during the first 4-5 weeks can preventinfection. Ducklings can be protected by maternal antibodies.To provide for this, parent stock has to be vaccinated,preferably twice.This will protect the progeny for two weeks, and mitigateinfection afterwards.Ducks without maternal antibodies should be vaccinated atday old.68Principal lesions found in the liver, showing fatty degeneration,yellowish and with many small or bigger haemorrhages.
  68. 68. Duck Plague(Duck Virus Enteritis)CauseDuck plague is caused by a herpes virus. Only one serotype isknown. There is a difference in virulence between strains.TransmissionDuck plague virus is excreted by affected birds throughfaeces and other body discharges. Via soiled drinking water,contaminated pound water or open water other birds areinfected.Species affectedDucks, geese and swans, of all ages.Clinical signsHigh mortality up to 100 %, sometimes sudden death. Droppyappearance, slow movements with hanging wings. Birds showbloody nasal discharges and conjunctivitis, diarrhoea andthey may make a hoarse noise. The birds are very thirsty.Birds often die in a rather characteristic position, with theneck twisted downwards, sidewards or backwards.In laying flocks egg production may drop 50 % or more.69During the diseasevascular damage,tissue haemorrhages,digestive mucosaleruptions, lesionsof lymphoid organsas well as degene-rative changes inparenchymatousorgans can occur.
  69. 69. Internal lesionsHaemorrhagic enteritis, haemorrhagic or pseudo-membranicpharingitis, oesophagitis and cloacitis, haemorrhagic ovaritis.DiagnosisThe gross lesions are rather characteristic for duck plague.Virus isolation and neutralization confirm the diagnosisto distinguish the disease from avian cholera (Pasteurellamultocida) or duck hepatitis.Treatment and controlThere is no treatment known. Prevention should includeclean drinking water and keeping wild, free-flying waterfowlaway. Vaccination with adapted strains can provide a reliableprotection. Even in an infected flock emergency vaccinationcan limit the damage, due to an interference phenomenonbetween the vaccine virus and the field virus.70
  70. 70. Parasitic Diseases • Coccidiosis • Endoparasites • Blackhead71
  71. 71. 72
  72. 72. CoccidiosisCauseCoccidiosis is caused by protozoa, unicellular parasites. Inchickens there are 9 different species of coccidia of whichthe main 5 are Eimeria acervulina, Eimeria necatrix, Eimeriatenella, Eimeria maxima and Eimeria brunetti.TransmissionInfected droppings, containing oocysts of coccidia are themain means of transmission, between birds. The incubationperiod is 4 to 6 days.Species affectedChickens have their own specific coccidiosis types which donot cross-infect other bird species.73Eimeria tenella
  73. 73. Clinical signs/DiagnosisCoccidiosis can be divided into 2 groups:The caecum is involved (Caecal coccidiosis).Mainly caused by E. tenella in chickens up to 12 weeks.Mortality may run as high as 50 %. Infected birds are listless,have bloody droppings, a pale comb and show a lack ofappetite. Laboratory examination will show haemorrhages inthe caecal wall. After severe bleeding a core will be formed inthe lumen.The small intestine is involved (small intestinal coccidiosis).Caused by E. acervulina, E. brunetti, E. maxima, E. necatrix.E. acervulinaMay affect birds of any age.E. acervulina is not normally very pathogenic, but in somecases considerable mortality may be seen.Birds infected show loss of weight, combs may be shriveledand a drop or even cessation of egg production in layers maybe seen.At necropsy, haemorrhagic lesions of E. acervulina are seenthroughout the upper portion of the affected intestine andalso grey or whitish patches may be present.74
  74. 74. E. brunettiMay affect birds of any age.E. brunetti is definitely pathogenic, in severe infectionsmortality can be high. Birds infected show emaciation anddiarrhoea.At necropsy a white cheese-like material is found in thelumen of the lower intestine and rectum.The caeca and cloaca are inflamed. The gut wall is thickened.E. maximaMay affect birds of any age.E. maxima is less pathogenic than E. acervulina, necatrix andbrunetti, mortality is generally low.Diarrhoea, loss of weight and a drop in egg production oflayers, will be seen; bloody droppings are common.At necropsy the lower portion of the small intestine is dilatedand the wall is thickened; the gut is filled with thick mucus,grayish, brownish or pinkish in color.75
  75. 75. E. necratixMainly in chickens up to 4 months of age.E. necratrix is very pathogenic. Infection with E. necratrixmay result in a two stage clinical outbreak of coccidiosis.In the acute stage mortality may be high in the first weekafter infection.In the chronic stage blood may be seen in the droppings,the birds are listless and lose weight. In layers a drop in eggproduction will be observed. At necropsy the middle portionof the intestine is affected, haemorrhage will be seen. Theunopened intestine looks spotty, white areas (schizonts)intermingled with bright or dull red spots (haemorrhages)will be observed.76Eimeria nectarix
  76. 76. Treatment and controlThis heading is most appropriate in the case of coccidiosis asthere is no disease group in poultry where both control andtreatment are employed more.The well established principles of good management andhusbandry are of basic importance.It is common practice to include low levels ofchemotherapeutics in the feed of birds. These chemicals arereferred to as coccidiostats and as such keep in check thedevelopment of the parasites so that a pathological situationdoes not develop. It should, however, be taken into accountthat coccidia can develop a resistance to all chemicals so farused for this purpose and for this reason it is necessary tochange from one chemical to another periodically. Treatmentof infected flocks may be carried out by the administrationof coccidiostats at a higher therapeutic level to theaffected birds. There are certain products available whichare specifically designed for treatment and which are notsatisfactory for prevention. These chemicals are sometimesreferred to as coccidiocidal agents.Whenever administering these products, particular attentionshould be paid to the dosage recommendation of themanufacturer.77
  77. 77. EndoparasitesWorms living in the intestines of chickens fall mainly into fourcategories.Roundworms (Ascarids), usually 5 to 7 cm (2-3 inches) long.Hairworms (Capillaria), only measure 1-1.5 cm long.Caecal worms (Heterakis), usually 1.5 cm long.Tape worms, usually 7 to 10 cm long, consisting of manysmall segments.78TapewormsVaccination toprevent coccidiosidis also possibleHairwormsRoundworms
  78. 78. Clinical signsMature roundworms are not a major cause of the disease, butthe larvae can damage the intestinal lining, causing enteritis,anaemia, decreased egg production and at times eggs withpale yolks.Capillaria cause more damage to the intestinal lining and cancause enteritis and anaemia with decreased egg productionand the appearance of pale egg yolks (“platinum yolks”).Caecal worms are found in the caeca and do not causeserious damage, except that their eggs can transmitblackhead – mainly in turkeys (see blackhead, page 80).Tape worms are infrequently found and do not causeserious damage, except that they use the nutrients of thehostchicken.DiagnosisExamination of the intestinal contents will reveal roundworms,caecal worms, and tape worms without difficulty.Capillaria can usually be found when intestinal contents arewashed through a fine mesh sieve.Treatment and controlRoundworms and caecal worm infections can be treated withpiperazine. Piperazine is not effective against tape worms andcapillaria for which other anthelmintics are required.79
  79. 79. Blackhead(Histomoniasis, Enterohepatitis)CauseA protozoan parasite, Histomonas meleagridis.TransmissionDirect transmission by infected water, feed, or droppings hasbeen proved.Indirect transmission by infected eggs of the caecal worm.Heterakis gallinarum, is also a major factor. Raising turkeysand chickens on wire and indoors decreases the incidence ofblackhead.Species affectedChickens, turkeys, and peafowl are natural hosts to blackheadinfection.Clinical signsAffected birds are depressed, stand or sit with ruffledfeathers, and have yellowish diarrhoea. Darkening of headparts, especially in turkeys, gave the name to the disease(blackhead). Gross lesions include circular necrotic areas inlivers with a crater-like center and cheesy cores in the caeca.Blackhead can cause high mortality, particularly in youngturkey poults, but the disease can also affect older birds. Inchickens the mortality from blackhead infection is usuallylower, young chickens being the most susceptible.80
  80. 80. Treatment and controlTreatment with protozoan chemotherapeutics is usuallyeffective. Such drugs can also be given at preventive levelsin turkeys starter and grower feed. Growing turkeys on wireand indoors can reduce the incidence of blackhead to a largeextent, but even so, strict hygiene and elimination of caecalworms are important control measures.81Necrotic liver infectedby Histomonasmeleagridis
  81. 81. 82
  82. 82. Some importantvitamin deficiencydiseases • Riboflavin • Vitamin E • Vitamin D383
  83. 83. 84
  84. 84. Riboflavin (Vitamin B2)Deficiency (Curly Toe Disease)Clinical signsYoung chicks, as early as 1-week-old, exhibit curling of thetoes, inability to walk and sometimes diarrhoea.Treatment and controlAdministering vitamin B preparations brings a rapid cure.Only in advanced cases will birds be dehydrated andemaciated, requiring further treatment.It is important to ensure adequate vitamin B levels not onlyin starter and grower diets, but also in the diet of parentbreeders.85Curly toe caused byriboflavin deficiency
  85. 85. Vitamin E Deficiency(Crazy Chick Disease, Encephalomalacia)Clinical signs and gross lesionsVitamin E deficiency in chickens affects the brain, causingdegeneration, oedema and haemorrhage, especially in thesmall brain (cerebellum).Affected young chicks appear unable to walk, they fall ontheir sides or stand with their heads between their legs.The cerebellum shows gross swelling, with yellow or browndiscoloration and pinpoint haemorrhages may be observed.Encephalomalacia can also be found in mature chickens.Treatment and controlAdequate levels of vitamin E and selenium in the diet ofchickens and their parent breeders is of prime importance.Treatment of affected birds with vitamin E preparations(alpha-tocopherol) is effective if the condition is not too faradvanced.86Brain lesionscaused by vitamin Edeficiency
  86. 86. Vitamin D3 Deficiency(Rickets, “Rubber Legs”)Clinical signs and gross lesionsYoung chickens, 2 to 5 weeks of age, with vitamin D3deficiency are unable to stand and have very soft, pliable,legs and beaks. The rib joints are swollen like beads andcurved inward, the breastbone often twisted.In layer chickens, vitamin D3 deficiency causes soft-shelledeggs and a drop in production.Treatment and controlVitamin D3 can be given as treatment, usually in combinationwith calcium and phosphorus.87Rubber legs
  87. 87. NopartofthisbrochuremaybereproducedinanyformwithoutwrittenpermissionfromIntervetInternational.Intervet/Schering-Plough Animal Health91-105 Harpin Street, Bendigo East VIC 3550Free Call: 1800 033 461 • Free Fax: 1800 817 •