Important poultry diseases 060058 cpc website


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Important poultry diseases 060058 cpc website

  1. 1. ImportantPoultryDiseasesImportantPoultryDiseasesResearch makes the difference060058©2009,IntervetInternationalbv,TheNetherlands.
  2. 2. IMPORTANT POULTRY DISEASESContentsForeword 3Infectious respiratory DiseasesChronic 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 631
  3. 3. Infectious Viral Diseases of ducksDuck Virus Hepatitis 67Duck Plague 69Parasitic DiseasesCoccidiosis 73Endoparasites 78Blackhead 80Deficiency DiseasesRiboflavin 85Vitamin E 86Vitamin D3 872
  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 info@intervet.comwww.intervet.com3
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  6. 6. INFECTIOUS RESPIRATORYDISEASES• Chronic Respiratory Disease (CRD)• Coryza• Aspergillosis• Newcastle Disease (ND)• Infectious Bronchitis (IB)• Infectious Laryngotracheitis (ILT)• Avian Influenza• Turkey Rhinotracheitis/SwollenHead Syndrome5
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  8. 8. Chronic respiratory Disease(CRD) (Airsacculitis)CauseThe underlying cause of CRD is Mycoplasma gallisepticum(Mg). The condition is frequently triggered by respiratory viru-ses such as ND and IB and subsequently complicated by bac-terial invasion. The main agents involved in the infection areMycoplasma 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 organism throughthe egg to their offspring. In addition, infection can occur bycontact or by airborne dust or droplets. The incubationperiod varies from 4 days to 3 weeks.Species affectedChickens and turkeys.7Airsacculitis
  9. 9. Clinical signsYoung chickens (broiler chicks or layer pullets) will showrespiratory distress. The birds frequently show a lack ofappetite, decreased weight gain and increased feed conver-sion 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 egg pro-duction in breeders and layers. In this way the overall econo-mic loss can be very great in broilers but less dramatic inbreeders 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 testing ofchickens, post-mortem examination and ultimately byisolating the causative Mg organism from tracheas or airsacsof affected birds.8
  10. 10. 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 be ofeconomic value. However, control by medication or vaccina-tion and eradication of Mg infections has been by far themost effective method of combating the disease. Fertile eggsfrom infected birds can be treated with antibiotics such astylosin to eliminate the Mycoplasma gallisepticum organisms.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.9Pericarditis, peritonitis andperihepatitis is frequently observedin birds with CRD
  11. 11. Infectious CoryzaCauseThe bacterium causing this disease is Hemophilus paragalli-narum.TransmissionThe disease spreads from bird to bird and flock to flock bycontact 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
  12. 12. 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
  13. 13. 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
  14. 14. 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 chicksshould be removed and destroyed. Strict hygiene in breederand hatchery management is necessary. Choice of littermaterial is important so that no spore-bearing wood shavingsare used.13Gross lesionsof the lungs
  15. 15. Newcastle Disease (ND)CauseNewcastle disease is caused by a paramyxovirus. Only oneserotype of ND is known. ND virus has mild strains (lentoge-nic), medium strength strains (mesogenic), and virulentstrains (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 (torticol-lis) are the main signs. Egg production will decrease 30 to 50% or more, returning to normal levels in about 2 weeks. Eggsmay have thin shells and eggs without shells may also befound. In well-vaccinated chicken flocks clinical signs may bedifficult to find.14
  16. 16. 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
  17. 17. 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 IBin chickens
  18. 18. 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 theflock.b. Isolation of the virus in the laboratory.c. A rising antibody titre when the serum is tested againsta 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
  19. 19. 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 caseous exu-date in larynx and trachea. When a caseous plug occludes thelarynx 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.18Haemorrhagiclesions in trachea
  20. 20. 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, with pos-sible coughing up of blood and mortality is indicative of ILT.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 vaccine isby far the best control method. Sometimes such vaccines areapplied 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
  21. 21. 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 equipmentare the 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
  22. 22. 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
  23. 23. 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, con-junctivitis, 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 mortality mayvary being usually higher in young poults. In chickens thepneumovirus may be involved in the so called “swollen headsyndrome” (SHS). In such cases affected chickens may showswelling of the periorbital and infraorbital sinuses, torticollis,cerebral disorientation and depression. Marked egg produc-tion losses can be associated with SHS.At necropsy the lesions seen may vary due to other microor-ganisms that may complicate the original picture. In cases ofSHS apart from oedema in the head also purulent or caseoussubcutaneous exudate can be found. Rhinitis, tracheitis andsinusitis are frequently noted in both chicken and 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
  24. 24. 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
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  26. 26. NEOPLASTIC DISEASES• Lympoid Leucosis• Marek’s Disease25
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  28. 28. 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 can alsooccur as blood leucosis. Such erythroid and/or myeloidleucemias are also quite rare.27Lymphoid Leucosis(big liver)Right: normalLeft: affected
  29. 29. 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 LL viruses(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 this virusare normally seen from sexual maturity onward and arefrequently located on the surface of bones such as the junc-tion of the ribs, sternum, pelvis, mandible and skull and maybe 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
  30. 30. 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 chicks areparticularly 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 some formof paralysis. Mortality varies from 5 to 50 % in unvaccinatedbirds. The classical form (paralysis) with leg nerve involve-ment causes a bird to lie on its side with one leg stretchedforward 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
  31. 31. 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 tumours offeather 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
  32. 32. 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
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  34. 34. AVIAN ADENOVIRAL DISEASES• Inclusion Body Hepatitis(Hydropericardium-HepatitisSyndrome)• Egg Drop Syndrome 1976(EDS ’76)33
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  36. 36. 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 ruffled feat-hers. Mortality is usually quite severe, up to 25 % in the first10 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
  37. 37. 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 Pakistan andwas referred to as “Angara disease”. The disease has mean-while been reported from several other countries, includingIndia and countries in the Middle East and Latin America.Hydropericardium-hepatitis syndrome is caused by a virusbelonging to the family of the fowl adenoviruses (FAV).Despite of the diversity in the geographical distribution of thedisease, in all areas the infection is caused by a virus belon-ging to FAV serotype 4. There are three features which under-line that this condition is a new disease, different from theknown IBH. IBH and hydropericardium accompany this syndro-me. Once outbreaks of HHS occur, it remains a problem forthe poultry industry. And while IBH is shown to be caused bystrains belonging to various FAV serotypes, HHS is, contraryto this, caused by FAV serotype 4. The infected flocks showhigh mortality rates and beside the lesions typical for IBH, amarked hydropericarditis is found in the affected birds.36
  38. 38. DiagnosisTypical mottled livers with pinpoint lesions, pale bone marrowand kidneys, small spleen and bursa are good indications ofthe disease. In the case of HHS the typical lesion (hydroperi-cardium) is also found. Histological examination (intranuclearinclusion bodies) of liver and/or virus isolation are helpfulmeans 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. during thefirst two weeks of life with an inactivated oil-emulsionvaccine.37Affected chickenshave mottled livers,pale bone marrowand sometimes gang-renous dermatitiscan be seen
  39. 39. 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 birdskept in 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
  40. 40. 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 show atransient diarrhoea and sometimes the food intake may bereduced. No increased mortality or other symptoms areobserved.Internal lesionsNo specific internal lesions have been observed.DiagnosisClinical signs provide the diagnosis for EDS ’76. Virus isola-tion and antibody tests can confirm this.39Misformed andsoft shelled eggs
  41. 41. 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 will elimi-nate 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
  42. 42. MISCELLANEOUS VIRALDISEASES• Fowl Pox• Avian Encephalomyelitis• Infectious Bursal Disease• Reovirus Infectious• Malabsorption Syndrome• Infectious Anaemia41
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  44. 44. 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 to near-by flocks. The incubation period varies from 4 to 20 days.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
  45. 45. 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 fowl poxhas been diagnosed, it is advisable to vaccinate the flockimmediately to stop further spread of the infection.44Fowl pox lesions on the headand appendages
  46. 46. 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 on thefarm. The incubation period varies from 5 to 14 days depen-ding 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 1 and 3weeks of age. Affected chicks sit on their hocks, do not movewell, and many fall on their sides. A fine, rapid trembling ofthe head and neck can be seen, but especially felt when affec-ted chicks are held in the hand. In laying and breeding flocks,AE virus infection causes a marked drop in egg productionwhich returns to normal in about 2 weeks. Mortality innaturally infected chicks varies and can be as high as 75%.45
  47. 47. 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 AE vaccinebefore egg production is the only effective means of AEcontrol. If a breeder flock has not been, or has been inade-quately, vaccinated against AE and an outbreak occurs, it isadvisable 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
  48. 48. 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 immunosuppressive effectof the IBD virus is now of more economic importance in thatthe immune system of the bird is damaged. Gumboro diseaserelated diseases such as inclusion body hepatitis are morefrequent in these birds. In broilers this form of the diseaseresults in bad performance withlower weight gains and higherfeed conversion ratios.47Normal (right) and affectedbursa three days post infection
  49. 49. DiagnosisIn acute cases the bursa of Fabricius is enlarged and gelati-nous, sometimes even bloody. Muscle haemorrhages and palekidneys can be seen. Infection by variant strains is usuallyaccompanied by a fast bursal atrophy (in 24-48 hours) wit-hout 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 of thebirds 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)
  50. 50. 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. Thebirds are reluctant to walk and when forced up have a painful,trembling gait. A distinct swelling of the tendons of theshanks 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 not asseverely 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 in the ten-don above the hock joint. When the infection is complicatedby Ms or Staphylococcus the fluid may appear yellow and cre-amy. In commercial egg-laying breeds of chickens, the disea-se is not as common as in broiler breeders and broilers.49
  51. 51. 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, but antibo-dies are of help in preventing secondary bacterial infections,particularly Staphylococcal infections.Vaccination of broiler breeders with certain live and inactiva-ted vaccines to ensure maternal immunity in their offspringappears to be of benefit to the birds themselves.50VA infected birds havemalpositioned feathers Swollen tendons
  52. 52. 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 disease com-plex involving avian Reoviruses and other viral and bacterialagents which may affect the digestive system resulting innutritional and deficiency signs and lesions.TransmissionOnly circumstantial evidence is present at the moment toindicate that the causal organism(s) may be vertically trans-mitted. Horizontal transmission also seems to play a role oninfected sites.Species affectedChickens and possibly turkeys.Clinical signsThe disease is mainly observed in broiler flocks. Many affec-ted broiler flocks have a history of diarrhoea, beginning asearly as a few days of age and lasting until 10-14 days of age.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 is varia-ble and in general as low as 4 %.51
  53. 53. 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 the intesti-ne. 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 the inciden-ce of the disease.52
  54. 54. Infectious AnaemiaCauseInfectious anaemia is caused by a very resistant small virusknown as CAV (Chicken Anaemia Virus).TransmissionThe major mode of transmission of infectious anemia is verti-cal 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 by incre-ased mortality and anaemia associated with atrophy of thehaematopoietic 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.
  55. 55. 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
  56. 56. MISCELLANEOUSBACTERIAL DISEASES• Infectious Synovitis• Fowl Cholera• Salmonella Pullorum Disease/Fowl Typhoid55
  57. 57. 56
  58. 58. Infectious SynovitisCauseThis disease is caused by Mycoplasma synoviae (Ms).TransmissionThe major mode of transmission of Ms is vertical (egg) trans-mission from Ms-infected breeder hens. Horizontal transmis-sion 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
  59. 59. DiagnosisBlood serum testing for specific Ms antibodies with Ms anti-gen and the findings of specific lesions are indicative of Msinfections. Isolation of the causative Ms organisms is decisivefor diagnosis.Differential diagnosisStaphylococcus arthritis can also cause swollen joints with acreamy exudate sometimes extending into the tendon she-aths. Reovirus infection can also cause swelling of joints andtendon 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, tiamu-lin). However, control of Ms has been largely successful byblood testing of breeder chickens and elimination of positiveMs reactors.58
  60. 60. 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 high inacute 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
  61. 61. 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 restoring eggproduction. However chronic carrier birds have been found inflocks of chickens after treatment. If clinical fowl cholera withmortality reappears in such flocks, one must treat again.Rodent control is also very important to prevent reintroduc-tion of the infection. Vaccines, both inactivated bacterins aswell as live vaccines are available.60
  62. 62. 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) breederhens through their eggs. Chicks that hatch from such infec-ted eggs will have typical pullorum disease (white diarrhoea)and high mortality. Infected chicks can also infect otherchicks via droppings.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 can con-tract both pullorum and fowl typhoid.Clinical signsPullorum in chicks causes typical white bacillary diarrhoea,with pasted cloacas and high mortality. Infected adult bree-ders do not have clinical signs of the disease but have intern-al lesions in the ovary (miss-shaped, dark coloured follicles).Fowl typhoid in adult chickens causes listlessness and sulfur-coloured diarrhoea. The birds have generalized infection withswollen livers, spleens, and kidneys and haemorrhages insuch tissues. Mortality is usually high: 25 to 60 %.61
  63. 63. 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 or tubeagglutination test with suitable S. pullorum antigen will detectinfected carrier birds which can then be culled. Such controlmeasures will stop the incidence of egg-transmitted pullorumdisease. If hatching eggs from tested pullorum-free breedersare kept free from contamination through infected eggs frominfected breeders or through contaminated equipment, chic-kens can remain after treatment. The best control method iseradication of infected birds. Breeder flocks should be bloodtested with antigen for typhoid. The typhoid carriers can thenbe 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
  64. 64. 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 the sinusinfraorbitalis. Broilers may also show respiratory signs afterinfection at around 4 weeks of age. A severe purulent pneu-monia, accompanied by airsacculitis and pericarditis may befound 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
  65. 65. 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
  66. 66. INFECTIOUS VIRAL DISEASESOF DUCKS• Duck Hepatitis• Duck Plague65
  67. 67. 66
  68. 68. 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 convul-sions, followed by quick death. Mortality up to 95 %.Internal lesionsPrincipal lesions found in the liver, showing fatty degenera-tion, yellowish and with many small or bigger haemorrhages.67Signs may includesomnolence andconvusions, followedby quick death
  69. 69. 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 prevent infec-tion. Ducklings can be protected by maternal antibodies. Toprovide for this, parent stock has to be vaccinated, preferablytwice.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.
  70. 70. 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, lesions oflymphoid organs aswell as degenerativechanges inparenchymatousorgans can occur.
  71. 71. 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 diagnosis todistinguish the disease from avian cholera (Pasteurellamultocida) or duck hepatitis.Treatment and controlThere is no treatment known. Prevention should include cleandrinking water and keeping wild, free-flying waterfowl away.Vaccination with adapted strains can provide a reliable protec-tion. Even in an infected flock emergency vaccination canlimit the damage, due to an interference phenomenonbetween the vaccine virus and the field virus.70
  72. 72. PARASITIC DISEASES• Coccidiosis• Endoparasites• Blackhead71
  73. 73. 72
  74. 74. CoccidiosisCauseCoccidiosis is caused by protozoa, unicellular parasites. Inchickens there are 9 different species of coccidia of which themain 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
  75. 75. 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
  76. 76. 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
  77. 77. 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
  78. 78. 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 of chemotherapeu-tics in the feed of birds. These chemicals are referred to ascoccidiostats and as such keep in check the development ofthe parasites so that a pathological situation does not deve-lop. It should, however, be taken into account that coccidiacan develop a resistance to all chemicals so far used for thispurpose and for this reason it is necessary to change fromone chemical to another periodically. Treatment of infectedflocks may be carried out by the administration of coccidio-stats at a higher therapeutic level to the affected birds. Thereare certain products available which are specifically designedfor treatment and which are not satisfactory for prevention.These chemicals are sometimes referred to as coccidiocidalagents.Whenever administering these products, particular attentionshould be paid to the dosage recommendation of the manu-facturer.77
  79. 79. 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
  80. 80. 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 transmit black-head – 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 round-worms, 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
  81. 81. 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 ruffled feat-hers, and have yellowish diarrhoea. Darkening of head parts,especially in turkeys, gave the name to the disease (black-head). Gross lesions include circular necrotic areas in liverswith 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
  82. 82. Treatment and controlTreatment with protozoan chemotherapeutics is usuallyeffective. Such drugs can also be given at preventive levels inturkeys starter and grower feed. Growing turkeys on wire andindoors 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
  83. 83. 82
  84. 84. SOME IMPORTANTVITAMIN DEFICIENCYDISEASES• Riboflavin• Vitamin E• Vitamin D383
  85. 85. 84
  86. 86. 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
  87. 87. 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
  88. 88. Vitamin D3 Deficiency(Rickets, “Rubber Legs”)Clinical signs and gross lesionsYoung chickens, 2 to 5 weeks of age, with vitamin D3 defi-ciency are unable to stand and have very soft, pliable, legsand beaks. The rib joints are swollen like beads and curvedinward, 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