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Avian pharmacology Dr Fares El-Khayat
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محاضرة اليوم الثالث د احمد البستاوي

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محاضرة اليوم الثالث د احمد البستاوي

  1. 1. AVIAN VIRAL AND BACTERIAL RESPIRATORY DISEASES Presented By Dr. Ahmed Ragab El-Bestawy BVs, MVs & Ph.D. Lecturer of Poultry Diseases Fac. Vet. Med., Damnhour Univ.
  2. 2. Diseases causing Resp signs: o Viral: AI, ND, IB,ILT, TRT, Adeno, Reo, Pox wet form and MD ( non specific) o Bacterial: IC, MG, Ecoli, FC, ORT and Chlamydia. o Fungal: Asperigellosis. o Parasitic: Syngamus trachea, Cryptosporidium o Nutritional: Vit A ↓. o Miscellaneous: Chilling and Ammonia
  3. 3. ‫إصاتح‬E.coli ‫ثاَىَح‬ ‫كإصاتح‬
  4. 4. Influenza Virus  Family Orthomyxoviridae  Three main types  Type A  Multiple species  Type B  Humans  Type C  Humans and swine
  5. 5. Influenza A  Multiple species  Humans  Avian Influenza  Most virulent group  Classification by surface antigens into subtypes  Hemagglutinin (H or HA)  Neuraminidase (N or NA)
  6. 6. Surface Antigens and Subtypes  18 HA and 11 NA for influenza A  Hemagglutinin (HA)  Function: Sites for attachment to infect host cells  Neuraminidase (NA)  Function: Remove neuraminic acid from mucin and release from cell
  7. 7. Influenza A
  8. 8. Avian Influenza  Pathogenicity based on genetic features and/or severity of disease in poultry  Low pathogenic AI (LPAI)  H1 to H18 subtypes  Highly pathogenic AI (HPAI)  Some H5 or H7 subtypes  LPAI H5 or H7 subtypes can mutate into HPAI
  9. 9. H9N2 infection
  10. 10. H9 subtype viruses generally exist as low pathogenicity influenza viruses causing mild to moderate disease. However, they have been associated with severe morbidity and mortality in poultry as a result of co-infection with other pathogens. The first H9N2 influenza virus was isolated from turkeys in Wisconsin in 1966. H9N2 subtype influenza viruses were isolated from pigs in Hong Kong in 1998 and subsequently from two sick children in 1999; six additional human infections were reported from China
  11. 11. Recent studies have shown that H9N2 viruses may have contributed to the genetic and geographic diversity of H5N1 viruses. During the last two decades, antigenic and genetic analysis of H9N2 isolates showed their gradual and complex evolution revealing extensive re-assortments to generate multiple novel genotypes (7) with gene segments from different lineages.
  12. 12. Transmission pathways:  Low biosecurity is a high risk.  Market systems  Mainly Air born
  13. 13. Pathogenicity: Severe morbidity and mortality in poultry results from: 1. co-infection with other pathogens. 2. Live Vaccines (ND &/or IBV) 3. Management factor.
  14. 14. Organ affinity:  Respiratory  Renal  Reproductive  Nervous
  15. 15. Clinical signs and PM lesions  Broilers: Swelling of head. Respiratory sound. Decreased feed in take. Intestinal ballooning. Pancreatitis Nephritis
  16. 16.  Layers and Breeders: Depression and slight to moderate decrease of egg production. Intestinal twisting and egg peritonitis Pancreatitis (Thickening of pancrease) Nephritis
  17. 17. H5N1 infection
  18. 18. H5N1
  19. 19. •‫انتش‬ ‫انصفح‬‫شَحُح‬: ‫انطُىس‬ ‫اَفهىَضا‬ ‫يشض‬ ٍ‫ف‬ ‫انتششَحُح‬ ‫انصفاخ‬ ‫أهى‬ ٍ‫ي‬(‫عاو‬ ‫تشكم‬)ٍ‫ه‬: .1‫وخىد‬ٌ‫احتما‬ٍ‫ف‬ ‫كًا‬ ‫انمصثاخ‬ ٍ‫ف‬‫انُُىكاسم‬، .2ً‫عه‬ ‫أَضفح‬‫انًعذج‬‫انغذَح‬‫األيعاء‬ ، .3‫سئىي‬ ‫انتهاب‬ .4‫تانثُكشَاط‬ ‫انتهاب‬ .5‫تانًثُط‬ ٌ‫احتما‬ .6‫وانمهة‬ ٍ‫انثط‬ ٌ‫دهى‬ ً‫عه‬ ‫أَضفح‬ .7‫انذ‬ ٍ‫ف‬‫خاج‬، ‫داكُح‬ ‫تُكضَح‬ ٍ‫أياك‬ ‫وخىد‬ ‫يع‬ ‫انثُط‬ ٍ‫ف‬ ‫َضف‬ ‫َالحظ‬ ‫انثُاض‬ .8‫انًثُط‬ ‫اَفداس‬ ‫َتُدح‬ ‫تانسىائم‬ ‫يًهىء‬ ٌ‫َكى‬ ٍَ‫انثشَتى‬ ‫انتدىَف‬ ‫كزنك‬. .9‫اندفاف‬ ‫عالياخ‬ ‫سىي‬ ‫َالحظ‬ ‫ال‬ ‫لذ‬ ‫انالحى‬ ‫انذخاج‬ ٍ‫ف‬‫أخشي‬ ‫تششَحُح‬ ‫صفح‬ ٌ‫أ‬ ٌ‫تذو‬ ‫انًصاتح‬ ‫اإلفشاخ‬ ً‫عه‬.
  20. 20. H9N2 vaccines  Inactivated vaccines  Must be Autogenous  Country/regional variation  Vaccine use will: Prevent clinical signs Reduce virus shedding
  21. 21. Dose of the vaccine 0.5 ml . Administration S/C lower back of the neck . Age of vaccination: Broiler one Dose at 7-10 day old . Breeder & layer 1st Dose 10 D.O 2 nd Dose 40 D.O 3 rd Dose 16-18wk .
  22. 22. Currently available H5 vaccine A. Inactivated homologous vaccine : B. Inactivated heterologous vaccines: The vaccine have the same H type as the field but heterologous neuraminidase. Clinical protection and reduction in viral shedding are ensured by the immune reaction caused by H and N used as marker of field infection.
  23. 23. Dose of the vaccine 0.5 ml . Administration S/C lower back of the neck . Age of vaccination: Broiler one Dose at 7-10 day old . Breeder & layer 1st Dose 10 D.O 2 nd Dose 40 D.O 3 rd Dose 16-18wk .
  24. 24. Marek‘s with H5 Fowl Pox with H5 Other vectors as ILT or lasota with H5
  25. 25. Avian Mycoplasmosis
  26. 26.  Mycoplasmas are bacteria that lack cell wall and belong to the class Mollicutes. ‫ّهزكجبد‬ ‫الجٌظليي‬ ‫هثل‬ ‫األدّيخ‬ ‫لجؼط‬ ‫هقبّهخ‬ ‫الويكْثالسهب‬ ‫إى‬ ‫الظلفب‬.
  27. 27. Species usual host A.Laidlawii Various M.Anatis Duck M.Anseris Goose M.Butenois Buteo Hawk M.Cloacale Turkey,goose M.Columbinasale Pigeon M.Columbinum Pigeon M.Columborale Pigeon M.Corogypsi Black Vulture M.Falconis Saker Falcon M.Gallinarum Chicken M.Gallinaceum Chicken M.Gallisepticum Chicken,turkey,house finish. M.Gallopavonis Turkey M.Glycophilum Chicken M.Gypis Griffon Vulture M.Imitis Duck,goose,partridge M.Iners Chicken M.Iowae Turkey
  28. 28.  Species usual host  M.Glycophilum Chicken  M.Gypis Griffon Vulture  M.Imitis Duck,goose,partridge  M.Iners Chicken  M.Lipofaciens Chicken  M.Meleagridis Turkey  M.Pullorum Chicken  M.Sturni European starling  M.Synoviae Chicken,turkey  M.Gallorale Chicken
  29. 29. Major mycoplasma species in poultry 1.M. gallisepticum: Chronic respiratory disease(CRD in chickens and infectious sinusitis in turkeys) embryo mortality, lameness, eye lesions. 2. M. Synoviae: Infectious tenosynovitis in chickens Respiratory disease(Turkeys), embryo mortality. 3. M. Meleagridis: Respiratroy disease, leg weakness, embryo mortality in turkeys. 4. M. iowae: embryo mortality, leg abnormalities in turkeys.
  30. 30. MYCOPLASMA GALLISEPTICUM INFECTION  Commonly known as chronic respiratory disease (CRD) of chickens and infection sinusitis in turkeys.  Characterized by respiratory rales, coughing, nasal discharge, ,conjunctivitis ,growth retardation and drop in egg production in layers.
  31. 31. ECONOMIC SIGNIFICANCE 1. Increased condemnations (air saculitis) (5-10%) 2. Increased downgrading of carcasses (10-25%) 3. Reduced feed efficiency(5-15%) 4. Reduced egg production (10-20%)& efficiency 5. Increased embryo mortalities (5-20%) 6. Increased mortality rate (5-30%) 7. Increased medication costs 8. Increased costs of prevention and control ,include surveillance (serology,culture,isolation, and identification)
  32. 32. ‫انعايم‬‫الوظجت‬Cause ُْ‫كبئي‬‫دقيق‬‫يحتل‬‫هزحلخ‬‫هتْططخ‬‫ثيي‬‫الجزاثين‬‫ّالفيزّطبد‬ٔ‫ّيظو‬ ‫هبيكْثالسهب‬‫غبليظيجتكن‬Mycoplama Gallispticum‫حيث‬َ‫ل‬ ‫ثؼط‬‫صفبد‬‫الجزاثين‬‫ّالفيزّطبد‬‫ّيختلف‬‫ػي‬ٔ‫األّل‬‫ّالثبًيخ‬ ‫ثجؼط‬‫الصفبد‬‫أى‬ٍ‫ُذ‬‫الكبئٌبد‬‫صغيزح‬ً‫ا‬‫جذ‬‫ليض‬‫لخليتِب‬‫غشبء‬. ‫تتلْى‬ً‫ب‬‫طلجي‬‫ثصجغخ‬‫غزام‬. ‫تتؼبيش‬‫الويكْثالسهب‬‫طجيؼيب‬ٔ‫ف‬‫صْرح‬‫غيز‬‫هوزظخ‬ٔ‫ف‬‫الجِبس‬ ٔ‫التٌفظ‬ْٓ‫الؼل‬‫للطبئز‬.
  33. 33. Transmission- MG/MS Vertical (transovarian) MG/MS are transmitted in eggs laid by infected breeders  Peak transmission is minimal < 3% of eggs
  34. 34. Horizontal Transmission: Dust, equipments, wild birds as sparrows, trucks, feed, workers, vet. doctors, insects as cats, dogs, contaminated vaccines.
  35. 35. Infected chickens transmit MG/MS through aerosols (short distances) contaminated feed and water MS spreads more rapidly than MG
  36. 36. FEED Skin: <4 hrs Ear: 4 hrs Nose: 1 day Hair: 3 days Feathers: 4 days Feed: 4 hrsRubber: 2 days Shavings: 8 hrs Wood: 1 day Cotton: 4 days Mechanical transmission and survival of MG
  37. 37. ‫الويكْثالسهب‬ ‫لوزض‬ ‫الوِيئخ‬ ‫الؼْاهل‬
  38. 38. ‫المعقد‬ ‫المسمن‬ ‫التنفسى‬ ‫المرض‬ CCRD ‫االجهاد‬ ‫عوامل‬ Stress ‫الثانوية‬ ‫البكتيريا‬ E coli‫الميكوبالزما‬
  39. 39. Stress ‫االخهاد‬ ‫عىايم‬  Bad ventillation ‫التِْيخ‬ ‫طْء‬  Cold ‫الجزّدح‬ (Temp. Variation)  High amonia ‫األهًْيب‬  Dust ‫األتزثخ‬  Mycotoxins ‫الفطزيخ‬ ‫الظوْم‬  Immunosuppression ٔ‫الوٌبػ‬ ‫التثجيط‬  Poor feed ‫الؼلف‬ ‫طحت‬ ‫قلخ‬  Overcrowding ‫التشاحن‬
  40. 40. Pathogenic Mycoplasma
  41. 41. MG is an intracellular microorganisms
  42. 42.  The latent status, i.e., when the mycoplasma is not recognized by the host immune system, may be explained by its intracellular location due to environmental pressure, as can be exemplified by the presence of antimicrobials in host tissues for the treatment of MG, MS or MM infection of birds.
  43. 43.  The frequent changes on surface antigens (antigenic variations due to defective DNA repair system) allow mycoplasmas to evade the host immune system, and facilitate their survival when adhered to the host respiratory tract
  44. 44. Their pathogenic mechanism for disease include adherence to host target cells
  45. 45. Destruction of cilia on endothelial cells
  46. 46. Mycoplasma gallisepticum Invades Chicken Erythrocytes during Infection
  47. 47. Clinical signs
  48. 48. INCUBATION PERIOD Varies from 6-21 days Varies depend on :  MG strain virulence  Complicating infection  Environmental and other stressors ‫ّالزّهي‬ ‫الذجبج‬ ‫قطؼبى‬ ٔ‫ػل‬ ‫األػزاض‬ ‫تظِز‬ ‫هب‬ ً‫ب‬‫غبلج‬ ‫الجيط‬ ‫إًتبج‬ ‫ثذء‬ ‫ػٌذ‬
  49. 49. 1.Coughing 2.Sneezing 3.Gasping 4.Rales 5.Ocular and nasal discharge 6.Decrease in feed consumption 7.Pale comb and head 8.Increased mortalities Broilers
  50. 50. Mycoplasmosis in Breeders  Reduce egg production (MG free hens laid 15 more eggs per hen housed than unvaccinated MG infected birds over a 45 week laying period)  lower fertility (MG & MS)  lower egg shell quality  Pipped embryo  poor chick quality  smaller chicks  greater cost per chick
  51. 51. PM lesions Catarrhal inflammation of sinuses, trachea, and bronchi. Air-sacculitis:
  52. 52. ‫انًاَكىتالصيا‬ ‫إصاتح‬ ‫دسخاخ‬: •‫درجخ‬‫صفش‬‫شفبفخ‬ ّ ‫ًظيفخ‬ ‫الِْائيخ‬ ‫االكيبص‬. •‫درجخ‬1‫الِْائيخ‬ ‫االكيبص‬ ‫في‬ ‫ػتبهخ‬. •‫درجخ‬2‫الِْائيخ‬ ‫االكيبص‬ ‫في‬ ‫تعخن‬. •‫درجخ‬3‫التِبثي‬ ‫ًعح‬ ‫ّجْد‬ ‫هغ‬ ‫لحوي‬ ‫هٌظز‬ ‫الِْائيخ‬ ‫االكيبص‬ ‫هي‬ ‫ّاحذح‬ ‫جِخ‬ ‫في‬. •‫درجخ‬4‫التِبثي‬ ‫ًعح‬ ‫ّجْد‬ ‫هغ‬ ‫لحوي‬ ‫هٌظز‬ ‫في‬‫الِْائيخ‬ ‫االكيبص‬ ‫هي‬ ‫جِتيي‬.
  53. 53. ‫صفش‬ ‫دسخح‬:‫َظُفح‬ ‫و‬ ‫شفافح‬ ‫انهىائُح‬ ‫االكُاط‬
  54. 54. Mycoplasma Score 1. No pericarditis and perihepatitis
  55. 55. ‫الهىائية‬ ‫االكياس‬ ‫في‬ ‫تضخم‬ ‫االكياس‬ ‫في‬ ‫نضح‬ ‫يىجذ‬ ‫ال‬ ‫االصابة‬ ‫درجة‬2Dr Lloyd Reeve-Johnson, PhD Thesis, Veterinary Epidemiology and Economics Research Unit, University of Reading
  56. 56. ‫مع‬ ‫الهىائية‬ ‫االكياس‬ ‫في‬ ‫تضخم‬ ‫إلتهابية‬ ‫إفرازات‬ ‫و‬ ‫نضح‬ ‫وجىد‬ ‫الكبذ‬ ‫و‬ ‫القلب‬ ‫على‬ ‫إصابة‬ ‫ال‬ Dr Lloyd Reeve-Johnson, PhD Thesis, Veterinary Epidemiolo and Economics Research Unit, University of Reading ‫درجة‬3:‫الهىائية‬ ‫لالكياس‬ ‫شاملة‬ ‫إصابة‬
  57. 57. ‫إصاتح‬E.coli ‫ثاَىَح‬ ‫كإصاتح‬
  58. 58. ٍ‫ساَُىف‬ ‫ياَكىتالصيا‬ Infectious Synovitis ‫االستطح‬ ‫و‬ ‫انًفاصم‬ ٍ‫ف‬ ‫انتهاب‬ ‫تُفسُح‬ ‫إصاتاخ‬
  59. 59. Eggshell Apex Abnormality
  60. 60. Options to assist in eradication effort or to reduce losses Medication Vaccination
  61. 61. Medication 1. Treat MG respiratory diseases 2. Reduce egg production losses 3. Reduce MG shedding and transmission. 4. Reduce severity of lesions and clinical signs. 5. Significantly reduce population of MG in the respiratory tract. Antimycoplasmal drugs have been used to :
  62. 62. Treatment .1ٍُ‫تهًُكىس‬ .2ٍُ‫تُايىن‬ .3ً‫دوك‬‫س‬ٍُُ‫كه‬-ٍُ‫تتشاسُكه‬ ً‫أوكس‬ .4ٍُ‫َىسفهىكساس‬-ٍُ‫سُثشوفهىكساس‬-ٍُ‫اَشوفهىكساس‬ .5ٍُ‫سثُشاياَس‬ .6ٍُ‫نُُكىياَس‬ .7ٍَ‫تاَهىص‬ .8ٍُ‫اسَثشويُس‬ ‫انمىنىَُح‬ ‫تانعصُاخ‬ ‫انثاَىَح‬ ‫األصاتح‬ ‫حانح‬ ً‫ف‬CCRD‫عًم‬ ‫َتى‬ ‫انحُىي‬ ‫انًعاد‬ ‫استخذاو‬ ‫َتى‬ ‫عهُه‬ ‫وتُاءا‬ ‫حساسُح‬ ‫اختثاس‬.
  63. 63. Antimycoplasmal Drugs MIC (μg/ml)Antimicrobial 0.048Tilmicosoin 0.006-0.39Tiamulin 0.04Doxycycline 0.05Enrofloxacin 0.06Ciprofloxacin 0.08Lincomycin 0.4-4Tylosin 0.08Erythromycin
  64. 64. ANTIMYCOPLASMA PLANNING BROILER Dose Days I 1,2,3 II 20,21,22 (With live vaccines (ND)
  65. 65. Antimycoplasma Planning Layer-Breeder Dose Days I 1,2,3 II For 3 days (20,21,22) III For 3 days during the 9th week IV For 3 days during the 17th week V Feed additive ( premix ) continously during laying
  66. 66. MG and MS Vaccination Vaccine types: MG 􀂾 F-strain MG 􀂾 Strain 6/85 􀂾 TS-11 􀂾 Bacterin – inactivated MS 􀂾 MS-H 􀂾 MG Bacterin- inactivated
  67. 67. Newcastle Disease Synonyms Pseudo fowl plaque Avian distemper Pests Avian pneumoencephilitis
  68. 68. Definition It’s usually an acute highly contagious septicemic disease of domestic and wild birds characterized by respiratory symptoms accompanied or followed by nervous manifestation with high losses in susceptible birds. (Disease common & serious in Egypt)
  69. 69. Strains of the virus vary in virulence (Pathogenecity): a) Velogenic strains: Texas, Herts, highly virulence used for challenge. Embryo receiving minimal lethal dose die ( 50hrs ). b) Mesogenic strains: Komarov, used as a vaccine. Moderate in pathogencity for CE (2-3 day) for ODO & 8-10 wks (death rarely). c) Lentogenic strains: F1, B1, lasota , low virulence used as a vaccine. Pathogenicity for CE die after 100 hrs. For ODO, 8-10 wks old in apparent disease. d) Apathogenic: Enteric strains
  70. 70. Pathotyping of NDV strains
  71. 71. ND
  72. 72. Avian Paramyxovirus – 1 (APMV-1) Order: Mononegavirales Family: Paramyxoviridae Sub-Family: Paramyxovirinae Genera: Avulavirus Serogroups: 9 Serogroups (APMV 1 – 9) (PPMV-1): Pigeons & Doves - Antigenic variant of NDV HN L, NP, P (V) Newcastle Disease Virus
  73. 73. NP: Nucleoprotein P: Phosphorilated protein (Overlapping V gene protein) M: Matrix F: Fusion with host cell membrane (Smaller spike) HN: Hemagglutinin / Neuraminidase activities (Largest spike) L gene: RNA-Directed RNA polimerase (Nucleocapside) NP P M F0 HN L Genomic Features Enveloped pleomorphic RNA virus 100-500 nm size Single-stranded; Non-segmented Negative sense (15kb) Helical nucleocapside symmetry (Herring-bone like structure) NDV Genome Features Lentogenic 112RRQRRF117 Velogenic
  74. 74. Although all NDV isolates characterized to date belong to a single serotype, the avian paramyxovirus serotype 1 (APMV-1), significant genetic diversity has been recognized among different NDV isolates. Historically, NDV isolates have been classified into two major groups (class I and II), based on their genome lengths and the nucleotide sequences of their genomes. Class I viruses are distributed worldwide and have been isolated mainly from waterfowl and shorebirds. Class II viruses have been divided into 11 genotypes (I to XI) with genotypes V, VI, VII, and VIII being the predominant genotypes circulating worldwide. Among these, genotype VII viruses are particularly important given that they have been associated with many of the most recent outbreaks in Asia, Africa, and the Middle East
  75. 75. Antigenicity and immunogenicity  Few antigenic variations  Cell mediated immunity (Local immunity: mainly IgA )  Humoral immunity  Antibodies against fusion protein  Antibodies against HN protein : HI Ab  Passive immunity of the chick
  76. 76. Respiratory Form 109
  77. 77. Neurotropic Form110
  78. 78. Enteric Form111
  79. 79. Egg Production114
  80. 80. ND
  81. 81. Kind of ND vaccines used for immunization of chickens in Egypt: A. Live lentogenic vaccines: Prepared from naturally weak strains. 1. F. strain vaccine: • It is used in chicks aged 1-10 days. • Via eye dropping , nasal instillation , beak dipping • Local prepared.
  82. 82. Kind of ND vaccines: 2. Hitchiner B1 vaccine: • Used for individual vaccination (Eye). • Massive vaccination (D.W) spraying. • Used in chicks aged 1-10 days. 3. Lasota vaccine:( Colone, Avinew ) • It is more virulent strain than F & B1. • It must used as a second vaccination after the first one with either F or B1 . • It’s used through DW., or spraying.
  83. 83. Kind of ND vaccines: B. Live mesogenic vaccine: • As Komarov vaccine, local prepared . • Administrated only by intermuscular I/M. • Used for birds aged not less than 4-6 wks. • Must be in good healthy condition and not in production.
  84. 84. Kind of ND vaccines: C. Inactivated vaccine (Dead vaccine): • Egg propagated (velogenic virus) killed with formaline with adjuvant. • chickens & turkeys I/M or S/C. • Used for vaccination of chickens previously vaccinated with ND live vaccine. • It gives immunity after 14 days and the immunity persist for 3-4 m in birds vaccinated at early age and for 10-12 m in birds vaccinated at the age of 18-22 wks. D. Recombonant vaccine : Its live HVT vaccine Carring F gene of NDV, not interfere with MDA, apply at 1 DO ,long protect.
  85. 85. Infectious Coryza (IC)
  86. 86. Def.  An acute, highly contagious catarrh mainly of growing or mature chickens usually in the cold winter time causing upper respiratory tract disease (nasal sinusitis), growth rate depression and drop of egg production.
  87. 87. Etiology Avibacterium paragallinarum (Haemophilus paragallinarum). H. paragallinarum is a gram-negative nonmotile bacterium. Culture on sheep blood agar is tiny dewdrop, non-hemolytic colonies ,require both X- (hemin) and V-(nicotinamide adenine dinucleotide —NAD) factors for growth A capsule may be demonstrated in virulent strains.
  88. 88. Strain Classification  The Page scheme was initially developed by using a plate or slide agglutination test to recognize the three serovars, A, B, and C . However, the use of hemagglutination-inhibition (HI) technology has been shown to be a much better method for identifying the Page serovar of field isolates.  It is widely accepted that the three Page serovars represent distinct ―immunovars,‖ since inactivated vaccines based on any one Page serovar provide no protection against the other two Page serovars
  89. 89. Susceptibility  Infectious coryza is an acute respiratory disease of chickens. Mature ages are susceptible.
  90. 90. Mode of transmission  The organism may be introduced by the airborne route Through direct contact Or indirect contact through feed and water contaminated with nasal discharge.  Infectious coryza occur frequently in fall and winter.  Chronic or healthy carrier birds are the main source of infection within 1—6 weeks after such birds are moved from the brooder house to growing cages near older groups of infected birds.  Introduction of carrier replacement pullets or males for spiking.  Multiple-age groups.
  91. 91. Vaccines:  Trivalent (A,B,C) thiomersal inactivated bacterins are more effective than formalin one.  A number of adjuvants have been shown to be effec-tive for IC bacterins, in particular, aluminum hydroxide gel, mineral oil, and saponin  108 colony-forming units/ml to be effective.  In breeders, at 18 and 22 weeks of age into the leg muscle.  In layers, at 10 and 14 weeks of age.  Significant immunity for about 9 months.
  92. 92. TREATMENT  oxytetracycline , Erythromycin and sulphonamides are commonly used antibiotics.  It should be noted that drug resistance does develop and hence the performance of antimicrobial sensitivity tests is recommended.  Strains of A. paragallinarum resistant to various antibiotics did not carry plasmids.  Relapse often occurs after treatment is discontinued and the carrier state is not eliminated.
  93. 93. Infectious Bronchitis
  94. 94. Clinical Forms of IB: 1.Respiratory Form (Classical) 2.Renal Form 3.Reproductive Form 4.Digestive Form 5.Muscular Form
  95. 95. IBV exists as scores, more than 360 serotypes. Most differ from each other by 20 -50% of S1 amino acids Classical strains: Massachusetts (M41, H). Connecticut (Florida, Clark 333, ArKansas 99), Georgia (SE17), Iowa 97, Iowa 609, New Hampashire and variant strains: Israel strain (Variant II) QX strain Dutch (D207, D3896, D3128, D212) Delawar (JMK, Halte, Gray) Australia T strain ( kidney lesions ). These strain share common antigen by AGPT. Show variable cross reactions with SNT.
  96. 96. Mode of infection and transmission 1. Air-borne disease. Infection occur through respiratory tract and spread readily by direct and indirect contact (with 48 hr. between infected and susceptible one). Carriers and vectors : Recovered birds may shed the virus for 4-9 weeks (49 days) re-infection may lead to persistence of infection and shedding of the virus for long periods.
  97. 97. Incubation period Naturally 3-10 days, experimentally 18-36 hrs. but natural spread about 36 hrs. it depend on: Dose. Aerosol , Route of inoculation. Symptoms and course : The severity of the clinical and pathological picture of the disease largely depend on : Virulence and organ-affinity of strain . Age and immune status of the birds. General health condition and presence of complicating secondary or inter- current infection, especially Mycploasma, E.coli, Haemophilus, Adenovirus, etc.
  98. 98. Symptoms and course In chicks under 6 wks age : A: Respiratory form Cause mortality of 5 to 10% up to 50%. With depression, ruffling, loss of appetite, gasping, rales, coughing, sneezing and wet eyes. Course of disease is usually 3-6 days.
  99. 99. Layers and breeders
  100. 100. Catarrhal trachitis , bronchitis and pneumonia are common. Red and yellowish caseaus plugs may be found in the lower part of the trachea and bronchi, Rhinitis and air-sacculitis are sometimes present. (Pericarditis, Peri-hepatitis, air-sacculitis in a complicating by inter-current MG, MS and secondary E.coli infection) PM Lesions
  101. 101. Respiratory and Kidney forms
  102. 102. Reproductive form
  103. 103. ‫ّالؼالج‬ ‫الْقبيخ‬ ‫انتىصُاخ‬‫تها‬ ‫انعًم‬ ‫َدة‬ ً‫انت‬: ٍ‫انذواخ‬ ‫عُاتش‬ ً‫ف‬ ‫انالصيح‬ ‫انصحُح‬ ‫االحتُاطاخ‬ ‫يشاعاج‬(ٍ‫ي‬ ً‫انصح‬ ‫انتخهص‬ ‫انُافمح‬ ‫وانطُىس‬ ‫انسثهح‬) ٍُ‫انتحص‬: ‫يصش‬ ً‫ف‬ ‫انًىخىدج‬ ‫انحمهُح‬ ‫انعتشج‬ ‫وتصُُف‬ ‫عضل‬ ً‫ف‬ ‫وَظائشها‬ ‫يصش‬ ً‫ف‬ ‫انحمهُح‬ ‫انًعضوالخ‬ ٍُ‫ت‬ ًُُ‫اند‬ ‫انتماسب‬ ‫يذي‬ ‫دساسح‬ ًُُ‫اند‬ ‫انثُك‬. ‫يغاَشج‬ ‫تعتشج‬ ‫االصاتح‬ ‫ظذ‬ ‫انتًُُع‬ ً‫عه‬ ‫لادسج‬ ‫انًتىفشج‬ ‫انهماحاخ‬ ٌ‫ا‬ ‫تحذَذ‬ ‫انعًهُح‬ ‫انتدشتح‬ ‫طشَك‬ ٍ‫ع‬ ‫رنك‬ ٍ‫ع‬ ‫عاخضج‬ ‫او‬ ‫خذَذج‬(ٍ‫انتًُُع‬ ‫انتصُُف‬ Protectotype)‫انهماحاخ‬ ٍ‫ي‬ ‫وعذد‬ ‫يصش‬ ً‫ف‬ ‫انحمهُح‬ ‫انًعضوالخ‬ ٍُ‫ت‬ ‫انًستخذيح‬. ‫أو‬ ‫انشش‬ ‫طشَك‬ ٍ‫ع‬ ً‫ه‬ ‫انفُشوط‬ ‫ظذ‬ ٍُ‫نهتحص‬ ‫طشق‬ ‫أفعم‬ ٌ‫أ‬ ً‫عه‬ ‫انتأكُذ‬ ٍُ‫تانع‬ ‫انتمطُش‬(‫تعذ‬ ‫ثى‬ ‫َىو‬ ‫عًش‬14‫َىو‬.)
  104. 104. Causes of failure Eye drop : 98-100% At 10 days PV DW vaccine: 56% protection ―10 day PV‖ Hand spray at hatchery : 32% (2wks PV), 86% (3 wks PV). Automatic spray : 93-97% .
  105. 105. ILT
  106. 106. Infectious Laryngotracheitis (ILT) is a viral upper respiratory tract infection of chicken which produces severe production losses due to mortality of infected pullets and adult birds and/or decreased weight gain and egg production. Severe epizootic forms of ILT show a great respiratory distress, gasping, expectoration of bloody mucus, and high mortality. Mild forms of infection, sometimes enzootic, are characterized by mucoid tracheitis, sinusitis, unthriftiness, and low mortality. History: ILT was reported in the USA in 1925 and its earliest recorded occurrence in the UK was in 1935 . It is now recognized worldwide . Introduction
  107. 107. ILT virus is a member of the family Herpesviridae in the subfamily Alphaherpesvirinae . The virus is taxonomically identified as Gallid herpesvirus 1 . • Characteristics: • INIB: Intranuclear inclusions in the trachea and on the chorioallantoic membrane • Types: only one, differentiated by PCR, Variation in virulence • Cultivation: pocks on the CAM and Syncytia in cell cultures • Latency: ILT virus becomes latent like other herpesviruses Etiology:
  108. 108. ILT virus strains appear to be antigenically homogenous based on serum-neutralization ,immunofluorescence tests and ELISA . Naturally occurring ILT virus strains vary in virulence from highly virulent strains that produce high morbidity and mortality in exposed chickens to strains of low virulence that produce mild to in-apparent infection .
  109. 109. Susceptibility: -Chicken is the primary natural host of ILT and occasionally pheasants and guinea fowl -All ages are susceptible ,the most characteristic signs are observed in adult birds. -In general males are more susceptible than females and the heavier breeds more susceptible than light.
  110. 110. Mode of infection : Natural portals of entry for ILT virus are through the upper respiratory and ocular routes . Ingestion can also be a mode of infection although exposure of nasal epithelium following ingestion is required with this route . Transmission: Horizontal transmission by Direct contact between infected birds with susceptible birds . Indirect contact through contaminated equipments and buildings with aerosol or expectorant of infected birds . Mechanical carriers such as personnel ,wild birds ,vermin ,cats and dogs . Recovered birds and even birds given attenuated live vaccines ,the birds become carriers .
  111. 111. • Horizontal spread: in droplets from infected birds - spread often slower than other respiratory diseases e.g. IB, ND. - other agents may exacerbate disease
  112. 112. Latency: ILT virus or vaccine becomes latent and can be re-excreted intermittently for many weeks reactivation due to stress, onset of lay, etc.
  113. 113. Incubation period: 6-12 ds. following natural exposure .
  114. 114. Gross lesions: Lesions may be found in the conjunctiva and throughout the upper respiratory tract of ILTV-infected chickens ,but they are most consistently observed in the larynx and trachea . A) In mild forms of ILT ,gross lesions may consist only of conjunctivitis ,sinusitis and mucoid tracheitis . B) In severe forms of ILT ,mucoid inflammation is observed early in infection with degeneration ,necrosis and hemorrhage occurring in later stages . -In some cases ,severe hemorrhage into the tracheal lumen may result in blood casts or blood may be mixed with mucus and necrotic tissue . -Diphtheritic changes commonly are seen as mucoid casts that extend the entire length of the trachea .
  115. 115. Prevention and control
  116. 116. Modified Live attenuated vaccines Used in areas of high risk Often where used routinely – ‗afraid to stop‘ • Application methods: ED, spray or DW • Live vaccines can become latent • Beware of adding vaccinated or recovered birds to a susceptible flock Vaccination
  117. 117. Vaccination program : Layers flocks generally are vaccinated twice before the onset of egg production ;vaccines typically are administered by eye drop at approximately 7 wks. of age and again at approximately 15 wks. (by eye drop ,spray or drinking water.)
  118. 118. Live attenuated ILT vaccines provide immunity when applied via intranasal instillation , eye drop, and orally through drinking water. However, application of ILT vaccines by eye drop method appears to be more protective than application by water or spray. Most vaccines when given by eye drop method had lower mean microscopic lesion scores and higher ELISA titers after one vaccination.
  119. 119. Fortunately, ILT is a slowly spreading (long IP) , controllable disease. If a diagnosis of ILT is obtained early in an outbreak, vaccination of unaffected birds may induce adequate protection before they become exposed. Emergency vaccination
  121. 121. The infection results in elevated mortality in flocks, lower egg production in commercial laying and breeder flocks, degraded broiler growth rate, and a marked reduction in carcass quality and elevated condemnation at processing. Healthy and sick broilers, layers, and breeders showed the incidence of APEC infection to be 17.7%, 38.6%, and 26.9%, respectively. Resistance to antibiotics was also found to be high
  122. 122. 43% of broiler carcasses condemned at processing had lesions of colisepticemia
  123. 123. Definition and Synonyms Colibacillosis refers to any localized or systemic infection caused entirely or partly by avian pathogenic Escherichia coli (APEC), including the following forms:
  124. 124. 1. Colisepticemia (hemorrhagic septicemia) S 2. Coligranuloma (Hjarre’s disease) S 3. Air sac disease S (chronic respiratory disease, CRD) 4. Swollen-head syndrome L 5. Venereal colibacillosis (Acute Vaginitis) L 6. Coliform cellulitis L (inflammatory or infectious process, IP) 7. Coliform peritonitis L/S 8. Coliform salpingitis L/S 9. Coliform orchitis L 10. Coliform osteomyelitis S 11. Coliform synovitis S (including turkey osteomyelitis complex) 12. Coliform panophthalmitis S 13. Coliform omphalitis/yolk sac infection L 14. Coliform enteritis L
  125. 125. Antigenic Structure and Toxins
  126. 126. Antigens H-antigens = Flagellar K-antigens = Capsular F-antigens = Pilus O-antigens = Somatic
  127. 127. Antigens O-antigens • Somatic (lipopolysaccharide or endotoxin released at cell lysis) • often used in serotyping and antigenic identification H-antigens • Flagellar (proteins not often used in antigenic identification) K-antigens • Capsular (polysaccharides associated with virulence) • Pilus (involved in attachment to cells)F-antigens
  128. 128. • Serotypes of E. coli are classified according to the Kauffmann scheme Currently there are approximately 180 O, 60 H, 80 K and 17F antigens • In most serologic typing schemes only the O and H antigens are determined (e.g., O157:H7). Antigenic structure
  129. 129. Colibacillosis Disease
  130. 130. Swollen Head Syndrome.  Swollen head syndrome (SHS) is an acute to subacute cellulitis involving the periorbital and adjacent subcutaneous tissues of the head.  Usually occurs following upper respiratory viral infections (e.g., avian metapneumovirus, infectious bronchitis virus) & Ammonia aggravates the disease
  131. 131. Pericarditis and green discoloration of the liver Salpingitis in a young bird caused by E. coli. Large caseated masses distending the oviduct (salpingitis). Goose breeder with acute peritonitis. Yolk in the peritoneum.
  132. 132. Omphalitis (Salmonella , Pseudomon , Streptococus facaeum, Proteous(
  133. 133. SHS (MG, IB, AI, IBD or high amonia as preliminary infection)
  134. 134. Arthritis
  135. 135. Panophthalmitis (amonia, Aspergillosis)
  136. 136. Treatment  Sensitivity test.  Ampicillin, fluoroquinolones, chloramphenicol, oxytetracycline, chlortetracycline, neomycin, gentamicin, ormethiprim-sulfadimethoxine, nalidixic acid,, polymyxin B, spectinomycin, streptomycin, sulfa drugs, apramycin, neomycin,.  monensin (anticoccidial) in feed reduced colonization with E. coli O157:H7.
  137. 137. Vaccination Types of Vaccines  A variety of vaccines and vaccination methods have been developed, including passive and active immunization: 1. Inactivated vaccines 2. live vaccines a. Recombinant vaccines b. Subunit vaccines 3. Immunization against specific virulence factors.
  138. 138. Mutant O2 and O78 APEC with deletions of the genes cya or crp, which are involved in energy production, were used as a spray vaccine to immunize broiler chickens. Similarly, strain O78 mutants with deletions of galE, purA, and aroA genes were found to be safe and immunogenic, but provided only moderate protection against homologous challenge with no protection against heterologous challenge
  139. 139. Def.  Ornithobacterium rhinotracheale infection is a contagious disease of birds mainly turkey and chickens that causes respiratory distress, mortality, and decreased growth.  The severity of clinical signs, duration of the disease, and mortality are extremely variable and are influenced by environmental factors, such as poor management, inadequate ventilation, high stocking density, poor litter conditions, and poor hygiene. Ornithobacterium rhinotracheale ORT
  140. 140. Economic importance of ORT in turkey industry • increased mortality • increased condemnation rates, • decreased growth, • decreased egg production,
  141. 141. Transmission O. rhinotracheale is highly contagious: • Infection by inhalation. • Transmitted horizontally by direct and indirect contact through aerosols or drinking water. • Vertical transmission occurs as ORT was isolated from ovaries, oviduct, hatching eggs, infertile eggs, dead embryos, and dead-in-shell poults and chicks.
  142. 142. Serotypes  18 serotypes (A- R).  Serotype A was the most prevalent serotype among chicken isolates (94%) and turkey isolates (57%) but not in USA and South Africa.  Serotype C is prevalent in chickens and turkey in South Africa and USA.
  143. 143. Colony Morphology  On blood agar, very small, non-hemolytic colonies circular, gray to gray-white, sometimes with a reddish glow, and convex with an entire edge.  ORT is a gram-negative, non motile, highly pleomorphic, short, plump rod-shaped, non sporulating bacterium.  No pili, no fimbriae, no plasmids, or specific toxic activities have been reported.
  144. 144.  Sprayed, live temperature-sensitive mutant of O. rhinotracheale vaccine. Treatment  Amoxycillin, ampicillin, Florfenicol.
  146. 146. Definition • An acute, very contagious, viral disease of young chickens characterized by destruction of lymphocytes in the Bursa of Fabricious and, to a lesser extent, in other organs.
  147. 147. Etiology • Infectious bursal disease virus is a member of the Birnaviridae family, named for the bi-segmented double stranded RNA nature of the genome of its members. • The family has 4 genera designated Aquabirnavirus, whose type species is infectious pancreatic necrosis virus (IPNV) of fish, molluscs, and crustaceans; Blosnavirus, whose type species is blotch snakehead virus or BSNV; Avibirnavirus, whose type species is IBDV, which infects birds; and Entomobirnavirus, whose type species is Drosophila X virus, which infects insects.
  148. 148. VP4 & 5
  149. 149. Viral proteins RoleProtein Encapsidation of viral particle VP1 RNA dependant RNA polymerase (Small amount in virus capsids) Contain antigenic region responsible for Serotype specific Elicit neutralizing antibodies (responsible mainly for protection) VP2 Main capsid protein Morphogenesis of the virus VP3 Other major structural protein nit exposed at the surface Viral protease (maturation of VP2 trimming peptides during virus assumbly) VP4 Viral relaseVP5
  150. 150.  IBD virus non-enveloped and resistant to environmental factors  Can persist for months in contaminated houses as once a house is contaminated with IBDV, the disease tends to recur.  Viruses exhibit different degrees of pathogenicity, variants are recognized
  151. 151. Antigenic types Pathotypes Serotype 1 A: Classical (standard) strains: • Mild • Intermediate • Intermediate plus • Very virulent or hyper virulent (VVIBDV) (Hot strain) B: Variant: (antigenically different from classical) and mostly low pathogenic causing only immunosuppression without specific lesions Serotype 1 (Pathogenic) Serotype 2 (Apathogenic)  IBDV serotypes 1 and 2 share only 30% antigenic relatedness
  152. 152. • Strains of IBD follow one of two courses of disease depending on the age at which chickens are infected • Subclinical course • Clinical disease
  153. 153. Variant Strains of IBD -Subclinical Form-  Infection of susceptible chickens less than 2 weeks of age when chickens are exposed to IBDV during the first two weeks post hatch and have sufficient maternal antibody at time of infection to prevent clinical disease but not viral replication in the bursa.  No clinical signs, No peak mortality as evidenced with clinical IBD, but permanent and severe immunosuppression  More economically important form  Majority of field infections are subclinical
  154. 154.  Subclinical form- Perminant immunosuppressive reduced antibody response to vaccination strong post-vaccine reactions  Increased susceptibility to concurrent or secondary disease as E. coli, Mycoplasma and NE  Inability to clear vaccine virus
  155. 155. Varian t strains Direct bursal atrophy
  156. 156. Standard Strains of IBD -Clinical Form-  Infection of susceptible chickens 3-6wks weeks of age:  Sudden onset, rapid increase in mortality  Clinical signs include ruffled feathers, diarrhea, vent pecking, dehydration, trembling, depression, transient immunosuppression
  157. 157. Clinical Signs 1. Anorexia, depression and ruffled feathers. 2.Whitish or watery diarrhoea. 3.The earliest signs is self vent picking and soiled vent feathers. 4. Dehydration and trembling. 5. In terminal stages of the disease, subnormal temperature, severe prostration and finally death.
  158. 158. Morbidity & Mortality In susceptible flocks, there is high morbidity rate usually approaching 80%. Mortality may be nil but can be high as 20- 30% and usually begin at 2nd day post infection and peaking and receding in a period of 5-7 days.
  159. 159. Gross Lesions Changes in cloacal bursa 2nd day post infection ----- bursa has gelatinous yellowish transudate covering serosal surface with prominent longitudinal striations. By 3rd-4th day ----- bursa is double in size and weight (due to edema and hyperemia). By 5th day -------- bursa returns to its normal weight but it continues to atrophy From 8th day forward --------- bursa is approximately 1/3 its original weight. Mortality rate Slightly higher Double Slightly lower Normal
  160. 160. 2. Dehydration. 3. Haemorrhages in mucosa at junction of proventriculus and gizzard. 4. Haemorrhages in thigh and pectoral muscles. 5. Increase mucous in intestine. 6. Spleen and liver slightly enlarged. 7.Pale kidney ,nephritis and ureter distended with urates.
  161. 161. Vaccination 1. Live IBD vaccines: (1-14 days) Divided according to virulence of strains: Mild strains Intermediate Intermediate plus Hot strains applied in drinking water, eye drop. 2. Oil-adjuvant, killed IBDV vaccines: Applied by injection S/C or I/M and used to booster or prolong immunity in breeder flocks.
  162. 162. In ovo vaccination  A more recent concept for the vaccination of chickens for IBD and other agents is in ovo vaccination at 18 days of incubation.  In ovo is a labor-saving technique and may provide a way for vaccines to circumvent the effects of maternal antibody and initiate a primary immune response.  The injected material is a live IBD vaccine, either alone or in combination with an anti-IBDV antibody to form immune complexes
  163. 163. Recombinant vaccines  live recombinant virus vectors expressing IBDV immunogens (VP2) as:  Herpes virus of turkey (HVT) Marek‘s disease virus  Fowlpox virus  Chick embryo lethal orphan (CELO) virus (Adenovirus)  Newcastle disease virus  Baculovirus
  164. 164.  Vaxxitek antigen = Faragher 52/70  Old classical strain  Transmune strain = Winterfield 2512 (= IBD Blen)  Very hot strain Recombinant vaccines Immune-complex vaccines
  165. 165. Control of outbreak *Supportive and symptomatic treatment : 1. Diuretics to increase efficiency of kidney and to prevent precipitation of urates . 2. Immunostimulant as vitamin E and levamisole . 3.vitamin K (for hemorrhage). 3.give coarse of antibiotic to prevent 2nd ry bacterial infection (but it‘s contraindicated in case of nephritis).
  166. 166. Other immun-suppressive diseases
  167. 167. CAV
  168. 168. Reo
  169. 169. Marek’s Disease
  170. 170. AL
  171. 171. Big liver Disease
  172. 172. H9N2
  173. 173. ‫نفُشوط‬ ً‫انًُاع‬ ‫انتثثُط‬H9N2 1. Atrophy of bursa of Fabricious and thymus gland 2. Ciliostasis and affect BALT 3. Decreased antibody production
  174. 174. MG
  175. 175. Enteric Bacteria
  176. 176. Salmonellosis
  177. 177. Infections caused by non-motile Salmonella serotypes (Salmonella entrica subspecies entrica serovar pullorum gallinarum) PD can cause 10-80% mortality during the first 2 weeks. FT can cause mortality as high as 26% in chicks during the first month of life.
  178. 178. Infections caused by motile Salmonella serotypes are called paratyphoid (PT) salmonellae. More than 2500 serotypes (of which 30% are caused by S. enteritidis and S. typhymurium).
  179. 179.  Salmonella infections cause: High mortality rate especially in young chicks Drop in egg production Decreased fertility and hatchability
  180. 180. Arthritis
  181. 181. Nephritis (IBD, ANV, Ochratoxins, High protein ration)
  182. 182. Heart nodules (MD, Coligranuloma and Aspergillosis)
  183. 183. Coliflower Oophoritis
  184. 184. Necrotic Enteritis
  185. 185. NE Caused By C. perfringens is an anaerobic, spore-forming, large Gram- positive rod, which is motile by pili. It is commensally live in the intestinal tract (lower gut & caecum ). There are five different types of CP {A-E} where A and C is mainly responsible for NE in broilers.
  186. 186. C. Perfringens Infection causes 1. Impaired FCR. 2. Reduced Weight Gain At Slaughter. 3. Reduced The Average Of Farmers Profit With 33% With High And Low Levels Of The Disease. 4. Increased Number Of Carcass And Liver Condemnation At Poultry Processing Plants.
  187. 187. Pre-disposing factors For NE:  Concurrent coccidial infections with scores 2-3  Removal of antibiotics growth promoter  Long anticoccidial withdrawal periods.  Feed and litter contamination with Clostridial spores have been incriminated as a source of infection.  Diet is believed to be an important:  Change Viscosity and PH (High level of wheat & Barley increasing SNSPS)  High Protein in ration  High level of animal by products i.e fish meal
  188. 188.  Direct damage to intestinal mucosa (coccidia infection, mycotoxicosis, bacterial over growth).  Immuno-suppressive such as: CAV, IBD, M.D.  litter high in fiber content, feeding programs e.g. skip a day starvation, overstocking).
  189. 189. Susceptibility: NE has been reported in many bird species but mostly in broilers 2-6 wks), layer pullets, adult layer, breeders and turkeys.
  190. 190. Subclinical NE
  191. 191. Subclinical NE
  192. 192. NE
  193. 193.  Pseudo-membranes covering the entire mucosa of large segments of SI which resemble a coarse yellow coating. Cholangiohepatitis:  Most common lesion CC by inflammation of bile tree (Intra-hepatic part most frequently).
  194. 194. 1. Gross intestinal lesions 2. Present of liver lesions 3. Microscopically exam of gut smears for coccidia. 4. Bacteriological examination: gut content should contain at least 1 million often 100-1000 million CP/gm) Differential diagnosis
  195. 195. Treatment of NE  Treatment of NE outbreaks can be effectively treated by administration of:  Ampicillin , Amoxicillin ,Lincomycin, Bacterin, and Streptomycin.  Metronidazol
  196. 196. Coccidiosis
  197. 197.  Species Specific (no cross-immunity exists between species of Eimeria ).  Host specific.  Tissue specific.  Simple, short and direct life cycle.  High reproductive potential of coccidia in poultry intensifies the potential for severe outbreaks of disease in the modern poultry house (New house disease).  It is a self limiting parasite. Characteristics of coccidian parasite:
  198. 198. Classification: - Chickens coccidiosis: I – Intestinal II- Caecal I - Intestinal. coccidiosis A- Anterior E. acervulina E. praecox B- Middle E. necatrix E. maxima C- Posterior E. brunetti II- Caecal coccidiosis E. tenella
  199. 199. Clinical signs: The Common Rule Says That: The species We Don't See Cause More Damage and More Loss. 1- diarrhea from (catarrhal to hemorrhagic,...etc.) 2- dehydration. 3- death.
  200. 200. Significantly damaged and therefore lesser absorbing ability of the intestine membrane. All of this leads to the weakening of the animal, a poorer usability of food and poorer conversion, flock disintegration and growth retardation, lesser body weight, poorer production results.
  201. 201. Diarrhea and dehydration are very common and depending on the type of coccidiosis as well as traces of blood in or bloody feces with consequential anaemia, as well as death of infected units where mortality may be expressed in a very significant percentage. Coccidiosis is primarily a disease affecting young animals.
  202. 202. E. acervulina & E. maxima: Poor weight gain, high morbidity, diarrhea, and sometimes mortality. There is often extreme emaciation, ruffling of feathers , anorexia. Killers (E. tenella & E. necatrix): bleeding, high morbidity and mortality, lost weight gain, emaciation, loss of skin pigmentation.
  203. 203. P.M. lesions Lesions of the intestine can vary from mild enteritis one score (+ve) to severe necrotic or hemorrhagic type scores (+++ve) and characterized by :- 1- sever inflam. in specific location according to Eimeria sp. 2- thicken of intestinal wall. 3- whitish yellow plaques (oocysts). Caecal coccidiosis may produce ballooning of the cecal pouches, which then fill with blood. A later stage involves cecae filled with material of cheesy consistency, streaked with blood (contains non sporulated oocysts) (whitish yellow plaques) or (caecal cords).
  204. 204. Lesions can often be seen from the serosal surface of the small intestine. The intestinal mucosa may at first be thin and covered with elongate white plaques, arranged transversely. The intestine may be pale and contain watery fluid. E. acervulina
  205. 205. E. acervulina
  206. 206. The intestine may be flaccid and filled with fluid, and the lumen often contains yellow or orange mucus. This condition has been described as ―ballooning.‖ E. maxima
  207. 207. E. maxima
  208. 208. E. necatrix older birds such as brooder pullets or layer pullets 9—14 weeks old. The intestine often is dilated to twice its normal size (ballooning), and the lumen may be filled with blood and fluid.
  209. 209. E. necatrix
  210. 210. Bloody cecal core E. tenella
  211. 211. Control of coccidiosis
  212. 212. I - Correct the managment: - avoid humidity. - avoid over crowdness - provide good ventilation. - proper temp. - Eradication of rodents, arthropods (vectors). - Disinfectant of the visitors, workers & shoes. - Separate the old from the young. birds - Control other disease. - through cleaning & disinfection before each new flocks. - periodical removal of litters wet letter should be changed either completely or partially as possible. Wet areas are found around drinkers, in corners or beside walls and … etc.
  213. 213. II- Destruction of oocyst - good hygiene - good disinfectant Ammonia fumigation or Ammonia solutions or Sodium hydroxide. or Calcium oxide III- Raise the vitality of the birds: - good balanced rations. - supplemented especially by vit K & vit A. - sufficient amount of ration.
  214. 214. IV – Feed additive compounds: - Used as protective coccidiostate: -Add from the first day of age to the end of the broilers flocks at ration and add from the first day of age to 12-16 weeks of age at ration in layers flocks. -Use for non diseased birds & not used as treatment. e.g.: 1- Chemicals coccidiostate Active principle 1- Halofuginon 2- Rubanoed 3- Dicelazoril
  215. 215. 2- Inophores coccidiostate Active principle 1- Monenzin 2- Salinomycin 3- Lasalocid 4- Maduramycin 5- Semduramycin - Coccidiostate permit descend of some oocysts which lead to partial immunity There are two main problems with chemotherapeutic approach to controlling coccidiosis, the emergence of drug resistance (which may be developed after repeated uses of the same drug) and residues. This problem is usually met by changing the anticoccidial drugs overcome the drug resistance as following:
  216. 216. Programs for coccidiosis control: 1- Continous use of single drug: using one particular anticoccidial in the feed from first day till withdrawal period 2- Shuttle programs (‫الواحدة‬ ‫الدورة‬ ‫خالل‬ ‫الكوكسيديا‬ ‫مضادات‬ ‫تبادل‬ ) Consists of starter medication, using one particular anticoccidial in the feed usually for the first 3 weeks of growth, followed by a change to another anticoccidial in the grower feed for the finishing period. 3- Rotation programs ( ‫تبادل‬‫مضادات‬‫الكوكسيديا‬‫بين‬‫الدورات‬ ) : using one particular anticoccidial in the feed for 2 cycles then change to another.
  217. 217.  Used for breeders and floor reared layers: Natural wild type vaccine: Coccivac,Immucox. Attenuated vaccine: Livacox, or Paracox. Vaccination
  218. 218. Immunogenicity of different species: Depending on the coccidian species considered, immunity will develop after one single exposure to the parasite or several exposures to the same species as shown in the following table: Species No. of Exposure to achieve Immunity. E. maxima 1 E. Praecox 1 E. brunetti 1-2 E. acervulina 2-3 E. mitis 2-3 E. tenella 3-4 E. necatrix 4-5
  219. 219. VI - Vaccination: - Administration via feed 3-5 days or spray (Cabin) 1 day old or eye of nasal drop 1 day old - Immunity after 3-4 weeks
  220. 220. Precautions after vaccination: -Never use a medication which affect any stage of Eimmeria sp. -Never change the litter for one month following vaccination. Examination for the chicks periodically to be sure from the presence of oocysts & absence of lesion scores.
  221. 221. Mycotoxicosis & their effect on poultry industry
  222. 222. Mycotoxicosis Mycotoxins are secondary metabolites produced by fungi that can enter the human and animal diet through direct or indirect contamination of cereals and grains. There are more than 350 type of mycotoxines
  223. 223. Mycotoxin Fungi Produced Commodities affected Aflatoxin(B1,B2,G1,G2) Aspergillus flavus Aspergillus parasiticus Corn, cotton seed, peanuts, soya Ochratoxin (A, B, C) Aspergillus ochraceus Aspergillus nigr Penicillium verrucosum Wheat, barley, oats, corn, others Trichothecenes (DON, T-2, DAS, etc) Fusarium graminearum Fusarium culmorum Corn, wheat, barley Zearalenone Fusarium graminearum Corn, wheat, barley, grass Fumonisin Fusarium verticillioides Fusarium proliferatum Corn Moniliformin Fusarium moniliforme Corn PR toxin, patulin Penicillium roqueforti Silage, Grass
  224. 224. Species Single oral doseLD50 mg kg -1 bodyweight Rabbit 0.30 Duckling (11 day old) 0.43 Chicken 6.30 Effect of bird species on toxicity of aflatoxin B1
  225. 225. Type of bird Age (days) LD50 (mg/Kg Bwt) Ducklings 3 0.5 Broiler chicks 1 2.14 Broiler chicks 21 3.6 Leghorn Chicks 1 3.3/3.9 Leghorn Chicks 3 3.4 Leghorn Chicks 10 10.67 Turkey poults 1 4.63 Turkey poults 3 5.9 Turkey poults 21 7.84 Japanese qual chicks 3 16.5 Effect of age on toxicity to LD50 of ochratoxin A (after single oral administration). Type of bird Age (days) LD50 (mg/Kg Bwt) Ducklings 3 0.5 Broiler chicks 1 2.14 Broiler chicks 21 3.6 Leghorn Chicks 1 3.3/3.9 Leghorn Chicks 3 3.4 Leghorn Chicks 10 10.67 Turkey poults 1 4.63 Turkey poults 3 5.9 Turkey poults 21 7.84 Japanese qual chicks 3 16.5 Effect of age on toxicity to LD50 of ochratoxin A (after single oral administration).
  226. 226. Level producing Immunodepression Regulations UE - USA Mycotoxins 5 ppb< 20 ppbAflatoxin 2ppb0-2 ppbOchratoxin 100 ppb< 500 ppbToxin T-2 < 500 ppbZearalenone 1000 ppb< 5000 ppbFumonisin 200 ppb< 1000 ppbVomitoxin(DON) MYCOTOXIN TOLERANCES (Synergism)
  227. 227. level , synergism & duration animal species , breed, sex, age, general health, immune status farm management( storage, Temp., & RH / infections ) • toxin-, • animal- • environmental- Factors influencing Mycotoxines depend on: related factors
  228. 228. Growth depression . Increased mortality . Increased susceptibility to disease . Decreased serum protein . Impaired blood coagulation (Decrease vit K absorption) . Fatty liver . Weakened bones (Decrease vit D absorption) . Poor nutrient absorption . Principle effects of aflatoxin in broiler
  229. 229. P. M.
  230. 230. 1. Pale bone marrow. 2. Regression of the bursa of Fabricius. 3. Mycotoxins can cause damage to mucosae with which they come in contact. 4. Gizzard erosions. 5. Enteritis of variable degree may be seen.
  231. 231.  Produced in moderate and colder climates.  It is stored in fatty tissues.  OTA is also known as a potent immunotoxic, teratogenic, and carcinogenic mycotoxin.  In addition, OTA ingestion induces intestinal injuries, including inflammation and diarrhea.  It is nephrotoxic.  Immunosuppressive: decrease immunoglobulin production and causes lymphocytopenia at 4 ppm. Ochratoxin
  232. 232. Citrinin:  Nephrotoxic.  Na and K increased excretion.  Inbalance in the minerals and salts PPT of uric acid crystals inside the kidneys.  At the final stage the nervous signs appear, (convulsions and death).
  233. 233. Trichothecenes: Mytotoxins produced by Fusarium sp. Includes more than 100 types. T--2 toxin LD50(4 mg/kg), HT-2 toxin Di-acetoxy-scirpenol Deoxy-nivalenol (DON) LD50(27 mg/kg) Neural toxicity Necrosis, odema, hemorrhage of intestinal tract
  234. 234. Prevention And Control Of Mycotoxicosis
  235. 235. 1. Quality control of the raw material all the way through feed mill, delivery, storage bins, at the farm, feed through, litter condition in poultry houses. 2. Storage time must be reduced to minimum esp., in starter feed. 3. Feed bin & handling equipment must be kept clean & disinfectant with 10% clorax.
  236. 236. • Decontamination for mold & mycotoxins infestation. -Ammoniation . -Cleaning “ all visible mold areas”. -Heating or roasting of feedstuffs. -Adding toxin binders (HSCAS) to feedstuffs. • Using of mold inhibitors (which inhibitor should be used & at what conc.?
  237. 237. Propionic acid was the only compound exhibiting cidal action. Ca. propionate had essentially no effect on mold growth . Sod. Propionate had essentially mild activity towards mold growth. The failure of these two compounds to exhibit marked anti fungal activity may be attributable to PH of medium since dissociation of these salts is PH dependent Mode of action of mold inhibitors:
  238. 238. Mycotoxin binders: An effective binder or sequestering agent is one that prevents or limits mycotoxin absorption from the gastro-intestinal tract of the animal. In addition, they should be free from impurities and odours. Be aware that not all are equally effective. Many can impair nutrient utilization and are mainly marketed, based on in-vitro data only.
  239. 239. Mycotoxin binding is achieved through both: 1- Physical adsorption Relatively weak bonding through hydrogen bonding 2- Chemical Adsorption (Chemisorption): It is a stronger interaction which involves ionic or covalent bonding.
  240. 240. Inorganic binders Organic adsorbents Inorganic binders Inorganic mycotoxin binders are silica based polymers. Examples could include: zeolites bentonites bleaching clays from the refining of canola oil hydrated sodium calcium aluminosilicates (HSCAS) diatomaceous earth numerous clays There are two types of chemical mycotoxin adsorbent/binder:
  241. 241. Extracts of yeast cell wall Such materials are biodegradable but can, in some cases, also be vectors of mycotoxin contamination. Benefits of yeast cell wall are low inclusion, high surface area and certainly no toxic contaminants. The efficacy of glucomannan-containing yeast products as mycotoxin adsorbents in feeds has been investigated globally with several studies with all animals. Organic Adsorbents Organic mycotoxin adsorbents are carbon based polymers.
  242. 242.  Bio-Transformation Bio-Agglutination Bio-Degradation How dose Bio-mycotoxin work against mycotoxins:
  243. 243. Bio-Transformation: Bio-Transformation is one of four processes involved in toxicokinetics
  244. 244. A substance biotransformed into a more toxic metabolite (bioactivated) is a greater hazard than a substance that is biotransformed into a less toxic or even non-toxic metabolite (detoxified). Bio-Transformation:
  245. 245. Some specially selected strains of Bacillus subtlus, Lactobacillus, S.faecium, S. cerevisiae and other technologies that Bio- Transform, (detoxify) mycotoxins. Bio-Transformation:
  246. 246. The process by which toxic or pathogenic substances ―stick‖ to long chain olygosacharide molecules Bio-Agglutination:
  247. 247. Degradation via enzymatic activity Bio-degradation:
  248. 248. ٍُ‫انتحص‬ ‫تشايح‬ ‫اعذاد‬ .1‫ثٌْػيِب‬ ‫االًفلًْشا‬. .2ٓ‫الوؼذ‬ ٔ‫الشؼج‬ ‫االلتِبة‬. .3ّ‫الجوجْر‬. .4‫الٌيْكبطل‬.
  249. 249. ‫الوزظيخ‬ ‫االصبثبد‬ ٔ‫ف‬ ‫التحكن‬ .1‫ثذقخ‬ ْٓ‫الحي‬ ‫االهبى‬ ‫ّطبئل‬ ‫اتجبع‬. .2‫الصحيخ‬ ‫ّالؼْاهل‬ ‫ثبلتزثيخ‬ ‫االُتوبم‬. .3‫جيذا‬ ‫ّاالدّيخ‬ ‫ثبلتحصيٌبد‬ ‫االُتوبم‬. .4‫الوزظيخ‬ ‫للوشبكل‬ ‫الظليوخ‬ ‫التشخيص‬ ‫ّطبئل‬ ‫اتجبع‬.
  250. 250. Thank you
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محاضرة اليوم الثالث د احمد البستاوي


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