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Avian Influenza History



Tables of poultry viral diseases Dr Fares El khayat

Tables of poultry viral diseases Dr Fares El khayat

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Tables of poultry viral diseases Dr Fares El khayat

  1. 1. Tables of Poultry Diseases ‫اد‬ ‫ا‬ ‫ا‬‫ر‬ ‫آ‬/‫ط‬ ‫ا‬ ‫رس‬ ‫ي‬ ‫ا‬ ‫ا‬ ‫وا‬ ‫ا‬ ‫اض‬ ‫أ‬ ‫ا‬ ‫آ‬
  2. 2. Viral Diseases of Poultry Dr Fares El-Khayat 1-Newcastle disease = Ranikhet disease = Pneumoencephalyetis = Pseudo fowl pest ‫ض‬‫آ‬ ‫ا‬ : Infectious, contagious, septicemic and zoonotic disease. The causative agent is a Hemagglutinating Paramyxovirus type-1 "PMV-1" ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫ا‬ which have five pathotypes (velogenic viscerotropic, velogenic neurotropic, mesogenic, lentogenic & asymptomatic enteric strains). It is an enveloped, RNA, 100-150 nm in diameter. It is propagated in 9-11 days old ECE via allantoic sac causing death of embryo in 2-6 days PI. Infection occurs by ingestion, inhalation of polluted air or feed. Transmitted by direct and indirect contact. There is minor antigenic variation. Host Signs & Lesions P & T P-Prophylactic Vaccination. Chicken, turkey, quails, ostrich & pheasant. ‫و‬٢٩٦ ‫ودا‬‫أ‬ ‫آ‬ ‫ض‬ ‫ا‬ ‫ا‬ ‫ا‬ ‫أ‬ ‫دة‬ ‫ا‬ ‫ا‬ ‫ا‬. I.P is 5-7 days. General signs: Rapid spread of morbidity & mortality. Enteric signs: Thrist, distended crop + bad-odered content, light bright greenish diarrhea. Resp. Signs: Nasocular discharge, wheezing sound, gasping, coughing & rales. Nervous signs: follow or associate the respiratory signs and include ataxia, tremors, circling, convulsions, torticallus, paresis & paralysis. In adults → moderate resp. signs + partial or complete drop in egg production that may reach zero with egg abnormalities. Flock signs last 2-3 wks. Hemorrhage on the tips of the gastric glands. Hemorrhagic ulcers in the duodenum, cecal tonsil. Hemorrhagic tracheitis, air sacculitis & pneumonia. Ureter is distended with urates. In adults, ovarian congestion with rupture of some ovules in the abdominal cavity. T- Emergency vaccination + supportive therapy. Prevention: Biosecurity measures + vaccination of chicks by live vaccines as Hitchner B1, LaSota, avenew, clone 30, clone 79, Komarov as well as Killed vaccines either single or combined. The method of applications of ND vaccines includes drinking water,
  3. 3. eye drop, spraying and injection. The choise of the suitable method is dependent on the size of the flock, the concurrent infection and the epidemiology of the disese. The most protective type of immunity is the mucosal or local type follwed by the cell mediated type "CMI", followed by the humoral type and the passive or maternal type protect the chicks for about 3 weeks. Intra-cerebral pathogenicity indexes or indices "ICPI" of the different vaccinal strains of NDV: Vaccinal NDV strains Pathotyping Standerd ICPI of pathotypes ICPI of the strain Tropism Ulcer strain Asypmtopatic enteric 0.04 -0.20 Enteric Phy LMV 42 Asypmtopatic enteric 0.0 -0.2 0.16 Enteric F1 strain Lentogenic 0.25 Respiratory Hitchner B1 Lentogenic 0.20 Respiratory Lasota strain Lentogenic 0.25 - 0.44 Respiratory Clone 30 Lentogenic 0.3 Respiratory Clone 79 Lentogenic 0.2 – 0.7 0.3 Respiratory Komarov Mesogenic 1.41 Respiratory Roakin Mesogenic 1.0 – 1.5 1.45 Respiratory Lasota strain is the best vaccine giving very potent and protective immune response against ND, but its disadvantage is the induction of severe post-vaccination reaction. This post-vaccination reaction is induced mostly due to the presence of a concurrent infection with avian mycoplasmosis. M.gallisepticum secret trypsin enzyme which makes artificial cleavage of the F epitope of the Lasota virus vaccine rendering it into a virus having a degree of virulence. To overcome this effect, we should use antimycoplamal drugs during the first 3 days of life and recyle this drug 20 days later. Control: Non specific treatment is present for the disease, but carrying out the sanitary measures regarding to the isolation of clinically diseased birds and the proper disposal of dead birds is helpful. Emergency vaccination in the face of an outbreak using LaSota, avenew strains are also used very useful in controlling the disease. Emergency vaccination is dependent on the induction of interference phenomena under the effect of the interferone production from the immune cells. Supportive therapy as spraying of minthol preparations and immunostimulant may give a good effect. The adminstration of broad spectrum antibiotics may give a good effect in controlling the secondary bacterial bacteria.
  4. 4. 2-Viscerotropic velogenic ND = Exotic ND: Hemagglutinating PMV-1 Host Signs & Lesions P & T Chicken I.P is 3-7 days. Sudden onset and rapid spread of high morbidity without any signs followed by facial swelling with sticky ocular and nasal exudates. They appear to have “black eyes”. Severe thrist, distended crop with bad-odered content, light bright greenish diarrhea and high mortality. Adults show partial or complete drop in egg production that may reach zero with egg abnormalities. Hemorrhage on tips of gastric glands. Hemorrhagic ulcers in the duodenum & cecal tonsil. In adults, ovarian congestion with rupture of some ovules in the abdominal cavity. As ND 3-Pigeon PMV1 infection = Paramyxovirosis: Pigeon PMV-1 is a sub-group of NDV which cross-reacts with the classic NDV. The pathotype of pigeon PMV-1 falls between the lentogenic and mesogenic NDV. All other biologic properties are the same as NDV. Host Signs & Lesions P & T Pigeon I.P is 2-7 days. There are thin broken solid droppings in a pool of liquid as light bright greenish diarrhea, fine tremor of eyes or head, staggering in gait, somersaulting in flight, crash landing, difficulty picking up seed, pecking and missing, tossing seed backwards, twisting neck, head upside down (torticollis, star gazing), paralysis of legs or wings, spiraling in flight, flying backwards, turning in circles and having fits. There are not respiratory symptoms in Paramyxovirosis. Petecheal hemorrhages on the heart, stomach and intestinal serosa. Cyanosis of skin and muscles. The course is 10-14 days. As ND, biosecurity measures and vaccination of pigeons against Pigeon PMV.
  5. 5. 4-PMV-2 infection “Yucaipa”: Hemagglutinating PMV-2. Infection occurs by ingestion, inhalation of polluted air or feed. Transmission is by wild birds and fomites. Wild birds are believed to be especially important. Vertical transmission does not usually occur. Host Signs & Lesions P & T P. Biosecurity and all-in/all-out production. Chicken & turkey and wide range of feral birds. Variable mortality, depending on the affected species and whether infection is complicated by other factors and diseases. In chickens it is mild, but turkeys are more severely affected. In uncomplicated cases, → mild respiratory signs + reduced egg production. Depression, inappetance, coughing. In the complicated cases due to any secondary bacterial pathogens as E.coli or any environmental stress as ammonia → severe respiratory disease + cesation of egg production + high mortality. No specific gross lesions are present in PMV-2 infection. T.None but supportive therapy give a good effect. Antibiotics to control secondary bacteria. 5-PMV-3 infection: Paramyxovirus PMV-3 infects turkeys, occasionally chickens and psittacine birds. The infection is transmitted by birds including wild bird and contact with fomites. Vertical transmission does not occur. Mortality is low. Hemagglutinating PMV-3 is serologically related with NDV. Infection occurs by ingestion, inhalation of polluted air or feed. Host Signs & Lesions P & T Turkey, psittacines & cage birds. In turkey, there are mild respiratory signs, depression, inappetance, coughing with drop in egg production and egg quality with loss of egg pigmentation. The effect on egg production depending on the presence or absence of the secondary bacterial agents and/or any environmental stressors. In psittacines, cage & feral birds, there are nervous symptoms with high mortality. As PMV-2 6-PMV-6 infection: it occurs in turkeys and inapparent in ducks & geese.. Infection is transmitted by direct contact with wild bird and indirect contact with fomites. Host Signs & Lesions P & T Turkey and exotic pet birds. Reduction in egg production with mild respiratory signs. Mortality is 0–5%. No specific lesions. As PMV-2
  6. 6. 7-Turkey Rhinotrachitis = TRT: A disease of turkeys caused by the viruses of Pneumovirus genus ‫ا‬ ‫ت‬ ‫و‬ ‫,ا‬ Paramyxoviridae. Two subgroups have been identified on the basis of the G-protein sequence(cross protection between them occur): A (original UK isolates) and B (original southern Europe isolates). There is rapid lateral transmission with infection by aerosol through the respiratory route; vertical transmission is uncertain. As for many infections, fomites can be important in moving infection between farms. Maternal antibody may protect. Pneumovirus is enveloped RNA, 80-100 nm in diameter. Isolated in tracheal organ culture from turkey embryo causing ciliostasis 4-5 days PI. Host Signs & Lesions (P) & (T) P.Biosecurity and chlorination of drinking water. L. vaccines. Turkey < 10 wks and turkey breeders Morbidity is 10-100% and mortality 1-30%. Decreased appetite, weight gain and feed efficiency, loss of voice, oculonasal discharge, conjunctivitis, snicking sound, dyspnoea and sinusitis with sudden drop in production that lasts 2-3 weeks and eggs depigmented and thin-shelled. Serous rhinitis and tracheitis, sometimes pus like material present in bronchi. If there is secondary E.coli infection then pneumonia, airsacculitis and perihepatitis. T.None but the supportive therapy give a good effect. 8-Swollen head syndrome = SHS = Dekkop ‫ض‬‫أس‬ ‫ا‬ ‫رم‬ : A viral disease of chickens, guinea fowl and possibly pheasants. It is caused by a Pneumovirus of the Paramyxoviridae family as TRT. Host Signs & Lesions (P) & (T) Chicken < 10 wks. The incubation period is 5-7 days, morbidity is 10-100% and mortality can be 1-10%. Reduced appetite, weight gain & feed efficiency, facial & head swelling, loss of voice, ocular & nasal discharge, snick, dyspnoea, conjunctivitis, sinusitis. Serous rhinitis and tracheitis. If secondary invasion as E.coli occur, pneumonia, airsacculitis & perihepatitis, congestion, edema & pus in the airspace of the skull occur in a proportion of affected birds. As TRT 9-Avian Influenza ‫ر‬ ‫ا‬ ‫ا‬ ‫:أ‬ A highly infectious and contagious avian disease caused by a Hemagglutinating Orthomyxovirus- Influenza A ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It has 16 H epitopes and 9 N epitopes with possible 144 serotypes. The virulent serotypes are those containing H5 and H7 epitopes. They cause a particularly severe course of AI, known as classical fowl plague (highly pathogenic AI, HPAI). HPAI is an acute disease of fowl-like birds with a mortality of up to 100%. Serotypes containing H9 epitopes
  7. 7. are immunosuppressive. It is characterized by antigenic drift "minor antigenic variation" and antigenic shift "major antigenic variation". It is enveloped with segmented RNA (8 segments), 80-100 nm in diameter. There are two pathotypes; low and high pathogenic AIV. It is propagated in 9-11 day old ECE via allantoic sac causing death of embryo in 1-2 days. Infection occurs by ingestion, inhalation, cloacal, conjunctival, wound and blood sucking insects. Transmission occurs via the miagratory birds, contaminated shoes, equipments, clothing, direct and indirect contact with infected birds. Host Signs & Lesions P & T All birds. The aquatic birds are clinically diseased and carriers). I.P is 1-3 days. According to the pathotypes; there 2 forms of the disease: Mild Form = Low pathogenic AIV: mild signs or no observable signs in chickens. In turkey, moderate mortality due to the higher chance of co-infection with mycoplasmosis that aggreviate the infection. Highly virulent Form = Highly pathogeniv AIV (fowl plague): severe disease take one of 2 coarses as follows: -Peracute form: Sudden high mortality without any symptoms or lesions. -Acute form: Sudden onset & rapid spread of high morbidity, sudden death, fever, marked inappetance, cessation of normal flock vocalization, depression, coughing, sneezing, nasal & ocular discharge, Sharp drop in egg production, swollen face due to edema in head region, severe cyanosis of comb & wattles, watery greenish diarrhea, nervous signs as paralysis, patchy hemorrhage in the shaft of long bone with very high mortality (up to 80-100% in 2-5 days in chicken & turkeys). Mortality increases in an exponential fashion i.e. 5-10 times as the preceeding day and peaks at the 6th -7th day of illness. Rapid rigor mortis, dehydration, S/C yellowish-red edema in the head region. Skin necrosis in the comb & wattles. Sinusitis, trachitis, conjunctivitis & air sacculitis. Hemorrhage on and in the pectoral muscle, inner surface of keel bone, coronary fat, proventriculus mucosa, under the cuticle of the gizzard & lymphoid tissue of intestinal tract. Hemorrhagic enteritis in the duodenum with blotchy hemorrhage in pancreas. Ovarian regression or hemorrhage. Turkey lesions is less marked than those of chickens, while ducks may be symptomless, lesionless (asymptomatic carriers). P-Proper cleaning & disinfection of pens with vaccination by inactivated vaccines. T- None but notification of the authorities is a must. Rapid culling of the stocks.
  8. 8. Differentiation between ND and HPAI: Criteria ND HPAI Incubation period 5-7 days 1-3 days HA of rabbit RBC -ve +ve Elution of HA Very fast. Very slow. Disease in pigeon +ve -ve Course of disease Few hours or more. 3 days or more. Histopathology No perivascular cuffing. Perivascular cuffing in brain. 10-Infectious Bronchitis ‫ي‬ ‫ا‬ ‫ا‬ ‫ب‬ ‫:ا‬ Highly infectious and contagious disease caused by Coronavirus ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It is an enveloped, ssRNA, 80-120 nm in diameter. It is originally non-hemagglutinating and can hemagglutinates RBC after chemical (tanic and phosphoric acid) or enzymatic treatment (trypsin). It is propagated in 9-11 days old ECE via allantoic sac causing dwarfing, curling and death of embryo after serial passages. The virus has classic and variant serotypes with or without cross protection. Massachusset's strains induce cross protection for all serotypes by about 45%. Infection occurs by inhalation of polluted air. It is transmitted via the polluted shoes, equipment, clothing as well as the direct & indirect contact with infected birds. Intercurrent diseases as ND, ILT, coryza, E.coli, CRD & H9N2 predispose to more severe and prolonged disease. IBV serotypes Isolates of IBV are divided into different serotypes based on the virus neutralization test in embryonated eggs, tracheal organ cultures or identified molecularly using RT-PCR and the RFLP test or nucleotide sequencing. In general, different serotypes of the virus do not cross-protect. However, some strains of the virus are quite effective at inducing cross protection against other serotypes or genotypes. Variant serotypes IBV has the ability to change rapidly resulting in new variant serotypes. The prevalence of variant IB serotypes must first be determined before the use of a vaccine containing these viruses. Variant viruses may be present when “IB-like” problems are seen in flocks properly vaccinated with Massachusetts type vaccines. On the other hand, existing vaccines may represent the protectotype needed in order to get protection against the variant strain. When currently available products prove to give insufficient protection against an emerging virus, the development of a homologous vaccine against the new variant is justified (e.g. IBV 4/91).
  9. 9. IB variant D1466 IB variant D1466, a strain belonging to D212 serotype, is of particular importance because it behaves somewhat differently from other important IBVs. Molecular analysis of the S1 spike of the virus genome has shown that D1466 is the least related genetically of the known IB variants. This is confirmed by protection studies which show that little cross protection is provided by heterologous vaccines. However, there was evidence of an increased incidence of disease problems associated with D1466 and some indication that these new isolates may have increased in virulence. A live and inactivated D1466 vaccine was developed for use in breeders and layers. The inactivated vaccine continues to be used, but currently no live attenuated D1466 vaccine is available to help control the disease outbreaks caused by D1466. Host Signs & Lesions (P) & (T) Chickens I.P is 18-36 hours. In chicks under 5 wks: Rapid onset & spread,gasping, rales with some gasping, sneezing,coughing, chirping, watery eyes & high mortality up to 25% especially if the condition is complicated by any bacterial invasion. The coarse is 3-6 days. In growing chickens (6-10 wks): Similar but milder than those in young chicks but with marked retardation in the growth. Low mortality (5-10%) in 7-10 days. In semi-mature & laying chickens: Very mild respiratory signs with drastic drop in egg production up to 50%. Egg abnormalities (small-sized, deformed, rough-shelled or soft- shelled & shell-less eggs & watery albumin). Return to full lay may take 4-6 wks but the expected potential production is nerver attained. Flock signs may last 10-14 days. False, blind or internal layers are commonly observed 8-10 wks after the onset of an outbreaks of IB in pullets. They are apparentlly healthy, visit the nest frequently but lay no eggs & easily detected by using the trap nests. Lesions of IB: Catarrhal tracheitis, bronchitis & pneumonia. In classic cases, there is a yellowish white caseous plug at the tracheal bifurcations which block the air passage and may cause asphxyation . Air sacculitis may or may not occur. In false layers, shortening & narrowing of oviducts with abdominal ovulation & egg peritonitis. P-Vaccination of chicks in the first week of life using live H120 vaccine. Vaccination of breeders and layers 4 weeks before lay if an important problem in your flock. T-None for treatment but all try supportive therapy.
  10. 10. 11-IB–793b Variant Sudden Death Syndrome in Broiler Parents: Host Signs & Lesions P & T Chickens Sudden death in affected birds. Muscular shivering, otherwise as for standard IB. Edema of the pectoral muscles and subcutaneously on abdomen. Lesions progress to necrosis and scarring of deep pectorals in convalescence. In layers the ovules are intensely congested. Other lesions of classic IB are encountered in this condition. As IB 12-Infectious nephritis nephrosis = INNS = Infectious uremia: Variant nephro-pathogenic strains of Cronavirus as T, Gray or Holte strains. All properties are similar to that of IBV. Heavy breeds, males and brown egg types are more severely affected. High protein% in feed espcially of meat meal is an exacerbating factor for the disease. Host Signs & Lesions P & T Chicken 3-9 wks (average 6 wks) are mostly affected but adults are also affected. I.P is 1-2 days. Rapid onset and spread of the disease. Mild respiratory signs followed by marked depression, loss of appetite, severe thrist, voiding urates in the droppings with high mortality up to 30%. In adults, drop in egg production up to 50% with lowered hatchability about 10-30%. Flock signs last 2-3 wks. Dehydration of carcass with dark-red discoloration of muscles. Marked kidney enlargement with urates accumulation and sometimes urolith in the ureters. In severe cases, urates is present in pericardium, peritonium and air sacs. P-Vaccination. T-None but all try supportive therapy & low protein% of feeds + ammonium chloride in feed "2- 3 kg/tonn" + acetyl salycilic acid in drinking waters. 13-QX strain infection of IB = IBV variant D388 (QX): Host Signs & Lesions P & T Chicken 4 weeks of age and layer birds Respiratory signs in broilers older than 4 weeks of age + low egg production rate with peak levels reaching only between 30-55% in apparently healthy flocks. The affected bird gas a penguin like position. Cystic oviducts with watery contents that could exceed one liter or partially atrophic oviducts with large cystic dilatations. Thin oviduct walls and transparent in the cystic areas. The ovaries in the birds are functional and look normal. P-Vaccination with H120 at one day old and 4/91 at 14 days. T-None but all try supportive therapy.
  11. 11. Protectotypes New serotypes may emerge as a result of small changes in amino acid sequence of the S1 gene of the virus spike. Although it appears to be a new serotype, most of the viral genome remains unchanged. This may be the reason why IB vaccines of a specific serotype can protect against strains of IB not belonging to the same serotype. From a practical point of view is more relevant to think in terms of protectotypes than serotypes. Studies have shown that vaccination with two different types of IBV vaccine can provide broad protection against different IBV types. The best combination of vaccines was reported to be MA5 at 1-day of age followed by 4/91 at 14 –days of age. 14
  12. 12. -Infectious Laryngeotrachitis = ILT ‫ا‬ ‫ا‬ ‫وا‬ ‫ة‬ ‫ا‬ ‫ب‬ ‫:أ‬ It is highly infectious and contagious respiratory disease caused by Herpesvirus ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It is an enveloped DNA virus. It is propagated in 9-11 days old ECE via CAM causing death of embryo within 2-12 days with the formation of plaques on CAM (2 days PI) and intranuclear inclusion bodies (36 hrs PI). Infection occurs by inhalation and ocular route. It is transmitted via direct and indirect contact with infected birds, carrier and vaccinated birds, contaminated shoes & equipments. Some recovered birds remain carriers for about 2 years. Host Signs & Lesions (P) & (T) Chickens, pheasants & their crosses. I.P is 4-12 days. The disease has two forms: 1-Epizootic = acute Form = Hot bird disease: Rapid spread of high morbidity (90-100%) and high mortality (10-25%). There is pump-handle respiration due to dysnea. Coughing, sneezing, nasal and ocular discharge with shaking of head to get rid of the mucous exudates present in the trachea. Gurgling sound with expecturation of blood-tinged mucus which is observed on the wall of the farm at the level of the head of affected birds. There is sharp drop in egg production up to 40%. The course may last 10-14 days. ILT recycling is reported in caged layers in which the disease affect most but not all of birds then in about 10-12 days a second wave of the disease sweeps through the flock. The recycling may occur in chickens vaccinated via drinking water. In early stage, catarrhal laryngitis and tracheitis with intranuclear inclusion bodies that is detected in this stage in 1-3 days postinfection. In later stage, hemorrhagic tracheitis with degeneration of tracheal mucosa with the presence of blood tinged mucus in the tracheal lumen. 2-Enzootic or mild Form: unthriftness of birds, drop in egg production up to 20%, watery eyes, conjuctivitis (may be hemorrhagic), pesistent nasal discharge and swelling of the infraorbital sinuses. Low morbidity (up to 5%) and very low mortality. Course may last 3-4 wks. Edema, conjuctival congestion and enlarged infraorbital sinuses are the only lesions of this form. P-Vaccinate, but only if a problem in your area and do not vaccinate unnecessarily. T-Emergency vaccination with supportive therapy may give good interferance.
  13. 13. 15-Avian encephalomyelitis = Epidemic tremors =AE ‫ا‬ ‫ش‬ ‫ر‬ ‫:ا‬ caused by Enterovirus ‫ا‬ ‫ت‬ ‫و‬ ‫ا‬ which is belonging to Picornaviridae ‫ا‬ ‫ا‬ ‫ه‬ ‫ر‬ ‫وآ‬ ‫ا‬ ‫ه‬ ‫ت‬ ‫و‬ ‫.ا‬ Non-enveloped, RNA, 16-25 nm. It is propagated in 5-6 days old ECE via yolk sac causing paralysis of legs & muscular dystrophy of the embryo after adaptation by 5-12 blind passages. It is also propagated by intra-cerebral inoculation in 1-day old chicks. The infection occurs by vertical transmission and horizontal route via direct contact with infected birds & indirect contact through ingestion of the contaminated feed or water. There is no antigenic difference between strains of the Enterovirus. Host Signs & Lesions (P) & (T) Chicken, turkey, pheasant & Japanese quail. All ages are affected but the nervous signs are only seen in 1-6 wks old (mainly 12-21 days of age). I.P is dependent on the route of infection. It is 1-7 days (vertical transmission) but it is 10-17 days (horizontal transmission). In young chicks (1-6 wks), there are nervous signs including ataxia, incoordination of gait, paresis or paralysis of the two legs with intermittent rapid tremors of the head & neck that particularly evident if the birds is held in palm of the hand, prostration (due to starvation) & death (due to trampling). Morbidity may reach 50% and mortality ranges from 5-20% (may reach 60%). Some recovered birds may develop blindness due to unilateral or bilateral opacity of pupil (catarct). In semi-mature and adult, no nervous signs but in adults, there is transient drop in egg production (10-15%) which lasts for 10-14 days. Low hatchability due to late embryonic mortality & hatched chicks have ataxia & paralysis of legs. In turkey & other species, the disease is similar but milder than that in chicken. No gross PM lesions belonging to AE. Microscopical involvement of brain "perivascular cuffing" and in the proventriculus, gizzard and pancreas "massive lymphocytic infiltration" with no involvement of peripheral nerves. P-Vaccination of layer & breeders at 12 wks old by live vaccine via drinking water or wing web sticking. Beta- propiolactone Killed vaccine also used at 8-16 wks old. T-None.
  14. 14. 16-Infectious bursal diseases = Infectious bursitis ‫ي‬ ‫ا‬ ‫آ‬ ‫ب‬ ‫أ‬=‫ج‬ ‫ا‬ ‫ز‬ ‫أ‬=‫رو‬ ‫ا‬ ‫ض‬ : A highly infectious and contagious disease caused by Birnavirus ‫زي‬ ‫ا‬ ‫وي‬ ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫.ا‬ It is non-enveloped, RNA, 60 nm in diameter. It has 2 serotypes; serotype-1 which is pathogenic to chicken and serotype-2 is apathogenic for chicken and isolated from turkeys. Serotype-1 has different subtypes "virulent = classic, very virulent and variant subtypes". It is propagated in 9-11 days old ECE via CAM causing death of embryo within 8 days PI that appear edematous, stunted in growth and show liver necrosis. It is also propagated in tissue cultures. Infection by ingestion and inhalation of the polluted air, feed and water. Transmission via direct and indirect contact with infected birds. The lesser meal worm (Alphitobius diapernus) harbors the virus for weeks. Host Signs & Lesions P & T Chickens (3-6 wks old) but it may occur up to 11 wks. -Subclinical Form: It occurs if the infection occurs in chicks under 3 wks of age either with classic or variant strains. It causes rapid profund bursal atrophy leading to severe persistent immuosuppression with no clinical signs. -Clinical Form: I.P is 2-3 days. It occurs due to infection of chicks older than 3 wks of age and has two phases: -Inflammatory stage: It is about 5 days. Sudden loss of appetite, tremors of the whole body, self-vent picking, incoordination with hunched up appearance of the affected birds that squate with their neck extended. Profuse watery yellowish-white diarrhea with oily texture soiling the vent region with straining during defecation. The course last 5-9 days. High morbidity (10-30%) with low mortality (1-20% - average 7%) in commercial broilers but in commercial layers & native breeds, the mortality may reach to 60%. Mortality occurs in a charactersitic spiking curve with peak mortality is reached in the 4th day of the disease and then gradually decline to zero during the next five days. Dehydrated mucles, ecchymotic hemorrhage on the thigh muscles. Patchy hemorrhage on the junction between the proventriclus and gizzard. Hepatomegaly with peripheral yellow infarct. Moderate splenomegaly. Marked enlargement of bursa of Fibricius to twice the normal size. The exterior of bursa is covered by gelatenous exudate. The interior of bursa is edematus, reddened or hemorrhagic with prominent plicae. -Resolution phase: it starts from theend of the 5th day of infection. In it, no mortality occur and the size of the BF reduced to one third iof its normal size. P-Biosecurity & vaccination. T-None but metaphylaxis or ring vaccination may be helpful using D-78 vaccine.
  15. 15. Gumboro-related diseases: These are diseases in which the incidence of it increases with the occurrence of Gumboro disease or with the vaccination with hot Gumboro vaccine. They include gangrenous dermatitis, inclusion-body hepatitis anemia syndrome and may include E.coli infections. Prevention: Biosecurity + getting rid of the lesser meal worm + trice vaccination of chicks with live vaccine via drinking water or eye drop "at 7, 13 and 20 days old in commercial broilers – 7, 14, 21 and 28 in chicks commercial layers and breeders + vaccination of layer and breeders at 18 wks old by Killed vaccine". The vaccination program depends on multiple factors, the most important of them are the degree and homogenicity of the MDA, the breed of birds, the type of vaccines and the half life time of the MDA. Control: No sepcific treatment is present for the disease but metaphylaxis or ring vaccination in multi-house system may be helpful using D-78 vaccine. The previous measures are tried in addition to the adminstration of potent diuretics and using a low protein % of feed to reduce the urate production.
  16. 16. 17-Chicken infectious anemia = CIA = blue wing disease ‫ج‬ ‫ا‬ ‫ا‬ ‫:ا‬ A disease caused by Circovirus. It is non-enveloped, ssDNA, 25 nm in diameter. It is propagated by IM inoculation in 1-day old chick and also in MDCC-MSB1 tissue culture cells (these are cell line derived from MD lymphoma). Vertical & horizontal infection occurs via the contact exposure shortly post-hatch via ingestion and inhalation of the polluted air, feed and water. Host Signs & Lesions P & T Chickens (2-3 wks old). I.P is 12-17 days. Diseased birds are anorexic, lethargic, depressed and markedly pallor due to the reduced erythrocytic number. Packed cell volume "PCV "is less than 25%, the blood smears reveal severe anemia and leucopenia. Blood is watery and clot slowly i.e. prolonged clotting time. The mortality is around 10% but may reach to 50% depending on the presence of the concurrent infections. CIA is a highly and deeply immunosuppressive disease due to its severe effect on the thymic tissue leading to very deep effect on the T-lymphocytes i.e. immunosuppressive on the CMI. Age resistance to disease begin at 1 wk old and is completed at 2 wks post-hatching but it can be overcome by CIA co-infection with other immunosuppressive agents as IBDV, MD, REV and mycotoxicosis. Pale organs, thymic and bursal atrophy, pale or yellowish discolord bone marrow. Hemorrhage may be present in or under the skin (especially at the tip of the wing hence its name Blue wing disease), skeletal muscles and other organs. Enlarged liver and gangrenous dermatitis may also be present. P- Vaccination of breeders at 11 wks old by live vaccine. T-None. 18-Pox: An infectious, slow spreading avian disease caused by Avipox virus. It is DNA virus, 300 nm in diameter. It has four strains; fowl pox virus, turkey pox virus, pigeon pox virus & canary pox virus. It is propagated in 9-12 days old ECE via CAM causing formation of greyish plaques of cell prolifiration on CAM and the formation of intracytoplasmic inclusion bodies (Bollinger’s body inside of which there very minute bodies known as Borrel's bodies).
  17. 17. The infection occurs by direct contact with infected birds, wound infection and mosquitoes bites. The disease has a seasonal incidence mostly in spring and summer due to the high mosquitos' populations. Host Signs & Lesions P & T Turkeys, Chicken Pigeons Canaries Pheasants Quails I.P is 4-10 days. Skin = cutaneous = dry Form: The presence of small yellow warts-like nodules on wattles, comb, face, legs around vent and under the wings. They increase in size and become dark brown scabs then drop off. Diphtheritic = Mucous membrane = Wet Form: The presence of yellow, cheesy necrotic lesions (Diphtheritic or pseudomembrane) on the Mucous membrane of mouth, nares, pharynx, larynex & trachea. It is diffecult to remove and leave hemorrhagic or eroded surface when forcely removed. It interferes with swallowing and respiration leading to starvation and suffocation. Mixed Form: both symptoms of the two forms are present. Naso-ocular Form → coryza-like signs. Mortality ranges from 3-10% up to 50% in case of complications. The course is 3-4 wks and may be 6-8 wks in case of complications. P-Vaccination in areas of high mosquito populations. Succsseful vaccination is detected by the presence of “takes”. T-Swab lesion with Tr. of iodine 5% after rubbing it against a hard object in addition to antibiotic oxytetracycline. Takes: It is a wart like lesion occurs as a post-vaccination reaction at the site of vaccination. It is formed 7-10 days post-vaccination. By mean of takes, the successful vaccination can be estimated. The presence of takes in the majority of taken sample means a successful vaccination. 19-Marek's disease = MD: It is a highly infectious, contagious and oncogenic poultry disease caused by Herpes B virus. It is highly cell associated virus due to which it escapes the effect of the antibodies after it once gains entry into the body. There are three serotypes: Serotype-1 is pathogenic for chicken, the serotype-2 is apathogenic for chicken and the serotype-3 is apathogenic for turkey. All these serotypes have the MD tumor associated surface antigen (MATSA) and so all of them can be used as a vaccinal virus. Infection occurs by inhalation of feather dander that contain fully infective enveloped virus.
  18. 18. Host Signs & Lesions P & T Chickens, very rare in turkey, pheasant, quail & pigeon. I.P is as short as 3-4 wks & as long as months. I-Classic form: occur in 3-5 months old although most cases occur around 3 months with affections in peripheral nerves or nerve plexuses & eyes. -Peripheral nerves involvements: -If sciatic neve involved, progressive lameness of legs with one stretched foreward & one is stretched backward as ballerna-like. -If brachial n. Involved; droopiness of wings. -If vagus & intercostal n. involved; dysnea + gasping. -If crop & gastric neve involved, there are crop impaction & digestive troubles & diarrhea. -If cervical neve involved→torticollis. In peripheral nerve affections, birds cann’t reach feed & water →loss of weight, pale comb & wattles & die from starvation. -Ocular form = Gray eye: Unilateral or bilateral concentric annular or spotty depigmentation or diffuse grayish fading of iris + irregular pupil (serrated, slit or pin-head like) leading to blindness. II-Acute form: → young birds raised intensively at 1.5-2.5 months with rapid coarse & high morbidity & mortality up to 50%. Affected birds are depressed, some birds show skin. tumors at the feather follicle & others may die suddenly without preceeding symptoms but, only small percent of birds show paralysis. The PM lesions are as follows: I-In classic Form, affected nerves show localized or diffuse swelling due to edema & mononuclear infiltration + loss of cross striations. II-In acute Form, lymphoid tumors in gonads (cauliflower), spleen, kidneys, lung, heart, liver, digestive tract, mesentery, skeletal muscles & skin with or without nerve lesions. P-Vaccination of 1 day-old chicks & nowadays the intraoval vaccination is used. T-None.
  19. 19. 20-Trnsient paralysis Host Signs & Lesions P & T Chickens (5-18 wks) It is uncommon encephalitic symptom of MDV infection in which birds suddenly develop various degree of paresis of legs, wings & neck. Mortality is low and the disease is characterized by spontaneous recovery. The signs usually disappear within 1-2 days. --- 21-Erythroleucosis = Erythroblastosis: It is one form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. The leucosis-sarcoma viruses are divided into 6 different subgroups; A,B,C,D,E & J. Egg borne i.e. transmitted to very young chicks from infected older birds. Host Signs & Lesions P & T Mature chicken over 6 months of age. I.P is 2-5 months. It is a sporadic cases characterized by neoplastic prolifiration of erythroid cells and their intravascular accumulation causes splenomegaly. Progressive anemia (pale yellowish discoloration of comb & wattles), weakness, emaciation, diarrhea and drop in egg production. Blood changes: Blood is pale, watery, slow to clot with reduced hemoglobin% Critaria Plasma WBC RBC Normal 55 1 44 Case 88 1 11 Diffuse splenomegaly, hepatomegaly, enlarged kidney, lung, heart with cherry red dicoloration of these organs. None
  20. 20. 22-Myeloblastosis = Granuloblastosis: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. Host Signs & Lesions P & T Mature chicken over 6 months of age. I.P is 2-5 months. It is a sporadic cases characterized by extravascular prolifiration of granulocytes which spread to internal organs causing diffuse splenomegaly, hepatomegaly and enlarged kidney with greyish mottling and granular appearance. The enlarged, granular, grayish brown liver is described as Morroco leather appearance of liver. Bone marrow is pale or pink. Anemia (pale comb & wattles),weakness, diarrhea, emaciation and drop in egg production. Blood changes: Blood is pale, watery, slow to clot with reduced hemoglobin%. Critaria plasma WBC RBC Normal 55 1 44 Case 16 69 15 None 23-Myelocytomatosis: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. Subgroup J. Egg borne. Host Signs & Lesions P & T Chicken (3-11 wks). I.P is 2-5 months. It is a sporadic cases that is characterized by tumor formation as small yellowish white solid friable like cheese along the inner surface of ribs, inside the keel bone, pelvis & cranium and sometimes in spleen, liver and bone marrow. Blood changes: absent None
  21. 21. 24-Osteopetrosis: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. Host Signs & Lesions P & T Mature chicken (2-3 months) more in male than in female. I.P is 2-5 months. Jerkey gait with bilateral, irregular thickening of the diaphysis long bones of legs then marked thickening of legs with “boot-like appearance”.Affected legs are warm. Blood changes: reduction of marrow tissues with relative or absolute lymphocytosis. Lesions: Bilateral thickenings of the diaphysis of the long bones of legs, wings, pelvic girdle & spines. The marrow cavity is narrowed or completely oblitrated. None. 25-Other sarcoma tumors: One form of sarcoma group caused by Retrovirus. Oncogenic RNA viruses. Host Signs & Lesions P & T Chicken I.P is 2-5 months. Nephroblastomas → tumor of epithelial tissue of kidney which occurs between 1.5-6 months of age. Endotheliomas → tumor of vascular organs " spleen, liver or bone marrow". Hemangiomas & teratomas are other types of tumors. None.
  22. 22. 26-Lymphoid leucosis = Visceral lymphomatosis = Big liver disease: Retrovirus. Oncogenic RNA viruses. Host Signs & Lesions P & T Chickens over 16 wks old More in females than in males. I.P is 2-5 months. Anemia manifested by pale comb & wattles with progressive emaciation of birds, green diarrhea and easily palpated hepatomegaly. Sick birds usually die. Blood changes: massive prolifiration of immature lymphoblastes. Lesions: There are 3 forms of LL: Focal = nodular Form: The formation of cicumscribed greyish tumors of various sizes in the liver, kidneys, heart (tigeroid heart), seosal surfaces, ovary, spleen and the lungs. Diffuse Form: The diffuse enlargement with greyish mottling of the same organs especially the liver giving rise to the so called “Big liver disease” in which the liver size may reach half of the whole body size. Mixed Form: the symptoms of both forms are present. None 27-Reticuloendotheliosis: Neoplastic disease caused by Retrovirus type C. Oncogenic RNA viruses that are serologically and genetically distinct from avian leucosis-sarcoma group. Infection occurs horizontally. Host Signs & Lesions P & T Chickens, turkeys, ducks, geese (15-20 wks) and quail (6-10 wks) Chronic neoplasia, a runting disease syndrome has occurred in flocks and some birds show a peculiar feathering abnormality “nakanuke” in which wing feathers have adhesions of the barbule to part of the feather shaft. Some birds show paralysis. REV is an immunosuppressive disease. It has 2 forms of neoplasia: Acute reticulum cell neoplasia. In liver, spleen, gonads, heart, kidney & pancreas. Chronic lymphoid neoplasia. In visceral organs plus peripheral nerves. None
  23. 23. 28-Lymphoproliferative diseases of turkey: Retrovirus type C. Oncogenic RNA viruses that distict serologically and genetically from avian retrovirus. Infection is horizontally and the incidence of infection is higher than that of the disease. Host Signs & Lesions P & T Turkeys (7-18 wks). Affected bird die suddenly after a period of depression. About 20% of birds may be affected. Marked splenomegaly that is pale and marbled. Moderate hepatomegaly that have miliary grayish white foci. Miliary or diffuse tumor infiltrations occur in gonads, intestinal wall, pancreas, lungs, myocardium & thymus. Peripheral nerves may be enlarged. Blood changes: Leucocytosis and leucopenia. None 29-Other tumors: Disease + Cause + host Signs & Lesions P & T Connective tissue tumors Fibroma & fibrosarcoma, Myxoma & myxosarcoma, Histiocytic sarcoma, Chondroma, Osteoma & osteogenic sarcoma None Epithelial tumors Nephroblastoma Embryonal nephroma, renal adenocarcinoma, adenosarcoma, nephroblastoma, cystadenoma, Nephroma Papillary cystadenoma, carcinoma of the kidney, Hepatocarcinoma, Adenocarcinoma of the pancreas, Thecoma, Granulosa cell carcinoma, Seminoma Adenocarcinoma of the testis, Squamous cell carcinoma. None Endothelial tumors Hemangioma Hemangiomatosis, endothelioma, hemangioblastomas, hemangioendotheliomas, Angiosarcoma, Endothelioma, Mesothelioma. None
  24. 24. 30-Avian adenoviruses ‫ا‬ ‫ت‬ ‫و‬ ‫:ا‬ It is icosahedral, non-enveloped DNA viruses. It is highly resistant viruses to the adverse environmental and chemical condition. It is divided into 3 groups: The first group or conventional adenoviruses: They are isolated from chicken, turkeys, geese, and other avian species. Its role as a primary pathogens is not well defined but they appear to have a role as a secondary pathogens in association with CIV and IBDV which the latters enhance the pathogenicity of the adenoviruses. Vertical transmission is very important but horizontal spread is also important. It hemagglutinates rat RBC. Incubation period is short (1-2 days). The diseases and disorders caused by or associated with viruses in this group are inclusion body hepatitis "IBHV in chickens - 70-90 nm), Mild Respiratory Disease (MRDV -- 70-90 nm), hydro-pericardium-hepatitis syndrome "HHS" = Angara disease and quail bronchitis "QBV - 69-75 nm). The second group: It includes: Hemorrhagic enteritis "HEV of turkey -70-80 nm", Marble spleen disease "MSDV of pheasant - 70-90 nm) and avian adenovirus splenomegaly "AASV of chicken – 70-90 nm). The adenoviruses of this group are transmitted mainly through oral and cloacal routes and unlike group I adenoviruses, there is no epidemiological evidence for egg transmission. The third group: It includes the viruses isolated from ducks and chickens with egg drop syndrome (75-80 nm). It hemagglutinates the avian RBC of chickens, ducks, turkeys, geese, pigeons and parrots. There are three types of egg drop syndrome: 1-Classic type: In which the route of transmission is mainly vertical route. 2-Endemic type: In which the route of infection is mainly the oral route and the infection is usually transmitted via the egg trays. 3-Sporadic type: In which the route of infection is mainly the oral route and the infection is usually transmitted via the wild ducks and geese.
  25. 25. Disease Host Cause Signs & Lesions P & T IBH Gumboro- related disease Commercial broilers (3-7 wks). Group-I Depression, inappetance, ruffled feathers, pale comb and wattles. Swollen yellowish mottled liver with petechiae and subcapsular hemorrhage. Kidneys and bone marrow are pale discolord. Blood is thin. Bursa and spleen are small sized. Microscopically – basophilic intranuclear inclusions. P.Biosecurety. T.None. MRD Chickens Group-I Mild snick and cough without mortality. Mild catarrhal tracheitis. P.Biosecurety. T.None. HHS = Angara disease Chickens Group-I QB Quail (1-5 wks) Group-I Respiratory distress, coughing, sneezing, rales, watery eyes and conjunctivitis with mortality may be 100% in birds < 2wks and up to 25% in birds > 4 wks. The disease course is 3-6 days. HE of turkey Turkeys Group-II Sudden death and bloody droppings from vent. The usual mortality is 0.5-3%. Immunosuppression with increased susceptibility to colibacillosis. Severe hemorrhage mostly in the upper part of intestine plus splenomegaly and mottling. P-Vaccination. T-None. MSD Pheasant Group-II It affects semi-mature and mature pheasants. Sudden death without signs. Splenomegaly with mottling (marbling) and massive lung edema. None AAS Chicken Group-II Splenomegaly with mottling (marbling). None. EDS 76 Chickens + Ducks Group-III Egg drop at peaking time or failure to peak (5-50%) and last for 3– 4 weeks. Rough, thin or soft-shelled eggs and shell-less eggs. Loss of shell pigment. Poor internal egg quality. Lack of signs in the birds themselves. No specific lesion – only a slight atrophy of ovary and oviduct. P.Vaccination with killed vaccine prior to lay. T.Supportive.
  26. 26. 31-Viral arthritis: Reo virus ‫ا‬ ‫ا‬ ‫ا‬ ‫ت‬ ‫و‬ ‫ا‬ infection. Reo means respiratory enteric orphan virus. Host Signs & Lesions P & T Commercial broiler and breeders IP is I-13 days. Lameness, low morbidity, poor growth. Hock arthritis, swelling of tendon sheath, unthriftiness, rupture of gastrocnemius tendon. Swelling and arthritis of digital flexor (footpads) and metatarsal extensor tendon sheaths (hock joints). The tendon sheaths contain yellowish or pus like fluid. Articular surfaces of tibia and metatarsal show erosions. Footpad is swollen. Articular cartilages is ulcerated. Tissues hemorrhage and fibrosis is present in chronic cases. 32-Runting syndrome = Helicopter Syndrome = Pale bird disease = femoral head necrosis: Reo virus infection Host Signs & Lesions P & T Chicken 1-2 week old birds About 5-20% show the disease with deaths not exceed 2-4% due to concurrent complications, due to immunodeficiency due to bursal atrophy. Externally there is poor feathering and poor shank pigmentation. Internally, intestinal tract is found distended with poorly digested food. Gall bladder remains distended with bile. BF & thymus remain small & atrophic. Pancreas may be atrophic or even fibrosed. Ceca filled with froth & gas. Proventriculus may also be inflamed. 33-Pasty Vent Disease (Cloacal Pasting): Reo virus infection. Host Signs & Lesions P & T Chicks 3-4 days old. White pasty excreta, which stick around the vent feathers, forming a lump. About 10- 15% chicks may be affected, causing 3-5% mortality. The disease subsides in about 2-3 weeks. Catarrhal enteritis and cloacal distension with white, pasty excreta. Small necrotic foci may be seen in the liver. The abdomenal distension due to the closure of the vent by the lump of the excreta.
  27. 27. 34-Respiratory disease due to reovirus: Reo virus infection Host Signs & Lesions P & T Chicks 3-4 days old. Some authors isolated a reovirus from cases of chronic respiratory disease (CRD) but their significance was overshadowed by the recognition of M. gallisepticum being mainly responsible for CRD. Others produced respiratory disease experimentally with reovirus. The real significance of this virus and the disease produced by it in nature has yet to be fully understood. 35-Rota virus infection: Rota virus Host Signs & Lesions P & T Chick in first week of life. Inappetance, diarrhea & increased mortality. Only diarrhea is observed in adult birds. Dehydration, intestines & ceca abnormally show fluid & gaseous contents. Cacking of feet and digits with dried faecal crusts is commonly seen. Mortality is around 5%. Viruses replicate mainly in mature villous epithelial cells. 38-Duck virus hepatitis: Host Signs & Lesions P & T All duck species except Muscovy ducks. It affects ages < 5 wks. I.P is 2-5 days. Sudden death of the affected birds, death in good condition, depression, fall on side, paddling of legs, arching of back, rapid deterioration and death occurs within an hour often in an opisthotonus position. Liver swollen with punctate/diffuse hemorrhages. Kidneys and spleen are swollen with diffuse hemorrhages. P.Vaccination of breeder to give MDA. T.Injection of antiserum of recovered birds (0.5 ml IM) or injection of hyper- immune yolk from eggs of vaccinated dam + effective antibiotics. Prevention: Vaccination of breeder by live vaccine at 70 day "primer dose" and 130 day "booster dode" to give high level of maternally derived immunity which protect the newlly hatched birds for about 1 month.
  28. 28. Control: Injection of hyper-immune antiserum of recovered birds (0.5 ml IM) or injection of hyper-immune yolk from eggs of vaccinated dam + effective antibiotics. 38-Duck virus Enteritis: Host Signs & Lesions P & T Duck & geese. I.P is 3-7 days. Sudden death of affected ducks with rapidly spreading disease. Drop egg production. Photophobia. Ataxia and tremor. The affected ducks hold its body in their wings. Closed eyes. Severe thirst and diarrhea, sometimes with dysentery. Dehydration. Paresis. Paraphemosis "penile prolapse in drakes". Cyanosis of the bill in the young. Severe enteritis, crusty plaques from esophagus to bursa (covered by yellowish plaques in later stages). Hemorrhage in intestine, body cavities, heart, pericardium, liver & spleen. Young ducks show thymic and bursal lesions. P.Vaccination. T.None, but Emergency vaccination is of value. 39-Goose Viral Hepatitis (Dorsey's Disease): Parvovirus ‫ا‬ ‫ا‬ ‫ه‬ ‫ر‬ ‫وآ‬ ‫ا‬ ‫ه‬ ‫ت‬ ‫و‬ ‫.ا‬ Vertical transmission resulting in congenital infection Host Signs & Lesions P & T Geese < 5 wks & Muscovy ducks up to 12 wks. I.P is age dependant; in very young it is 3-5 days but in older it is 5-10days. For goslings < 1 wk of age the signs are anorexia, reduced feed intake, excessive water intake, swollen eyelids, ocular & nasal discharge, profuse white diarrhea & prostration. Mortality with deaths occurring in 2-5 days. Older birds depending on the level of MDA exhibit anorexia, polydipsia, weakness with reluctance to move, nasal & ocular discharge, swollen & red uropygial gland, eyelids & profuse white diarrhea. Membrane covering tongue, loss of down, reddened skin especially at the cloacal region. Pericardial effusion "about 5-10 ml of faint yellow discolord fluid" with fibrinous pericarditis, pale myocardium, swelling & congestion of liver, spleen & pancreas. Ascites, & perihepatitis. P.Vaccination of breeder to give MDA. T.Injection of antiserum of recovered birds (0.5 ml IM) or injection of hyper- immune yolk from eggs of vaccinated dam + effective antibiotics.
  29. 29. 40-Muscovy ducks Parvovirus: Muscovy ducks Parvovirus is distinct from GVH virus. It is transmitted by horizontal and vertical routes. Host Signs & Lesions P & T Muscovy ducks. I.P is 4-7 days. Inappetance, thrist, crowding, conjuctivitis & nasal discharge. The feed & water are refused completely before death. The recovered birds are stunted. P.Vaccination of breeder to give MDA. T-None.
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Tables of poultry viral diseases Dr Fares El khayat


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