| Avian Encephalomyelitis | Incubation Period 2 to 4 days | Duration 1 to 3 weeks | | Primarily a viral infection of poultry, chickens, turkey and pheasants. First reported in 1932, the virus grows in the yolk sac and brain of the chicken embryo in eggs from nonimmune hens. Most prevalent in chickens 1 to 6 weeks of age. Susceptible chickens more than 5 weeks old will develop antibodies to AE, but do not show clinical signs at the time of infection. AE occurs world wide and occurs in all seasons of the year, but most cases are reported from Jan to June. Egg-passage transmission from infected hen to chick is the most common mode of spread, but direct contact of susceptible hatchlings with infected birds accounts for spread within the flock. Indirect spread via fecal contamination of feed and water also occurs. The virus can survive at least 4 weeks in droppings. Clinical signs appear at 7 to 10 days of age. Tremors of the head and neck are presumptive of the disease in the flock hence the name "Epidemic tremor". Affected chicks first may show a dull expression of the eyes, followed by progressive in coordination, sitting on hocks, tremors of the head and neck, and finally paralysis or prostration. Muscular tremors are best seen by exercising the bird. Affected birds are inactive; some may refuse to walk or walk on their hocks. Diagnosis is confirmed by fluorescent antibody test, virus isolation and agar gel precipitin test. AE must be differentiated from other encephalitic diseases such as ND, EEE, MD etc. There is no treatment for acute outbreaks. Control is through prevention. Affected birds should be removed, killed and incinerated. Recovered chicks are unthrifty. Prove good nursing during outbreaks will help with mortality. Prevention is by selecting hatching eggs from immune breeder flocks. Lifetime immunity is acquired through vaccination or recovery from a natural outbreaks. | | |
| | | Coronaviral Enteritis | Incubation period 2 to 3 days | Duration 10-14 days | | Coronaviral enteritis is an acute, highly contagious disease of turkeys of all ages. Cornavirus, a small RNA virus survives for long periods in frozen feces. The virus tends to localize in the intestine and bursa of Fabricius of young poults. The disease is recognized only in turkeys and mortality in young flocks may reach 50%. Exact distribution of the disease is not known, but it probably exists in all major turkey growing areas of the US and Canada. The disease in natural outbreaks appears to be transmitted by ingestion of contaminated materials. Feces from infected birds are rich in virus. The virus is not egg-transmitted. Spread is by direct and indirect contact. Clinical signs are sudden onset and rapid spread. Sick birds chill and chirp and seek heat. Other signs are depression, loss of appetite and weight, diarrhea, dehydration, cyanosis and death . Fecaes show mucous threads and urates. Morbidity and mortality can approach 100% in uncontrolled outbreaks. Diagnosis is based on farm history and gross autopsy findings, absence of other causes and positive fluorescent antibody (FA) test on frozen intestinal tract sections. Treatment is to medicate the feed with antibiotics and vitamins. Also the use of calf milk replacer and/or potassium chloride in the drinking water. Prevention is eradication only. | | | | | | Egg Drop Syndrome | Incubation period 3 to 5 days | Duration 4 to 10 weeks | | Egg drop syndrome is an infectious disease of laying hens caused by a hemagglutinating adenovirus and characterized by thin shelled and shell less eggs in otherwise healthy birds. The natural hosts for EDS virus are ducks and geese, but has become a problem with chickens of all ages . The disease is most severe in bro9iler breeders and brown egg layer strains, less so in white egg breeds. EDS was first introduced into chickens through contaminated vaccine. Transmission occurs by any of the conventional methods of disease spread. Infected birds excrete the virus in the feces. Vertical transmission is considered the primary mode of spread. Clinical signs are loss of color in pigmented eggs, followed by thin shelled or shell less eggs. Egg production drops by 40 percent. Virus isolation should be done in duck or goose embryos or cell cultures of duck or goose origin. Harvested allantoic fluid or cell culture should be checked for hemagglutinating activity in chicken RBC . There is no successful treatment . The endemic form in breeders can be controlled by washing and sanitizing incubators and egg trays before reuse. In layers, molting will restore egg production. Prevention is through the control of vertical transmission. Endemic EDS is associated with the egg-packing stations, as contaminated egg trays can be a major factor in spread. Virus is also present in fecal material, so hygienic procedures are required. | | | | | | Equine Encephalitis in Birds | Incubation period 2 to 5 days | Duration 2 to 4 weeks | | A contagious disease of birds, mammals, horses, and people caused by a virus. Two forms affect birds, eastern and western encephalitis. All birds are susceptible though EE is rarely diagnosed in confinement reared domestic poultry. Due to present day transporting of livestock, both disease have been diagnosed across the nation. Generally, each remains endemic to its original areas. The virus increases in titer in the mosquito, although increased titer is not necessary for transmission. Birds are the major source of the virus for vectors because birds develop higher titer than mammals. Infected mosquitoes are the primary vectors. The clinical signs of EEE and WEE are identical, signs include inappetence, staggering and paralysis. Surviving birds may be blind, have unilateral or bilateral paralysis of muscle groups and difficulty in holding up the head. Damage to the birds central nervous system varies slightly with species. Flock mortality is up to 95%. Diagnosis is by history, typical microscopic lesions, virus isolation or positive serology. The preferred serological test is virus neutralization using tissue-culture systems. Prevention is immunize birds with vaccine prepared for horses. Do not immunize birds until 6 weeks of age. | | | | | | Infectious Bursal Disease | Incubation period 3 to 4 days | Duration 4 to 7 days | | Acute contagious viral immunosuppressive disease of young chickens characterized by mild respiratory symptoms, white watery droppings, severe depression, vent picking and inflammation followed by atrophy of the bursa of Fabricius. All chicken are susceptible, but mostly affects chicks up to 12 weeks of age. Occurs world wide. Transmission is from bird to bird or by contact with contaminated environment. The virus is shed in exudates and excrements of infected birds. Spreads by air on dust particles within the poultry house. Clinical signs are sudden onset, rapid drop in feed and water consumption. Mucoid diarrhea with soiling of the vent feathers, feathers are ruffled, chicks are listless, pick at their own vent and sleep with beak resting on the floor. Surviving chicks remain unthrifty and are more susceptible to secondary infections because of imunosuppression. Diagnosis is confirmed on microscopic tissue study, fluorescent antibody test, virus isolation from bursa, and virus neutralization tests. No specific treatment and antibiotics, sulfonamides and nitrofurans have little or no effect. Vitamin-electrolyte therapy is helpful. . Prevention is with attenuated commercial vaccine. | | | | | | Avian Lymphoid Leukosis | Incubation period 3 to 16 weeks | Duration Chronic in flocks | | Avian lymphoid leukosis is a neoplastic disease of chickens caused by a virus of the leukosis/sarcoma group and characterized by tumor formation of the bursa of Fabricius with metastasis to other tissues and all abdominal organs. There are several manifestations : Lymphoid leukosis, myeloid leucosis (myeloblastosis, granuloblastosis), erythroid leukosis (erythroblastosis) hemangioendothelioma (tumors comprised of blood vessels), and osteopetrosis (bone leukosis). Susceptibility starts in ovo but decreases with age of the bird. Birds are most susceptible when young, but LL is seldom seen in broilers due to the long incubation period. The female is more susceptible than the male to all forms of LL except osteopetrosis, to which the cockerel is more susceptible. Stresses from other diseases increase the severity of leukosis. Because the virus has a long incubation period, signs are not noticeable until birds are 16 weeks or older. The disease produces progressive weakness, regression of comb, paleness, enlarged abdomen, emaciation and death. Greenish diarrhea develops in terminal stages. Diagnosis based on flock history and tumors, confirmed by typical progression of disease and differentiation from other diseases. There is no treatment. Prevention is to obtain chicks from LL-free sources, rear birds in isolation with adequate ventilation and biosecurity, prevent stress and control other diseases. | | | | | | Marek's Disease | Incubation 14 days | Duration chronic in flocks | | Marek's disease is a herpes virus-induced neoplastic disease of chickens characterized by tumor formations in nerve, organ, muscle and epithelial tissue with pleomorphic lymphoid cells. Affects chickens 2 to 16 weeks of age, stresses from other disease increase severity of MD. Herpes virus is cell associated and shed in skin scales and feather dander. Birds remain viremic for life but infected carriers may or may not be clinically ill. vaccination protects against tumor formation but not against MD infection. Occurrence is world wide wherever poultry is produced. Transmission is primarily by air within the poultry house, in feather dander, chicken house dust, feces and saliva. Infected birds carry virus in blood for life and are a source of infection to susceptible birds. Transmission by egg is of no significance. Clinical signs "gray eye" caused by tumors in the pupils and blindness, tumors of the liver, kidneys spleen, gonads, pancreas, lungs, muscles and skin. Birds develop tumors, emaciation and death. Diagnosis is based on history of no vaccination, presence of typical tumor pattern and affected birds. There is no treatment. Prevention is by vaccination at the hatchery, but vaccination only prevents tumor formation, not MD infection. All Marek's Disease vaccine must include HVT. |
|
