VIRAL DISEASES OF POULTRY (NONRESPIRATORY)
MAREK’S DISEASE
Synonyms: acute leukosis, neural leukosis, range paralysis, gray eye (when eye affected)
Species affected: Chickens between 12 to 25 weeks of age are most commonly clinically affected. Occasionally pheasants, quail, game fowl and turkeys can be infected.
Clinical signs: Marek’s disease is a type of avian cancer. Tumors in nerves cause lameness and paralysis. Tumors can occur in the eyes and cause irregularly shaped pupils and blindness. Tumors of the liver, kidney, spleen, gonads, pancreas, proventriculus, lungs, muscles, and skin can cause incoordination, unthriftiness, paleness, weak labored breathing, and enlarged feather follicles. In terminal stages, the birds are emaciated with pale, scaly combs and greenish diarrhea (see Table 2).
Marek’s disease is very similar to Lymphoid Leukosis, but Marek’s usually occurs in chickens 12 to 25 weeks of age and Lymphoid Leukosis usually starts at 16 weeks of age.
Learn MoreTransmission: The Marek’s virus is transmitted by air within the poultry house. It is in the feather dander, chicken house dust, feces and saliva. Infected birds carry the virus in their blood for life and are a source of infection for susceptible birds.
Treatment: none
Prevention: Chicks can be vaccinated at the hatchery. While the vaccination prevents tumor formation, it does not prevent infection by the virus.
LYMPHOID LEUKOSIS
Synonyms: visceral leukosis, leukosis, big liver, LL
Species affected: Although primarily a disease of chickens, lymphoid leukosis can infect turkeys, guinea fowl, pheasants, and doves, but not on a large scale.
Clinical signs: The virus involved has a long incubation period (4 months or longer). As a result, clinical signs are not noticeable until the birds are 16 weeks or older. Affected birds become progressively weaker and emaciated. There is regression of the comb. The abdomen becomes enlarged. Greenish diarrhea develops in terminal stages (see Table 2).
Transmission: The virus is transmitted through the egg to offspring. Within a flock, it is spread by bird-to-bird contact and by contact with contaminated environments. The virus is not spread by air. Infected chicken are carriers for life.
Treatment: none
Prevention: The virus is present in the yolk and egg white of eggs from infected hens. Most national and international layer breeders have eradicated lymphoid leukosis from their flocks. Most commercial chicks are lymphoid-leukosis negative because they are hatched from LL-free breeders. The disease is still common in broiler breeder flocks.
INFECTIOUS BURSAL DISEASE
Synonyms: Gumboro, IBD, infectious bursitis, infectious avian nephrosis
Species affected: chickens
Clinical signs: In affected chickens greater than 3 weeks of age, there is usually a rapid onset of the disease with a sudden drop in feed and water consumption, watery droppings leading to soiling of feathers around the vent, and vent pecking. Feathers appear ruffled. Chicks are listless and sit in a hunched position. Chickens infected when less than 3 weeks of age do not develop clinical disease, but become severely and permanently immunosuppressed (see Table 2).
Transmission: The virus is spread by bird-to-bird contact, as well as by contact with contaminated people and equipment. The virus is shed in the bird droppings and can be spread by air on dust particles. Dead birds are a source of the virus and should be incinerated.
Treatment: There is no specific treatment. Antibiotics, sulfonamides, and nitrofurans have little or no effect. Vitamin-electrolyte therapy is helpful. High levels of tetracyclines are contraindicated because they tie up calcium, thereby producing rickets. Surviving chicks remain unthrifty and more susceptible to secondary infections because of immunosuppression.
Prevention: A vaccine is commercially available.
EQUINE ENCEPHALITIS
Synonyms: EE, EEE, WEE
Note: This disease should not be confused with St. Louis Encephalits (SLE). Chickens are used as sentinels (test animals) in SLE suspect areas, such as southern Florida. While SLE is also carried by mosquitos, that is where the similarities between the two encephalitis diseases end. Chickens do not get SLE. Refer to Factsheet VM71 (St. Louis Encephalitis—The Role of Chickens) for more information on SLE.
Species affected: Equine encephalitis is a contagious disease of birds (especially pheasants), mammals (especially horses), and people. Birds are the major source of the virus.
Clinical signs: Two forms affect birds: eastern equine encephalitis (EEE) and western equine encephalitis (WEE). The clinical signs are identical and include reduced feed consumption, staggering, and paralysis. Surviving birds may be blind, have muscle paralysis, and have difficulty holding their head up. Damage to the bird’s nervous system varies with species. In pheasants, there is pronounced leg paralysis, twisting of the neck, and tremors. Mortality is high. Chukar partridges and turkeys show drowsiness, paralysis, weakness, and death.
Transmission: Infected mosquitoes are the primary source of the virus. The Culiseta melanuria mosquito is the primary transmitter of the virus to poultry. Other mosquito species transmit the disease too, but feed mostly on other animals. Cannibalism of sick or dead birds by penmates is a major source of transmission within pens.
Treatment: none
Prevention: Remove the source of infection by establishing mosquito control: keep weeds mowed in a 50-foot strip around bird pens. This removes cover and resting areas for mosquitos. Eliminate mosquito breeding areas. Fog areas with malathion.
It is possible to immunize birds, especially pheasants, with the vaccine prepared for horses. The recommended dose is one-tenth of a horse dose per bird.
Read also: Economic Benefits of Biosecurity in Poultry
AVIAN ENCEPHALOMYELITIS
Synonyms: epidemic tremor, AE
Species affected: The disease is most prevalent in chickens less than 6 weeks of age. Pheasants, corturnix quail, and turkeys are natural hosts as well, but less susceptible than chickens. Ducklings, young pigeons, and guinea fowl can be experimentally infected.
Clinical signs: Signs commonly appear during the first week of life and between the second and third weeks. Affected chicks may first show a dull expression of the eyes, followed by progressive incoordination, sitting on hocks, tremors of the head and neck, and finally paralysis or prostration. Affected chicks are inactive. Some may refuse to walk or will walk on their hocks. In advanced cases, many chicks will lie with both feet out to one side (prostrate) and die. All stages (dullness, tremors, prostration) can usually be seen in an affected flock. Feed and water consumption decreases and the birds lose weight. In adult birds, a transitory drop (5–20 percent) in egg production may be the only clinical sign present. However, in breeding flocks, a corresponding decrease in hatchability is also noted as the virus is egg- transmitted until hens develop immunity. Chickens which survive the clinical disease may develop cataracts later in life (see Table 2).
Transmission: The virus can be transmitted through the egg from infected hen to chick, accounting for disease during the first week of life. The disease can also be spread through a flock by direct contact of susceptible hatchlings with infected birds, accounting for the disease at 2–3 weeks of age. Indirect spread can occur through fecal contamination of feed and water. Recovered birds are immune and do not spread the virus.
Treatment: There is no treatment for outbreaks. Infected birds should be removed, killed and incinerated. Recovered chicks are unthrifty.
Prevention: A vaccine is available.
EGG DROP SYNDROME
Synonyms: egg drop, egg drop syndrome 76, EDS-76
Species affected: The natural hosts for EDS virus are ducks and geese, but EDS has become a major cause of reduced egg production in chickens in many parts of the world. No illness has been observed in ducks or geese. Chickens of all ages and breeds are susceptible. The disease is most severe in broiler-breeders and brown-egg layer strains.
Clinical signs: There are no reliable signs other than the effects on egg production and egg quality. Healthy-appearing hens start laying thin-shelled and shell-less eggs. Once established, the condition results in a failure to achieve egg production targets. Transient diarrhea and dullness occur prior to egg shell changes. Fertility and hatchability are not affected (see Table 2).
Transmission: It is believed that the syndrome was first introduced into chickens from contaminated vaccine. Vertical transmission occurs from infected breeders to chicks. Newly hatched chicks excrete the virus in the feces.
Treatment: There is no successful treatment. Induced molting will restore egg production.
Prevention: Prevention involves a good biosecurity program.
INFECTIOUS TENOSYNOVITIS
Synonyms: viral arthritis, tenosynovitis, teno, reovirus enteritis, reovirus septicemia, malabsorption syndrome, helicopter disease
Species affected: turkeys and chickens
Clinical signs: Several serotypes of the reovirus have been identified. Some localize in the joints (tenosynovitis) while others target respiratory or intestinal tissues (septicemic form) (see Table 2).
The principal sign of tenosynovitis is lameness with swelling of the tendon sheaths of the shank and area extending above the hock (see Table 2). Affected birds are lame, sit on their hocks, and are reluctant to move. Rupture of the tendon can occur in older roaster birds, resulting in permanent lameness of the affected leg. If more than two joints are affected, the entire carcass will be condemned.
Infection can also play a part in broiler stunting, the result of malabsorption syndrome. In chicks, malabsorption due to viral enteritis is called “helicopter disease” because feathering is affected. Wing feathers protrude at various angles. A reovirus is believed to play only a secondary role in this syndrome.
In commercial layer flocks, increased mortality may be the first sign of the septicemia form (see Table 2). Egg production will decrease by about two to three times the mortality rate. For example, a mortality rate of 5 percent will be accompanied by a 10–15 percent drop in egg production. In the septicemic form, joint involvement is present but less pronounced. Affected birds become cyanotic (blue) and dehydrated. The tips of the comb turn purplish. The entire comb darkens as the disease progresses.
Transmission: The infection spreads rapidly through broiler flocks, but less rapidly in caged layers. Spread is by respiratory and digestive tract routes. The virus is shed in the feces.
Treatment: There is no satisfactory treatment available. With hens, tetracycline, molasses, and oyster shell therapy is helpful.
Prevention: A vaccine is available for use in endemic areas or on endemic farms.
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