VIRAL DISEASES
(Exclusive of Respiratory Diseases)



AVIAN POX

AVIAN LEUKOSIS

EPIDEMIC TREMOR

INFECTIOUS BURSAL DISEASE

INCLUSION BODY HEPATITIS (I.B.H.)

TRANSMISSIBLE ENTERITIS OF TURKEYS

A number of viral diseases of poultry produce symptoms and lesions primarily exclusive of the respiratory system. Among them are some of the most devastating diseases of chickens and turkeys. Considered in this group are avian pox, leukosis, avian encephalomyelitis (epidemic tremor) and bluecomb disease.

AVIAN POX
(Fowl pox, Canker, Avian diphtheria)

Avian pox is a relatively slow-spreading viral infection of birds, characterized by wart-like nodules on the skin and diphtheritic necrotic membranes lining the oral cavity and upper respiratory system. It has been present in birds since the earliest history and is universal in distribution. It may cause severe economic loss in chickens and turkeys due to poor growth, feed efficiency, reduced production, increased cull rates and downgrading. Mortality usually is not significant unless the respiratory involvement is marked. The disease may occur in any age bird any time during the warm months, particularly when mosquito populations are high.

Cause: Avian pox is caused by a viral agent. There are at least three different strains or types of avian pox virus: fowl pox virus, pigeon pox virus and canary pox virus. Although some workers include turkey pox virus as another distinct strain, many feel that it is identical to fowl pox virus.

Each virus strain is infective for a number of species of birds in addition to its primary host. For example, among others, fowl pox virus may infect chickens, turkeys, pheasants, quail and ducks; pigeon pox virus may infect pigeons, chickens and turkeys; and canary pox virus may infect canaries, chickens, pigeons and sparrows.

Natural occurring pox in chickens, turkeys and other domestic fowl is considered to be caused by fowl pox virus.

Transmission: Fowl pox can be transmitted by direct or indirect contact. The virus is highly resistant in dried scabs, and under certain conditions may survive for months on contaminated premises. The disease may be transmitted by a number of species of mosquitoes, this being the usual manner by which the infection is introduced to a premise. Mosquitoes may harbor infective virus for a month or more after feeding on affected birds. After the infection is introduced, it spreads within the flock by mosquitoes as well as by direct and indirect contact. Recovered birds do not remain carriers.

Symptoms and lesions: Since fowl pox usually spreads slowly a flock may be affected for several months. The course of the disease in the individual bird is 3 to 5 weeks. Affected young birds are retarded in growth. Laying birds experience a drop in production. Birds of all ages which have oral or respiratory system involvement have difficulty eating and breathing.

The disease manifests itself in one or two ways.

Cutaneous or dry pox: Lesions start as small whitish foci which develop into wart-like nodules. The nodules eventually are sloughed and scab formation precedes final healing. Lesions are seen most commonly around the featherless facial parts (comb, wattles, ear lobes and eyes) but may be found on the body.

Diptheritic or wet pox: Lesions are associated with the oral cavity and the upper respiratory tract, particularly the larynx and trachea. The lesions are diptheritic in character and involve the mucous membranes to such a degree that when removed, an ulcerated or eroded area is left.

Diagnosis: Fowl pox readily is diagnosed on the basis of flock history and presence of typical lesions. In some instances, laboratory diagnosis by tissue or transmission studies is necessary.

Prevention and treatment: There is no treatment for fowl pox. Disease control is accomplished best by preventive vaccination since ordinary management and sanitation practices will not prevent it. Several kinds of vaccines are available: pigeon pox, pigeon pox-like and fowl pox vaccine. The pigeon pox vaccine is of questionable value and its use usually is not recommended. The pigeon pox-like vaccines are newer and have wider acceptance. Fowl pox vaccine is an efficient product and is in common use in Texas. Its use varies according to the type of operation, but generally the following recommendations apply:

Broilers: Vaccination usually is not required; but in some areas where the mosquito population is high, as in parts of Texas, it may be necessary to prevent the disease. In such instances, the vaccine is applied to chicks (as young as 1 day) using the wing-web method but using only one applicator needle.

Replacement birds: Vaccinate all replacement chickens against fowl pox. One application of fowl pox vaccine results in permanent immunity. Birds can be vaccinated at any convenient time during the growing period, usually between 6 and 10 weeks of age.

Turkeys: Fowl pox vaccine does not produce lasting immunity in turkeys. Vaccinate turkeys when they are between 4 and 10 weeks of age. Turkeys to be retained as breeders should be revaccinated as adults. This usually is done as the breeding flock is selected. Birds not selected and vaccinated should be marketed within a day or two.

Examine vaccinated birds for "takes" about 7 to 10 days following vaccination. A high percentage showing a reaction indicates a satisfactory vaccination.

AVIAN LEUKOSIS

The diseases which make up the avian leukosis complex are transmissible virus diseases of birds characterized by tumor formations. The diseases are widespread and have been the most devastating of those affecting mature laying chickens. In recent years these diseases have become an increasingly significant cause of losses in broilers and growing birds.

Of the separate and distinct diseases which form the complex, lymphoid leukosis and Marek's disease produce the most losses.

Lymphoid Leukosis (L.L.)

Characteristically, lymphoid leukosis is a disease of adult chickens; however, the disease appears to be of increasing importance in turkeys and other species such as the pheasant. Although the virus of lymphoid leukosis may produce various responses (for example: blood forms - erythroblastosis and myeloblastosis; bone forms - osteopetrosis), the lymphoid tumor response is the most common.

Cause and transmission: Lymphoid leukosis is caused by a group of enveloped RNA viruses which closely resemble those of the myxovirus group. The disease is transmitted in a number of ways. The agent is eliminated naturally from the body of the infected bird via eggs and feces. The virus may be transmitted mechanically from infected birds to susceptibles by blood-sucking parasites or by man in such procedures as fowl pox vaccination.

Most infections are acquired during the first few weeks of life. This suggests that most flocks acquire the disease by egg transmission or by direct or indirect contact with older infected birds during the early brooding period.

Manifestations of disease: Lymphoid leukosis is characterized by the formation of lymphoid tumors, particularly in the liver and spleen. Affected birds may die without preliminary symptoms, but the disease usually is chronic in nature with affected birds showing loss of appetite, progressive emaciation and diarrhea. Clinically affected birds invariably die. Although losses due to the disease may be most severe shortly after the onset of production, losses in the affected flocks continue as long as it is retained and may total 20 percent or more during the productive life of the flock.

Autopsies of affected birds reveal tumors. Although the liver and the spleen are commonly involved, other visceral organs may be affected. The neoplastic process may be diffuse involving 100 percent of the affected organ, or it may be a nodular type. Affected structures, the liver in particular, may be greatly enlarged.

Osteopetrosis is the bone form of the disease. Until recently it was thought to be a disease primarily of older birds, particularly males; however, it is now known to be quite common in young chickens and is one of the more serious causes of broiler condemnations. The disease is characterized by a thickening and deformation of bone, the long bones in particular. This frequently results in lameness and faulty body conformation.

Blood forms of L.L. are diagnosed infrequently.

Diagnosis: The clinical diagnosis of L.L. is based upon flock history and disease manifestations. The lymphoid disease cannot be readily distinguished from the visceral response to Marek's disease (M.D.); however, there are some features which aid in differential diagnosis. Some of these features are outlined in the table at the top of the next column.

It should be kept in mind that the clinical differentiation of L.L. and M.D. is often presumptive at best. Histopathological differentiation is more accurate, but not completely so.

Treatment and prevention: There is no treatment for lymphoid leukosis. Although the disease cannot be prevented completely, there are certain steps which can be taken to help control the level of infection in a flock.
Some of these are listed below.

  1. Buy resistant strains of birds. Most reputable breeders have invested a great deal of time and money breeding for L.L. resistance,
  2. Brood in isolation. Most L.L. is acquired early (under 6 weeks of age). If replacement birds are brooded in strict isolation, contact transmission (direct and indirect) from adult carriers will be minimal,
  3. Keep incubator sanitary,
  4. Control blood-sucking parasites, and
  5. Do not use gimmicks in disease control (e.g. explosive outbreaks of L.L. have occurred following indiscriminate use of turkey blood in M.D. "control" programs).

DIFFERENTIAL DIAGNOSIS OF L.L. AND M.D.
FEATURE LYMPHOID LEUKOSIS MAREK'S DISEASE
Incubation period Prolonged Short
Usual age incidence Over 6 months Under 6 months
Visceral lesions Most commonly liver & spleen Generalized
Skin lesions No Yes
Ocular lesions No Yes
Neural lesions No Yes

Marek's Disease (M.D.)

Marek's disease characteristically is a disease of young chickens; however, the disease commonly is seen in adult birds. In contrast to L.L., the tumor response of M.D. is limited to the lymphoid type. However, the response may be much more diverse in location than that usually seen in lymphoid leukosis.

Cause and transmission: Marek's disease is caused by a virus belonging to the Herpesvirus group. Much is unknown about the transmission of the virus; however, it appears that the virus is concentrated in the feather follicles of affected birds and is shed in dander. The virus apparently has a long survival time in dander, and viable virus may be demonstrated in depopulated houses months after infected birds have been removed. The usual mode of transmission is by aerosols containing infected dander and dust. As with L.L., young birds are most susceptible to infection with M.D.; however, since the incubation period of M.D. is short, clinical disease can appear much earlier than is the case with lymphoid leukosis.

Manifestations of disease: Marek's disease may produce a variety of clinical responses, all lymphoid in character. These are acute visceral, neural, ocular and skin; or commonly a combination of the responses may be seen.

Marek's disease of the visceral type may be characterized by widespread involvement. The lesions most commonly are associated with the gonads (testes or ovaries), liver, spleen and kidney; however, other organs such as the lungs, heart and musculature are commonly involved. The disease often is acute, with apparently healthy birds dying very rapidly with massive internal tumors. The disease may appear in broiler-age birds and be a significant cause of death loss and condemnations. More commonly the disease produces the most severe losses in replacement pullets near or at the onset of production. At this time, the disorder is seen frequently in birds with acute coccidiosis, leading some to suspect there is a relationship between the two diseases. Presently the only relationship is considered to be that of a bird with coccidiosis or M. D., whichever the case, being more susceptible to the other disease.

Marek's disease of the neural type is the classical type, Neural leukosis was the first disease known as M.D. before the etiologic relationships of the various diseases in the leukosis complex were established. Neural leukosis is characterized by a progressive paralysis of the wings, legs and neck. Loss of body weight, anemia, labored respiration and diarrhea are common symptoms. When affected birds are autopsied, lesions, if observed in uncomplicated cases, are confined to the nerve trunks and plexuses innervating the paralyzed extremities. Affected nerve tissue is swollen as a result of an accumulation of lymphocytes and tissue fluids. Frequently no gross lesions are observed.

Ocular leukosis (gray eye) is responsible for much of blindness in chickens. This type of M.D. usually is seen in early maturity. Morbidity and subsequent mortality usually are low, but in some instances approach 1 5 to 25 percent. Ocular leukosis is characterized by spotty depigmentation or diffuse graying of the iris caused by lymphocytic infiltrations. The pupil develops an irregular shape and fails to accommodate to light. Emaciation, diarrhea and death usually follow because of partial to complete blindness.

Skin leukosis is the form of M.D. that produces the most severe losses in broilers. Losses more commonly are due to condemnation at processing time. The disorder is characterized by enlargement of the feather follicles due to accumulations of lymphocytes. As stated, most infective virus is produced in the regions of the feather follicle and is shed with skin dander.

Course of disease: Acute M.D. can be extremely rapid in its course, producing mortality in apparently healthy birds. However, it has been demonstrated that the lesions of M.D. (particularly of skin leukosis) may regress, and clinically affected birds may make complete recoveries.

Diagnosis: The clinical diagnosis of M.D. is based upon flock history and disease manifestations (refer to table under the diagnosis of lymphoid leukosis). Accurate diagnosis may depend on the employment of sophisticated laboratory procedures.

Prevention and treatment: As is the case with L.L., there is no treatment for Marek's disease, and until recently there have been no effective preventive measures.

A vaccine is now available which appears to be extremely effective (90 percent) in the prevention of M.D. The vaccine is made with a Herpesvirus of turkeys (H.V.T.) that prevents the virus of M.D. from transforming cells to produce tumors. It is applied to day-old chickens by injections in strict accordance with the manufacturer's recommendations. Other approaches to control include the genetic and management/sanitation.

EPIDEMIC TREMOR
(Avian Encephalomyelitis)

Avian encephalomyelitis is a viral infection which affects chickens of all ages, but usually produces clinical manifestations only in young birds. In recent years, the disease also has been observed in turkeys. Signs of infection include incoordination, nervousness, a jerky or irregular gait, falling over on the side with outstretched wing and muscular tremors especially noticeable in the head and neck. The commonly used term epidemic tremor is misleading because muscular tremors are not evident in many otherwise typical outbreaks.

This disease, reported first in New England in 1932, now exists in all poultry-producing areas of the United States and has been reported in several other countries.

The custom of hatcheries to adjust for losses due to epidemic tremor has led other segments of the poultry industry to regard the disease as of minor importance and significant primarily to hatcherymen. Such losses are costly, troublesome and reduce efficiency in all operations, especially in breeder and broiler flocks. Thus, epidemic tremor poses a major problem for the entire poultry industry.

Cause: Epidemic tremor is caused by a relatively small virus which produces microscopic lesions in the bird's nervous system.

Transmission: The virus is transmitted to the chick through eggs of infected parent flocks. Such outbreaks in parent flocks often are unnoticed and usually last 21 to 30 days. It appears that affected flocks do not remain carriers and are not susceptible to the disease again for a reasonable time; consequently such flocks are desirable as hatchery supply flocks.

Apparently, other modes of transmission are responsible for outbreaks in production flocks. The disease can be transmitted by direct or indirect contact, but this is not of major significance.

Symptoms and lesions: In a small percentage of outbreaks, the disease may be suspected because of poor hatchability or morbidity in birds at hatching time. The incubation period varies from 5 to 40 days with an average of 9 to 21 days. The typical outbreak becomes noticeable when birds are 17 to 21 days old. Some individuals in flocks exposed during hatching may develop clinical evidence of infection up to 7 weeks later. Morbidity rates vary from only a few individuals to 30 percent, but average 5 to 10 percent.

Outbreaks in young chicks are characterized by an inability to walk normally. Affected birds may become paralyzed and lie propped on one wing. Visible trembling of the head and neck may be present, but is not apparent in many outbreaks. Affected birds usually do not recover, but they will survive for long periods if food and water are provided. New cases developing after the fifth or sixth week are rare. Mortality usually is negligible but visibly affected individuals should be removed and destroyed.

No lesion is visible with the naked eye. Microscopic lesions are widespread and are a diagnostic aid.

In adult flocks, there may be no evidence of infection other than a 5 to 10 percent drop in egg production, with a decrease in hatchability. Most outbreaks in adult flocks are not suspected unless the caretaker is a keen observer and keeps good records.

Diagnosis: The disease usually is diagnosed on the basis of case history and typical signs. Atypical cases present diagnostic problems and every reliable aid must be used to make an accurate diagnosis.

Treatment and prevention: The disease readily is prevented by vaccinating breeder replacements prior to the onset of production. Vaccine is applied in drinking water when the birds are approximately 10 to 14 weeks old. The vaccination of breeder stock in this way prevents subsequent infection and egg transmission of the virus.

There is no treatment. Remove and kill all birds showing clinical evidence of the disease, since they do not develop into profitable birds.

INFECTIOUS BURSAL DISEASE
(Gumboro)

Infectious bursal disease (I.B.D.), commonly referred to as Gumboro disease, is an acute, highly contagious viral disease of young chickens. It is found most often in the highly concentrated poultry producing areas of the state. It causes marked morbidity and mortality in affected flocks but usually disappears after 1 to 2 weeks.

Cause: A virus or virus-like agent referred to as the infectious bursal agent causes this disease.

Transmission: The transmission or spread of the disease can occur by direct contact (bird to bird), contaminated litter and feces, caretaker, contaminated air, equipment, feed, servicemen and possibly insects and wild birds. It is extremely contagious.

Symptoms and lesions: Birds have ruffled feathers, a slight tremor at onset of the disease, strained defecation, loss of appetite and are dehydrated. Affected birds have a tendency to sit, and when made to move have an unsteady gait. Vent picking is common. Early in the disease there is a rise in body temperature, but it soon becomes subnormal. This often is followed by prostration and death. The litter of contaminated houses becomes sticky during the course of the disease.

Postmortem lesions include dehydration and changes in bursa, skeletal muscle, liver and kidney. All affected birds have some bursal changes commonly characterized by swelling change in shape (oblong), color (pink, yellow, red, black) and the formation of gelatinous film around the bursa.

Diagnosis: The diagnosis of I.B.D. usually is based on flock history and postmortem lesions. Laboratory procedures may be used to substantiate the diagnosis.

Prevention and treatment: Management and sanitation practice alone cannot be relied upon to prevent the occurrence of the disease.

Early exposure (before 14 days of age) to the agent of I.B.D. apparently acts as an immunization procedure, and many flocks that are exposed and infected do not develop noticeable disease symptoms.

Vaccines are available but must be given under the supervision of a poultry pathologist or regulatory official. If given correctly, good control can be obtained.

There is no specific treatment for I.B.D. In fact, indiscriminate medication with certain drugs (e.g. the sulfonamides) may severely aggravate mortality. Supportive measures, such as increasing heat, ventilation and water consumption, are beneficial.

INCLUSION BODY HEPATITIS (I.B.H.)

Inclusion body hepatitis is an acute infectious disease of chickens characterized by sudden onset, marked depression, jaundice of the unfeathered skin and high mortality. The disease was first reported in 1963 as a rare condition in chickens. However, at the present time the disease appears to be widespread among commercial flocks.

Cause: The etiological agent of I.B.H. is an adeno virus.

Transmission: How the disease is introduced into a flock is not fully understood. Some researchers believe the virus is egg transmitted. Horizontal transmission may take place by direct or indirect contact with infected birds, litter and equipment.

Signs and lesions: The disease has a sudden onset. A dramatic increase in mortality in an apparently healthy flock of birds may be the only sign observed. Mortality rate remains high during the first 3 to 5 days and then declines. Total mortality may range between 2 and 10 percent. As the disease progresses in a flock, affected chickens may be seen. Signs at this time include anemia, jaundice of the unfeathered skin, marked depression, weakness and prostration. Birds showing signs of the disease usually die within a few hours. It is often observed that sick birds selected for diagnosis die on their way to a diagnostic laboratory if more than a few hours of travel is required.

Gross lesions of I.B.H. include discoloration (paleness) of liver, bone marrow depletion, swelling and discoloration of kidneys, along with atrophy of spleen and bursa of Fabricius. Hemorrhagic areas generally are evident in various organs and muscles. The hematocrit value may be one half to one tenth of the normal value.

Diagnosis: I.B.H. tentatively can be diagnosed on the basis of history, clinical signs and lesions. Virus isolation and agar gel precipitin test is performed to confirm the diagnosis.

Treatment and control: There is no treatment for I.B.H. At present no vaccine is available for preventive immunization of susceptible birds.

TRANSMISSIBLE ENTERITIS OF TURKEYS
(Bluecomb)

Transmissible enteritis is an acute to chronic disease of turkeys characterized by sudden onset, marked depression and severe diarrhea. Death losses may be high, particularly in young poults, but heaviest losses in adults are due to loss of condition. The disease at one time was considered to be the same as so-called "bluecomb" of chickens. Now it is recognized as a distinct entity.

Cause: The etiologic agent of turkey bluecomb is now known to be a corona virus. Substantial evidence exists; however, the disease as seen in the field is the result of an interaction of several agents, among which the virus is considered to be primary.

Transmission: The disease spreads by contact with infected birds or premises. Droppings of infected birds are especially rich in virus. No specific environmental factors appear to influence the occurrence; however, the stress of adverse weather conditions may be a factor in the severity of the disease in range birds.

Symptoms and lesions: When the disease strikes young poults under 3 to 4 weeks of age, onset is sudden. Affected poults appear cold and seek heat. Feed and water consumption drops markedly, and poults lose weight rapidly. Morbidity and mortality may approach 100 percent in uncontrolled outbreaks.

Young poults show few lesions other than those associated with the intestinal tract. Intestines usually are distended and lack muscle tone. Intestinal contents are fluid and gaseous (foamy).

Morbidity is variable in older flocks of turkeys. It may be extremely low in some flocks but extremely high in others. Feed intake drops markedly and birds may lose up to 5 pounds of body weight in just a few days. Birds usually have profuse diarrhea. Cyanosis of the head parts is common.

When older birds are autopsied, the following lesions may be seen. The body musculature is dehydrated. Minute hemorrhages may be seen on the viscera and necrotic foci seen on the liver. Kidneys commonly are swollen and contain an excess of urates. Severe catarrhal enteritis is seen often, and mucous casts may be present. The pancreas usually presents multiple chalky white areas. The crop frequently is distended and contains sour-smelling contents.

Diagnosis: Transmissible enteritis must be differentiated from common bacterial infections such as paratyphoid, fowl cholera, fowl typhoid and erysipelas. Diagnosis usually is based on history, symptoms, lesions and negative bacteriological findings for the common bacterial infections.

Prevention and treatment: Until more is known about the spread of bluecomb, no specific recommendations for prevention can be made. However, consider recovered birds as potential carriers. Clean and disinfect houses in which outbreaks have occurred. Leave vacant for at least 30 days. Apply routine management and sanitation practices for disease prevention.

During outbreaks older turkeys can be flushed with molasses at the rate of 1 pint molasses to 5 gallons of drinking water for 1 day. Then give antibiotics in feed or drinking water at the rate of at least 200 grams/ton of feed or 200 to 400 milligrams/gallon of water. Continue treatment for at least 5 to 7 days.

Do not flush young turkey poults. Give antibiotics at the rate of up to 400 grams/ton of feed or 1 gram/gallon of drinking water. Give this high level for 2 or 3 days, after which time antibiotics may be reduced, depending on flock response. Total treatment period should be at least 5 to 7 days.

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