Chapter 4 Diseases caused by Viruses

 

 

             

 Among the most troublesome diseases to which poultry are susceptible are those caused by viruses. Some of these filterable agents are extremely virulent and the diseases induced by them are capable of causing severe losses to flock owners. Newcastle disease, and fowl pest are among the most important diseases in this group. Viruses are obligate parasites with no enzymes system to complete their biologic functions. 

4.1 The structure of a virus consist of:

• 1. Nuclei acid core
• 2. Capsid: Protein in nature, composed of various numbers of capsomeres.
• 3. Envelope: Altered host cell membrane component, sensitive to fat solvents. 

4.2 Classification of viruses depend upon:

1. Type of nucleic acid:

DNA

All known DNA viruses are double stranded, except parvovirus, kilham rat virus and Feline panleukopania.

RNA

All known RNA viruses are single stranded, except reovirus.

2. Capsid symmetry:

DNA

Icosahedral

RNA

Helical

3. Presence or absence of an envelope

4. Acid or alkalhle lability (Helicals are sensitive)

5. Ether and chloroform sensitivity, again helicals are sensitive.

6. Number of capsomeres. (only in icosahedral).

7. Viron sizes by using x-ray, filtration and E.M.

8. Molecular weight of the viron.

Major virus group:

4.3 Newcastle Disease.

a. Synonyms:

ND. pneumonencephalitis, pseudofowl pest, Nine day flu.

b. Definition:

Acute, rapid spreading, viral, contagious respiratory disease of birds of all species. Characterized by respiratory symptoms and/or encephalitis. High mortality in young chicks and caused a severdrop in egg production in mature fowl. There are four forms, caused by viruses that are similar in morphology and immunogenicity.

c. Etiology:

• 1. The etiologic agent is a virus designated as Tortor furens, RNA, paramyxovirus.
• 2. It is readily cultivated in developing chick embryo.
• 3. ND virus is very resistant, live in dust for 255 days (81/2months)

d. Susceptibility:

• 1. Chickens and turkeys of all ages, are naturally affected.
• 2. Others such as pheasants, ducks, geese, pigeons, quail, partridges, sparrows etc. are also susceptible.
• 3. The infection of human beings has been recognized only as a relatively mild pink-eye-like infection contracted by handlers of sick or slaughtered birds of by diagnosticians or laboratory personnel working with virus.

e. Occurrence:

The disease occurs in many countries of the world, and is very prevalent in the United States having been reported from practically every state. However, the most virulent form (exotic Newcastle) is presently eliminated from the U.S.

f. Epizootiology:

• 1 Air borne: Transmission within the flock.
• 2. Cirulent and vaccine straim of virus are excreted through feces for about 3 weeks.
• 3. Vaccinated birds can survive challenge, but can become infected with VVMD, and shed virus in feces and respiratory tract for 14-17 days.
• 4. Isolation of the virus from yold-sacs of young chicks, dead embryos, and from infertile eggs laid by infected hens offer plenty of supporting evidence that egg transmission does occur.

g. Signs and lesions of different forms of MD.

• 1. Peracute to acute, rapid spreading, highly virulent, mortality usually over 90%
• 2. Incubation period is about 5-7 days course of the disease averaged 3-4 days.
• 3. Generalized edema and hemorrhage. Edema significant around the eyes, neck and head.
• 4. Respiratory system: ND virus multiplies at site of entrance (trachea), virus released into blood circulation. Later NDV multiplies in visceral organs causing lesions in digestive system. This respiratory symptoms are seen before nervous symptom.

  Common symptoms are:

  Outstretched head, bubbling,grasping, long inhalation, sneezing, loss of appetite.

  Production declines rapidly, brown egg shells may change to white, poor egg shell quality, water egg whites, sour crop and diarrhea. 

  Lesions:

  mucous in the trachea may be tinged with blood. Air sacs may be cloud, yellowish or whitish. Cheesy pellets or frothy slimy exudation the windpipe, and congestion of lungs.

• 5. Digestive system: Hemorrhage of mucosal layer of the pro-ventricular, gizzard fat, liver, and intestinal tract.
• Catarrhal enteritis. Hemorrhage and necrosis of the intestinal lymphoid follicles.
• 6) Nervous system:
• Signs: Loss of equilibrium, leg paralysis, in coordination, walk in circles, posterior propulsion etc. Mortality is so rapid that nervous symptoms are seldom seen in this form.
• Lesion: No gross CNS lesions.
• Other systems:
• Hemorrhage of heart muscle, skeletal muscle and ova. Liquid yolk in the abdominal cavity also noted.
• 7) Histopathology: Necrosis and hemorrhage of the spleen liver, gall bladder, intestine and heart muscle. None separative encephalitis in CNS. Proliferative changes in lung and iris.
• 8) VVND-Velogenic Viscerotropic Newcastle disease, also known as exotic ND.
  • 1. Beach's form, described in 1942 characterized by acute respiratory and CNS involvement, Hemorrhage absent from digestive tract.

    Disease cause by certain velogenic strains.

    2. Mesogenic form. Mesogenic form, Beaudette's from. Acute respiratory and sometimes lethal nervous infection of young chicks.

    • 1. Less virulent, rapid spread, mortality varies from 5-15%
    • 2. Respiratory distress, greenish diarrhea. Paralysis of wings and legs or torticollis.
    • 3. Drop in egg production, some may drop to zero. The egg shell is often discolored, imperfect, or misshapen, the eggs become smaller.
    • 4. Lentogellic form. Hitchner's form. Mild respiratory infection.
      • 1 Mild form, mortality usually low.
      • 2 Impairment of appetite.
      • 3. Mild respiratory symptoms.
      • 4. Rapid drop in egg production, (characteristic)
      • 5. Mild tracheitis is the only observable lesion .

h. Diagnosis

• 1. Has signs similar to coryza, CRD, LT, IB, Fowl cholera and Fowl plague. Differential field diagnosis based on history, signs and necropsy finding should be considered.
• 2. One of the two diseases actually affect egg quality. (IB, MD)
• 3. Field differential diagnosis. 

CharactersCoryza	---	CRD	LT	IB	ND
Age	Any	4 wks	Growing	Days+	Days
Spread Fast	Fast	---	Slow	(+) Fast	(++) Fast
Duration Wk+	wks+	---	wks +	1 wk	1-2 wk +
Coughing	Some	Some	Some	Some	Some
Gasping	+	+	+	+	+
Rattling	-	+	+	++	++
Air Sacs	-or +	+++	-	+	++
Trachea	Mucous	Mucous	M blood	Mucous	M blood
Nervous	-	-	-	-	+
Egg Quality	-	-	Slightly	++	++
Odor +	-	-	-	-	-

• 4. Laboratory diagnosis is considered essential to confirm filed cases. In making a laboratory diagnosis, the following procedures are used:
  • l) Virus isolation. Round wooden sterile sticks without cotton tips were used for swabbing trachea, spleen-lung composite, brain or cloaca. The swabbing is washed with brain-heart infusion (BHI) broth, refrigeration over- night.
  • 2) Chick embryo inoculation The above material is then inoculated into the chorioallantoic cavity of ten-days old chick embryos. In the case of VVND virus, the embryo should die within 5 day. Collect the allantoic fluid from dead embryos for further study.
  • 3. Serological test. The allantoic fluid collected is used for hemagglutination and hemagglutination inhibition test, to identify the Virus.
  • 4.Animal inoculation. Allantoic fluid from (2) is inoculated, introaocularly or through the cloaca, to 4-7 weeks-old susceptible chickens. The inoculated chickens should develop typical ND signs within 10 days.
  • 5. Diagnosis with sentinel birds. Chicken flocks recently vaccinated with Newcastle vaccine will prevent mortality and severe losses in the flock. However, these birds are still susceptible to infection of VVND virus and eventually excrete viruses that would endanger unvaccinated flocks. Under this condition, sentinel birds (very susceptible to VVND) are used to detect the presence of VVND virus.
  • 6 Other methods such as serum neutralization test (this test is more sensitive than HI test, but costs more and required longer time for the test), fluorescent antibody technic, tissue culture technic for typical plague formation are also employed.

i. Method of control and prevention

Eradication program.

• (l) Slaughter infected and exposed flocks to eliminate sources of virus excretions. Thoroughly clean and disinfect the premises.
• (2) Establish surveillance and reporting system.

Collection of dead poultry from commercial ranches for necropsy examination and virus isolation. Educate owners to report any disease condition of contagious nature. Place sentinel birds in selected commercial as well as backyard poultry flocks.

Vaccination Program . Vaccination of unexposed poultry can slow down the spread of VVND. Lasota, Roakin, B, TCND and kimber are the common vaccine strains used for immunization However, as mentioned above, vaccination reduces loss due to mortality, but does not prevent a flock from becoming infected. Vaccination is the best method to control Newcastle disease other than VVND.

l) Strains of virus for vaccination.

• a. Bl strain is the most common and mild strain.
• b. La Sota slightly cirulent, both strain can be applied either in the eye, nostril or through drinking water.
• c. Koakin strain - more virulent strain, injection on wing web.
• d. GB strain - a very virulent strain, usually used to challenge immune birds.

2) Two types of vaccine

KILLED VIRUS:

Site of injection

Breast muscle. 

Age:

Any age.

Advantage:

No danger of bringing the disease to the farm.

Duration of immunity: Immunity started about one week after vaccination, peak at 2-3 weeks, started to drop fast at 6-8 weeks, disappear in about 6 months.

LIVE VIRUS VACCINE:

Age:

As young as days.

Site:

Eye is preferred over the nostril. Can be used as combination with IB vaccine in water.

Revaccination should be done at 4 weeks and 4 months.

J. Treatment:

No effective treatment. 

4.4 INFECTIOUS BRONCHITIS

a. Synonyms:

IB, broncllitis, cold.

b. Definition:

It is a highly infectious condition and widely disseminated. 

This is the most contagious respiratory disease in chicken due to short incubation period (18 hours).

c. Etiology:

The causative agent of infectious bronchitis is an RNA corona virus. The viral particle is surrounded by crownlike projections.

d. Susceptibility:

Chickens only.

e. Transmission:

The virus is present in the bronchial, tracheal, and nasal exudates of affected birds, spread by air, contaminated cloth, equipment, crates. However it does not spread by egg transmission.

f. Symptoms:

• 1. Age: A few days old to mature birds.
• 2. Action: Peracute to acute.
• 3. Disease spread, fast, last about 2 weeks. Watery eyes.
• 4. Evidence of tracheitis, bronchitis with sneezing and coughing and "crackle" breathing is often heard.
• 5. Growth of broiler is significantly retorted.
• 6. In chicks under 2 weeks of age may cause permanent damage to the oviduct resulting later in false layers.
• 7. Mortality in very young chicks may he as high as 70-80%, but in chickens over 6 weeks of age, mortality is negligible.
• 8. Mature birds, the outstanding symptoms are gasping, tracheal rales, and coughing.
• 9. In laying flocks, egg production will decline (30-50%), and misshapen, rough, and soft shelled eggs may be found. Laying of poor quality eggs and lowered hatchability may continue in some flocks even after recovery of full production.

g. Lesions:

• 1. Serous or catarrhal exudate is observed in the trachea.
• 2. Catarrhal or fibrinous inflammation of the air sacs.
• 3. In chicks that die, yellowish caseous plugs may be found in the lower trachea and bronchi.
• 4. Very young chicks also have a catarrhal inflammation of the nasal passages and sinuses, cuasillg nasal discharge, wet eyes, and occasionally swollen sinuses.
• 5. T strain IB virus causes swollen kidneys with tubules and ureter extended with uric acid.
• 6 Histopathology: Significant changes occur in the respiratory tract. Lost of cilia, shorting of columnar epithelium (coboidal). Hyperplasia and vacuolatio of epithelial cells, and hemorrhage inlsubmucosa Thickened tracheal mucosa and submucosa due to edema and diffuse infiltration of mononuclear cells.

h. Diagnosis.

• 1. Field diagnosis.(Based on the history of the flock, and rapid spreading of the disease)
• 2. Less swelling than coryza, no odor
• 3. No blood in trachea.
• 4 Laboratory diagnosis:
  • 1. Intratracheal inoculation into baby chicks with tracheal and lung material of sick birds, characteristic, symptoms developed in 18-36 hours.
  • 2. Isolation of the virus in chick embryos. The characteristic embryo changes are seen several days after inoculation of the virus. During Candling, only slight movement of a dwarfed embryo is seen curled into a spherical form with the thickened amnion closely,
  • 3. Negative for HA and HI test.
  • 4. Detection of antigodiesagainst bronchitis virus. Use embryo adapted virus as antigen in serum neutralization 
  • 5. Fluorescent antibody test.

i. Prevention:

• 1. Purchase chicks from immune hens. (Parental immunity lasts for about 2 weeks).
• 2. Vaccination programs have been extensively used particularly in the immunization of replacement laying flocks.

   Site:

  Intraocular or drinking water. Use live virus.

  Age:

  • 18-35 days of age (4-5 weeks).
  • Re-vaccination at 12-16 weeks of age.
  • May be re-vaccinated every 4 months.

   

  • 5. When PPLO is present- vaccination with bronchitis virus may trigger the outbreak of CRD . It is a stress factor for CRD , thus vaccination should be delayed.

j. Treatment:

• 1. No effective treatment.
• 2. Increase room temperature and keep it warm
• 3. Increase ventilation but keep draft out.
• 4. Feed high antibiotic crumble feed. 

4.5 . INFECTIOUS LARYNGOTRACHEITIS (LT)

a. Synonyms:

LT, Larynogo or ILT.

b. Definition:

Infectious laryngotracheitis is an acute, highly contagious disease of chickens characterized by respiratory distress, rapid spread, and in many cases, high mortality.

 c. Etiology:

This disease is caused by an DNA herpes virus.

d. Susceptibility:

The primary natural host is chickens, but pheasants are also susceptible.

e. Occurrence:

• Usually a problem within an endemic or localized area.
• In 1959 this disease spreaded to the South.

F. Transmission:

• 1. The virus is found in abundance in the respiratory tract of affected birds. Thus, the natural route of infection is by way of the respiratory tract.
• 2 Apparently healthy carrier fowls serve as a ready means of transmission. Recovered chickens remain carriers up to 24 months.
• 3. Transmission of the disease indirectly by way of one or two occurred prior to the onset of respiratory symptoms throughout the flock.
• 4. Quiet, dull, sitting With eyes closed.
• 5. Intermittent gasping.
• 6. Coughing sometimes with blood discharge. Sneezing, during which the fowl shakes its head vigorously in an attempt to dislodge the offending exudate which has accumulated in the larynx and trachea.
• 7. Rale, at inspiration, the head and neck are raised and extended, the mouth is opened, in an effort to take in as much air as possible.
• 8. No appetite
• 9. Mortality high.
• 10 Slight lose in egg shell thickness
• 11 Mild in young birds.

h. Lesions:

• 1. Confined to respiratory tracts
• 2. Mucoid exudate in nostrils, which may be dried into flakes.
• 3. A sticky mucus is present in the throat and the larynx is inflamed, swollen and edematous.
• 4. Varying amount of blood and blood-streaked exudate are found adhering to its wall, Pin point hemorrhage may also be seen in the lining membrane of the inflamed larynx and trachea.
• 5. In the course of the disease had been somewhat subacute, there is often present adhering to the rim of the larynx, a yellowish cheesy exudate which may practically fill laryngeal opening.
• 6. Histopathology: Tracheal mucosa started with cloudy swelling, then edema, lymphocytic infiltration, and hemorrhage. Internuclear inclusion bodies inepithelial cells (characteristic).

i. Course and Mortality.

• 1. Average course of the disease is about 2 weeks with extremes of 1 to 4 weeks.
• 2. Mortality may range from less than 5% to as high as 60%.

j. Diagnosis

• 1. Based upon the rapid spreading of the condition in the flock.
• 2. Hemorrhages of the upper respiratory tracts are characteristic.
• 3. Laboratory diagnosis: 
  • 1. Intracheal inoculation of susceptible and immune male chicks with a broth suspension of trachea exudate from a suspected case.
  • 2. Inoculate embryonation chicken eggs at 9 to 12 days of age. LT virus produces area of grayish thickening on the choriolallantoic membrane by the third day . Inclusion bodies can be observed between the first and third days in sections of the membrane.
  • 3. Intranuclear inclusion bodies in the trachea.

k. Prevention and Control.

• 1. Sound management practices. The introduction of the disease on the farm can be avoided by adding new stock only from disease free sources.
• 2. Recovered and carrier birds should be marked.
• 3. Vaccination program: Immunization of chickens against infectious laryngotracheitis can be accomplished by inoculating birds with virulent or modified virus vaccines. Birds should be vaccinated 4-5 weeks of age and older.

  l) Virulent vaccine:

  • Vaccinated birds are carries, recommended to be used only in endemic areas.

    Site:

    Cloaca

    Method:

    Brush needle and drop method.

    Examination:

    Examine the inoculation site 4-5 days after vaccination, a swelling of the cloacal lips and reddening of mucosal membrane is positive or "take".

    Duration of immunity: 12 weeks to a year

  2) Modified virus vaccine:

  • The modified live virus vaccine will not cause clinical disease, administered by the eye drop method. (American Scientific Labs.)

L. Treatment:

• 1. No good treatment
• 2. Keep birds in high antibiotic feed.
• 3. Clean up, depopulate, leave the house empty for 2 months.

 

4.6 FOWL POX 

a. Synonyms:

Sore head, avian diphtheria, contagious epithelium, camper, chicken pox. 

b. Definition:

Avian pox is a chronic viral infection of birds characterized by discrete, proliferative lesions, mucous membrane of the mouth and upper respiratory tract.

c. Etiology:

• 1. Avain pox is caused by a virus of the pox group. The virus particle is large, oval, or brick-shaped, about 150 to 200mu. by 265 to 350 mu. in size.
• 2. It is a DNA containing enveloped virus, which develops in the cytoplasm of infected epithelial cells.
• 3. Infected cells characteristically contain large acidophilic intracytoplasmic inclusions (Bollinger bodies), made out of elementary bodies called Borrel bodies.
• 4. At least four different viruses or strains virus causing pox among birds.
  • 1. Borreliota avium - fowl pox virus .
  • 2. Borreliota meleagridis - turkey pox virus, the strongest
  • virus in this group.
  • 3. Boreliota fringillae - canary pox virus, weakest virus.
  • 4. Borreliota columbae - pigeon pox virus.

d. History:

Because they produce obvious lesions, pox infections in both domestic and wild birds were among the earliest described avian diseases.

e. Susceptibility:

Most, if not all ,avain species are susceptible to one or more pox strains. Domestic chickens are highly susceptible to fowl pox, but the disease also affects turkeys, and to a less extent ducks, geese, pheasants, quail, canaries and hawks. Mammals are not susceptible to natural infection with avian pox virus.

f. Occurrence:

Fowl pox is prevalent where poultry is raised. The disease some-

times assumes an exceptional virulent form, affecting large numbers of fowls and causing serious losses. It is most prevalent during the fall and winter months, but may occur at any seasons of the year. 

g. Transmission:

• 1. Pox virus is unable to penetrate unbroken skin, but small abrasions are sufficient to permit infection.
• 2. Culex pipiens and aedes aegypti are capable of transmitting the disease from infected chickens, as lesions developed from 5 to 10 days after the infected mosquito was allowed to feed on a susceptible chicken. The mosquitoes are considered to be mechanical carriers. 

h. Symptoms:

1. Skin form (dry form) or cutaneous form.

• l) Age: Any age, usually couple of weeks old.
• 2) Action: Subacute.
• 3) Season: Late summer during the mosquito season.
• 4) Characterized by the appearance of cutaneous eruptions or wart like nodules on the unfeathered parts of fowl, eg, comb wattle, eyelid, feet, cloacal aperture, and under the wings.
• 5) In young chicks, corner of mouth, nostril and eyelids. Removal of the pox scale (local epithelialhyperplasia). resulted in bleeding.
• 6) The cutaneous nodules may be very numerous or few in number and they do not necessarily erupt at the same time. At first, the nodules appear as small, whitish foci which rapidly increase in size and become yellowish in color as they develop.
• 7) In some instances closely adjoining lesions may coalesce, and the large developing lesions are rough, and gray or dark brown in color.
• 8) After about 2 weeks of development, the lesions may show area of inflammation at their base and become hemorrhagic. The lesion then undergoes a process of desiccation and scar formation which may last for another week or possible two weeks.
• 9) In uncomplicated cases the process ends with desquamation of the degenerated parts of the epithelial layer. If the desiccated scab is removed in the mean time, a moist seropurulent exudate is found underneath, covering a bleeding, granulating surface. When the scab drops off, a smooth scar may be present
• 10) The specific process is often modified by the invasion of bacteria which propagate in the degenerated epithelium and may reach the deeper layer of mucous membrane where they catlse supportive or necrotic processes with the formation of fibrinous deposits. tSpherophorus necrophorus)

2. Diptheritic (wet) form.

• 1. The type is not as common as the cutaneous form.
• 2. The eruptions on the mucous membranes are white, opaque, slightly elevated nodules.
• 3. These process rapidly increase in size, often coalescing to become a yellowish, cheesy, necrotic material with the appearance of a pseudomembrane.
• 4. Where these pseudomembranes are removed they leave bleeding erosions.
• 5. The invasion by contaminated bacterial aggravates the diphtheritic form of the disease. The inflammatory process may extend from the mouth region into the sinuses, particularly the intraobital sinuses, resulting in a tumorlike swelling, and may extend into the pharynx, resulting in respiratory disturbance.

i. Histopathology :

Avian-pox infections cause localized proliferation of epithelial cells. Affected cells become hyperplasic and hypertrophic. The increase rate of multiplication occurs in ten basal germinal layer of cells in the epithelium.

• 1. Hypertrophy and the appearance of large granular acidophilic intracytoplasmic inclusions appears as the cells mature in layers of the epithelium above the stratum germ;nation.

j. Diagnosis:

The presence of typical wart-like nodules on the comb, wattles and other unfeathered areas.

• 1. Yellowish, adherent, membranous or cheesy patches; in the mouth and throat
• 2. Differential diagnosis: Pox - bleeding when scab is removed , no odor.Coryza - watery eye, foul odor.
• 3. Histopathological examination, with demonstration of typical intracytoplasmic inclusions is usually for a diagnosis.
• 4. Isolation and propagation of virus on chrioallantoic membranes of chicken embryos. Incubated 12-day old embryos were incubated for 4 to 5 days and the chiorallantoic membranes were collected. Gross lesions ("pocks") were visible as early as 48 hours after inoculation. 

K. Prevention:

• 1. Control the population of mosquitoes
• 2. Vaccination:

The chick embryo origin vaccine contains live, nonattenuated fowl pox virus capable of producing infection in a flock if used improperly.

• l) Vaccination for broilers and replacement flocks. In problem areas birds may be vaccinated at one day of age. However, it is usually done at 1-2 months of age by the wing web stick method.
• 2) Vaccination for turkeys.
  • May be vaccinated by wing web stick method, but the virus may spread to and infect the head region. The site of choice for vaccination is midway on the thigh.. Turkeys are vaccinated when they are 2-3 months old.
• 3). Laying birds.
  • Pigeon pox virus vaccine is mild for chickens and
  • turkeys, thus it is used for vaccination of laying
  • hens, turkeys and future layers.

Lesions, "take", should be examined 7-10 days after vaccination. Welling of follicles and inoculation site and development of scabs are indications of "take". zen-twenty per cent of the birds should be examined, 90% of these birds should develop "take".

Type of vaccine used in relationship to duration of immunity.

Type	Species	Immunity
Pigeon Pox	Pigeon	Life
-	Chicken	6 months
Fowl Pox	Chicken if vaccinated	Almost life
-	-	10-12 wks
-	Turkeys	6 months

l. Treatment:

• 1, No Satisfactory treatment.
• 2. Removal of lesions which interfere With eating and drinking may be helpful. The raw areas resulting from this treatment should be painted with tincture of iodine or With mercurochrome to facilitate healing. 

4.7 INFECTIOUS BURSAL DISEASE

a. Synonyms:

Gumboro disease 

b. Definition:

• Acute viral contagious disease of young chickens characterized by mild respiratory symptoms, white diarrhea, severe depression and death.

c. Etiology:

• Infectious bursal agent (IBA) believed to be a Reovirus, double stranded RNA. Quite resistant to the environment.

d. Susceptibility:

Only in chickens

e. Occurrence: 

First diagnosed in Delmava area of Delaware now all over the world.

f. Transmission:

• 1. Contact
• 2. Air
• 3. Contaminated feed and requirement.

g. Symptoms:

• 1. Age: Usually 3-6 weeks old.
• 2. Action: Acute, incubation period is about 5 days. Duration is 4 days
• 3. Mortality: 0.5-30%, average 5%
• 4. Slight head and body tremor, unsteady gait.
• 5. Affected birds show signs of general depression and loss of appetite.
• 6. The feathers around the cloaca are often soiled and the feces are watery and whitish.
• 7. Picking at the vent 
• 8. Severe]y affected birds refuse to move, sitting with eyes closed and head lowered with bread buried into the litter. (Nervous after recovery).

h. Lesions:

• 1. Inflammation of the bursa of Fabricius is typical for this disease. In birds that die or in severe infection the bursa usually atrophied, pinkish, hemorrhagic, inside of the bursa filled with creamy content. However, in less severe affected birds the bursa was enlarged(2X), surrounded by yellowish whitish pin point necrotic foci may be seen in both serosa mucosa.
• 2. Histopathology of the bursa. Necrosis of lymphoid cells and regeneration later, severe edema and hemorrhage.
• 3. General dehydration of the chicken. Reddish of skeletal muscle (hemoconcentration).
• 4. Massive intramuscular hemorrhage of beast, thigh and wing muscle in dead birds.
• 5. Kidneys of birds that die, had urate deposit, prominent and highly extended tubules.
• 6. Gizzard hemorrhage - between the glandular stomach and the gizzard.
• 7. Rectum full of urate. Catarrhal enteritis. 

h. Diagnosis:

• 1. Base on mortality pattern.
• 2. Base on postmortem - bursal infection
• 3. Base on laboratory transmission of the disease.

i. Prevention and Control.

• 1. In previously affected flocks, subsequent flocks must be vaccinated with either virulent or modified IBA vaccine at early age, (3-7).
• 2. Previously unaffected flocks, keep out of traffic between infected flocks. Servicemen should attend the affected flocks last.
• 3. Destruction of the bursa of fabricuous may result in hindering the development of resistance of birds against other diseases In recent studies, there were evidence that birds from IBA susceptible flocks will he infected with IBA early in their lives, resulted highly susceptible to inclusion body 4 hepatitis; gangrenous dermatitis etc.

j. Treatment:

• 1. No effective treatment.
• 2.Keep sick birds away from apparently normal birds. Give sick birds plenty of water.

7.8 AVIAN ENCEPHALOMYELITIS

a. Synonyms:

Epidemic tremor, AE.

b. Definition:

Avian encepllalomyelitis affects primarily young chickens, characterized by ataxia and tremor of the head and neck.

c. Etiology:

AE is caused by a small virus classified as enterovirus, belong to the family of Picornaviridae (RNA).

d Susceptibility:

Chickens (appear to be the only species of birds naturally affected). the disease has been reported only in young chicks with susceptibility being greater in birds from one to three weeks of age. Similar disease condition is also reported in turkey.

e. Occurrence:

Throughout United States. It has been found in Australia. In the outbreaks so far observed, the greatest incidence has been in the wintenmonths with a few sporadic outbreaks appearing during the fall.

f. Transmission:

• 1. Through the eggs for about 3-4 weeks after infection.
• 2. Through contact of contaminated fecal material virus excrete through feces one week before showing symptoms.

g. Symptoms:

• 1. Age: 1-2 weeks.
• 2. Action: Acute, incubation period is about 10 days.
• 3. Affected young chicks will show a slightly dull expression of the eyes which is followed by a progressive ataxia or incoordination of the leg muscles
• 4. Unsteady gait, inclination to sit on their haunches When disturbed, may move out exhibiting little control over the speed and movement of their gait.
• 5. Some chicks may refuse to move or they may walk on their hocks and shanks.
• 6. The full expression becomes more pronounced, accompanied With weakened cry or an inability to cry. Tremor of the head may become evident.
• 7. Exciting or disturbing the chick may bring on the tremor.
• 8. Blindness
• 9. Normal appetite, but unable to move close to the feed.
• 10. Mortality from 0-50%, due to starvation.
• 11. Morbidity varies, usually form 10-20% birds affected.

  2. In hen.

  • 1 Slight drop of egg production for 6-12 days after exposure, egg production might drop 5-10
  • 2. Unnoticeable mortality

h. Lesions:

• 1. No significant gross pathological changes.
• 2. The principle histopathologic changes are distributed among the CNS, manifested by gliosis, perivascular infiltrations. neuronal degeneration Chromatolysis and nonsupportive encephalitis.
• 3. In the viscera, hyperplasia of the lymphoid follicles involving primarily themyocardium, proventriculus and ventricular muscles and the pancreas.
• 4. Neuronal degeneration was most striking and common among lesions distributed throughout the CNS, especially in the region of the lumbosacral enlargement.

i. Prevention.

• 1. Hens are immuned three weeks after exposure to the virus
• 2. Parental immunity lasted about 6-8 weeks.
• 3. Buy chicks from immuned hens.

j. Treatment:

No effective treatment

k. Vaccination:

Immunize parent stock and prevent egg production loss in commercial layers

Chicken-Vaccinate replacement pullets when they are at least 10 weeks of age, but no later then 4 weeks before they start to lay.

Turkey:

Vaccinate after they have been selected for breeding, but no later than 4 weeks before eggs are taken for hatching.

The vaccine is administered through the drinking water.

Warning:

Eggs for hatching should not be taken from the flock until 4 weeks have passed following vaccination.

4.9 Avian influenza infection:

a. Synonyms:

AI, Flu, Influenza, Fowl Plague

b. Definition:

Infectious respiratory disease of the avian species, Characterized by respiratory symptoms, depression, lowered production and hatchability.

c. Etiology:

Avian influenza type A virus, belong to orthomyxovirus group, RNA virus. There are more than 80 species of influenza viruses associated with avian influenza.

d. Susceptibility

Turkey, chickens, pheasants, ducks, geese and wild birds. Mature turkeys are the most severely affected species in the united States. Fowl plague in chicken was eradicated from the U.S. in 1929.

e . Occurrence: Nationwide.

f. Transmission:

• 1, Contact
• 2. Through air.

g. Signs and Postmortem Lesions.

1. Turkeys.

• Incubation period: Varies from a few hours to 2-3 days..
• Signs are. extremely variable, listless, mild to severe respiratory signs, eg. coughing, sneezing. rale, excessive lacrimation. Egg production and hatchability dropped sharply.
• Postmortem Lesions: Mild tracheitis, airsacultis, sinusitis with caseous exudate, lung congestion. Ovarian regression misshapen ova, and involution of the oviduct.

2. chickens (Fowl Plague or Fowl Pest).

Fowl plague virus affects chickens, turkeys and other fowls.

Action:

Acute to peracute.

Incubation period:

3-7 days

Mortality:

Started 2-4 days after showing signs ranging from 50-100%

Common signs are:

Depression - droopiness, head drawn in eyes closes, irregular gait, recumbence and die.

Swollen comb wattle, eyelids, cyanotic.

Difficulty respiration:

• Sneezing or rattling due to accumulation of exudates ever: 100° - 112°F.
• Diarrhea common
• Sudden drop in egg production
• Postmortem lesions:

Mucoid exudate in and around nostrils. Subcutaneous accumulation of gelatinous exudate (edema) and dotted with hemorrhage. (Pathognomonic) Hemorrhage: Lining of proventriculus, under side of keel bone underlying surface of gizzard, larynx, trachea, pericardial fat, and abdominal fat.

Catarrhal enteritis.

Histopathology:

• Edema, hyperemia and hemorrhage of various organs.
• Perivascular lymphoid cuffing of myocardium, spleen, lung, brain, wattles, and to lesser extend liver and kidney.
• Necrosis - spleen, liver, kidney and brain.

h. Diagnosis:

• 1. Differential diagnosis: Newcastle disease, Para-influenza, orinthosis in turkey, infectious bronchitis, laryngotracheitis and fowl cholera in chicke
• 2. The extreme acuteness, nigh death rate and generalized hemorrhage suggest the presence of fowl plague.
• 3. Laboratory diagnosis:

Isolation, cultivation and identification of the viral agent. Serum neutralization, HA, HI, gel diffusion and fluorescent antibody technic.

i. Control and Eradication.

• 1. If fowl pest is suscept, the proper regulatory officers should be notified at once so that control measures may be instituted immediately in an effort to limit the spread of the infection.
• 2. All sick and exposed birds should be killed and destroyed by burning.
• 3. All equipment with which the diseased birds have been in contact should be thoroughly cleaned and disinfected.

4.10 QUAIL BRONCHITIS

a. Synonyms: QB

b. Definition:

Acute, highly contagious, respiratory disease of bobwhite quail.

c. Etiology:

QBV is classified as an avian adenovirus, DNA, it grows readily in inoculated chicken embryos, causing lesions and mortality patterns similar to those caused by infectious bronchitis virus of chicken.

d. Susceptibility:

Young bobwhite quail (American species) are highly susceptible,The Japanese Coturniz quail are resistant,

e. Transmission:

• 1. In bobwhite quail only contact transmission of virus has been demonstrated experimentally.
• 2. Based on flock histories that airborned and mechanical transmission are factors in the spread of the disease

f. Symptoms:

• 1. Natural infection in quail under 4 weeks of age is characterized by a sudden onset and the rapid spread of tracheal rales, coughing, and sneezing
• 2. Depression, huddling and ruffled feathers may be observed.
• 3. Neural signs - twisting or bending the neck over the back or between the legs - may appear in a few birds.
• 4. Signs persist 1 to 3 weeks, and mortality ranges from 10-100%, often being over 50%

g. Lesions.

• 1. Tracheitis and bronchitis, inflammation of airs.
• 2. Conjuntivities and congestion of the nasal or infra-orbital sinuses.

h. Diagnosis:

• 1. Based on symptoms.
• 2. High mortality within 2 weeks of age. In birds over 4 weeks of age,the signs may be less severe, spread slower, and the mortality less than 10%.
• 3. Excess mucus in the air sac.
• 4. Accurate diagnosis is based on isolation and identification of QBV. Curling and stunting of the embryos inoculated, thickening of the amniotic membrane, necrotic foci or patches in the liver and ureter collections in the kidneys are typical effects of QBV infection, similar lesions are seen in IBV infection.

i. Prevention:

• 1. Preventing entry of the agent onto the premises.
• 2. Preventing transmission the agent from one group of birds to another,

j, Treatment:

No effective treatment.

4.11 DUCK VIRUS HEPATITIS

a. Synonym: DVH

b. definition:

A highly fatal disease of young duck. Characterized contagious, sudden onset, rapid course, high mortality in duckling of less than 3 weeks age.

c. Etiology:

An RNA, entero virus of the Picornavirus group.

d. Susceptibility:

Natural outbreaks only in ducklings less than 3 weeksof age. Chicken and turkeys are resistant.

e. Occurrence:

First described in 1950 in Long Island, N.Y. Now recognized in several states.

f. Transmission:

Contact transmission .

g. Symptoms:

• 1. Onset and spread of the disease is rapid. (Short incubation period 1-3 days).
• 2. Mortality occurring within 3-4 days. (Morbidity 100%, mortality variable).
• 3. Birds stopped moving, and squatted down with eyes partially closed.
• 4. The ducklings fell on their sides, kicked spasmodically with both legs and died with heads drawn back. (Opisthotomus).

h. Lesions:

• 1.The liver is enlarged and contained punctate or ecchymotic hemorrhages
• 2. Reddish .discolorations or mottling of the liver.
• 3. Spleen enlarged and mottled.
• 4. Kidneys are swollen, renal vessels injected.
• 5. Microscopic examination - necrosis of the hepatic cells and proliferation of the bile epithelium. Various stages of inflammation and hemorrhages.

i. Diagnosis:

• 1. Sudden onset, rapid spread, and acute course of the disease.
• 2. Lesions in the liver of young ducklings up to 3 weeks of age.
• 3. Isolation of virus in chicks embryos. Use 9 day old embryo, stunted growth and edematous, died 5th day after inoculation.

j. Prevention and control.

• 1. Serum therapy proves to be highly successful.
• 2. Immunize breeders with DVH (attenuated or killed virus vaccine).
• 3. Immunize ducklings with attenuated or formalin-killed vaccine.

4.12 DUCK ENTERITIS

a. Synonyms:

Duck Plague, DVE.

b. Definition:

Duck plague is an acute, contagious herpesvirus infection of ducks, geese, swans. Characterized by vascular damage with tissue hemorrhages and free blood in the body cavities, enanthematous lesions of the digestive mucosal surface, lesions of the lymphoid organs, and retrograde changes of the parenchyma.

c. Etiology:

• 1. DNA herpesvirus.
• 2. Initial isolation can best be made by cultivation of the virus on chorioallantoic membrane of 12 day-old embryonated duck eggs. The virus has also been propagated in duck embryo cell cultures.

d. Susceptibility

Natural outbreaks in only ducks, geese, and swans.

e. Transmission:

• 1 Direct contact between infected and susceptible birds, and indirectly by contact With contaminated environment.
• 2. Water appeared to be the natural medium of transmission of the cirus form infected to susceptible individuals.
• 3. The disease can be transmitted experimentally via the oral, intranasal, intravenous, intraperitoneal, intramuscular, and dorsal foutes of administration.

f. Symptoms:

• 1. Incubation period 3-7 days. Once overt signs of the disease appear death usually follows within 1 to 5 days. Mortality ranged form 5-100%.
• 2. All ages are susceptible. Sudden high and persistent flock mortality is often the first reported observation. Prolapse of the penis may be evident in dead mature male breeders.
• 4. In laying flocks a drop in egg production of 25 to 40% may be during period of greatest mortality.
• 5. Photophobia (associated with half-closed, pasted eyelids), inappetence, extreme thirst, droopies, ataxia, ruffled feathers, nasal discharge, soil vents, and a watery diarrhea. weakness and depression. Dehydration.

g. Lesions:

• 1. Enathematous (an eruption upon a mucous surface) lesion in specific location on the mucosal surface of the gastrointestinal tract, lesions of lymphoid organs, and retrograde sequela in parenchymatous organs are pathgnomonic.
• 2. Hemorrhage heart muscles, mesentery, liver, pancreas, in testines, lung, and kidney.
• 3. All lymphoid organs are affected. Hemorrhage and necrosis or thymus, spleen and lymph follicles. The bursa of Fabricius is edematous, the serosal and mucosal walls have pinpoint hemorrhage and necrotic areas.
• 4. The intestinal annular bands appear as intensely reddened rings. yellow pinpoint spots can be observed on the mucosal surface.

h. Diagnosis:

• 1. Base on gross lesions. Should differentiate from duck hepatitis.
• 2. Histopathological studies. Hepatic cells with intranuclear inclusion body, and spherical bodies within the cytoplasm
• 3. Isolation and identification of the virus. Serum neutralization test.
• 4. Reportable disease, suspected cases should be submitted to a state laboratory.

i. Prevention

Vaccination

j. Control

The disease can be controlled in domestic ducks by depopulation, sanitation, disinfection and removal of the birds from the infected environment. All possible measures should be taken to prevent dissemination of the virus by free-flowing water.

*Annular bands (AB) are 4 normal, regularly space lymphoid organs that are located in the anterior and posterior portions of those regions of the intestines commonly referred to in mammals as the jejunum and ileum. They are anterior and posterior jejunal annular band, and anterior and posterior ideal annual band.

K. Transmissible enteritis of turkeys.

• a. Synonym: Blue comb, mud fever.
• b. Definition: Acute highly infectious disease affecting turkeys. Characterized by anorexia, weight loss and wet droppings.
• c. Etiology: Believed to be caused by corona (RNA) virus.
• d. susceptibility: Turkeys
• e Transmission: Both unfiltered and filtered intestinal material of sick turkeys can reproduce the disease by oral or rectal route.
• f. Occurrence: Common in turkey rearing area
• g. Symptoms:
  • 1. A highly infectious and fatal disease of newly hatched poults.
  • 2. Severe catarrhal enteritis. Shanks are cold and veins are clearly visible due to sever dehydration.
  • 3. Incubation period 2-5 days.
  • 4. Mortality may be 25-50%, or even higher in young poults. Morbidity nearly 100%
  • 5. In growing mature turkey. Rapid decline in feed and water consumption.
  • 6. Hematology: Monocytosis.

l. Lesions:

• 1. Severe catarrhal, mucoid enteritis, gelatinous contents of the duodenum, jejunum and ceca.
• 2. The pancreas have a chalky appearance with numerous whitish area. Urate deposit may also seem in kidneys.
• 3. Histopathology:

The adrenals are completely obliterated due to large numbers or found cells With hyperchromatic nuclei.

The pancreas showed numerous foci of acinar cells, (hydropic degeneration). Cytoplasm contain eosinophilic inclusions decrease in microvillus length, decrease in goblet cells, separation of epithelium from the propria.

m. Diagnosis:

• 1. Based on history of outbreak, course of the disease and gross lesion.
• 2. Confirmation by virus isolation.
• 3. Differential diagnosis: Separate this disease from hemorrhagic enteritis and non-specific bacterial enteritis.

n. Treatment:

Antibiotic treatment reduce mortality greatly. Bacitracin and neomycin therapy give best results.

o. Prevention:

Strict sanitation and management.

4.14 AVIAN MONOCYTOSIS (Pullet disease, Blue comb disease, X-disease, or New Wheat disease) .

1. Etiology:

• 1. Unknown, recently a gram negative bacilli was isolated, proven to be related to this disease.
• 2. Nephrotoxin, wheat poisoning.
• 3. Waller (1942, 1944) reported the isolation of a filterable agent from the blood, liver, feces, and eggs of birds affected with the acute from. The virus could be cultivated on the chorioallantoic membrane of 8- to 9-day old chicken embryos when it produced a compace of circular lesion with radiating process, stunting of the embryo, and death in about 12 per cent.

2. Susceptibility:

Chickens

3. Occurrence:

Nationwide. Seasonal disease in hot weather. The disease may occur, as if often does, at the time new grains come into the ration, especially wheat.

4. Transmission. Unknown.

5. Symptoms:

• 1. Age 1 month to 2 years. Usually 5-7 months old, when they are in prime laying condition.
• 2. Since it often strikes without warning and affects a high percentage of the flock, it can be very costly interims lowered egg production (60%), and stay out for 30 days.
• 3. Action: Acute
• 4. Depression, lack of appetite, marked cyanosis or darkening or the comb and head, and a watery diarrhea. Refuse to eat grain.
• 5. The crop is often distended with food and water which do not move into the lower digestive tract. The food in the crop soon turns sour with an offensive odor. There is usually a high degree of dehydration, shown by dry skin and thin legs and shanks. Veins in the shanks (metatarsal vein) often become plainly visible.

6. Lesions:

• a. Muscular dehydration and degeneration is evident.
• b. Blood becomes thickened and there is an increased white blood cell count.
• c. Liver congestion, pancreas chalky appearance, Enlarged kidneys, accumulations of urates, distended ureters which often are clogged with crystals of uric acid .
• d. Histopathology:
  • 1. Nephrosis - cloudy swelling, pyknois, desquamation of epithelial cells in tubules, hyaline casts, pseudogiant cells.
  • 2. Catarrhal enteritis
  • 3. Pancreas - cloudy swelling of acinar lobules.
  • 4. Breast muscle - Zenker's necrosis.

7. Diagnosis:

1. Differential field diagnosis is possible.

Characteristic	Blue comb	Cholera
Temperature	Normal to subnormal	110-112°
Thirsty	no	Yes
Loss of appetite	yes	yes--No
Crop( full)	yes	No
Ratting	No	yes
comb	Dark	Dark
Dehydrated	+	-
Action	Acute	Acute
Mortality	Low	High-Low
Spleen	Atophy	Normal size
Liver	(OK)	Necrotic
Heart	Normal	Petechial
Pancreas	+	-

---

2. Blood Count:	Total Leukocyte Counts
Monocytes	-
Blue Comb - 8,000/mm3	40,000/mm3
Normal - 1,700/mm3	15,- 35,000/m~3

8. Control

Providing an abundance of clean, readily available water and coo, well-ventilated quarters, and in reducing consumption of grain.

9. Treatment:

• 1. Do not flush
• 2. Antibiotic treatment, best with tetracycline.

4.15 EQUINE ENCEPHALOMYELITIS (EEE).

a. Definition:

Serious disease associated with arbovirus infection is uncommon in birds.

b. Etiology:

Two antigenically different viruses causes encephalitis in horses in North America. The EE and WEE virus. RNA. The viruses are classified as Alphavirus of the Togaviridae group

c. Occurrence:

• 1. These viruses have a wide host range, readily infecting most laboratory animals when inoculated intracerebrally.
• 2. Mice and guinea pigs are especially susceptible, dying of encephalitis within 2 to 5 days (EE), and in 4-7 days (WEE).
• 3. Infections, both natural and experimental, and usually subclinical, have been reported in a very large number of indigenous birds.

d. Transmission:

It is transmitted in nature by several species of vector mosquitoes.

The most important biological vector among birds are Culex spp and Aedes spp. Wild birds are considered to be important reservoir of EEV .

e. Symptoms:

• 1. Chickens more than 4 weeks of age, show no clinical signs of disease when infected by these viruses.
• 2. Day-old chicks succumb rapidly to infection without showing signs of CNS involvement. Signs in young chicks consist of diarrhea and extreme prostration.

g. Lesions:

• 1. No gross lesions.
• 2. Histopathologically nonsupportive encephalitis. They consist of vasculitis, focal or patch necrosis, perivascular leukocyte infiltration, swelling proliferation of glial cells- meningitis and degeneration and necrosis of neuro
• 3. Young birds: Mycarditis.

h.Diagnosis:

• 1. Based on isolation and identification of the virus or demonstration of a rise specific serum antibody during Convalescence.
• 2 For isolation of virus, either blood taken during the stage of viremia of a suspension of brain tissues may be inoculated into the allantoic chambers of embryonating eggs, intracerebrally inoculated into suckling or weaning laboratory mice. CPE in tissue cultures.

i. Control and Prevention:

• 1. Birds which survive infection become solidly immune, can be demonstrated by HI, CF, and SN tests.
• 2. Chick embryo vaccine for horses, can be used for pheasants. I.M. injection.
• 3. Control is based on attempts to break the cycle of vector transmission from reservoir species to other susceptible birds.

4.16 INCLUSION BODY HEPATITIS (IBHC) or infectious anemia.

• a. Definition: Viral infection with liver degeneration, aplastic anemia and hemorrhaged.
• b . Etiology: Adenovirus.
• c. Susceptibility: Chicken
• d. Transmission: Contact, egg transmission.
• e. Signs:
  • 1. Age: 4-8 weeks.
  • 2. Sudden increase in mortality, pale comb, wattles and facial skin.
  • 3. Hematology: Normocytic, normochromic anemia,, RBC count below 1.5 million/mm , IYBC 20,000 to O/mm

f. Postmortem:

• 1. Liver - Discoloration (Yellow-tan), softening and hemorrhagic.
• 2. Hemorrhage in skin, muscle and viscera
• 3. The spleen and bursa are frequently shrunken.
• 4. Bone marrow pink to whitish.
• 5. Microscopically: Liver and kidney cell degeneration. Intanculear inclusion bodies in liver cells

g. Diagnosis:

• 1. Intranuclear inclusion bodies in hepatic cells.
• 2. Cultivation and identification of the adenovirus.
• 3. Serological test. Virus neutralization tests.

h. Prevention and Control:

Unknown.

• a. Synonyms: Tenosynovitis
• b. Etiology: RNA, Reo-virus.
• c. Susceptibility: Chicken
• d. Transmission: Contact
• e. Signs:
  • 1. Lameness at 6-7 weeks o£ age.
  • 2. Swelling of the tendon sheath.
  • 3. Petechial in the synovial surface.
  • 4. Retarded growth.

f. Lesions:

• 1.Swelling of digital flexor tendon and metatarsal extensor tendon.
• 2. The hock or elbow joint usually contains a small amount of straw colored exudate.
• 3. Conronic case showed hardening and fusion of the tendon sheaths.

g. Diagnosis:

• 1. Presumptive diagnosis may be on the basis of signs and lesions.
• 2. FA test, PPLO test.

h. Treatment, prevention and control.

• 1. No effective treatment.
• 2. all in all our management methods.

 

4.18 TURKEY VIRAL HEPATITIS:

a. Definition:

• Acute, highly contagious, typically subclinical disease of turkeys which produces lesions of the liver and less frequently of the pancreas.

b. Etiology:

• Virus, Enterovirus of the Picornaviridae group

c. Susceptibility:

• Turkey.

d. Transmission:

• Contact, egg transmission possible.

e. Signs - Subclinical

f. Lesions

• 1. Liver - focal gray, depressed, several mm diameter lesions. necrosis, mononuclear infiltration.
• 2. Pancreatic lesions less frequent.

g. Diagnosis

• 1. Base on lesion
• 2. Animal inoculation

h. Treatment

No effective treatment