Avian pathology

Avian Pathology Viral Diseases By Prof Dr. Al-Sayed R. Al-Attar Professor of Pathology Fac.of Vet.Med. Zagazig University

Neoplastic diseases Mareks disease

It is a common lymphoproliferative disease of chickens usually characterized by mononuclear cellular infiltrates in peripheral nerves and various organs and tissues including iris and skin.

Etiology: MDV is a cell-associated herpes virus with lymphotropic properties There are 3 serotypes .Serotype 1 (Gallid herpes virus 2) isolate from chicken ,Serotype 2 (Gallid herpes virus 2) isolate from chicken .Serotype 3 ( Meleagnd herpes virus) isolated from turkey MDV refers to serotype, strains can be sub divided into (according to pathogenicity) (mild, virulent and very virulent ) .Virulence or oncogenicity with only serotype 1 MDVs. Natural hosts: Virtually all chickens including game fowl are susceptible to MDV infection and tumor development (natural host) Quail, turkeys, pheasants and some species of ducks and geese are also susceptible to natural infection and disease.

Transmission: MDV is transmissited horizontally and readily by direct or indirect contact between chickens by air borne route (from residual feather dust and dander in growing or adjacent houses, fomites or personnel).

Incubation period: Experimental infection: early mononuclear infiltration after 5 days but clinical signs and classical lesions not before 3-4 weeks PI. Natural infection: MD outbreaks sometimes occur in young unvaccinated chickens of 3-4 weeks. But most of serious causes begin after 8-9 weeks and common after egg production especially in broiler breeders, or subsequent to molting.

Clinical signs: It varies according to the specific syndrome Paralysis syndromes (MD lymphoma): Progressive paresis and later complete spastic paralysis of one or more of extremities.

Involvement of the vagus nerve can result in paralysis and dilation of crop and/or gasping.

Incoordination or stilted gait may be the first observed sign.

The characteristic sign is a birds with one leg stretched forward and the other back, some birds may appear clinically normal and others depressed or comatose prior to death.

Nonspecific signs as emaciation paleness, anorexia and diarrhea could be seen. Some birds develop nervous signs as torticollis.

Some chickens may exhibit ataxia and flaccid neck paralysis.

Acute fatal deaths may occur follow by paralysis Ocular syndrome: characterized by blindness (unilateral or bilateral).

Morbidity and mortality: Most birds develop clinical disease die. Mortality is low Some flocks experience disease outbreaks despite vaccination (mortality take periods 4-10 weeks). Acute cytolytic infection or transient paralysis can be developed in some flocks.

Gross lesions: It consists of mainly : Nerve lesions Visceral lymphoma No brain lesion but spinal ganglia Nerve lesions: Severally affected peripheral nerves (cervical ,sciatic and brachial) show loss of cross striation, gray or yellow discoloration and sometimes edematous appearance with unilateral or bilateral localized or diffuse enlargement (2-3 times normal size). Autonomic nerves as celiac nerves are highly affected than peripheral nerves.

Visceral organs: Lymphomatous lesions in gonads (ovary), lung, heart, mesentery, kidney, liver, spleen, bursa, thymus, adrenal gland, pancreases, proventriculus, intestine iris, skeletal muscles and skin.

Visceral lesions can occur with nerve lesions Visceral lesions either is diffuse enlargement (white or greyish discolorations) or nodular growths of varying sizes of firm grey to white nodules with smooth cut surfaces. Lesions in immature ovaries appear as small or large translucent areas or cauliflower like growth in mature ovaries. Other viscera showed focal greyis foci or large nodules to diffuse enlargement.

Cutaneous from: Due to involvement of skin (feather follicle) either scattered follicles (whitish nodules) or diffuse (brownish crust).

Erythematous involvement of skin shank in broiler due to virulent disease called Alabama red leg. Also swelling of comb and wattle due to skin lymphoma.

Ocular form: changes include loss of pigmentation of iris, irregularity of pupil. Conjunctivitis, multifocal hemorrhages and corneal edema.

Other syndromes: Acute cytolytic infection characterized by degenerative and cytolytic changes in lymphoid organs.

Splenomegaly due to nonneoplastic response of viral replication.

Occulsive atherosclerosis (vascular syndrome) grossly fatty atheromatous lesions in large cornories, aorta and other large arteries.

Local lesions (experimental, some nodular growths at the site of inoculation)

Microscopic pathology: Nerves: it includes 2 lymphoproliferative lesions Type A lesions: It consists of CD4 T lumphocytes and some B cells . Lesion consists of infiltration by proliferating lymphoblasts, large, medium and small lymphocytes, and macrophages, and appears to be neoplastic in nature. In some cases, demyelination and schwann cell proliferation.

Type B lesions: It is called inflammatory It characterized by diffuse, light to moderate infiltration by small lymphocytes and plasma cells usually with edema and sometimes ith demyelination and Schwann cell proliferation. A few macrophage may be found.

Two types may be found in different nerves of the same bird Type A lesions were seen in the absence of paralysis or demyelination.

Type C lesions: The C-type lesion consists of mild scattering of small lymphocytes, often seen in birds that show no gross lesions or clinical signs; this is thought to be a regressive inflammatory lesion Brain lesions: In classical and acute transient paralysis are similar and represented by mild, persistent perivascular cuffing . Gliosis without primary demyelination may be seen Visceral organs: lymphoproliferative lesions as diffuse proliferation of small to medium T-lymphocytes and lymphoblasts, natural killer cells, B cells and macrophages with rarely plasma cells.

Tumor cells are characterized by large, pleomorphic nucli with prominent nucleoli.

The majority of transforormed T. cells express MHC-11 and CD 4

Integument lesions: Lymphoproliferative nodules often around feather follicles that contain MDV viral antigens and intranuclear inclusions in the FFE .These lesions appear largely inflammatory but also may be lymphomatous around feather follicles (Massive prolferative lesion may cause disruption of the epidermis resulting in ulcer) Eyes: early lesion characterized by: Arachnoid layer of optic nerve and ciliary nerves infiltrated by T-cells heterophils and macrophages together with vaculitis and hypertrophy, of endothelial cells.

Late lesions: characterized by uveitis, keratitis and retinal necrosis with infiltration by CD4 and CD8 T-lymphocytes, macrophages, plasma cells and granulocytes.

Unusual severe ocular lesions include uveal change(damage), congestion, swelling of iris, severe inflammatory changes, edema of cornea, including intanuclear inclusion bodies.

Lymphodegenerative syndromes: (acute mortality syndrom) in cloacal bursa and thymus (transient acute cytolytic changes) Bursal lesion characterized by degeneration, necrosis and deplation of lymphocytes and cyst formation (bursal atrophy). Thymic atrophy is often severe due to degeneration necrosis depletion from cortex and medulla with presence of intranuclear inclusions.

Vascular syndromes: Atherosclerosis changes in aorta and other main arteries. Characterized by intimal l and medial foam cells, extracellular lipid, cholesterol clefts and calcium deposits (fatty proliferative lesions).

Local lesions and tumors transplants: Tumor transplants are composed of uniforms lymphoblastic cells .In regression tumors or transplants, small lymphocytes, heterophils vascular invasion and necrosis may be present at the site of inoculation (wing web or pectoral M.).

Leukosis/ sarcoma group

Definition:- The leukosis / sarcoma (LIS) group of diseases designates a variety of transmissible benign and malignant neoplasma of chickens caused by viruses (Retroviridae).

Etiology: Viruses are placed in the alphaeteroviruses genus of the family retroviridiae ALSv that occur in chickens have been divided into 6 envelop subgroups A, B, C, D, E and J on the basis of their viral envelope glycoproteins which determines antigenicity.

Natural hosts: Chickens are the natural hosts for all viruses of LIS group.

Transmission: Vertical from hen to progeny through the egg Horizontal from bird to bird by direct or indirect contact.

Incubation period: It dependents up on many factors. It may be long (14-30 weeks). Filed infection not before 14 weeks age or higher.

Clinical signs: Are mostly nonspecific .They include inappetence, weakness, diarrhea, dehydration and emaciation. In L.L. there may be abdominal enlargement. The comb may be pale, shriveled ‫ذابل‬or occasionally cyanotic. In erthroblastises and myeloblastosis, hemorrhage from feather follicles may occur. After appearance of signs, the course is usually rapid and birds die within a few weeks. Other affected birds may die without showing obvious signs.

There are other signs according to the type of sarcoma

Clinically , It is characterized by a gradual beginning, persistent low mortality in the flock and diffuse or focal neoplastic growths of lymphoblasts in viscera. The neoplastic changes begin always from the bursa of Fabricius, where various-sized lymphomas are detected . Clinically, pale comb and wattles, sometimes swelling of the abdomen because of the highly enlarged liver are observed. Diffuse or nodular neoplastic growths could be detected in many organs, but they are more common in the liver, the spleen, the kidneys, the heart and the ovary. Spontaneous rupture of the neoplastically grown spleen, leading to extensive loss of blood.

LL is widely distributed worldwide in countries with developed industrial poultry breeding. It is usually observed in birds at the age of 16 weeks and older.

Pathology Lymphoid leucosis (L.L): Gross lesions: Visible tumors invariably involve the liver, spleen and cloacal bursa.

Other organs often grossly involved include kidney, lung, gonad, heart, bone marrow and mesentry. Tumors are soft, smooth and glistening, acute surface appears greyish to creamy white and seldom has areas of necrosis. Tumors growth may be nedular, mainly diffuse or a combination of there forms.

Microscopic: All tumors are focal and multicentric in origin The tumors cells proliferate, displace and compress cells of the organs rather than infiltrate between them. Nodules in the liver usually are surrounded by aband of fibroblast like cells (remnants of sinusoidal endothelium). In bursa, the tumor growth had a follicular pattern.

Tumors consist of aggregates of large lymphoid cells (lymphoblasts) that may vary in size but all of the same developmental stage. They have a poorly cytoplasmic membrane. Much basophilic cytoplasm and a vesicular nucleus (cell have margination and clumping of the chromatin and one or more conspicuous acidophilic nucleoli) Tumor cells contain a large amount of RNA ( it stains red with methyl green pyronin) indicating the cells are immature and rapidly dividing It also have cells antigen markers and produce and carry surface IgM. Other forms: They include erythroblastosis, myloblastosis and other bengin or malignant neoplasms (hemangioma, nephroma, nephroblastoma, fibroma and fibrosarcoma). Â

the bursa of Fabricius, a characteristic intrafollicular hyperÂŹplasia is observed.

Histopathology, (a) Myelocytes were accumulated in dilated Disse’s space of liver, X100, (b) Myelocytes were accumulated in stroma of granulosa cells in ovary, X100, (c) Focal aggregates of myelocytes was raised on myocardium of the heart, X40 and (d) High magnification of myelocytic cell with bright eosinophilic granules and peripheral nucleus, X630 H and E

Reticuloendotheliosis It is agroup of pathologic syndromes caused by the reticuloendotheliosis virus (REV) group of retroviruses in several avian species.

Etiology: stocks of T strain contain a non-defective helper REV. (REV-A).

Natural hosts: turkeys, chickens, ducks, geese, pheasants, Japanese quail and peafowl.

Transmission: Horizontal transmission by direct physical contact with infected birds. Insect transmission recorded. Vertical transmission infection via eggs to their progeny.

Clinical signs: Chickens with runting disease syndrome may be stunted and pale (loss of weight). Some birds with abnormal feather development termed nakanuke (wing feather with adhesion of the barbs to a localized section of the shaft. Lameness or paralysis is rare.

Low mortality and birds developed chronic lymphoma become depressed prior to death.

Pathology Runting disease syndrome: The principle lesions in chickens including runting, atrophy of thymus and cloacal bursa, enlarged pripherail nerves, abnormal feather development Proventriculitis (acute hemorrhagic or ulcerative), enteritis, anemia and necrosis of liver and spleen. Other forms as (chicken bursal lymphoma, chicken non bursal lymphoma, turckey lymphoma, lymphoma of other species) multiple syndromes, acute reticulum cell neoplasia , chronic lymphoma were recorded. This syndrome may occur in ducks and turkeys. Microscopic picture: Peripheral nerve of chicken in runting syndrome usually infiltrated with mature, immature lymphocytes and plasma cells and often occur in the absence of other neoplasms.

Reticuloendotheliosis virus (REV) belongs to the retrovirus family, genus Gammaretrovirus. The genome of retroviruses consists of single-stranded RNA with positive polarity and present in two copies .

The genomic structure of REV consists of a group-specific antigen (gag), protease (pro), polymerase (pol), and envelope (env) regions flanked by long-terminal repeats (LTRs) . The gag gene encodes five structural proteins, p10, p12, pp18, pp20 and p30. The p30 (30 kDa) protein is the major REV group-specific antigen. The env gene encodes two envelope glycoproteins, gp90 and gp120 . The pol gene encodes a reverse transcriptase similar to those of mammalian type retroviruses and differs from the Avian Leucosis–Sarcoma Virus REV is immunologically, morphologically and structurally distinct from the leukemia/sarcoma group. REV can cause acute reticular cell neoplasia, chronic neoplasia of lymphoid tissues and other organs, immunosuppression and runting disease syndrome in domestic poultry as well as other avian species. However, natural outbreaks of REV in commercial poultry are rare

The REV infections can cause various pathologic lesions. The most common clinical diseases induced by REV are including runting-stunting disease syndrome, characterized by growth retardation and poor feathering with acute reticular cell neoplasia and chronic B-cell and T-cell lymphomas. The losses and mortalities in affected flocks with REV can be significant due to tumor and or immunosuppression. Although REV is wide spread, REV-induced clinical disease is infrequently diagnosed in commercial flocks. Reticuloendotheliosis cases have been rarely diagnosed in commercial chicken flocks, even though REV infection has been identified in a high proportion of chicken farms by serology and virus isolation

Histopathological pictures: Multiple nodules were observed in the liver, spleen and intestine consisted of homogeneous immature lymphocytes. The head region showed presence of collagen fibers in circular and in parallel or interlake arrangement, hypercellularity, clusters of lipoblasts of varying size, intercellular transudate, dilated blood vessels and aggregation of inflammatory cells surround the blood vessel .

Some areas were more cellular than others, these cells mainly fibroblasts, which separated from each other by intercellular transudate and focal localized aggregation of inflammatory cells mainly lympho-reticular cells, lymphocytes and histocytes.

Aggregation of inflammatory cells surrounded congested blood vessels . The dilated blood vessels sometimes contain transudate and inflammatory cells . Mitotic figures of fibroblast were observed.

Unusual tumor formation in the head region gross lesions of head region of cross-bred chicken 25 weeks of age with tumors formation

Congested and enlarged liver, proventriculus and gizzered with whitish nodular infiltrations organ obtained from chicken with 25 weeks age

Pathological changes in the head showing the (a) Collagen fibers in circular, (b) In parallel or interlake in tumor mass arrangement in tumor mass, (cd) Hypercellularity in tumor mass, (e) Clusters of lipoblasts of varying size in tumor mass, (f) Intercellular transudate in tumor mass, (g) Dilated blood vessels and (h) Aggregation of inflammatory cells surround the blood vessel

Duck hepatitis

Its highly fetal and rabidly spreading viral infection of young duckling characterized primarily by hepatitis Etiology: Three types' of DHAV, closely related picornaviridae virus (DHAV1, 2 and 3) Transmission: Horizontally and by contact of infected ducks and highly contagious (rapid spread) Incubation period: lasts 1 to 2 days Clinical signs: DHAV1:- spread rapidly and all mortalities occurred within 3-4 days The infected duckling fails to keep up on the broad.

Is stop moving and squat down with eyes partially closed Birds full on their sides and keck spasmodically with both legs and die with head drawing back Morbidity 100% and mortality variable Gross lesions: Mainly in liver (enlarged liver with punctate or ecchymotic hemorrhages and reddish discoloration or mottling of liver surfaces Spleen enlarged and mottling, kidney swollen and congested

Microscopic changes: Acute disease, necrosis of hepatic cells Chronic cases, wide spread bile duct hyperplasia Inflammatory cells responses and hemorrhages . Regeneration of liver parenchyma Duck hepatitis type 2: Clinical signs: Infectious via oral cloacal and subcutaneous routs This is within 1-4 days .Polydipsia with loose dropping, excessive rate of excretion.

Sometimes, convulsions and acute opisthotonons Mortality (10-50%) dependence up on age Mature ducks are refractory to the disease Gross lesions: Target organs liver and kidneys .Liver pale pink with multiple, small punctate hemorrhages .Spleen may be enlarged and sagolike due to scattered pale foci.

Kidneys are often swollen with injected blood vessels (congested) .No food in alimentary tract Small hemorrhage in intestinal wall and heart fat.

Microscopic changes: Extensive necrosis of the hepatocytes Bile duct hyperplasia N.B survivors of DH type 2 were immune to further infection.

Duck hepatitis type 3: Clinical signs: Duckling dying from DHV type 3 show the typical appearance of type 1 infection.

Outstretched legs and opisthotonos Mortality nearly exceeds 30% Gross and microscopic lesions: They are similar to those caused by DHAV-1

Duck virus enteritis (duck plague)

It is an acute contagious herpes virus infection of ducks, geese and swans characterized by Vascular damage ,Tissue hemorrhage ,Digestive mucosal emptions Degenerative changes in parenchymatous organs Etiology: The causative agents of DVE is a herpes virus Transmission: By direct contact between infected and susceptible birds or indirectly from contaminated environment Incubation period: In domestic ducks, it ranges from 3-4 days Clinical signs: In breeder ducks: Sudden, high, persistent flock mortality is often the first observation Mature ducks die in good flesh ,Prolapse of the penis in dead mature males In laying flocks, a marked drop in egg product .Lateron, photophobia associated with half closed pasted eyelids In appetence, extreme thirst, droopiness, ataxia, ruffled feathers, nasal discharge, soiled vents and watery diarrhea. Affected ducks are unable to stand; they mention a posture with drooping outstretched wings and head down.

Young duckling: Dehydration, loss of weight, blue beaks, conjunctives, lacrimation, nasal exudate and a blood stand vents. Mortality and morbidity: total mortality in domestic ducks rang from 5-100%

Gross lesions: Lesions of DVE are associated with DIC .Necrotic degenerative changes in GIT mucosa and sub mucosa, lymphoid organs and parnchymaous organs Petechial, ecchymotic or layer extravasited of blood on myocardium, viscera, mesentery and serous membrane On the epicardium, closely pucked petechiae on the coronary grooves give the surface a red paint brush appearance (in mature breeder ducks) Endocardial mural and valvular hemorrhages In laying hemorrhage's may be observed in deformed, discolored ova rian follicles and massive hemorrhage from ovary may fill abdominal cavity Lamina of intestines and gizzard are often filled The esophageal proventricular sphilicter appears as a hemorrhage raing.

Oral cavity, esophageal, ceca, rectum and cloaca showed the following changes Initially, macular surface hemorrhages Later coverd by yellow, white erusty plaques Folloed by, superficial green scab .It may be formed diphtheritic membrane (thick yellow white membrainous) Meckels diverticulum may be hemorrhage and contain a fibrinous core All lymphoid organs (spleen, thymus and bursa) may be normal or smaller in size, dark and mottled. Sometimes, petechiae or necrotic areas could be seen.

In geese, intestinel lymphoid disks (button like ulcers) are common.

Microscopic picture: Wall of blood vessels (smaller blood vessels, venules and capillaries) shoed endothelial disruption and edema and perivascular hemorrhages Hemorrhages are common in proventriculus, liver, lungs, intestines and kidnyes.

Degenerative and necrotic changes in visceral organs (parnchymatous organs lymphoid T. ) Esinophilic intranuclear and cytoplasmic inclusions in epithelial cells.

Lymphoid organs showed necrosis and hemorrhages Oviduct, congestive, hemorrhagic and necrotic lesions. Testes hemorrhages.

Influenza (fowl plague) It is highly infectious and contagious severe fatal disease

of poultry and humans caused by A influenza viruses. Bird flu: a simplified alternative to avian influenza by the media to describe infections in poultry, human and other mammals with type A influenza viruses derived from birds.

Etiology: Orthomyxoviridae family, genus influenza A (RNA viruses).

Virus influenza have a high frequency of antigenic in the surface glycoproteins (HA and NA) because of 2 phenomena, drift and shift.

Antigenic drift is minor antigenic changes in the coding proteins ,these may be due to vaccination which vessels in improper, in complete or inadequate population immunity, may play a role in selecting antigenic variants (drift variant). In LPM antigenic shift in HA and /or NA subtypes has been documented.

Antigenic shift arise from genetic reassotrment between gene segments of two influenza viruses that infect the same cell and result in the acquisition of Noval HA and /or NA antigenic combination in a virus that can infect a population with no preexisiting immunity.

It is reported for HPAI viruses in Asia chickens and geese. Also wild ducks have coinfection with different influenza viruses.

Pathotype: based on pathogenicity (IVPI- intravenous pathogenicity index test) Highly pathogenic (HPNAI) viruses , include H5 and H7 viruses. Low pathogenic (LPNAI) viruses all naturaly occurring H1-4. H6 and H 8-16 viruses have low virulence for chickens when given by the natural route of challenge.

Natural hosts: All viruses naturally infect a wide variety of wild and domestic birds especially free-living birds occupying aquatic habitats.

Incubation period: Natural infection from 3 days to 14 days. Experimental infection a few

Biology of Influenza A Virus Influenza viruses are RNA viruses in the family Orthomyxoviridae, which includes four genera: Influenza A, B and C viruses and Thogotovirus, as recently proposed by the International Committee on Taxonomy of Viruses (ICTV) . They are enveloped negative-stranded RNA viruses that can be distinguished on the basis of antigenic differences in nucleocapsid (N) and matrix (M) proteins .

Influenza A viruses are roughly spherical (120 nM) with glycoprotein spikes on the surface and genome consisting of eight RNA fragments that encode 10 proteins. The haemagglutinin (HA), neuraminidase (NA) and matrix (M2) proteins are embedded in the envelope lipid bilayer derived from the host cell . The M1 protein underlying the envelope is the major determinant of virion morphology . The nucleoprotein (NP) associates with each RNA segment to form the ribonucleoprotein (RNP) complex, which also contains small amounts of the three polymerase subunits. The nonstructural proteins NS1 and NS2 are found only in infected cells .

Antigenic shift is the process by which two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains.

The term is often applied specifically to influenza, as that is the best-known example, but the process is also known to occur with other viruses, such as visna virus in sheep.Antigenic shift is a specific case of reassortment or viral shift that confers a phenotypic change.

Antigenic shift is contrasted withantigenic drift, which is the natural mutation over time of known strains of influenza (or other things, in a more general sense) which may lead to a loss of immunity, or in vaccine mismatch.

Antigenic drift occurs in all types of influenza including influenzavirus A, influenza B and influenza C. Antigenic shift, however, occurs only in influenzavirus A because it infects more than just humans.Affected species include other mammals and birds, giving influenza A the opportunity for a major reorganization of surface antigens. Influenza B and C principally infect humans, minimizing the chance that a reassortment will change its phenotype drastically.

The hallmark of influenza viruses is antigenic variation, which comes in two forms: antigenic shift and antigenic drift. Antigenic shift, which is seen only with influenza A viruses, results from the replacement of the hemagglutinin and sometimes the neuraminidase with novel subtypes that have not been present in human viruses for a long time. The source of these new genes is the large reservoir of influenzaviruses in waterfowl, in which 15 antigenically distinct subtypes of hemagglutinin and 9 subtypes of neuraminidase have been identified. The consequences of the introduction of a new hemagglutinin into human viruses is usually a pandemic, or a worldwide epidemic, resulting in hundreds of thousands or millions of influenza-related deaths. the phenomenon of antigenic drift. Drift is a subtler(perfect), process than shift and involves the accumulation of mutations within the antibody-binding sites in the hemoagglutenin, neuraminidase, or both that abrogate the binding of some antibodies. Because of these mutations, the resulting viruses cannot be inhibited well by antibodies against previous strains, and it is easier for them to spread throughout a partially immune population. Antigenic drift occurs in both influenza A and influenza B viruses, but the pattern observed is somewhat different fo perfect r the different viruses. Whereas drift variants of A (H1) viruses and B viruses often cocirculate with multiple coexisting lineages, influenza A viruses of the H3 subtype evolve more rapidly. Antigenic-drift variants of the H3 viruses occur more often, and new variants tend to replace older variants quickly, so that the evolution of the H3 hemagglutinin is more linear than that of other subtypes.

The extent of antigenic drift is usually assessed by determining the nucleotide sequence of the hemagglutinin of new variants and evaluating the ability of antiserum against the old virus to inhibit the new virus.

Avian Influenza is a potential zoonosis. It can result in inapparent infection, conjunctivitis or severe pneumonia. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets. The first avian influenza in humans was reported in Hong Kong in 1997. It was called avian influenza (H5N1). The outbreak was linked to chickens. Since then there have been human cases of avian influenza A in Asia, Africa, Europe, Indonesia, Vietnam, the Pacific, and the near East.

Hundreds of people have become sick with this virus. Up to half of the people who get this virus die from the illness.

Signs Sudden death. Marked loss of appetite, reduced feed consumption. Cessation of normal flock vocalisation. Drops in egg production. Depression. Coughing. Nasal and ocular discharge.

Swollen face. Cyanosis of comb/wattles. Diarrhoea (often green). Nervous signs such as paralysis.

Post-mortem lesions Inflammation of sinuses, trachea, air sacs and conjunctiva. Ovarian regression or haemorrhage. Necrosis of skin of comb and wattles. Subcutaneous oedema of head and neck. Dehydration. Muscles congested.

Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract.

Turkey lesions tend to be less marked than those of chickens, while ducks may be symptomless, lesionless carriers of highly pathogenic virus.

Pigs can also be infected with human, avian, and swine influenza viruses, allow for mixtures of genes (reassortment) to create a new virus, which can cause an antigenic shift to a new influenza A virus subtype which most people have little to no immune protection Avian influenza strains are divided into two types based on their pathogenicity: high pathogenicity (HP) or low pathogenicity (LP).The most well-known HPAI strain, H5N1, appeared in China in 1996, and also has low pathogenic strains found in North America. Companion birds in captivity are unlikely to contract the virus and there has been no report of a companion bird with avian influenza since 2003. Pigeons do not contract or spread the virus.

In the approximate four years from early 2013 to early 2017, 916 lab-confirmed human cases of H7N9 were reported to the World Health Organization (WHO).

On 9 January 2017, the National Health and Family Planning Commission of China reported to WHO 106 cases of H7N9 which occurred from late November through late December, including 35 deaths, 2 potential cases of human-tohuman transmission, and 80 of these 106 persons stating that they have visited live poultry markets. The cases are reported from Jiangsu (52), Zhejiang (21), Anhui (14), Guangdong (14), Shanghai (2), Fujian (2) and Hunan (1). Similar sudden increases in the number of human cases of H7N9 have occurred in previous years during December and January.

Clinical signs: It usually variable and depend on other factors including host species, age, sex, concurrent infections acquired immunity and environmental factors.

Low pathogenic avian influenza virus: In chicken and turkeys: mild to severe respiratory signs (coughing, sneezing, rales, rattles and excessive lacrimation).

In layers and breeding an increase in broodiness and decreased egg production and general signs as huddling, ruffled feathers, listlessness, decreased activity, leathery, decreased feed and water consumption and diarrhea.

High pathogenic avian influenza viruses: In wild and domestic water fowl: Few clinical signs but HPAL (H5N1) can induced neurological signs, depression, anorexia and sudden deaths.

Domestic chickens, turkeys and related galli forms: Sudden death may be early clinical signs In severely infected birds (3-7 days) nervous signs as tremors of head and neck, in ability to stand, torticollis, opisthotossis and other usually position of head and appendeges.

Beside listlessness peak of mortality taking 10 – 15 days.

In ducks, mortality varied according age & virus strain .

In ostriches, LP and HPAI varies according , strain of virus and age of the bird.

Pathology: Gross lesions: Extremely variable with regard to their location and severity.

LPAI viruses: (chickens and turkeys): Catarrhal, fibrinous, serofibrinous, mucopurulent or fibrinopurulent of respiratory tract and sinus Tracheal mucosa can be edematous with congestion and occasionally hemorrhage and trachea exudates may be vary forms serous to Caseous with occlusion of air ways.

Fibrino or fibrinopurulant air saculitis Infraorbital sinuses may swollen and muco to mucopurulant nasal discharge.

Fibrinopurulants bronchopneumonia where secondary bacterial infections.

Fibrinous or egg yolk peritonitis may be observed Catarrhal or fibrinous enteritis in cecal and/ or intestine especially in turkey.

Exudate in or induct of laying birds A few eggs laid with reduction in calcium deposition of egg shalls (misshapen and fragile) with loss of pigmentation.

Ovaries may show hemmorages of large follicles , regressions and progression to colliquation.

The oviduct may be edematous and showed catarrhal to fibrinous luminal exudat , before involution(shrinkage) Rarely, swollen kidney with urates.

Sporadically, firm pancreas with pale mottling and hemorrhage usually in turkeys.

In domestic ducks and geese, sinusitis, conjunctivitis and other lesion. Coinfections with bacteria are common.

HPAI virus: Virus produce a variety of lesions mainly edema, hemorrhage and necrotic lesions in visceral organs and skins.

Pre acute death, no detectable gross lesions Swelling of the head, face, upper neck and feet may be observed due to subcotunius edema may be seen.

Necrotic foci, hemorrhages and cyanosis of the non-feathered skin especially wattles and combs.

Visceral organs, hemorrhages on serosal and mucosal surface and necrotic foci in the parenchymatous organs (liver, kidneys, spleen and heart) necrotic foci with hemorrhages on the eoicardium, pectoral muscles of provrntrculus and ventriculus.

Necrosis and hemorrhages of peyer patches of the small intestine and sometimes, sever congestion, hemorrhage and edema of lungs.

Atrophy of bursa and thymus and splenomegaly could be seen.

In ostriches: Edema of head and neck . Hemorrhagic enteritis Enlarged and firm pancreas Mild to severe air saculitis, hepatitis, Peritonitis, renomegaly and splenomegaly.

Microscopic lesions: Low pathological viruses: Lesions mainly in respiratory tract and sinuses Pulmonary (fibrinocellular to peribronchiolar lymphocytes) Heterophilic to lymphocytic trachitis and bronchitis Nephrosis and nephritis In turkey, pancreatitis with acinar necrosis Lymphoid depletion and necrosis of lymphoid organs High pathogenic viruses: Multi-organ necrosis and/or inflammation mainly in brain, heart, lungs, pancreas and primary and secondary lymphoid organs.

Vasculitis, perivascular to generalized edema and necrosis of capillary endothelium could be seen beside microthrombi in some blood vessels.

Lymphocytic meningo encephalitis with focal gliosis neuronal necrosis and nuronophagia beside edemal hemorrhage were common.

Necrosis, apoptosis and depletion of lymphoid organs.

Respiratory tract lesions varied from mild to severe . non feathered skin have edema and microthrombi with vesicle formation to necrosis in feather shaft and follicle epithelium.

Infectious bursal disease (gumbro disease)

It is an acute highly contagious viral infection of young chickens (3 weeks of age and older) Etiology: It is caused by virus (a member of the Birnaviridae family) nemed for the bisegmented double-stranded RNA nature of the genome of its members (serotype 1 IBDv) Natural hosts: Chickens are the natural hosts of virus Incubation period: It is short 2-3 days Clinical signs: The earliest sign of infection, some birds have tendency to pick at their own vents. Anorexia, depression, whitish or watery diarrhea and soiled venthers, trembling, severe protrations and finally death.

Late stage of the disease, dehydration and subnormal temperature.

In susceptible birds, high morbidity (100%) with high mortality 2050%mainly due to infection with VVIBDV.

Pathology Gross lesions: Dehydration with darkened discoloration of pectoral muscles.

Hemorrhages are present in the intestine and pectoral muscles.

There is increased mucus in the intestine and renal changes.

The cloacal bursa begins to increase in size and weight because of edema and hyperemia (double in size and weight within 4 days of infection) after that became atrophied.

In early stages, it has a gelatinous yellowish transudate covering the several surface and prominent longitudinal striations with cream color. Transudate disappear and bursa become gray in color.

Necrotic foci with petechial or ecchymotic hemorrhages on the mucosal surface or throughout the entire bursa and birds may void blood in their droppings.

The spleen may be slightly enlarged and often has small gray foci on the surface.

Hemorrhages in the mucosa at the junction of proventriculus and venriculus(gizzard) and may cause melena (black digestive content from digested blood) Different lesions in thymus, cecal tonsils, spleen and bone marrow.

Microscopic lesions: It occurs in lymphoid tissues (clocal bursa, spleen, thymus, harderian gland and cecal tonsils) Bursa, degeneration and necrosis of lymphocytes in the medulla of bursal follicles followed by replacement of heterophils, pyknotic debris and hyperplastic reticuloendothelial cells.

Hemorrhages often appear, severe edema, hyperemic and marked accumulation of heterophils.

Lateron, cystic cavities developed in medullary areas of follicles, phagocytosis of heterophils and plasma cells occurred and fibroplasia of interfollicular C.T. moreover, proliferation of the bursal epithelial layers produced a glandular structure of columnar epithelial cells containing glorioles of mucus.

Avian encephalomyelitis (epidemic tremors)

It is an infectious viral disease affecting young chickens, pheasants, quail and turkeys.

Etiology: It is an member of picornaviridae family . There are 2 distinct pathotypes of virus.

Natural field strain (enterotropic) non pathogenic Neurotropic (embryo adapted strain) it causes severe neurologic signs.

Natural hosts: Chickens, pheasants, coturnix quail, pigeons and turkeys are susceptible to natural infection.

Transmission: Horizontal: in natural infection, AE is essentially an entric infection (infection by ingestion) Vertical: in field infection.

Incubation period: In vertical transmission, it was 1 to 7 days In horizontal transmission, the minimum incubation period is 10 days

Clinical signs: In natural outbreaks, the signs usually appear 1-2 weeks of age and characterized by dull expression of the eyes followed by a progressive ataxia from incoordination of the muscles which may followed by an inclination to sit on their hocks. Finally, they fall on their sids, some may refuse to move or may walk on their hocks and shnaks. Also, dull expression, a weakened cry and tremors of the head and neck by irregular intervals. In some cases only tremors has been observed.

Ataxia usually progress followed by inanition prostration and finally death. Chickens with marked ataxia and prostration are frequently trampled by their penmates. Some survivors later develop blindness from an opacity (bluish discoloratation to the lens). Mature birds may show temoporary drop in egg production (5-10%) but no nurological signs.

N.B: there is age resistance to clinical signs in birds exposed after they are 2-3 weeks of age.

The morbidity in young chicks 40-60% which comes form infected flock.

The mortality averages 25%.

Pathology Gross lesions: The only gross lesions are whitish areas in the muscularis of the ventriculus.

Microscopic lesions: The principal changes are in CNS and some viscera CNS lesions include a disseminated, nonpurulent encephalomyelitis and aganglionitis of the dorsal root ganglia (pathognominic lesions is central chromatolysis, axonal reaction) of the neurons in the nuclei of the brain stem (medulla oblongata) Viseceral lesions include: Hyperplasia of lymphocytes aggregates scattered in the birds.

In the porventriculus and ventriculus aggregates of a few small lymphocytes become obvious dense nodules within the muscular wall.

In pancreas, an increase in number several time of circumscribed lymphocytic follicles.

Myocardium, lymphocytes aggregates mainly in the atrium.

Infection laryngotracheitis

It is a respiratory tract infection of chickens caused by Gallid herpes virus type 1.

Natural and experimental hosts: The chickens are the natural host of Gall V-1, and although the disease affects all ages, the mast characteristic signs can be observed as early as 3 weeks of age.

Recentally a case of natural infection in turkey and a subclinical infection in ducks with seroconversion were reported.

Transmission, carriers and vectors: Natural portal of entry for Gall V-1 are through the upper respiratory and ocular routes.

Ingestion also can be a mode of infection. No vertical (egg) transmission was reported. Direct bird to bird transmission occurs more readily from acutely infected bird than through contact with clinically recovered carrier birds. Indirect transmission from contaminated equipment's and infected carcasses was recorded.

Incubation period: In natural infection, it ranged from 6-14 days and 2 days after intracheal experimental infection.

The clinical signs: In chicks in early epizootics form, an acute respiratory signs as dyspnea with expectoration of blood stained mucus and moderate to severe conjunctivitis were common in sever forms of the disease.

Mild enzootic forms characterized by unthrifitiness, decreased egg production, watery eyes, conjunctivitis, swelling of infraorbital sinuses, mild mucoid trachitis, persistent nasal. The course of in infection varies with the severity of lesions (recovery occurs after 10-14 days in natural infection).

Morbidity and mortality: In sever epizootic forms, high morbidity (90-100%) and variable mortality (10-20%) were recorded.

Mild epizootic forms, low morbidity (5%) and very low mortality (0.1-2%) were recorded.

Gross pathology: Lesions located mainly in the conjunctiva and the respiratory tract of chickens.

Lesion in larynx and trachea varied form mild (excess mucus) or sever with hemorrhagic and /or diphtheritic changes (mucoid or bloody casts that extend the entire length of the trachea) or blood may be found in with mucus and necrotic tissue.

Inflammation may extend down the bronchi, into the lungs and air sacs.

In mild forms, moderate mucoid tracheitis with varying degrees of hemorrhages localized in larynx and upper trachea. Edema and congestion of conjunctiva, frothy ocular secretion, nasal discharge and swelling of the infraorbital sinuses.

Microscopic changes: The changes vary with the stage of the disease.

After 2 days pI, tracheal mucosa revealed loss of cilia, infiltration of mucosa with inflammatory cells After progression of viral infection, respiratory and conjunctival epithelial cells enlarged and become edematous with formation of multinucleated cells (syncytia).

Lymphocytes, histiocytes and plasma cells migrate into mucosa and submucosal after 3 days.

Inclusion bodies could be seen in early stages of infection (15 days) and disappear with progression of infection due to necrosis and desqumation of epithelium.

Lateron, mucosal surface will be reduced to a thin layer of basal cells or will lack any epithelial covering.

Blood vessels within the lamina propria may protrude into the tracheal lumen and hemorrhage may be occurring after epithelial destruction.

Infectious bronchitis Avian infectious bronchitis is an economically highly contagious acute, upper respiratory tract disease of chickens and other fowl, caused by the avian coronavirus infections bronchitis virus.

Rout of infection:Inhalation or direct contaminated litter, equipment or other fomites.

Vertical transmission not recorded but infection contaminated shell surface from the oviduct or GIT. Natural hosts: Chickens are the only host for IBV. All ages are susceptible but the disease is most severe in chicks. As age increases, chickens become more resistant to nephropathogenic effects, oviduct lesions and mortality due to infection.

Incubation period: IBV spreads rapidly among chickens in a flock with short incubation period 18- 36 hours after intra tracheial inoculation dose dependent after ocular application.

Clinical signs: Nonspecific respiratory signs in susceptible chicks are gasping, coughing, sneezing, tradual rales and nasal discharge.

Watery eyes may be observed with swollen sinuses Depression of chicks and may huddled under gain are significant reduced.

The severity of signs is influenced by the climate, housing and kind of bird, vaccination program and coinfection.

Broiler chickens infected with a nephropathogenic virus may appear to recover from the respiratory phase and then show signs of depression, ruffled feathers, wet dropping, increase water intake and mortality.

In laying flocks, decline in egg production up to 70% and quality are seen with respiratory signs.

Respiratory sings may be absent or vary mild Production of eggs with pale, unpigmented shells abnormally shelled eggs (egg weight and internal egg quality also affected) for different period.

Drop in egg production may be mild (1-2 week or sever 6-8 week) and return to preinfection level and sometimes never attained.

Flocks with false layers (birds look healthy without production) fail to attain peak of production due to cystic oviducts.

Morbidity and mortality: It varies according to virulence and patho type of infecting strain, age of infection immune status, stress (cold) and secondary bacterial infection.

The highest mortality is usually seen with infections of nephropathogenic strains in young birds.

Gross pathology:

Serous, catarrhal or caseous exudate in trachea, nasal passage and sinuses Foamy air sacs in acute infection then become cloudy and may contain yellow caseous exudate Areas of pneumonia around large bronchia Nephrogenic infection produce swollen and pale kidneys with tubules and urters distended with urates.

Fluid yolk material within the abdominal cavity in laying flocks Cystic oviducts were common due to IBV infection in very young ages → false layers (reduction in length and weight of oviduct in the infected birds) as well as regression of the ovaries.

Microscopically: Tracheitis characterized by edema, loss of cilia, rounding and sloughing of epithelial cells, minor heterophils and lymphocytes infiltration (18 hours). Regeneration of epithelium start of ten 48 hours hyperplasia followed by massive lymphoid cells aggregation in lamina preperia forming follicles Air sacs showed edema, epithelial desquamation and fibrinous exudate. Later, heterophils with lymphoid nodules and fibroblasts proliferation and regeneration by cuboidal epithelium.

Hardarian glands, an increase in plasma cells ,hyperemia and extension lymphoid follicles formation.

Kidney lesions are principillay interstitial nephritis and urolithiasis.

Oviduct (Infection of mature hens) has decreased height and loss of cilia, dilation of tubular glands, infiltration by lymphocytes and other mononuclear cells, heterophils edema and fibroplasia of mucosa of all regions of the oviduct.

Entrotropic G strain induce mild rectum lesion mainly with co-infection.

Newcastle disease Avian paramyxo viruses & avian metapneumonia virus infections:Definition: Newcastle disease is defined as an infection of birds caused by virus of avian paramyxo virus serotype 1 (A PM-1) that means one of the following criteria for virulence.

The virus has an intracerebral pathogenicity index (ICPI) in day old chicks of 0.7 or greater.

Multiple basic amino acids have been demonstrated.

The velogenic virus infect poultry species naturally (chicken and turkey) and pigeons, cormorants and psittacines.

Etiology:Members of the paramyxoviridea Virus have the following biological properties: Hemagglutination activity Neuraminidase activity Cell fusion and hemolysis

Pathogenesis:-

There are different serotypes according to ICPI (intracerebral pathogenicity index)in day old chicks and virulence of the virus: Velogenic strains: the virus with high virulence Mesogenic strains: the virus with moderate virulence Lentogenic strains: the virus with low virulence Recently molecular assays and sequencing were created based on results from pathogenicity assays.

NDV virulence is a complex trait due to the effect of multiple genes mainly F gene.

Natural and experimental hosts: Natural hosts: Chicken and turkey but turkeys require a higher infectious dose of NDV to become infected. Infection with NDV has been documented are least 241 species (all avian species are susceptible to infection).

Transmission: Horizontal transmission has been documented by inhalation or ingestion of contaminated dusts or aerosolized virus.

Vertical transmission from natural infected hens resulted in death of embryo before hatching, but chicks may be infected from contaminated feces or environment.

Incubation period: It depends upon, host species and the immune status, age of the host, the virulence and dose of the virus and the route of exposure.

Incubation period in natural exposures varies between 2 to 5 days (average around 6 days) but may take 3-4 weeks.

In experimental infection with virulent viruses tropic NDV in chickens usually 1 to 4 days depending upon challenge dose.

Aerosol exposure has a shorter incubation time than ingestion.

signs:-

Neither the clinical signs nor the gross lesions are pathognomonic for ND. Non vaccinated chickens infected with virulent viscerotropic isolates become listless and depressed 2 days after infection ending with 100% mortality by the third or fourth day.

Bilateral conjunctivitis with some facial swelling could be seen with oculonasal infection route.

Often clear mucus will pour from the mouths of infected birds if their heads droop toward the ground, leaving the bird gasping for air as it tries to clear the oral cavity of fluid.

(Croup fluid). The feces may be green and watery. The comb may become blue Infection with virulent neurotropic virus resulted in hyper excitability 3-4 days post infection, after 5 days, head or muscular tremors, torticollis and paralysis of wing or leg may occur, these birds dies within 9 days because they unable to reach food and water.

Mortality ranged 50% or more in younger birds.

Mesogenic strains result in low or no mortality in 4 week old chickens and may develop neurological signs such as head tremors, torticollis and paralysis. Pigeon isolates in chickens may lead to no clinical signs.

Low virulent strains usually do not cause disease in adult birds. However young birds may present with serious respiratory distress following application of Lasota vaccine or high ammonia levels or due to smaller aerosolized droplet of vaccine which are delivered deep into lung tissue during vaccination.

The clinical signs varies according to species the older of most to least susceptible showing the fewest clinical signs are chickens, turkeys, pigeons and ducks. Pheasant are susceptible as chickens. Ostriches usually present with various signs and mortality present only in young birds. Chickens are elates in pigeons may cause body tremors.

Gross lesions: Lesions are not pathognomonic for ND Lesions will likely be absent in vaccinated birds and possibly in nonvaccinated birds.

Necrosis and hemorrhagic lesions in the lymphoid dependent areas of the intestines (lower eyelid, cecal tonsils and pyer patches) in chickens and turkeys due to virulent viscerotrepic isolates Chickens will occasionally present with moderate splenic congestion and mild thymic atrophy after infection with virulent neurotropic NDV without CNS gross lesions.

No lesion in respiratory tract except thickening of air sacs due to secondary bacterial infection.

Egg yolk peritonitis with atrophied follicles and degenerated oviducts in laying birds.

Microscopic lesions: Necrosis and depletion of lymphoid organs Histiocytic or lymphohistocytic air saculitis Glios is with perivascular cuffing in medulla, cerebllum and brain stem.

Yolk peritonitis with foamy macrophages of sub-serosal space of oviduct.

Necrotic myocarditis Bone marrow necrosis Pancreatic, thymic and hepatic necrosis Necrosis and ulceration of intestinal epithelium Hemorrhagic, ulceration tracheitis or lymphoplasmatocytic tracheitis with deciliation.