inclusion body hepatitis pigeon herpes virus infection duck viral … · 2019-10-01 · pigeon...

Viral diseases with hepatitis

• inclusion body hepatitis

• pigeon herpes virus infection

• duck viral enteritis

• avian hepatitis-E-virus infection

Inclusion body hepatitis

Pathogen:– different serotypes of a type-1 adeno virus

• Predisposing factors are needed

• immunosuppression– infectious bursitis

– infectious (viral) chicken anaemia

– mycotoxicosis

• appears in 28-30 days old chicken

• Other avian species susceptible are:– Young adult turkeys

– Young guinea fowl, quail, pigeon

• Main feature of the disease: viraemia– hepatitis is consequence of the viraemia!

Inclusion body hepatitis

Pathological lesions:

• multiple hemorrhages (per diapedesin)

• swollen, pale liver (fatty infiltration)– with necrotic foci

• pale bone marrow– anaemia

• in the pancreas:– hemorrhages and necrotic foci

• Histopathology (liver):– hemorrhages

– basophil and eosinophil inclusion bodies in the nuclei of the hepatocytes

Pigeon herpes virus

infection• The pathogen is

– pigeon herpes virus 1 (PHV 1)

• disease of young (2-6 months old) pigeons– it can occur in older age group too

• Infection:– with direct contact

– infected hen transmits the infection

– aerogen route

• Predisposing factors:– other diseases at the same time:

• chlamydophilosis, salmonellosis

• E. coli infection, mycoplasmosis

• pasteurellosis, pigeon pox

• other stress factors (demanding excercise – distant flying)

Pigeon herpes virus

infection

Pigeons survived the disease are carriers of the virus!

• the symptomless carriers shed the virus– after stress

• in birds infected with herpes virus– viraemia develops

– lesions occur in different organs and mucous membranes

• Appearance of the viraemia:– enteritis

– serous hepatitis, liver dystrophy

• + intranuclear inclusion bodies in the hepatocytes

– multifocal pancreatitis

– mild encephalitis

Pigeon herpes virus

infection• Pathological changes appear

– in the nasal cavity, oro-pharyngeal cavity, esophagus

– in the larynx, trachea

– in the cloaca, in the conjunctiva

• Pathological lesions:– catarrhal rhinitis with pseudomembrane formation

• + sinusitis

– fibrinous inflammation in the oro-pharyngeal cavity

– croupous pseudomembrane in the larynx

– acute catarrhal or fibrinous tracheitis

• intranuclear inclusion bodies in the epithelial cells

– necrosis and ulceration can occur

– necrotic inflammation in the cloaca

– sero-fibrinous conjunctivitis

• with cohesive eyelids

Duck viral hepatitis

• disease of young (7 - 10 day-old) ducks– sometimes appear in older (3-4 week-old) ducks too

– In case:• feed contains high amount of peroxide

• lack of lipotrop substances

• Pathogen: astro virus

• Forms:– peracute: acute hemorrhagic liver dystrophy

– acute: acute serous hepatitis

– prolonged: subacute-chronic hepatitis with cholangiolitis

• The young ducks– die suddenly without any clinical symptoms

– OR

– die after short period of drowsyness and lack of appetite

– the ducks in agony straighten their legs backwards and bend their neck (opistotonus)


• peracute form– the liver is bright yellow

– hemorrhagies are seen in the liver• in some case destruction due to bleeding can occur

– centrolobular necrosis of the hepatocytes• sometimes on other areas of the lobules too

• karyolysis

– the necrotized hepatocytes detach from the liver row and become rounded eosinophil structures

• Councilman-bodies

– the necrotized and dying hepatocytes contain large amount of fat droplets

– structure of the lobules becomes homogenous, and distructed

Duck viral hepatitisPeracute form

• In the hepatocytes and in the Kupffer cells, and in the reticulum cells of the spleen

• cytoplasmic inclusion bodies– red

– rounded-oval

– solitary or multiple

Acute form

• less hemorrhages in the liver

• dilated Disse-spaces, due to serous exudate accumulation

• necrobiotic fatty infiltration in the hepatocytes– liver dystrophy

• multifocal necrosis of the hepatocytes– the lobules are less destroyed

• perilobular perivascular serous infiltration of the interstitium – infiltration by heterophil granulocytes and lymphocytes

• activity and mild proliferation in the small bile capillaries


• Prolonged form– extensive proliferation of the small bile vessels

• in the perilobular interstitium

– perivascular fibrosis (connective tissue proliferation)

• In other organs– acute enteritis

– multifocal interstitial nephritis

– edema in the myocardium

– in some cases splenitis

• Muscowy ducks and mallard ducks– are not susceptible

– they do not show symptoms!!!

Avian hepatitis-E-virus infection

in layer and parent flocks

Other names of the disease

• big liver and spleen disease

• hepatitis-splenomegalia (USA)

Pathogen

• avian hepe virus

• avian hepatitis-E-virus

Main feature of the disease:

• viraemia with hepatitis

Pathogenesis:

• symptoms appear after the start of the egg production

• lasts for several weeks



Pathogenesis:• infection?

– most probably happened earlier

– carries on? gets infected later?

• egg laying as predisposing factor is important

Clinical signs:• decreased feed uptake

• drowsyness

• diarrhea

• drop in egg production(up to 20%)

• fertility and hatchabilityalso decreases

• anaemia

• increased mortality(more than 1% / week)– lasts for 3-4 weeks



Pathological changes:

• In acute case– multiple hemorrhages

– hydrops in the serous body cavities (yellowish-red fluid)

– acute serous hepatitis (hepatomegaly)• with hemorrhages in the parenchyma

– splenomegaly, with hemorrhages in the parenchyma

– hemorrhages in the parenchyma of the pancreas

• Later– hepatitis - liver dystrophy

• subcapsular hemorrhages and necrotic foci

– splenomegaly (more than 1g / bwkg)

– hemorrhages and necrotic foci in the spleen

– hemorrhages and necrotic foci in the pancreas

– degeneration and rupture of the follicles• consequential peritonitis

Pathology of the serous

membranes and serous body

cavities

Topics

• 17. Pathology of serous membranes. Anatipestifer-

disease, Derzsy’s disease

• 18. Pathology of the pericardium.

Hydropericardium-ascites syndrome,

hydropericardium-hepatitis syndrome (Angara

disease)

• 19. Pathology of the myocardium. Sudden death of

broilers, spontaneous cardiomyopathy in turkey,

perirenal hemorrhages in turkey

• 20. Pathology of the blood vessels. Hemorrhagic

nephritis and enteritis in young geese, aortic

rupture in turkey

Pathology of the serous

membranes

• Abnormal content

– corpora libera, egg, serous exudate

• Circulatory disturbances

– hyperaemia, hemorrhage, oedema

• Regressive changes

• Proliferative changes

• Inflammations

• Tumors

– mesothelioma

Important diseases

• Anatipestifer-disease

– riemerellosis

• Derzsy’s disease

Anatipestifer-disease

• Riemerellosis

• Pathogen: (does not stain according to Gram)– Bacillus septicaemiae anserum exsudativae

– Pfeiffer influenza bacterium

– Pfeifferella anatipestifer

– Pasteurella anatipestifer

– Schigella septicaemiae

– Haemophilus anserisepticum

– Moraxella anatipestifer

– Riemerella anatipestifer

• Infection

– aerogen (aerosol)

– per os (oro-fecal)

– per cutan (open woulds)

• in case of individual identification (cutting the nails, cutting or clipping the webbed toes)

Riemerellosis

Pathogenesis (main features):

• the bacteria live together with the birds– facultative pathogens

• after predisposing factors the bacteria get to the blood circulation

• septicaemia develops in the weakened organism

• usually occurs in young age– In goslings: between 2-3 week-old age

– In ducklings: at the same age and later, in 7-8 week-old birds

Riemerellosis

Predisposing factors

• one of the most important is

– the young age

• other stressors:

– problems related to husbandry or malnutrition

– long transport, weather fronts, cold

• other concurrent infectious diseases

– Derzsy’s disease

– influenza viruses

– mycoplasmosis

– chlamydophilosis

Riemerellosis

The main feature of the disease:

• exsudative serositis – sero-fibrinous inflammation of the serous membranes

– with the sero-fibrinous inflammation of

– the joints and tendonsheats,

– the leptomeninx

Clinical signs:• respiratory symptoms

– lacrimation, serous nasal discharge, rhinitis and sinusitis

– well visible in ducks (missing in geese)

• nervous signs– ataxia, tremor, backing, opistotonus

– listing, lurching, lying on their back and kicking

Riemerellosis

Pathology:• sero-fibrinous

– peritonitis, air sacculitis, pericarditis

– leptomeningitis

– arthritis and tenosynovitis

• serous inflammation and hemorrhage in the subcutaneous connective tissues of the leg – in prolonged cases: necrotizing dermatitis

• acute catarrhal enteritis

• rhinitis, conjunctivitis, sinusitis in the infraorbital sinus

Histoptahological examination:• sero-fibrinous inflammation in the leptomeninx

– under the lining ependyma-layer in the cerebral ventricules and canalis centralis

Photo: Dr. Dobos-Kovács, Mihály

Derzsy’s disease

• Main feature of the disease: viraemia

– following viral replication in the GI tract

• Pathogen: goose parvo virus

• Susceptible:

– goose amd Muscowy duck

• Infection:

– vertical (through egg)

– horisontal (oro fecal route)

Derzsy’s disease

• Other (old) names of the disease:

– goose plague

– goose viral enteritis

– goose infectious myocarditis

– goose infectious hepatitis

– goose infectious ascites

– goose infectious hepato-nephritise

– so called „goose influenza”• to differentiate it from the goose influenza

• from the anatipestifer disease– or riemerellosis

Derzsy’s disease

Pathogenesis:

• after per os infection– the virus replicates in the GI tract of susceptible

young geese

– the virus prefers to proliferate in the nucleus of the Lieberkühn crypt cells

• viral enteritis develops– followed by a viraemia and the virus reaches all

organs

• the virus replicates in the nuclei of the young parenchyma cells of all the organs

• some names refers to this feature– infectious hepatitis

– infectious hepato-nephritis

Derzsy’s disease

during viraemia

• degeneration of the vessel walls occurs– Leakage of the plasma to the extravascular spaces

and to the serous body cavities

– The name refers to it: infectious ascites

during viraemia

• the virus reaches the heart muscle– replicates in the nucleus of the new myocardial cells

• myocardial necrosis (myocardosis)

– around the necrotized cardiomyocytes reactive inflammation starts

• myocarditis

– because of that it was called infectious myocarditis

Derzsy’s disease

Morbidity:

• all young susceptible geese become sick up to 4 week-old age

Mortality: up to 30-40% or even more– in case of proper maternal immunity the ratio is

maximum 3-5%

• infection in geese after 4 weeks of age– no clinical signs, but they carry the virus!!!

• susceptibility does not disappear with age!!!– inapparent infection, no clinical signs

– but the infected goose sheds the virus!

Pathology of the Derzsy’s disease


Derzsy’s disease

• In the surviving geese…..

– decreased immuncapacity

– secondary infections

• salmonellosis

• colibacillosis

• Anatipestifer-disease

• and others

Pathology of the circulatory

system

Organs of the blood and lymph

circulation

• pericardium

• myocardium

• endocardium

• chambers of the heart

• blood vessels

• blood

• organs of the lymph circulation

Pathology of the pericardium

• Circulatory disturbances

– hemorrhages

• Abnormal content

– Hydropericardium-ascites syndrome

– Hydropericardium-hepatitis syndrome

(Angara-disease)

• Inflammations

– serous, fibrinous, purulent, ichorous

– caused by bacteria, viruses, chemicals

• Bacteriaemia, septicaemia, viraemia, uricosis

Hydropericardium-ascites syndrome

• disease of the broiler chickens

• uniform disease– unclear pathogenesis

• Cause– the broilers eat constantly

– the GI tract is always full

– the lungs is permanently squeezed

– this results in high pressure

– increased load on the right ventricule

– high blood pressure in the small circulation

• increased pulmonary arterial pressure disease

• right-sided heart failure and ascites

Hydropericardium-ascites syndrome

Pathology

• Dilatation of the heart

– especially the right ventricule

– often hypertrophy of the right ventricule also occur

• stagnation fluid in the abdominal cavity and pericardium

• hyperaemia and edema in the lungs

Hydropericardium-hepatitis syndrome

(Angara disease)

• It was described first in 1987 in Pakistan

• Pathogen: serotype IV. avian adenovirus– similar disease was caused in Mexico by an

adenovirus (serotype VIII.)

• Main feature: viraemia caused by adenovirus– hepatitis

– multifocal degeneration and necrosis of the myocardium

• with hydropericardium

– tubulonephrosis

– lung edema

Pathology of the myocardium

• Regressive changes

– acute swelling, fatty infiltration

– necrosis, Zenker necrosis

• Sudden death of broilers and layers

• Spontaneous cardiomyopathy

– in turkeys

• Sudden death of turkeys with perirenal

hemorrhages

• Imflammations, accomodation, tumors

Sudden death of broilers

• sudden death syndrome

• In 1-8 week-old age– most often between 2-3 weeks of age

• The primary cause of death: ventricular fibrillation

Cause of the disease: complex

• metabolism of the organism

• genetic effects– in fast growing meat-type chickens the myocardium is

more sensitive

– the heart is more sensitive in cocks than in hens

• environmental factors– increase the manifestation:

• overcrowding

• too large flocks

• failure of the microclimatic factors

Sudden death of broilers

Metabolism of the organism

• everything influences the manifestation of the disease– which allows the birds the exploitation of the possible growth

rate

• the form of the feed (loose, firm)

• the way of feeding

• the light program (lenght of exposure)

• the myocardium is especially sensitive for changes in the acid-base balance

• disturbances of lipid metabolism– these fast-growing genetic lines are very sensitive for lack of

biotin (B7 or vitamin H)

• biotin is necessary for the normal function of the liver in lipid metabolism

– influences unfavorably the function of sarcoplasmatic reticulum transport in the cardiomyocytes

Spontaneous cardiomyopathy

• Genetic disorder

– Toxicosis (furazolidone, nitrite)

• Turkey: 2-3 weeks old

– sometimes up to 14 weeks of age

• spontaneus

– no previous regressive changes

• Pathology:

– enlarged heart

– dilated chambers (especially the right ventricule),

streched wall

– lung hyperemia and edema

– congestion in the liver

Spontaneous cardiomyopathy

• Histopathology of the myocardium:

– hyperemia

– acute swelling, vacuolar degeneration

– multifocal lymphocytic infiltration in the

interstitium

– endocardial sclerosis

• proliferation of collagen and elastic fibres

– similar lesions in the liver

• vacuolar degeneration, necrosis

Sudden death of turkeys with

perirenal hemorrhages

• in 8-14 weeks old males

• Good body condition!

– High blood pressure - angiopathies

• Pathology

– Circulatory disturbances

• hyperaemia of the organs, lung edema

• hemorrhages: kidneys, lungs

– due to the special portal circulation of the kidney

– Hypertrophy of the cardiac septum

• Cause of death: arrythmia

Blood vessels

• Hemorrhagic nephritis and enteritis in

goslings

– Pathogen: polyomavirus (around 40nm, DNA)

– Infection:

• vertical (through egg)

• horizontal (oro-fecal, per os)

– Pathogenesis

• Aortic rupture in turkey

Hemorrhagic

nephritis and

enteritis

in goslings

Photos: Dr. Dobos-Kovács, Mihály

Photos: Dr. Dobos-Kovács, Mihály

Aortic rupture in turkey

• in any parts of the aorta the rupture can occur

– in the large vessels exiting the aorta too

• losses reach usually 1-2 %

– in some special cases 50 % mortality occured

• Forms:

– spontaneous rupture of the aorta

• the aorta is intact

• extremly high blood pressure

– secondary (pathological) rupture of the aorta

• primary regressive changes in the wall of the aorta


Multifactorial disease

• constitutional factors– in lines developing large pectoral muscles for meat

– cumulative appearance in some genetic lines

• physiological specialties– between 7-24 week (mostly between 12-16 weeks)

– mainly the males are affected• more often seen around the sexual maturation

• malnutrition– high protein content in the first weeks of age

– lack of some important nutrients

• husbandry conditions– in case of irritation, too many stimuli

– in case females are males are kept together


Pathologic rupture of the aorta

• at the time of sexual maturation the diethystilboestrol level decreases in the blood– the possibility for aneurysm development increases

• lack of elastic fibers due to decreased production– copper-deficiency (primary, secondary)

– lack of vitamin C

– lack of essential amino acids

– beta-aminoproprionitrile intake

• in the seeds of sweetpea, Lathyrus odoratus

• or degenerative changes develop in the wall of the aorta– degeneration of the elastic fibers

– fat accumulation in the wall

– intima proliferation

inclusion body hepatitis pigeon herpes virus infection duck viral … · 2019-10-01 · pigeon...

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