adeno virus infections -...
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Adeno Virus Infections
(AV)
Dr./ Wafaa Abd El-ghany
Assistant Professor of poultry dis.,
Fac. Vet. Med., Cairo Univ.
Definition Adenoviruses are common infectious agents in
poultry. Many AVs are potential pathogens but require the presence of some other agent to allow them to cause disease.
The co-infection with IBDV or CIAV enhanced the pathogenicity of some avian adenoviruses.
Most of the viruses replicate in healthy birds with little or no signs.
Some AVs are primary pathogens e.g., turkey hemorrhagic enteritis virus, quail bronchitis virus, and egg drop syndrome virus.
Most of AVs replicate readily in nucleus of avian cell cultures with formation of inclusions.
Economic importance
AVs cause economical losses due to:
1. Mortalities.
2. Drop in egg production.
3. Complicating other affection through their
latency, contamination of live vaccine,
and immunosuppressant.
The virus
Adeno viruses are double stranded DNA, non enveloped, grow in cell nucleus with intranuclear inclusion bodies.
Resistant to lipid solvents (ether and chloroform, sodium deoxycholate, trypsin, 2% phenol, and 50% Alcohol). variations in pH (3 and 9) but are inactivated by a 1:1000 formaldehyde, exposure to 56°C for 30 minutes.
Adeno viruses don’t agglutinate chickens RBCS; except EDS and CELO who agglutinate rats and human type O.
Pathogenesis Adenovirus replication is divided into 2 well-
defined phases.
The early phase involves the entry of virus into
the host cell and the transfer of the virus DNA to
the nucleus, transcription and translation, coding
for the virus structural proteins and assembly of
the viral proteins into complete virions.
The late phase is disruption of the nuclear
membrane and release of virus by cell
destruction.
Adeno virus groupsGroup 1: AV isolates share a common group antigen
from chicken, turkey, geese and other avian species.
A. Quail bronchitis or Chicken Embryo Lethal Orphan virus (CELO).
B. Inclusion body hepatitis (IBH).
Group 2:These viruses share a common group antigen distinct from group I.
A. Turkey haemorrhagic enteritis (THE). Marble spleen disease (MSD). Adeno virus spleenomegaly in chickens.
Group 3: Viruses of this group partially share a common antigen with group I.
A. Egg drop syndrome (EDS).
B. Similar viruses from ducks.
Laboratory host system1) E.C.E: AVs multiply in the embryonated egg; the chorioallantoic
membrane route of inoculation is more sensitive for virus isolation and growth. Signs and lesions produced in the embryo were death, stunting, curling, hepatitis, splenomegaly, congestion and hemorrhage of body parts, with urate accumulations in the kidneys. Hepatocytes usually contained basophilic or eosinophilic, intranuclear inclusion bodies..
2) TC :
Most chicken AVs grow in chick kidney (CK) or chicken embryo liver (CEL) cells. Some turkey AVs grow only in turkey cells. It is important to use cell system homologous to the examined species.
Epidemiology &
transmission Vertical transmission is important in the spread of adenoviruses.
AVs are transmitted through the embryonated egg and are often reactivated in cell cultures prepared from embryos and young chicks taken from infected flocks. AV infections can remain latent and undetected for at least one generation in an SPF flock.
Viruses are excreted from week 3 onward.
In broilers, peak excretion occurred between 4 and 6 weeks of age.
In layer replacements, virus excretion was at a maximum level from 5-9 weeks following infection but was still at 70% of cases after 14 weeks and there is a second period around peak of egg production due to reactivation of the virus by stress associated with egg production or the increased levels of sex hormones. This would ensure maximum egg transmission to the next generation.
Epidemiology &
transmission Horizontal spread of virus is also important. Virus
is present in highest titers in feces, and secretions of the trachea and nasal mucosa, and kidneys.
Virus may be present in semen.
Horizontal spread within a flock occurred mainly by direct fecal contact.
Spread by fomites, personnel, and transport is important.
Avian adenoviruses are distributed widely throughout the wild and domestic avian species of all ages.
Quail Bronchitis
It is an acute, highly contagious, fatal
respiratory disease of young bobwhite quail,
characterized by rapid onset, high
morbidity, and high mortality and mainly
affects captive-reared birds.
Etiology Quail bronchitis (QBV) and chicken embryo lethal orphan
(CELO) serves as the type strain for group I/serotype 1 avian adenoviruses (both are considered to be the same agent).
QB virus is readily propagated in embryonated chicken eggs and in CK or CL cells.
Sometimes several blind passages are required before development of typical lesions and mortality.
Infection of the embryo by the yolk sac or allantoic cavity results in dwarfing, curling, stunting, thickening of the amnion, necrotic foci, or mottling of the liver, and accumulation of urates in the mesonephros within 2-4 days. Affected embryos reveal hepatitis with intranuclear inclusion bodies.
Experimental subcutaneous inoculation of hamsters leads to various kinds of neoplasms including fibrosarcomas, hepatomas, or hepatic carcinomas.
Susceptibility and transmission
Bobwhite quail are the main host. Clinical
disease has been reported in Japanese
quail, chickens and turkeys.
QB is highly contagious and transmitted
probably by aerosol.
Fecal-oral or mechanical transmission is
possible.
Clinical signs QB is often a catastrophic disease of captive reared
bobwhite quail, manifested by respiratory distress leads to death in young quail.
Morbidity and mortality frequently exceed 50% to reaching 80% in birds younger than 3 weeks of age.
Sign is a sudden increase in mortality, closer inspection, decreased feed consumption, ruffled feathers, huddling under brooders, wing droop, open-mouthed breathing, “snicks,” and nasal-ocular discharge. Infection severity varies depending on the age.
Asymptomatic infection in older birds is believed to be widespread.
Lesions Nasal and ocular discharge.
Opacity and filling of trachea with moist necrotic
exudates with thick tracheal mucosa.
Necrotic exudates in the anterior air sacs.
Red consolidated areas around bronchi of the
lungs.
Mottled pale pinpoint to 3 mm necrotic foci on the
liver.
Mottled and slightly enlarged spleen.
CELO virus infection in
chickens
It is a contagious disease of chicken
characterized by respiratory signs in
young birds and drop in egg production in
layer or latent infection.
CELO virus is related to QB Adenovirus
group 1 serotype 1.
Clinical signs
IN young birds:
The infection is characterized by respiratory signs including rales, coughing, sneezing, nasal and ocular discharge, depression, ruffled feather and decrease food intake. Morbidity is high but mortality is very low not exceeding 1-2% in uncomplicated cases.
In layer:
Mild respiratory signs can be seen followed by 20-30% drop in egg production in lasted for 3-4 weeks. The laid eggs contain spotted, soft shell and shell less eggs.
Lesions Young infected birds:
catarrhal treachitis, mucoid secretion in nasal
passage and multifocal pneumonic patches in
lung. Hyperamia in lung, petechial hemorrhages in
larynx and treacha as well as cloudy air sacs can
be also seen in uncomplicated cases.
Layer chickens:
produce changed eggs show lesions of
inflammatory changes in oviduct.
Diagnosis
Signs and lesions are suggestive.
Isolation and identification form
suspensions of trachea, air sacs, liver or
lungs.
Isolated virus must be neutralized by
specific QBV or CELO virus antiserum for
identification.
Differential diagnosis
QB must be differentiated from pulmonary
aspergillosis, pox, Newcastle disease.
CELO virus infection must be clarified from
atypical ND, Infectious bronchitis, EDS,
Pnemovirus, and neutritional causes of
drop in egg with change in shell quality
Control Slightly increase the brooder or housing
temperature.
Adequate ventilation without draft.
Avoid overcrowdness.
All in –all out (avoid mixing between different ages
and species).
Housing should be stopped until 2 weeks after
signs disappearance to provide a break in the
presence of susceptible young's (prevent
transmission from group to another).
No available vaccine.
Inclusion Body Hepatitis
(IBH)
It is adeno virus type (1).
It is a disease affecting chickens of young ages and it is characterized by sudden onset, sharp increase in mortality, short course, anemia, hepatitis with intranuclear inclusion bodies and immunosuppression.
Many virus serotypes of adenovirus group I (FAdV-1) are incriminated. At least 19 serotypes had been reported.
Susceptibility
IBH mainly affect meat-type chickens aged 3-7 weeks. Cases of IBH and pancreatitis were reported in pigeons.
This virus induce sever signs, severe growth retardation, lesions and immunosuppression in presence of IBDV or CIAV.
IBH was isolated from chicken, turkeys, geese, ducks and pigeons.
Clinical signs Meat-type chickens aged 3-7 weeks are mostly
affected and show of sudden onset of mortality peaking after 3-4 days and may be stopped on day 5 or continued for 2-3 weeks.
Morbidity is usually low; sick birds adopt a crouching position with ruffled feathers and die within 2 days or recover.
Mortality ranged from 10% to 30%.
Outbreaks of IBH have been reported in chickens less than 3 weeks and as old as 20 weeks.
Certain chicken breeder flocks are more susceptible.
Lesions The skin is pale, ecteric with hemorrhages on
legs and breast.
Hemorrhage on muscles and serous membranes.
The liver is swollen, pale, friable with hemorrhage mottling.
The kidneys are swollen, pale with cortical hemorrhage.
The bone marrow is pale.
The blood is watery and thin.
Spleen and bursa are atrophied small
Turkey Haemorrhagic Enteritis
(THE)
It is an acute viral disease of turkeys 4 weeks of age and older characterized by rapid progression of depression, bloody droppings, and death. Clinical disease usually persists in affected flocks for 7-10 days.,
Due to the immunosuppressive nature of HE, secondary bacterial infections may extend the course of illness and mortality for an additional 2-3 weeks.
Cause HE virus ,MSD virus, and AAS virus are
serologically related and under and designated as avian adenovirus group (type) II.
HEV, MSDV, and AASV have been classified according to source (turkeys, pheasants, or chickens), and referred to a svirulent or avirulent based on the degree of pathology.
Serial passage of HEV and MSDV in turkey lymphoblastoid B-cell line derived from a Marek’s induced tumor which is considered standard system viral isolation as well as HE and MSD vaccine production.
Susceptibility Hemorrhagic enteritis has been a serious
problem as infection with HEV is widespread
among adult turkeys aged 6-12 weeks old.
Turkeys, pheasants, and chickens were the only
known natural hosts for HEV and related
viruses..
Generally, poults younger than 3- 4 weeks of
age are considered refractory to HEV infection.
This is due to the presence of maternal antibody
that in some cases has been reported to last out
to 6 weeks of age.
Transmission
THE virus can be transmitted orally by
feces contaminated litter.
HEV is transmitted mechanically from
infected to susceptible flocks via
movement of infectious fecal or litter
material.
Clinical signs Rabid progression in signs within 24 hrs.
Affected birds show depression, bloody droppings and death.
Feces with blood on skin and feathers of vent.
Bloody faeces can be forced from vent if moderate pressure is applied to the abdominal area.
Most birds with diarrhea mostly die within 24 hours in well fleshy conditions or recover completely.
Mortality up to 60% in average 10 days.
Lesions Dead birds are in well fleshy conditions with pale skin and
massive hemorrhages.
Small hemorrhages on heart, muscles, liver and proventriculus.
The intestine is filled with blood.
Duodenal mucosa is congested and in some individuals covered with a yellow, fibrinonecrotic membrane.
The spleen is enlarged, friable and marbled or mottled.
The lung is congested.
Enlarged livers.
Intra nuclear inclusion bodies can be seen in liver, spleen, bone marrow, pancreas, lug intestine and blood lymphocytes.
Marble spleen disease
(MSD)
It is a condition affecting confinement-reared pheasants 3-8 months of age.
The causative virus is serologically indistinguishable from that of HE virus.
The clinical disease, however, is predominantly respiratory in nature with death occurring due to lung edema, congestion, and subsequent asphyxia.
Susceptibility
MSDV has been documented in
confinement pheasant.
Marble spleen disease in pheasants
occurs naturally in birds 3-8 months of age.
Pheasants are refractory to infection up to
4 weeks of age, either as a result of
undetectable, low maternal antibody levels
or a developmental lack of target cells.
Signs
Death of pheasants infected with MSDV is
considered to be per-acute or acute due to
respiratory compromise.
depression, weakness, and progressive dyspnea.
Occasionally, a premortem nasal discharge has
been noted.
Mortality rates in pheasants naturally infected with
MSDV have been reported to be 5-20% over a
period of 10 days to several weeks
Lesions Enlarged, mottled (marbled) spleens.
Edematous, congested lungs.
Intestinal lesions have not been noted.
The virus produce intranuclear inclusions
in liver, lung, kidney, bursa, and bone
marrow no inclusions are seen in the
gastrointestinal tract.
Avian adenovirus splenomegally
(AAS)
It has been described in broiler breeder
chickens characterized by splenomegaly,
pulmonary edema, and congestion.
In chickens, infection with AASV has been
observed in broiler breeders 20-45 weeks of
age.
Transmitted orally by feces contaminated litter.
AASV transmitted mechanically from infected to
susceptible flocks via movement of infectious
fecal or litter material.
Signs
Death of chickens infected with AASV is
considered to be per-acute or acute due to
respiratory compromise.
Depression, weakness, and progressive
dyspnea.
Occasionally, a premortem nasal
discharge has been noted.
In mature chickens with AAS, 8.9%
mortality has been reported.
Lesions
In broiler breeder chickens infected with AASV, Spleens of infected birds are characteristically enlarged, friable, and marbled or mottled in appearance.
Congested lungs.
AASV produce typical adenoviral intranuclear inclusions in liver, lung, kidney, bursa, and bone marrow no inclusions are seen in the gastrointestinal tract.
Diagnosis Isolation and Identification of causative virus
large concentrations of HEV can be found in sanguinous intestinal contents or splenic tissue obtained from dead or moribund poults.
Positive identification of HEV, MSD, and AASV is commonly by the use of AGP method in which splenic tissue (fresh or frozen).
Detection of viral DNA in fresh or frozen tissues by standard , and nested PCR assays PCR.
THE virus antibodies can be detected in plasma or serum of recovered birds by AGP while, ELISA for HEV is commercially available.
Differential diagnosis
In turkeys, reticuloendotheliosis or lymphoproliferative, colibacillosis, salmonellosis, gastrointestinal bleeding and mucosal hyperemia with acute septicemic, viremic, or toxemic conditions. Parasitism such as coccidiosis.
Pheasants and chickens die acutely with signs of respiratory distress but without enlarged, marbled spleens should be tested for Newcastle disease, avian influenza, infectious laryngotracheitis, and in the case of chickens, infectious bronchitis. Splenic enlargement and marbling without MSDV or AASV antigen on AGP should tested for neoplastic diseases as Marek’s, lymphoid leukosis, or reticuloendotheliosis.
Treatment For THE: At the first signs, inject 0.5 to 1ml/ bird S/C of
convalescent immune serum (collected from turkeys at slaughtering).
Vitamin K to stop the haemorrhages.
Antibiotic for 2nd infection primarily colibacillosis, selection of an appropriate antimicrobial based on culture and sensitivity .
Electrolytes as potassium chloride to prevent dehydration from diarrhea.
correction of management deficiencies, and vaccination for other primary agents that may be exacerbated by exposure to field and vaccine strains of HEV (i.e., Bordetella avium, Newcastle disease virus) must not be neglected.
Prevention Convalescent immune serum (collected from
turkeys at slaughtering) could be used as prophylactic (passive immunization) in endemic areas S/C or I/M 0.5-1m/bird.
Prevent transportation of infected litters from one flock to another.
Contaminated facilities may be cleaned and then disinfected with 0.0086% sodium hypochlorite solution or other viricidal agents.
Avoid contact between different species (turkeys, chickens and pheasants) and multiages.
In case of MSD, vaccinate 3-4 wk old birds with living attenuated vaccine in the drinking water.
Egg Drop Syndrome (EDS)
The disease is characterized by transient respiratory signs and drop in egg production with changes in color, thin-shelled or shell-less eggs by healthy birds and a failure to achieve production targets. Vertically infected flock show these signs at 50% or peak egg production.
Losses due to drop in egg production and increased costs of vaccination and preventive methods.
Cause EDS virus is classified as an adenovirus (member of the
subgroup III), unrelated to the subgroup I and subgroup II viruses, and only one serotype is recognized as duck adenovirus type 1 (DAdV-1), variations have been demonstrated in its isolates.
EDS virus agglutinated erythrocytes of chickens, ducks, turkeys, geese, pigeons, and peacocks but did not agglutinate rat, rabbit, horse, sheep, cattle, goat, or pig erythrocytes.
The hemagglutinin (HA) is resistant to heating at 56°C.
EDS virus replicates in the nucleus of infected cells where intranuclear inclusions were observed.
The virus is of one serotype, but there are chicken (EDS76) and duck (BC14) isolates.
Host
EDS virus replicated to high titers in duck
kidney, duck embryo liver, and duck embryo
fibroblast cell cultures.
The virus grew to high titers in goose cell
cultures and allantoic sac of embryonated
duck or goose eggs producing HA titers.
Susceptibility
EDS virus has been isolated from chickens.
The natural hosts for EDS virus are ducks and geese.
Natural outbreaks affect broiler breeders and heavy breeds producing brown eggs are more severely affected than white-egg producers.
Chickens of all ages are susceptible to EDS virus infection.
The disease at around peak egg production may be due to reactivation of latent virus.
In many cases, chicks infected in ovo did not excrete virus or develop HI antibody until the flock had achieved greater than 50% egg production.
Quail is susceptible to infection and to develop classic signs of EDS.
Transmission It is possible to divide EDS outbreaks into three
types:
1. Classic form: vertical spread of virus via embryonated egg is the main method.
2. Endemic form: Infection resulted from spread of excreted virus of classic form led to contamination of litter, egg trays and trucks. Needles or blades used for vaccination or bleeding of viremic birds can transmit infection.
3. Drinking water form: Spread of virus by droppings of water fowls to hens through contaminated drinking water.
Pathogenesis1. Infection of adult with limited replication of the
virus in nasal mucosa mild respiratory signs (not observed) and viremia within 3-4 days post infection (PI).
2. The virus reaches and replicates in lymphoid tissues (thymus and spleen) 7-20 days (PI).
3. The virus reaches shell gland pouch, replicates and induces inflammation (salpingitis) (Abnormal shell eggs).
EDSV IS NOT REPLICATE IN THE INTESTINAL MUCOSA AND PRESENCE OF VIRUS INFECTION DUE TO CONTAMINATION FROM OVIDUCT EXUDATE.
Clinical signsIn chickens and ducks:
Mild transient respiratory signs.
Loss of egg colour in pigmented eggs (depigmentation).
Soft shell, thin shell or shellless eggs.
Small eggs.
Granular roughening at one end of the egg “SAND PAPER LIKE TEXTURE”.
Drop in egg production at the peak of production (re-activation of latent infection) up to 40% for 4-10 weeks “HEN LOST10-16 EGGS/BIRD”.
Delay the onset of laying.
No change in fertility or hatchability.
Mild diarrhea due to exudate from the oviduct.
Lesions In-active ovary.
Deformed or atrophied oviduct.
Uterine edema.
Exudates in shell gland pouch.
Ova of different size in abdominal cavity.
Mild spleenomegally.
Flaccid ovules.
Ova with different sizes in the abdomen (egg peritonitis).
NB.
Intranuclear inclusions can be detected in shell gland cells
and in nasal mucosa and spleen infected chickens.
The egg on the left (brown) is normal, while
the egg on the right (right) is abnormal
This discoloration is caused by
abnormal pigment deposition of
the egg while in the oviduct of
infected chickens
These deformities are
especially evident in the
egg pictured in the top
center of this photo
soft misshapen eggs.Egg shell is roughened and
areas of discoloration
soft-shelled (fragile) and misshapen,
These eggs have thin shells that are
sometimes misshapen and easily broken .
Rough shell egg
Diagnosis Falls in egg production and changes in eggs
shell without mortalities.
Samples from blood at viremia or shell gland, oviduct secretion or egg albumin.
Isolation in duck embryo or TC.
Identification of HA virus with HI test.
Detection of antibodies is serum by ELISA, HI and AGPT.
EDS must differentiated from; ND, IB, SHS, CELO and non infectious causes of eggs shell changes.
Prevention1. Replacement birds should be derived from
uninfected flocks.
2. Drinking water must be away from ducks and geese.
Eradication:
A) chickens produced from EDS virus-infected eggs may be latently infected and fail to develop antibody;
B) The virus will become reactivated and will be excreted at around the time of peak egg production, and EDS antibody will develop, which will prevent or reduce further excretion.
C) lateral spread is poor.
Prevention1- The eradication program was based on the elite and grand
parent flocks aged 40 weeks or more. At this stage, these flocks had produced abnormal eggs and had EDS HI antibody.
2- Chicks hatched from these eggs were divided into small groups of about 100 (separated by netting wire). Ten to twenty-five percent of the chicks were HI tested for EDS antibodies by HI test at about 6-week intervals.
3- If one or two reactors were found, they were removed; 100% of the birds in the pen and 100% of adjoining pens were then tested twice at weekly intervals. If HI test positive reactors were found or if positive reactors.
4- kept appearing within a single pen, the whole pen was then removed and the in-contact pens of birds were tested. At 40 weeks, 100% of the birds were tested by HI test, and eggs were collected for the next generation. This program was successful, and subsequently, the grandparent and parent flocks were found to be free of infection.
Prevention Hygienic measures.
prevent contact of chickens with water fowl as ducks (reservoirs).
Avoid use of contaminated water sources by the excreta of infected water fowl.
Water chlorination or use water from wells.
Bleeding needle and needles used for vaccination should be sterilized between uses as infected birds have viraemia.
Egg sanitation (cleaning and disinfection of egg packing stations to avoid contamination of egg trays).
Testing of breeder flocks.
There is an inactivated vaccine given by injection at 14-16 weeks of age ( 4-6 weeks before egg production).
PreventionVaccination:
An oil-adjuvant inactivated vaccine is widely used and gives good protection against clinical EDS.
The birds are vaccinated between 14 and 16 weeks of age.
If uninfected birds are vaccinated, EDS HI titers of 8-9 log2 can be expected.
If the flock has been exposed previously to EDS virus, HI titers of 12-14 log2 may be found.
Vaccinal immunity lasts at least 1 year.
Vaccinated birds are protected against disease and do not appear to excrete EDS virus.
When vertical or lateral transmission of EDS virus is a possibility, flocks in danger can be protected by vaccination in the growing period.
If one or more houses on a multiage laying site become infected due to lateral spread of the virus, careful evaluation must be undertaken before vaccinating the healthy birds during lay.
