Avian Reo Virus

Plan of Talk
 Introduction
 Economic importance
 Virus characteristics
 Transmission
 Clinical sings and PM lesions
 Treatment and control

Introduction
1954
 The initial avian reovirus was isolated by Fahey and Crawley
from the respiratory tract of chickens.
1957
 Olsen et al. Isolated a reovirus from chickens with naturally
occurring synovitis that were unrelated to MG or MS.
Late 70s – early 80s
 Nonspecific malabsorption syndrome due to avian reovirus
was described.

Cont. …
 Avian reo viruses are ubiquitous viruses in nature.
 They are commonly isolated from a variety of tissues in
poultry affected by multiple disease conditions such as:
1. Viral arthritis/tenosynovitis.
2. Stunting syndrome.
3. Respiratory disease.
4. Enteric disease.
5. Malabsorption syndrome.

Cont. …
 Reovirus infections are prevalent
worldwide in chickens and turkeys.
 Viral arthritis/tenosynovitis is found
primarily in meat-type chickens and
turkeys.
 Reoviruses are commonly found in the
digestive and respiratory tracts of
clinically normal chickens and turkeys.

Cont. …
Highly contagious
15% susceptible chicks are enough to
spread through entire flock in the 1st
week.

Cont. …
Age-dependent susceptibility
Earlier the infection is associated
with more severe and permanent
weight suppression.

Cont. …
 10-30% weight suppression, without
complications.
 Up to 50% weight suppression, when
complicated with other stressors.

Economic Importance
Reovirus-associated Diseases;
1. Weight suppression (malabsorption)
Infections in the first week of age.
2. Viral arthritis/ tenosynovitis
Infections in naive birds (any age, but especially young).
3. Runting & stunting syndrome
– Infections in the first week, reovirus + other agent(s).
– Femoral head necrosis, brittle bone disease, acute mortality.
4. Respiratory disease.
5. Enteric disease.
6. Immune suppression.

Cont. …
Broiler
1. Increase mortality.
2. Viral arthritis and tenosynovitis.
3. General lack of performance;
1. Diminished weight.
2. Poor feed conversion.
3. Uneven growth rate.
4. Reduce marketability of affected birds.

Cont. …
Breeder
(viral arthritis prior to the onset or during egg production)
1. Lameness.
2. Increased mortality.
3. Decrease egg production.
4. Suboptimal hatchability and fertility.
5. Vertical transmission to progeny.

Virus Characteristics
 Family: Reoviridae
 Genous: Orthoreovirus
 Icosahedral symmetry
 Non enveloped
 10 ds RNA

Cont. …
Persistent pathogen:
1. Resistant to high temp 60c for 8 hrs.
2. Tolerates pH 3-9.
3. Non sensitive either.
4. Slight sensitive for chloroform.
5. The virus can survive for up to 10 days on feathers, wood
shavings, glass, rubber and galvanized metal, and for 10
weeks in water, with limited effect on infectivity.

Cont. …
Sensitive to:
1. 70% ethanol.
2. 0.5% organic acid.
3. 5% hydrogen peroxide.

Virus Target Tissue
The epithelial cells of:
1. Small intestine
2. Bursa of Fabricius
are the main sites of primary infection
and portal of entry of the virus which
rapidly spreads to other organs within
24-48 hours of infection.

Cont. …
 The site where virus replication has the most serious
consequences is the tibiotarsal-tarsometatarsal (hock) joint.
 At this site, the virus replication and long-term persistence
induce a series of processes leading to joint damage and in
the most severe cases, tendon rupture.

Virus Kinetics
 Experimental infection of adult SPF hens via the nasal,
tracheal or esophageal routes, showed distribution of virus to
all areas of the respiratory, enteric and reproductive tracts
and the tendon of the hock joints (viraemia).

Cont. …
 The virus was recovered from the plasma, erythrocyte and
mononuclear cell fractions of blood within 30 hours.
 By 3 to 5 days, virus had been distributed throughout the
body.
 Despite this widespread tissue dissemination, the principal
site of virus replication is the enteric tract.

Transmission
1. Vertical transmission, occurs at a low rate.
2. Most chicks become infected at an early age from:
 Small nucleus of congenitally infected hatch-mates.
 Environment.

Cont. …
Horizontal transmission
1. Intestinal tract (fecal contamination)
2. Respiratory tract.
3. Age related resistance.
4. Reoviruses may enter broken skin of the feet of chicks from
the litter and become established in the hock joints.
Vertical Transmission
1. Egg transmission low (<2.0%)
2. Hens infected via oral, tracheal, and nasal inoculation were
able to transmit reovirus to their progeny.

Clinical Signs – Post Mortem lesions
Viral arthritis/tenosynovitis
Viral arthritis/tenosynovitis
The first signs of reovirus infection are usually observed in
broiler breeder chickens between 6 and 10 weeks of age.
Broilers

Cont. …
1. Lameness.
– Birds are reluctant to walk and
when forced up have a painful,
trembling gait.
2. Joint swelling.
– A distinct swelling of the
tendons of the shanks and also
above the hock joint can be
observed.
3. Thickened/ruptured tendons. Swollen tendons

Cont. …
4. Affected birds have malpositioned
feathers, especially on the wings.
Malpositioned feather

Cont. …
5. The hock joint may be somewhat swollen, but usually not as
severely as with Mycoplasma synoviae or Staphylococcus
infections.
6. Upon opening the legs, the tendons usually appear
discolored, brown or blood-tinged, with straw colored fluid
between them.

Cont. …
7. Ruptured tendons may occur and, in older broiler breeders
(29-30 weeks old), one may feel a hard scarry knot in the
tendon above the hock joint.
8. When the infection is complicated by MS or Staphylococcus,
the fluid may appear yellow and creamy.

Clinical Signs – Post Mortem lesions
Malabsorption Syndrome
The disease is mainly observed
in broiler flocks.

Cont. …
1. History of diarrhea, beginning at few days of age and lasting
until 10-14 days of age.
– Light or dark brown, foamy droppings can be found with undigested
food particles.
2. Runting/Stunting.
3. Abnormal feathering.
– Several affected broilers in a flock may exhibit malpositioned feathers,
especially on the wings.

Cont. …
4. Skeletal abnormalities.
– Early rickets with extreme paleness of legs and heads can be
observed.
5. At a later age (5-6 weeks) osteoporosis becomes clinically
evident.
– Frequently unilateral causing the birds to limp.
6. Delayed growth of the affected birds.
7. Mortality is variable and in general as low as 4 %.

Treatment and Control
 Treatment is impossible.
 Vaccinating breeders helps reduce problems in the progeny.
 Strict hygienic and sanitary measures will reduce the
incidence of the disease.

Purpose of Vaccination
1. Prevent infection of breeders.
2. Prevent egg transmission to progeny.
3. Produce maternal antibodies for the progeny.
Layers

Time of Vaccination
Broiler progeny need high MDA to prevent early infections,
Infection before 7 days leads to malabsorption, runting
and stunting.
Infection before 14 days leads to leg problems (FHN and
ruptured tendons).

Vaccination Program
For the development and persistence of high levels of maternal
antibody, Giambrone recommended the use of:
1. Live vaccine as a primer early in life.
2. Inactivated vaccine given at 6 weeks of age and again
prior to lay.

Cont. …
In areas of high exposure
 Chicks are susceptible during the first weeks of life, and early
vaccination becomes mandatory.
 In these areas, vaccination should begin at 7 days of age.
 Re-vaccination is recommended at 5 to 7 weeks of age and
again at 9 to 11 weeks.

Cont. …
In areas where there is less exposure
 Vaccination should be carried out at 5 to 7 weeks of age and
again at 9 to 11 weeks.
 To complete this program for breeding birds, the
administration of an inactivated Reovirus vaccine is
recommended between 16 to 18 weeks of age.

Vaccine Strains
Strain Association Live/Killed
S1133 Tenosynovitis Live and Killed
UMI 203 Tenosynovitis Live
2408 Malabsorption/Tenosynovitis Killed
1733 Malabsorption/Tenosynovitis Killed
CO8 Malabsorption Syndrome Killed
305 Malabsorption/FHN/BBD Killed
ss412 Malabsorption/proventriculitis Killed

Virus Strains
Strain Disease or Syndrome Signs and Symptoms
1133
Causes tenosynovitis (VA), an
infection of the synovial sheath of
the tendon.
Leg and or joint swelling, difficult
in walking and bruised
appearance of the leg and thigh
muscles due to tendon rupture.
2408
Associated with VA and
Malabsorption Syndrome (MAS), a
condition where nutrients are not
absorbed in the intestine.
Early mortality, reduced weight
gains, poor feathering, poor
pigmentation, runting and
stunting.
3005
Associated with MAS, femoral
head Necrosis (FHN), and brittle
bone disease.
Deterioration of the top of the
thigh bone can be seen during a
post mortem examination.

Vaccine Administration
Route of Administration Efficacy
Subcutaneous (SQ) Good
Wing web Good
Water Good
In Ovo Poor

Why do we use live vaccines for REO virus?
Are they used just as a primer or do they protect
vaccinated birds against symptoms?

 Live REO vaccines can induce protection against symptoms in
young birds, but only when there are no maternally-derived
antibodies (MDA) present to neutralize the vaccine.
 Vaccines will not be effective in young birds with MDA against
REO.
 Early REO infections are the most dangerous ones.
 The most effective protection against them is by inducing high
levels of antibodies in the parent stock, to protect the
offspring by MDA.

 High antigen content inactivated REO vaccines are the most
effective, inducing high titres in parent stock.
 Priming such parent flocks with a live REO vaccine will further
increase the effect of the inactivated REO vaccine.
 Individual and average titres are higher and more uniform.
 Most importantly, the percentage of breeder birds that has
low or zero titres diminishes.
 This live priming of the young breeder birds can be done
when MDA have waned (after approximately six weeks of
age).

Mal-absorption syndrome (MAS) is still a current
problem in broiler flocks worldwide. Can it be
minimized by REO virus vaccination of parent stock?

 MAS is a complex of symptoms occurring when the intestines
of the broiler are not able to absorb sufficient nutrients,
resulting in deficiencies and growth retardation.
 Certain REO strains cause MAS like symptoms.
 This does not mean that all MAS is caused by REO infections:
 Any pathogen that disturbs the optimal balance in the intestinal flora,
can cause symptoms of MAS.
 In cases of MAS caused by REO infections, REO vaccination of the
parent stock is the most effective way of prevention.

Are different strains of REO virus responsible for
different symptoms or syndromes in the infected
birds?
Why do some inactivated vaccines contain different
REO virus strains?

 REO virus isolates have been associated with a great variety of
symptoms.
 This has enabled the categorization of REO-related infections
into different syndromes such as:
1. Viral arthritis (VA)
2. Brittle bone syndrome
3. Mas
4. Runting/stunting syndrome
5. Helicopter disease.

 The S1133 (Lvd-Heijden) strain is reported to be isolated from
a case of VA.
 The 1733 strain is isolated from a case of classic MAS.
 The 3005 from a case of brittle bone.

 However, a REO isolate from one specific syndrome will not
necessarily always cause similar symptoms.
 Neither is it possible to differentiate various isolates by
current serological methods: the REO antibodies do not make
a distinction.
 In fact, the immune system does not distinguish between the
one and the other pathotype: antibodies induced by one
isolate will protect equally against the other pathotypes.
 Inclusion of isolates of two or more syndromes in a vaccine
does not give a broader protection.

 Moreover, it would be un-practical to include isolates of all
syndromes, associated with REO virus infections.
 However, including more antigen per dose can increase the
immune response, measured in titers.
 A higher titer sometimes can induce a more effective
protection, which in itself could induce a higher titer and a
better protection.

Avian Reo Virus

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