avianinsight

A L O H MA N N A N I MA L H E A L T H N E WS B R I E F
Deep South Experiences with an Autogenous
Novel Reovirus Vaccine
The U.S. commercial
broiler industry started
reporting a resurgence
of clinical reoviral
infections in broilers as
early as 2000 (Tim
Cummings, Reovirus
Survey Summary,
AAAP Epidemiology
Committee, AVMA 2002). Classic reovirus clinical
signs include unthrifty, rufed appearance, swollen
shanks, lame birds with angular leg deformities, low
average ock weight and uneven bird sizes at
harvest. At that time, the southeast and southwest
reported more evidence of reovirus than other
regions. No interventions appeared to be successful,
whether using current commercially available live
vaccines in broilers, killed vaccines in breeders or
palliative treatments for lameness.
It was 2012 before there were reports of reoviral
infections in Sanderson Farms, Inc. (SFI) broiler
ocks, first in south Georgia (Riley, et al., 2013 ECVC).
Individual houses on a given broiler farm were
affected on multiple farms. It was relatively simple
to track progeny back to source hen ocks. Apparent
shedding hen ocks did not have any clinical signs or
elevated reovirus titers to indicate time or infection
or shedding pattern. Like most viral diseases, reovirus
was evident in progeny for 4 to 6 weeks, but then
unlike other viral diseases, progeny would be affected
intermittently for the duration of hen ock egg
laying cycle.
Affected and unaffected houses of reovirus-suspect
broiler ocks were bled as well as tissues harvested
for virus isolation from affected birds. Reovirus ELISA
serology demonstrated a strong immune response in
affected birds, especially when compared to
unaffected houses. Reovirus isolation was more
successful from leg quarters submitted to diagnostic
laboratories rather than tendons removed in the
field (Stayer, et al., 2014 AVMA). Reoviruses isolated
were not related to commercially available vaccines
(Sellers, 2013 ECVC) but closely related to one
another, regardless of hen source ock.
Later in 2012, and into 2013, more reovirus-affected
broilers were found in SFI ocks in Mississippi and
Texas. As with the south Georgia distribution,
individual houses of broilers on a given farm shared
clinical signs with similar progeny distributed to
houses on other farms. Serology and virus isolation
yielded the same results as south Georgia, in fact, the
reoviruses isolated in all three states (Georgia,
Volume 3, 2014
inside
Both challenge
studies supported
field observations
that progeny
from pullets
vaccinated one
time with killed
autogenous MG1
reovirus vaccine,
after three live
reovirus primes
and simultaneous
commercial 2-way
killed IBDV +
reovirus vaccine,
are protected
from novel
reovirus infection.
Autogenous Novel Reovirus Vaccine
in the Deep South, p.1
Notes from the Director of Sales, p.4
Philip A. Stayer, D.V.M., M.S., A.C.P.V.
Corporate Veterinarian,
Sanderson Farms, Inc.
Mississippi and Texas) shared the same
genotype, molecular group 1 (MG1), as
tested by Dr. Sellers (Riley, et al., 2013
ECVC). At this point, the veterinary staff at
SFI asked Lohmann Animal Health to assist
them in making a killed autogenous
reovirus vaccine with one of the original
viruses of the shared MG1 genotype.
By June 2013 SFI started to vaccinate all
pullet ocks with autogenous MG1 reovirus
vaccine. The standard vaccination program
involved 3 live priming reovirus
vaccinations at day of age, 3 weeks and 6
weeks, followed by two commercial killed
combined Infectious Bursal Disease Virus
and Reovirus vaccines administered
simultaneously at 15 weeks of age. The
autogenous MG1 reovirus vaccine replaced
one of the commercial killed combined
products so that the new program had the
same 3 live priming vaccinations, but only
one commercial killed combined vaccine
and one autogenous killed MG1 reovirus
vaccine administered simultaneously at
15 weeks.
Pullet and hen titers on the new vaccination
program did not show any difference from
the previous program in mean titers or
coefficient of variation of the titers. Broiler
progeny titers remained low as they had
on previous hen vaccination schedule. The
only elevated broiler titers in the ensuing
months were those from affected progeny
out of hens that did not receive the
autogenous MG1 reovirus vaccine. At the
time of writing this report, there have been
no clinical cases of reoviral infections in
broilers from hens receiving the
autogenous MG1 reovirus vaccination.
Of course the question remains, Were we
lucky or were we good? To address this
question two challenge studies were
conducted at the Poultry Disease Research
Center (PDRC) in Athens, GA under Dr. Holly
Sellers supervision. The first trial tested
the progenies protection from homologous
challenge, that is, using the original MG1
reovirus isolated for vaccine manufacture
as challenge virus in offspring whose
mothers received the same virus in killed
vaccine form (Alvarado, et al., IPSS 2014).
The second trial tested the progenies
protection against challenges of both the
homologous MG1 reovirus and the
commercially available modified live
reovirus vaccine strains (Stayer, et al.,
ECVC 2014).
For the first study, day of age broiler chicks
were obtained from the North Carolina SFI
hatchery where no broiler reoviral
infections had been reported. One group of
chicks came from hens that received the
autogenous MG1 reovirus vaccine and
another group of chicks came from hens
within 4 weeks of hen age to the first
group but that did not receive autogenous
MG1 reovirus vaccination. Both sets of
chicks were bled at day of age and weighed
to document the starting point of the trial.
Some chicks from both groups were
challenged with MG1 reovirus at 12 days of
age when footpad and tendon
measurements were made. The trial was
completed at 42 days of age when all birds
were euthanized, measurements taken
again and gross lesions recorded
from necropsy.
The results of the first trial indicate that
vaccination with autogenous MG1 reovirus
vaccine was protective against MG1
challenge. ELISA serology and body
weights were not significantly different at
the start of the trial. Footpad and digital
tendon thicknesses were not significantly
different between treatments. The most
significant finding at the end of the trial
were the gross lesions seen on necropsy.
Fig. 1. Figure 1. Macroscopic lesions observed in treatment groups from progeny originating
from broiler breeders vaccinated once with the MG 1 autogenous vaccine.
The MG1 vaccinated progeny had 10X
fewer birds with severe tendonitis than
their non-MG1 protected peers.
The second study used the same North
Carolina SFI sources of broiler chicks to
avoid any inadvertent exposure to novel
reovirus infection. Again, one group of
chicks came from hens that were
vaccinated with autogenous MG1 reovirus
vaccine at 15 weeks of age as pullets and
another group of chicks from hens within
four weeks of age to the first group, but
this hen ock did not receive the
autogenous vaccine. Chicks from both hen
ock sources were separated into six
challenge environments: mock tracheal
challenge (Neg/IT), mock footpad
challenge (Neg/FP), tracheal 1133 virus
challenge (1133/IT), footpad 1133 virus
challenge (1133/FP), tracheal MG1 virus
challenge (Gp1/IT), and footpad MG1 virus
challenge (Gp1/FP). The trial was
terminated 10 days after challenge at 12
days of age so that chicks in all treatments
were kept for a total of 3 weeks.
Some chicks from both hen sources were
bled at the beginning of the second trial.
Chicks from the MG1 vaccinated source
had higher ELISA reovirus titers (4,707
geometric mean titers (GMT), 56%
coefficient variation (CV)) than those from
the non-MG1 vaccinated hens (2,105 GMT,
89.8% CV). Chicks from the MG1 vaccinated
hens started smaller and remained smaller
throughout the trial, most likely due to
source hens being four weeks younger
than the non-MG1 vaccinated hens.
Thicknesses of exor tendons and footpads
did not differ significantly among
treatments for the duration of the trial,
probably due to the short duration of
the trial.
Gross clinical lesions, especially pericardial
effusion and visibly swollen tendons, did
differ between treatments at the
termination of the second trial (see figures
1 & 2). MG1 chicks had few clinical lesions
from intra-tracheal challenges with either
1133 or Gp1 reovirus. Non-MG1-sourced
chicks were protected from intra-tracheal
1133 challenge but showed clinical lesions
of reovirus infection with intra-tracheal
Gp1 reovirus challenge. Within each ock
source, footpad challenges with either
1133 or Gp1 virus produced more gross
lesions in either MG1 or non-MG1 chicks
than intra-tracheal challenges. MG1-source
chicks had fewer affected chicks with
either challenge virus or route of infection
than non-MG1-source chicks with similar
virus and similar route of infection.
The superior protection of MG1-source
chicks to both viruses demonstrated the
efficacy of the MG1 autogenous vaccine
and lack of interference with standard
reovirus vaccines.
Both challenge studies supported field
observations that progeny from pullets
vaccinated one time with killed autogenous
MG1 reovirus vaccine, after three live
reovirus primes and simultaneous
commercial 2-way killed IBDV + reovirus
vaccine, are protected from novel reovirus
infection. Since implementation of the
autogenous MG1 reovirus vaccination, only
chicks from non-MG1 vaccinated hens have
had clinical signs of reovirus infection.
Fig. 2. Macroscopic lesions observed in treatment groups from progeny originating from
broiler breeders not vaccinated with the MG1 autogenous vaccine.
Autogenous vaccines provide a
platform to help the poultry
industry battle disease challenges
not covered by commercial
vaccines. Autogenous vaccines
have been and will continue to
be an important tool for poultry
health professionals and poultry
producers. Our vaccine production
facility has been producing high-
quality autogenous vaccines for
the industry for multiple decades and makes them with the
same standards as our commercial vaccine line.
We want to thank Dr. Stayer and his team for contributing this article
and more importantly, for allowing us to work together on this industry-
wide Reo issue. It is a compliment when we are asked to provide
resources and to partner with our customers and hope that the value
we place upon those relationships is evident. To all the people we
have worked with over the years under the Lohmann Animal Health
banner, we thank you for your continued support and trust. We cherish
those relationships and are looking forward to growing them with our
new Elanco team, providing even greater opportunity with innovative
and necessary tools and resources to support our industry.
Please visit with your Elanco Animal Health representative to learn
more about our autogenous capabilities.
Notes from the Director of Sales
Tim Hopson
Director of Sales, US & Canada
Lohmann Animal Health
International, Inc.
for more information:
avianinsight
(+1) 207-873 3989 (+1) 800-655 1342 www.lahinternational.com
Pullet, hen and progeny reovirus titers
remain low at the writing of this article
now that all breeding stock have been
vaccinated with MG1 vaccine.
Our autogenous MG1 reovirus vaccine
appears to be efficacious for the reovirus
challenge that our ocks face from Texas
to North Carolina. We intend to continue
using autogenous reovirus vaccines until
there is a commercial product available
with similar efficacy. It is imperative that
commercial reovirus vaccine candidates
have broad enough protection to cover
current reovirus challenges. Hopefully
years will pass again before new reoviruses
appear to create the same issues as these
novel reoviruses.
References
1. Alvarado, I., P.A. Stayer, E. G. Riley, J.
David French, H. Sellers, Evaluation of
Progeny Protection against a Novel
Reovirus Strain associated with
Lameness and Poor Performance, 2014
International Poultry Scientific Program,
Atlanta, GA; January 28, 2014, (T97).
2. Cummings, T.S., Reovirus Survey
Summary, AAAP Epidemiology
Committee report, 139th Annual
Convention of the American Veterinary
Medical Association, Nashville, TN;
July 13, 2002.
3. Riley, E.G. and P.A. Stayer, Viral
Arthritis: This aint your Daddys
reovirus, 2013 Emerald Coast
Veterinary Conference, Sandestin, FL;
June 29, 2013.
4. Sellers, H.S., Emergence of a novel
reovirus in broilers 2012, 2013 Emerald
Coast Veterinary Conference,
Sandestin, FL; June 29, 2013.
5. Stayer, P.A., E.G. Riley, J.D. French,
I. Alvarado, J. Stockam and H.S. Sellers,
Deep South Experiences with
an Autogenous Vaccine for Novel
Reovirus, 2014 Emerald Coast
Veterinary Conference, Sandestin, FL;
June 20, 2014.
6. Stayer, P.A., E.G. Riley, J.D. French, P.J. Ferro,
A. Banda, H.S. Sellers, and R.E. Mock,
Virus Isolation Experiences Across
the Chicken Belt, 151st Annual
Convention of the American Veterinary
Medical Association, Denver, CO;
July 29, 2014; 2014 AAAP Scientific
Program Abstracts