hmmm that link doesn't work even cut and pasted!
Not an Emergency...Marek's in the Flock
- Thread starter Haunted55
- Start date
Ahhh...
retrofitted, MacGyvered and more Power...
Four more glorious words strung together could never be written...lol !!!
-kim-
retrofitted, MacGyvered and more Power...
Four more glorious words strung together could never be written...lol !!!
-kim-
I'll cut and paste.
That looks like a file that is hosted on your home computer. You'll have to either upload it somewhere or find a link to a copy online.
Some could get real carried away when it comes to what stresses a chicken. I'll bet the list is endless and unrealistic.
This was the article I tried to link
Marek's disease is a lymphoproliferative and neuropathic
disease of domestic chickens, and less commonly, turkeys and
quails, caused by a highly contagious, cell-associated,
oncogenic herpesvirus (7). As a disease occurring world-wide,
with increasing reports of vaccination failures and emergence 546 Rev. sci. tech Off. int. Epiz., 19 (2)
of more virulent pathotypes, MD poses a severe threat to the
poultry industry. Developing strategies for the control of MD
remains a significant challenge.
The pathogenesis of MD is complex. The infection is thought
to be transmitted by the respiratory route from the inhalation
of infected dust in poultry houses. Although the very early
events in the disease are not yet clear, the pattern of events
after infection with an oncogenic MDV in susceptible birds
can be divided into the following stages:
a) early cytolytic infection
b) latent infection
c) late cytolytic infection with immunosuppression
d) neoplastic transformation (6).
Marek's disease virus is a lymphotropic virus and targets
lymphocytes, the principal cells of the immune system.
B-lymphocytes, the cells of the antibody-forming arm of the
immune system, are first targeted by the virus in a lytic
infection. Following this, cytolytic infection occurs in the
activated T-lymphocytes that are involved in cell-mediated
immune responses. These early cytolytic events result in
atrophic changes in the bursa of Fabricius and thymus,
leading to severe debilitation of the immune system and
marked immunosuppression. The cell-associated viraemia
that develops during this period is believed to be the route by
which the virus spreads throughout the body, including the
feather follicle epithelium, the only site where a fully
productive infection occurs which allows shedding of the
virus into the environment. After the early cytolytic phase, the
infection switches to a latent phase in the infected T cells, and
the regressive changes in the lymphoid organs start resolving,
largely restoring the architecture of these lymphoid organs.
Following this, some of the latently infected T cells become
targets for neoplastic transformation resulting in
lymphomatous lesions in various visceral organs. Due to the
complex nature of the pathogenesis with varying periods of
latency, the incubation period of MD from the point of
infection to the onset of clinical disease can vary from a few
weeks to several months.
Generally, four different clinical forms of the disease are
recognised in flocks infected with MDV, as follows:
a) the classical or neural form, where a large proportion of
the birds show signs of paresis or paralysis involving the legs,
wings and sometimes the neck. These cases, also referred to as
'fowl paralysis' or 'range paralysis', are usually seen in birds of
two to twelve months of age;
b) the acute form, a more virulent form of the disease where
lymphomatous lesions of various organs develop and high
mortality occurs in the affected flocks. Birds as young as six
weeks can be affected, with losses commonly occurring
between three and six months. Involvement of the eyes and
nerves as well as lymphomatous lesion of the skin is also
evident in some cases. Visceral and skin lesions due to MD
are important causes of carcass condemnation in
slaughterhouses;
c) transient paralysis, an uncommon condition in flocks
infected with MDV, usually occurring between five and
eighteen weeks of age. This is an encephalitic expression of
infection characterised by sudden onset of paralytic
symptoms that often only last for approximately 24 h to 48 h,
although in some instances death can occur;
d) acute mortality syndrome, a form of the disease observed
more recently, where the affected birds die with an early acute
cytolytic disease well before the onset of lymphomas. The
affected birds show characteristic atrophy of the bursa of
Fabricius and thymus. This form of the disease is thought to
be due to infection with highly virulent pathotypes of the
virus.
Aetiology
Viru s structur e an d replicatio n
The isolation of cell-associated herpesvirus from MD tumours
in the late 1960s (8) was an important historical landmark
which led to an improved understanding of the disease and
development of effective vaccines. Due to the lymphotropic
nature of the virus, MDV was originally classified as a
gammaherpesvirus together with Epstein-Barr virus, and the
oncogenic herpesviruses of non-human primates, herpesvirus
saimirí and herpesvirus ateles. However, on the basis of the
genomic organisation, MDV is currently classified together
with alphaherpesviruses such as the herpes simplex vims
(HSV) in the family Herpesviridae. The deoxyribonucleic acid
(DNA) of MDV is a linear double-stranded molecule of
approximately 170 kilobases, consisting of a unique long
region (UL) flanked by a set of inverted repeat (TRL
and IRL )
regions and a unique short region (US) flanked by another set
of inverted repeat regions (IRS
and TRS ) (34). Thus, the
genomic structure of MDV from left to right can be described
as TRL-UL-IRL-IRS-US-TRS and is similar to that of other
alphaherpesviruses. The viral genomes in the infected cells are
maintained either as circular episomes or as integrated forms.
The viral genome has the capacity to encode at least seventy
proteins, sixty of which have counterparts in HSV, including
structural proteins, metabolic enzymes and transactivating
proteins such as VP 16 and ICP4 (34). However, at least ten
MDV genes have no homologues in other herpesviruses.
Similar to those of other herpesviruses, MDV genes also
belong to three kinetic classes of immediate early, early and
late genes, based on the requirements for viral protein
synthesis and DNA replication. Compared to the extensive
expression of genes, during the lytic infection, the
transcription in latently infected and transformed cells has
been largely restricted to the repeat regions of the MDV
genome. Some of the important genes recognised within the
repeat regions that could potentially be associated with
transformation include the BamHI-H family transcripts, pp38,
ICP4 sense and antisense ribonucleic acid (RNA) transcripts,
and the meq gene. fíev, sci. tech. Off. int. Epiz., 19 (2| 547
The main types of interaction that occur between the virus
and the cell in MDV infection include the following:
a) a semiproductive infection similar to that which occurs in
vivo in lymphoid organs and in vitro in cultured cells which
results in the production of non-enveloped virions
b) a fully productive infection which occurs in the feather
follicle epithelium with production of infectious enveloped
virions
c) a non-productive infection which is commonly seen in
tumours and lymphoblastoid cell lines where the viral
genome is not expressed or is expressed to a limited extent
only.
Marek's disease virus serotypes and pathotypes
The first isolation of MDV in 1967 was followed by the
description of a number of isolates from different parts of the
world. Subsequently, these isolates where divided into three
distinct serotypes, as follows:
a) serotype 1, which includes all the pathogenic or oncogenic
strains of MDV in addition to the attenuated strains of these
viruses
b) serotype 2, which includes naturally non-pathogenic
strains of MDV
c) serotype 3, which includes the herpesvirus of turkeys
(HVT), the non-oncogenic MDV-related virus, isolated from
turkeys.
In addition to differences in biological properties, these
serotypes can also be distinguished by serological methods
using polyclonal and monoclonal antibodies, DNA and
polypeptide analysis as well as by the polymerase chain
reaction (PCR).
A large diversity exists within serotype 1 concerning the
oncogenic potential, with strains varying from highly to
mildly oncogenic. Recently, serotype 1 MDV strains have
been further classified on the basis of the ability to induce MD
lesions in vaccinated chickens. Strains are classified as mild
(mMDV), virulent (vMDV), very virulent (vvMDV) and very
virulent + (w+MDV) pathotypes (Table I). The emergence of
these pathotypes is thought to represent a continuous
evolution of MDV towards greater virulence. Some of these
pathotypes show an increased propensity to produce acute
Table I
Serotypes and pathotypes of Marek's disease virus
Serotype Pathotype Representative strains
Mild (mMDV) HPRS-B14, CU2, Conn-A
Virulent (vMDV) HPRS-16, JM, GA
Very virulent (wMDV) RB1B, ALA-8, Md5, Md11
Very virulent + (w+MDV) 61 OA,648A
Non-oncogenic SB-1, HPRS-24.301B/1
Non-oncogenic HVT-FC126, HPRS-26
cytolytic disease with atrophic changes in the lymphoid
organs, the severity of which directly correlates with the
virulence.
Epidemiology
Prevalence of infection and disease
Marek's disease virus infection mainly occurs in domestic
chickens and is ubiquitous among poultry populations
throughout the world. The infection in other species is rare,
but occasionally the disease occurs in turkeys and quails. In
commercial chicken houses, where the infection is rampant,
virtually all birds become infected, commonly within the first
few weeks of life, although on occasions infection may be
delayed. Because of the prevalence of serotype 1 viruses of
varying pathogenicity and of non-pathogenic serotype 2 in the
poultry house environment, birds can be infected with more
than one MDV strain. Evidence suggests that the frequency of
isolation of non-pathogenic viruses becomes higher as the age
of the birds increases. Natural infection by non-pathogenic
strains of MDV can provide immunity to subsequent infecüon
by a virulent strain.
Transmission of infection
The transmission of MDV occurs by direct or indirect contact,
apparently by the airborne route. The epithelial cells in the
keratinising layer of the feather follicle replicate fully
infectious virus, and serve as a source of contamination of the
environment. The shedding of the infected material occurs
approximately two to four weeks after infection, prior to the
appearance of the clinical disease, and can continue
throughout the life of the bird. The virus associated with
feather debris and dander found in dust in the contaminated
poultry house can remain infectious for several months.
Although the inhalation of infected dust from poultry houses
remains the most common route of disease spread, other less
common mechanisms of indirect transmission, such as those
involving darkling beetles (Alphitobius diaperinus), could also
play minor roles in transmission. However, no evidence exists
to suggest that vertical transmission of MDV occurs through
the egg.
Flock infection
Because of the ubiquitous nature of the infection and the
ability to survive for long periods outside the host, flock
infections usually occur early in the life of a bird. In addition,
in most flocks, the hatched chicks usually have
maternally-derived antibodies. This antibody disappears in
most chickens by three to four weeks of age. The rate of the
spread of MD within a flock can vary greatly and depends on,
among several factors, the level of initial exposure and the
concentration of susceptible birds. A number of stress factors,
including those from handling, change of housing and
vaccination, are thought to increase the disease incidence. The
existence of genetic resistance to MD among chickens has
long been recognised and the genetic constitution of the flock
influences the outcome of MDV infection. The outcome of
infection is also influenced by sex, as females are usually more
susceptible to the development of tumours. 548 Rev. sci. tech. Off. int. Epiz., 19 (2|
Diagnostic methods
Diagnostic procedures for avian tumour viruses include both
pathological and virological methods. Pathological diagnosis
identifies the nature of the tumour that is causing mortality,
whereas virological diagnosis identifies viruses that are
present in a bird or flock. As MDV, ALV and REV occur
commonly, virological diagnosis does not necessarily establish
the cause of the tumour. Nevertheless, histopathological
identification of a tumour often determines the likely cause.
However, in some cases, the presence of an infection in a flock
may need to be established in the absence of tumour
mortality.
Pathological diagnosis
The main gross and histopathological features of the
neoplasms under review are summarised in Table II. In
general, while gross appearance can provide indications of the
nature of the neoplasm, histopathological diagnosis is
essential for accurate diagnosis. Histopathological diagnosis
requires tumour material from birds which have died very
recently and from several cases from an affected flock; this
material should be placed in fixative. For the diagnosis of MD,
the most useful set of tissues to collect include the liver,
spleen, bursa of Fabricius, thymus, heart, proventriculus,
kidney, gonads, nerves, skin and other gross tumour tissues.
Although clinical signs associated with MD can occur in
chickens from four weeks of age, signs are most frequently
seen between twelve and twenty-four weeks of age, and
sometimes later. Significant diagnostic features of the classical
and acute forms of MD are described below.
Classical form
In the classical form of the disease, with mainly neural
involvement, mortality rarely exceeds 10%-15%, occurring
over a few weeks or many months. The most common clinical
sign is partial or complete paralysis of the legs and wings. The
characteristic pathological lesion is the enlargement of one or
more of the peripheral nerves. The most commonly affected
nerves that are easily seen on post-mortem examination are
the brachial and sciatic plexus and nerve trunks, coeliac
plexus, abdominal vagus and intercostal nerves. The affected
nerves are grossly enlarged, and often two or three times the
normal thickness. The normal cross-striated and glistening
appearance of the nerves is lost, instead, the nerves have a
greyish or yellowish appearance and are oedematous.
Lymphomas are sometimes present in this form of the disease,
most frequently as small, soft grey tumours in the ovary,
kidney, heart, liver and other tissues.
Acute form
In the acute form of the disease, where formation of
lymphomas in the visceral organs usually occurs, the
incidence of the disease is frequently between 10% and 30%,
and in major outbreaks can reach 70%. Mortality can increase
rapidly over a few weeks and then cease, or can continue at a
steady or falling rate over several months. The typical lesion in
this form of the disease is the widespread, diffuse
lymphomatous involvement of visceral organs such as the
liver, spleen, ovary, kidney, heart and proventriculus.
Lymphomas are also occasionally seen in the skin around the
feather follicles and in the skeletal muscles. Affected birds may
also show involvement of the peripheral nerves similar to that
seen in the classical form. The liver enlargement in younger
Table II
Principal gross and microscopic features of importance in the differential diagnosis of the leukoses and Marek's disease lymphoma
Feature Lymphoid leukosis Erythroid leukosis Myeloid leukosis
(myeloblastosis)
liver
Spleen
Bursa of Fabricius
Bone marrow
Blood
Cytology and
histopathology
Other organs and
tissues often grossly
involved
Greatly enlarged; diffuse,
miliary or nodular tumours;
moderately firm
Usually enlarged; diffuse,
miliary or nodular tumours;
soft
Usually enlarged; nodular
tumours
Often tumorous; diffuse or
focal
Occasionally lymphoblastic
leukaemia
lymphoblasts; mainly
extravascular infiltrations
Moderately enlarged;
diffuse infiltration;
cherry-red colour; soft
Often enlarged; cherry-red;
smooth; very soft
No changes
Semi-liquid; cherry-red
Kidneys, ovary
Erythroblastic leukaemia;
immature erythrocytes;
anaemia; thin buffy coat
Erythroblasts;
intravascular
Kidneys; may be
haemorrhages in muscles
Myeloid leukosis
(myelocytomatosis)
Marek's disease
lymphoma
Greatly enlarged; diffuse
infiltration; mottled;
granular surface; firm
Often enlarged; diffuse
tumour; mottled; smooth;
soft
Sometimes tumorous
Diffuse, reddish-grey
tumour infiltration
Myeloblastic leukaemia;
thick buffy coat
Myeloblasts in
intravascular and
extravascular locations
Kidneys, ovary
Often yellowish white
nodular or diffuse tumours
Often nodular or diffuse
tumours
No changes
Usually diffuse
yellowish-grey tumour
infiltration
Myelocytic leukaemia;
thick buffy coat
Myelocytes in
intravascular and
extravascular locations
Kidneys, ovary, thymus,
surface of bones (sternum,
ribs, skull)
May be moderately to
greatly enlarged; miliary
or nodular tumours; firm
Often atrophic; may be
enlarged; usually diffuse
tumours
May be diffusely
enlarged
No changes
May be lymphocytosis or
lymphocytic leukaemia
Pleomorphic, sometimes
blastic, lymphoid cells in
perivascular locations
Nerves, kidneys, ovary,
proventriculus, heart,
muscle, skin, iris Rev. sci. tech. Off. int. Epiz., 19 (2) 549
birds is usually moderate compared to that in adult birds
where the liver is greatly enlarged and the gross appearance is
very similar to that seen in lymphoid leukosis. Nerve lesions
are less frequent in adult birds.
Features common to the acute and classical forms
The peripheral nerves in both forms of the disease are affected
by proliferative, inflammatory or minor infiltrative changes
that are termed A-, B- and C-type lesions respectively. The
A-type lesion consists of infiltration by proliferating
lymphoblasts, large, medium and small lymphocytes, and
macrophages, and appears to be neoplastic in nature. Nerves
with B-type lesions show oedema and infiltration by small
lymphocytes and plasma cells with Schwann cell
proliferation; in this case the lesion appears to be
inflammatory. 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. Demyelination, which is frequently seen
in nerves showing A- and B-type lesions is thought to be
principally responsible for the paralytic symptoms.
Lymphomas seen in the visceral organs and other tissues are
similar cytologically to the lymphoproliferations in the nerve
A-type lesions. The lymphoid cells are usually of the mixed
type, with a preponderance of small and medium
lymphocytes. However, large lymphocytes and lymphoblasts
may occasionally predominate, especially in adult birds. The
polymorphic population of the lymphoid cells, as seen in
impression smears or tissue sections of MD lymphomas, is an
important feature in differentiating MD from lymphoid
leukosis.
Virologica l diagnosi s
Isolation of Marek's disease virus
Marek's disease virus infection in a flock can be detected by
isolating the virus from the infected tissues. Materials,
commonly used for the isolation of the virus are buffy coat
cells from heparinised blood samples, or suspensions of
lymphoma and spleen cells. As Marek's disease virus is highly
cell-associated, the suspensions must contain viable cells.
These cell suspensions are inoculated into monolayer cultures
of chick kidney cells or duck embryo fibroblasts. Chicken
embryo fibroblasts (CEF), although less sensitive for the
primary isolation of serotype 1 MDV, can be used to isolate
serotypes 2 and 3. Evidence of MDV replication in the culture
can be seen as plaques which appear in three to four days.
Less commonly, feather tips, from which cell-free MDV can be
extracted, are also used for virus isolation.
Characterisation of Marek's disease virus serotypes
Serotypes of MDV isolated in culture can be differentiated
fairly accurately on the basis of the time of appearance, rate of
development and morphology of the plaques. Plaques of HVT
usually appear earlier and are larger than serotype 1 plaques,
whereas serotype 2 plaques appear later, and are smaller than
the serotype 1 plaques. The serotype specificity of the plaques
can also be confirmed by using specific antibodies in
immunological tests. Recently, PCR tests have been developed
which allow the differentiation of oncogenic strains of
serotype 1 virus, and strains of serotypes 2 and 3 (3, 35).
Detection of virus infection in tissues
The methods commonly employed for the detection of
virus in tissues include immunofluorescence and
immunohistochemical methods using polyclonal and
monoclonal antibodies, in situ hybridisation using
MDV-specific nucleic acid probes, PCR and electron
microscopy.
Serological tests
The presence of antibodies to MDV in birds from
approximately four weeks of age is an indication of infection.
Antibodies detected in birds before this age are likely to
represent maternally derived antibodies and are not
considered evidence of active infection. Although no
serological test has been prescribed for the detection of
MDV-specific antibodies, the agar gel immunodiffusion
(AGID) test is usually employed for this purpose. The antigen
used in the test is either disrupted MDV-infected tissue
culture cells, extract of the feather tips or skin containing
feather tracts from infected chickens. The viruses, antigens
and antisera are usually available from OIE Reference
Laboratories for MD. A modification of the AGID test to detect
MDV antigen in the feather tips by reactivity with MDV
hyperimmune serum is also used. Other serological tests,
such as the indirect immunofluorescence test, enzyme-linked
immunosorbent assay (ELISA) and virus neutralisation (VN)
have been described, but are used mostly for research
purposes rather than for routine diagnosis.
Surveillance
Marek's disease is a ubiquitous virus infection occurring in
commercial poultry operations world-wide. Because the virus
is able to survive for long periods both in the host and in the
environment of the poultry house, the disease is unlikely to be
completely eradicated. Control of the disease therefore
depends essentially on the use of successful vaccination
strategies. The vaccine strains are non-pathogenic viruses that
establish a permanent infection in the vaccinated birds. The
vaccines are capable of preventing lymphoma formation and
clinical disease, but do not prevent superinfection by
pathogenic MDV strains. Hence, surveillance for MD should
verify that the birds do not suffer from clinical disease and are
properly vaccinated. To achieve this, various tests mentioned
under the section on diagnosis can be applied. In addition,
importing countries should require the exporter to provide
international animal health certificates (24) to ensure that
imported chickens and day-old chicks are free from clinical
disease and are vaccinated against MD and that the hatching
eggs originate from a vaccinated source and have been
shipped in clean unused packages. As MDV is not vertically
transmitted, these measures are sufficient to prevent
introduction of infection through day-old chicks or hatching
eggs. However, vaccination and freedom from clinical disease 550 Rev. sci. tech. Off. int. Epiz.. 19(2)
would not exclude the possibility of introduction of
pathogenic MDV isolates when importing older birds.
Marek's disease virus could persist in the skin (in feather
follicles) of imported carcasses and portions, and in feathers,
but is unlikely to be present in poultry meat and eggs. Live
poultry should not be exposed to such potentially infected
materials. Heat treatment (cooking) will destroy MDV.
Public health implications
The identification of MDV and the widespread use of live
vaccines against MD have raised some concerns that exposure
to MDV from the environment or from consumption of
poultry meat could be a cause of cancer in humans. However,
a large body of evidence in both avian and human virology,
serology, pathology and epidemiology strongly supports the
conclusion that no aetiologic relationship exists between avian
herpesviruses and human cancer (31). Recently, there has
been speculation that MDV infection might be associated with
multiple sclerosis (MS), principally based on serological
findings. However, in detailed studies using sensitive methods
such as PCR, no MDV-related sequences could be detected in
the DNA of patients with MS, ruling out the involvement of
MDV (16).
Prevention and control methods
Vaccinatio n
The development of vaccines for the control of MD was a
significant landmark both in avian medicine and basic cancer
research, as this was the first example of a neoplastic disease
controlled by the use of a vaccine. Currently and at least for
the foreseeable future, vaccination represents the principal
strategy for the prevention and control of MD, although other
approaches, such as increasing the genetic resistance of birds
and improving hygiene and biosecurity, should form valuable
adjuncts for control programmes.
Live virus vaccines, used since 1970, remain the basis of
disease control programmes. These are usually administered
to day-old chicks at hatching to provide protection against the
natural challenge the chicks are exposed to early in life from
the infected poultry house environment. With the
introduction of in ovo immunisation methods, an increasing
number of birds are vaccinated by this route. Marek's disease
vaccines are highly effective, often achieving over 90%
protection under commercial conditions. Vaccines available
vary from country to country. In the United States of America
(USA), strains of MDV belonging to all three serotypes have
been licensed as vaccines (Table III).
In many countries, HVT continues to be widely used as a
monovalent product because it is inexpensive, available as
cell-free and cell-associated forms, and effective when the field
exposure is not severe. The HVT and SB-1 strains comprised
the first commercial bivalent vaccine based on the protective
synergism demonstrated between serotypes 2 and 3 viruses.
The CV1988 strain Rispens vaccines and modified versions are
Table III
Strains of Marek's disease virus licensed to be used as vaccines in the
United States of America
Vaccine strain Serotype
FC126 (HVT) 3
SB-1 2
301B/1 2
CVI988 clone C 1
CVI988/C/RB 1
CVI988 (Rispens) 1
R2/23 (Md 11/75) 1
widely used in many countries and appear to be effective
against some of the w+MDV pathotypes.
Although MD vaccines have been successful in controlling
major losses from the disease, threat of vaccine failure has
continued to cause concern. The reasons for these possible
failures include the following:
a) challenge with virulent viruses before the development of
vaccinal immunity
b) interference with the development of immunity by the
maternal antibodies
c) improper use of the vaccine
d) the use of a non-protective vaccine strain.
Vaccinating alternate generations with different types of
vaccines can reduce the effects of interfering passive
antibodies. Early exposure to MDV can be significantly
prevented by improved hygiene and biosecurity measures.
Despite the success achieved by vaccines in controlling MD,
the continuous evolution of MDV strains towards greater
virulence leading to the emergence of vv and vv+ pathotypes
of MDV is threatening to pose problems in the future (45).
The development of more effective vaccines through
recombinant DNA technology (33), and the use of
immunomodulatory approaches to enhance the response to
vaccines should improve vaccination strategies in the future.
Selectio n fo r geneti c resistanc e
Genetic resistance to MD is well documented, and susceptible
and resistant lines can be developed by progeny testing,
selection from survivors of MD challenge, or blood typing.
Two distinct genetic loci that play a major role in controlling
resistance have been identified. The best characterised
association is the one between the chicken major
histocompatibility complex (MHC) and resistance to MD, the
most notable being the association with the B 2 1
allele. This
association develops early in life and is accompanied by
reduced numbers of infected T-cells. A second type of
resistance associated with non-MHC genes is provided by the
observation that RPL (Regional Poultry Laboratory) line 6 and
7 chickens, which are both homozygous for the same MHC Rev. sci. tech. Off. int. Epiz., 19 (2) 551
allele, differ markedly in MD susceptibility. Mapping of genes
associated with such resistance is in progress and evidence
suggests that the NK region within chromosome 1 contains a
resistance gene, which has been designated MDV1 (5). As
aditional tools for selection for genetic resistance become
available, the opportunities for genetic selection against MD
will be extended.
Hygiene measures
The use of vaccines should never be an excuse for poor
management or lack of biosecurity measures. Removal of used
litter and disinfection of buildings are important aspects of
disease control, especially in view of the possibility of
selection for pathogens with increased virulence.
Furthermore, placing chicks in an environment heavily
contaminated with virus, before solid immunity can be
developed, can lead to vaccination breaks. Strict biosecurity is
also necessary to prevent the introduction of new MDV strains
onto a farm.
Marek's disease is a lymphoproliferative and neuropathic
disease of domestic chickens, and less commonly, turkeys and
quails, caused by a highly contagious, cell-associated,
oncogenic herpesvirus (7). As a disease occurring world-wide,
with increasing reports of vaccination failures and emergence 546 Rev. sci. tech Off. int. Epiz., 19 (2)
of more virulent pathotypes, MD poses a severe threat to the
poultry industry. Developing strategies for the control of MD
remains a significant challenge.
The pathogenesis of MD is complex. The infection is thought
to be transmitted by the respiratory route from the inhalation
of infected dust in poultry houses. Although the very early
events in the disease are not yet clear, the pattern of events
after infection with an oncogenic MDV in susceptible birds
can be divided into the following stages:
a) early cytolytic infection
b) latent infection
c) late cytolytic infection with immunosuppression
d) neoplastic transformation (6).
Marek's disease virus is a lymphotropic virus and targets
lymphocytes, the principal cells of the immune system.
B-lymphocytes, the cells of the antibody-forming arm of the
immune system, are first targeted by the virus in a lytic
infection. Following this, cytolytic infection occurs in the
activated T-lymphocytes that are involved in cell-mediated
immune responses. These early cytolytic events result in
atrophic changes in the bursa of Fabricius and thymus,
leading to severe debilitation of the immune system and
marked immunosuppression. The cell-associated viraemia
that develops during this period is believed to be the route by
which the virus spreads throughout the body, including the
feather follicle epithelium, the only site where a fully
productive infection occurs which allows shedding of the
virus into the environment. After the early cytolytic phase, the
infection switches to a latent phase in the infected T cells, and
the regressive changes in the lymphoid organs start resolving,
largely restoring the architecture of these lymphoid organs.
Following this, some of the latently infected T cells become
targets for neoplastic transformation resulting in
lymphomatous lesions in various visceral organs. Due to the
complex nature of the pathogenesis with varying periods of
latency, the incubation period of MD from the point of
infection to the onset of clinical disease can vary from a few
weeks to several months.
Generally, four different clinical forms of the disease are
recognised in flocks infected with MDV, as follows:
a) the classical or neural form, where a large proportion of
the birds show signs of paresis or paralysis involving the legs,
wings and sometimes the neck. These cases, also referred to as
'fowl paralysis' or 'range paralysis', are usually seen in birds of
two to twelve months of age;
b) the acute form, a more virulent form of the disease where
lymphomatous lesions of various organs develop and high
mortality occurs in the affected flocks. Birds as young as six
weeks can be affected, with losses commonly occurring
between three and six months. Involvement of the eyes and
nerves as well as lymphomatous lesion of the skin is also
evident in some cases. Visceral and skin lesions due to MD
are important causes of carcass condemnation in
slaughterhouses;
c) transient paralysis, an uncommon condition in flocks
infected with MDV, usually occurring between five and
eighteen weeks of age. This is an encephalitic expression of
infection characterised by sudden onset of paralytic
symptoms that often only last for approximately 24 h to 48 h,
although in some instances death can occur;
d) acute mortality syndrome, a form of the disease observed
more recently, where the affected birds die with an early acute
cytolytic disease well before the onset of lymphomas. The
affected birds show characteristic atrophy of the bursa of
Fabricius and thymus. This form of the disease is thought to
be due to infection with highly virulent pathotypes of the
virus.
Aetiology
Viru s structur e an d replicatio n
The isolation of cell-associated herpesvirus from MD tumours
in the late 1960s (8) was an important historical landmark
which led to an improved understanding of the disease and
development of effective vaccines. Due to the lymphotropic
nature of the virus, MDV was originally classified as a
gammaherpesvirus together with Epstein-Barr virus, and the
oncogenic herpesviruses of non-human primates, herpesvirus
saimirí and herpesvirus ateles. However, on the basis of the
genomic organisation, MDV is currently classified together
with alphaherpesviruses such as the herpes simplex vims
(HSV) in the family Herpesviridae. The deoxyribonucleic acid
(DNA) of MDV is a linear double-stranded molecule of
approximately 170 kilobases, consisting of a unique long
region (UL) flanked by a set of inverted repeat (TRL
and IRL )
regions and a unique short region (US) flanked by another set
of inverted repeat regions (IRS
and TRS ) (34). Thus, the
genomic structure of MDV from left to right can be described
as TRL-UL-IRL-IRS-US-TRS and is similar to that of other
alphaherpesviruses. The viral genomes in the infected cells are
maintained either as circular episomes or as integrated forms.
The viral genome has the capacity to encode at least seventy
proteins, sixty of which have counterparts in HSV, including
structural proteins, metabolic enzymes and transactivating
proteins such as VP 16 and ICP4 (34). However, at least ten
MDV genes have no homologues in other herpesviruses.
Similar to those of other herpesviruses, MDV genes also
belong to three kinetic classes of immediate early, early and
late genes, based on the requirements for viral protein
synthesis and DNA replication. Compared to the extensive
expression of genes, during the lytic infection, the
transcription in latently infected and transformed cells has
been largely restricted to the repeat regions of the MDV
genome. Some of the important genes recognised within the
repeat regions that could potentially be associated with
transformation include the BamHI-H family transcripts, pp38,
ICP4 sense and antisense ribonucleic acid (RNA) transcripts,
and the meq gene. fíev, sci. tech. Off. int. Epiz., 19 (2| 547
The main types of interaction that occur between the virus
and the cell in MDV infection include the following:
a) a semiproductive infection similar to that which occurs in
vivo in lymphoid organs and in vitro in cultured cells which
results in the production of non-enveloped virions
b) a fully productive infection which occurs in the feather
follicle epithelium with production of infectious enveloped
virions
c) a non-productive infection which is commonly seen in
tumours and lymphoblastoid cell lines where the viral
genome is not expressed or is expressed to a limited extent
only.
Marek's disease virus serotypes and pathotypes
The first isolation of MDV in 1967 was followed by the
description of a number of isolates from different parts of the
world. Subsequently, these isolates where divided into three
distinct serotypes, as follows:
a) serotype 1, which includes all the pathogenic or oncogenic
strains of MDV in addition to the attenuated strains of these
viruses
b) serotype 2, which includes naturally non-pathogenic
strains of MDV
c) serotype 3, which includes the herpesvirus of turkeys
(HVT), the non-oncogenic MDV-related virus, isolated from
turkeys.
In addition to differences in biological properties, these
serotypes can also be distinguished by serological methods
using polyclonal and monoclonal antibodies, DNA and
polypeptide analysis as well as by the polymerase chain
reaction (PCR).
A large diversity exists within serotype 1 concerning the
oncogenic potential, with strains varying from highly to
mildly oncogenic. Recently, serotype 1 MDV strains have
been further classified on the basis of the ability to induce MD
lesions in vaccinated chickens. Strains are classified as mild
(mMDV), virulent (vMDV), very virulent (vvMDV) and very
virulent + (w+MDV) pathotypes (Table I). The emergence of
these pathotypes is thought to represent a continuous
evolution of MDV towards greater virulence. Some of these
pathotypes show an increased propensity to produce acute
Table I
Serotypes and pathotypes of Marek's disease virus
Serotype Pathotype Representative strains
Mild (mMDV) HPRS-B14, CU2, Conn-A
Virulent (vMDV) HPRS-16, JM, GA
Very virulent (wMDV) RB1B, ALA-8, Md5, Md11
Very virulent + (w+MDV) 61 OA,648A
Non-oncogenic SB-1, HPRS-24.301B/1
Non-oncogenic HVT-FC126, HPRS-26
cytolytic disease with atrophic changes in the lymphoid
organs, the severity of which directly correlates with the
virulence.
Epidemiology
Prevalence of infection and disease
Marek's disease virus infection mainly occurs in domestic
chickens and is ubiquitous among poultry populations
throughout the world. The infection in other species is rare,
but occasionally the disease occurs in turkeys and quails. In
commercial chicken houses, where the infection is rampant,
virtually all birds become infected, commonly within the first
few weeks of life, although on occasions infection may be
delayed. Because of the prevalence of serotype 1 viruses of
varying pathogenicity and of non-pathogenic serotype 2 in the
poultry house environment, birds can be infected with more
than one MDV strain. Evidence suggests that the frequency of
isolation of non-pathogenic viruses becomes higher as the age
of the birds increases. Natural infection by non-pathogenic
strains of MDV can provide immunity to subsequent infecüon
by a virulent strain.
Transmission of infection
The transmission of MDV occurs by direct or indirect contact,
apparently by the airborne route. The epithelial cells in the
keratinising layer of the feather follicle replicate fully
infectious virus, and serve as a source of contamination of the
environment. The shedding of the infected material occurs
approximately two to four weeks after infection, prior to the
appearance of the clinical disease, and can continue
throughout the life of the bird. The virus associated with
feather debris and dander found in dust in the contaminated
poultry house can remain infectious for several months.
Although the inhalation of infected dust from poultry houses
remains the most common route of disease spread, other less
common mechanisms of indirect transmission, such as those
involving darkling beetles (Alphitobius diaperinus), could also
play minor roles in transmission. However, no evidence exists
to suggest that vertical transmission of MDV occurs through
the egg.
Flock infection
Because of the ubiquitous nature of the infection and the
ability to survive for long periods outside the host, flock
infections usually occur early in the life of a bird. In addition,
in most flocks, the hatched chicks usually have
maternally-derived antibodies. This antibody disappears in
most chickens by three to four weeks of age. The rate of the
spread of MD within a flock can vary greatly and depends on,
among several factors, the level of initial exposure and the
concentration of susceptible birds. A number of stress factors,
including those from handling, change of housing and
vaccination, are thought to increase the disease incidence. The
existence of genetic resistance to MD among chickens has
long been recognised and the genetic constitution of the flock
influences the outcome of MDV infection. The outcome of
infection is also influenced by sex, as females are usually more
susceptible to the development of tumours. 548 Rev. sci. tech. Off. int. Epiz., 19 (2|
Diagnostic methods
Diagnostic procedures for avian tumour viruses include both
pathological and virological methods. Pathological diagnosis
identifies the nature of the tumour that is causing mortality,
whereas virological diagnosis identifies viruses that are
present in a bird or flock. As MDV, ALV and REV occur
commonly, virological diagnosis does not necessarily establish
the cause of the tumour. Nevertheless, histopathological
identification of a tumour often determines the likely cause.
However, in some cases, the presence of an infection in a flock
may need to be established in the absence of tumour
mortality.
Pathological diagnosis
The main gross and histopathological features of the
neoplasms under review are summarised in Table II. In
general, while gross appearance can provide indications of the
nature of the neoplasm, histopathological diagnosis is
essential for accurate diagnosis. Histopathological diagnosis
requires tumour material from birds which have died very
recently and from several cases from an affected flock; this
material should be placed in fixative. For the diagnosis of MD,
the most useful set of tissues to collect include the liver,
spleen, bursa of Fabricius, thymus, heart, proventriculus,
kidney, gonads, nerves, skin and other gross tumour tissues.
Although clinical signs associated with MD can occur in
chickens from four weeks of age, signs are most frequently
seen between twelve and twenty-four weeks of age, and
sometimes later. Significant diagnostic features of the classical
and acute forms of MD are described below.
Classical form
In the classical form of the disease, with mainly neural
involvement, mortality rarely exceeds 10%-15%, occurring
over a few weeks or many months. The most common clinical
sign is partial or complete paralysis of the legs and wings. The
characteristic pathological lesion is the enlargement of one or
more of the peripheral nerves. The most commonly affected
nerves that are easily seen on post-mortem examination are
the brachial and sciatic plexus and nerve trunks, coeliac
plexus, abdominal vagus and intercostal nerves. The affected
nerves are grossly enlarged, and often two or three times the
normal thickness. The normal cross-striated and glistening
appearance of the nerves is lost, instead, the nerves have a
greyish or yellowish appearance and are oedematous.
Lymphomas are sometimes present in this form of the disease,
most frequently as small, soft grey tumours in the ovary,
kidney, heart, liver and other tissues.
Acute form
In the acute form of the disease, where formation of
lymphomas in the visceral organs usually occurs, the
incidence of the disease is frequently between 10% and 30%,
and in major outbreaks can reach 70%. Mortality can increase
rapidly over a few weeks and then cease, or can continue at a
steady or falling rate over several months. The typical lesion in
this form of the disease is the widespread, diffuse
lymphomatous involvement of visceral organs such as the
liver, spleen, ovary, kidney, heart and proventriculus.
Lymphomas are also occasionally seen in the skin around the
feather follicles and in the skeletal muscles. Affected birds may
also show involvement of the peripheral nerves similar to that
seen in the classical form. The liver enlargement in younger
Table II
Principal gross and microscopic features of importance in the differential diagnosis of the leukoses and Marek's disease lymphoma
Feature Lymphoid leukosis Erythroid leukosis Myeloid leukosis
(myeloblastosis)
liver
Spleen
Bursa of Fabricius
Bone marrow
Blood
Cytology and
histopathology
Other organs and
tissues often grossly
involved
Greatly enlarged; diffuse,
miliary or nodular tumours;
moderately firm
Usually enlarged; diffuse,
miliary or nodular tumours;
soft
Usually enlarged; nodular
tumours
Often tumorous; diffuse or
focal
Occasionally lymphoblastic
leukaemia
lymphoblasts; mainly
extravascular infiltrations
Moderately enlarged;
diffuse infiltration;
cherry-red colour; soft
Often enlarged; cherry-red;
smooth; very soft
No changes
Semi-liquid; cherry-red
Kidneys, ovary
Erythroblastic leukaemia;
immature erythrocytes;
anaemia; thin buffy coat
Erythroblasts;
intravascular
Kidneys; may be
haemorrhages in muscles
Myeloid leukosis
(myelocytomatosis)
Marek's disease
lymphoma
Greatly enlarged; diffuse
infiltration; mottled;
granular surface; firm
Often enlarged; diffuse
tumour; mottled; smooth;
soft
Sometimes tumorous
Diffuse, reddish-grey
tumour infiltration
Myeloblastic leukaemia;
thick buffy coat
Myeloblasts in
intravascular and
extravascular locations
Kidneys, ovary
Often yellowish white
nodular or diffuse tumours
Often nodular or diffuse
tumours
No changes
Usually diffuse
yellowish-grey tumour
infiltration
Myelocytic leukaemia;
thick buffy coat
Myelocytes in
intravascular and
extravascular locations
Kidneys, ovary, thymus,
surface of bones (sternum,
ribs, skull)
May be moderately to
greatly enlarged; miliary
or nodular tumours; firm
Often atrophic; may be
enlarged; usually diffuse
tumours
May be diffusely
enlarged
No changes
May be lymphocytosis or
lymphocytic leukaemia
Pleomorphic, sometimes
blastic, lymphoid cells in
perivascular locations
Nerves, kidneys, ovary,
proventriculus, heart,
muscle, skin, iris Rev. sci. tech. Off. int. Epiz., 19 (2) 549
birds is usually moderate compared to that in adult birds
where the liver is greatly enlarged and the gross appearance is
very similar to that seen in lymphoid leukosis. Nerve lesions
are less frequent in adult birds.
Features common to the acute and classical forms
The peripheral nerves in both forms of the disease are affected
by proliferative, inflammatory or minor infiltrative changes
that are termed A-, B- and C-type lesions respectively. The
A-type lesion consists of infiltration by proliferating
lymphoblasts, large, medium and small lymphocytes, and
macrophages, and appears to be neoplastic in nature. Nerves
with B-type lesions show oedema and infiltration by small
lymphocytes and plasma cells with Schwann cell
proliferation; in this case the lesion appears to be
inflammatory. 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. Demyelination, which is frequently seen
in nerves showing A- and B-type lesions is thought to be
principally responsible for the paralytic symptoms.
Lymphomas seen in the visceral organs and other tissues are
similar cytologically to the lymphoproliferations in the nerve
A-type lesions. The lymphoid cells are usually of the mixed
type, with a preponderance of small and medium
lymphocytes. However, large lymphocytes and lymphoblasts
may occasionally predominate, especially in adult birds. The
polymorphic population of the lymphoid cells, as seen in
impression smears or tissue sections of MD lymphomas, is an
important feature in differentiating MD from lymphoid
leukosis.
Virologica l diagnosi s
Isolation of Marek's disease virus
Marek's disease virus infection in a flock can be detected by
isolating the virus from the infected tissues. Materials,
commonly used for the isolation of the virus are buffy coat
cells from heparinised blood samples, or suspensions of
lymphoma and spleen cells. As Marek's disease virus is highly
cell-associated, the suspensions must contain viable cells.
These cell suspensions are inoculated into monolayer cultures
of chick kidney cells or duck embryo fibroblasts. Chicken
embryo fibroblasts (CEF), although less sensitive for the
primary isolation of serotype 1 MDV, can be used to isolate
serotypes 2 and 3. Evidence of MDV replication in the culture
can be seen as plaques which appear in three to four days.
Less commonly, feather tips, from which cell-free MDV can be
extracted, are also used for virus isolation.
Characterisation of Marek's disease virus serotypes
Serotypes of MDV isolated in culture can be differentiated
fairly accurately on the basis of the time of appearance, rate of
development and morphology of the plaques. Plaques of HVT
usually appear earlier and are larger than serotype 1 plaques,
whereas serotype 2 plaques appear later, and are smaller than
the serotype 1 plaques. The serotype specificity of the plaques
can also be confirmed by using specific antibodies in
immunological tests. Recently, PCR tests have been developed
which allow the differentiation of oncogenic strains of
serotype 1 virus, and strains of serotypes 2 and 3 (3, 35).
Detection of virus infection in tissues
The methods commonly employed for the detection of
virus in tissues include immunofluorescence and
immunohistochemical methods using polyclonal and
monoclonal antibodies, in situ hybridisation using
MDV-specific nucleic acid probes, PCR and electron
microscopy.
Serological tests
The presence of antibodies to MDV in birds from
approximately four weeks of age is an indication of infection.
Antibodies detected in birds before this age are likely to
represent maternally derived antibodies and are not
considered evidence of active infection. Although no
serological test has been prescribed for the detection of
MDV-specific antibodies, the agar gel immunodiffusion
(AGID) test is usually employed for this purpose. The antigen
used in the test is either disrupted MDV-infected tissue
culture cells, extract of the feather tips or skin containing
feather tracts from infected chickens. The viruses, antigens
and antisera are usually available from OIE Reference
Laboratories for MD. A modification of the AGID test to detect
MDV antigen in the feather tips by reactivity with MDV
hyperimmune serum is also used. Other serological tests,
such as the indirect immunofluorescence test, enzyme-linked
immunosorbent assay (ELISA) and virus neutralisation (VN)
have been described, but are used mostly for research
purposes rather than for routine diagnosis.
Surveillance
Marek's disease is a ubiquitous virus infection occurring in
commercial poultry operations world-wide. Because the virus
is able to survive for long periods both in the host and in the
environment of the poultry house, the disease is unlikely to be
completely eradicated. Control of the disease therefore
depends essentially on the use of successful vaccination
strategies. The vaccine strains are non-pathogenic viruses that
establish a permanent infection in the vaccinated birds. The
vaccines are capable of preventing lymphoma formation and
clinical disease, but do not prevent superinfection by
pathogenic MDV strains. Hence, surveillance for MD should
verify that the birds do not suffer from clinical disease and are
properly vaccinated. To achieve this, various tests mentioned
under the section on diagnosis can be applied. In addition,
importing countries should require the exporter to provide
international animal health certificates (24) to ensure that
imported chickens and day-old chicks are free from clinical
disease and are vaccinated against MD and that the hatching
eggs originate from a vaccinated source and have been
shipped in clean unused packages. As MDV is not vertically
transmitted, these measures are sufficient to prevent
introduction of infection through day-old chicks or hatching
eggs. However, vaccination and freedom from clinical disease 550 Rev. sci. tech. Off. int. Epiz.. 19(2)
would not exclude the possibility of introduction of
pathogenic MDV isolates when importing older birds.
Marek's disease virus could persist in the skin (in feather
follicles) of imported carcasses and portions, and in feathers,
but is unlikely to be present in poultry meat and eggs. Live
poultry should not be exposed to such potentially infected
materials. Heat treatment (cooking) will destroy MDV.
Public health implications
The identification of MDV and the widespread use of live
vaccines against MD have raised some concerns that exposure
to MDV from the environment or from consumption of
poultry meat could be a cause of cancer in humans. However,
a large body of evidence in both avian and human virology,
serology, pathology and epidemiology strongly supports the
conclusion that no aetiologic relationship exists between avian
herpesviruses and human cancer (31). Recently, there has
been speculation that MDV infection might be associated with
multiple sclerosis (MS), principally based on serological
findings. However, in detailed studies using sensitive methods
such as PCR, no MDV-related sequences could be detected in
the DNA of patients with MS, ruling out the involvement of
MDV (16).
Prevention and control methods
Vaccinatio n
The development of vaccines for the control of MD was a
significant landmark both in avian medicine and basic cancer
research, as this was the first example of a neoplastic disease
controlled by the use of a vaccine. Currently and at least for
the foreseeable future, vaccination represents the principal
strategy for the prevention and control of MD, although other
approaches, such as increasing the genetic resistance of birds
and improving hygiene and biosecurity, should form valuable
adjuncts for control programmes.
Live virus vaccines, used since 1970, remain the basis of
disease control programmes. These are usually administered
to day-old chicks at hatching to provide protection against the
natural challenge the chicks are exposed to early in life from
the infected poultry house environment. With the
introduction of in ovo immunisation methods, an increasing
number of birds are vaccinated by this route. Marek's disease
vaccines are highly effective, often achieving over 90%
protection under commercial conditions. Vaccines available
vary from country to country. In the United States of America
(USA), strains of MDV belonging to all three serotypes have
been licensed as vaccines (Table III).
In many countries, HVT continues to be widely used as a
monovalent product because it is inexpensive, available as
cell-free and cell-associated forms, and effective when the field
exposure is not severe. The HVT and SB-1 strains comprised
the first commercial bivalent vaccine based on the protective
synergism demonstrated between serotypes 2 and 3 viruses.
The CV1988 strain Rispens vaccines and modified versions are
Table III
Strains of Marek's disease virus licensed to be used as vaccines in the
United States of America
Vaccine strain Serotype
FC126 (HVT) 3
SB-1 2
301B/1 2
CVI988 clone C 1
CVI988/C/RB 1
CVI988 (Rispens) 1
R2/23 (Md 11/75) 1
widely used in many countries and appear to be effective
against some of the w+MDV pathotypes.
Although MD vaccines have been successful in controlling
major losses from the disease, threat of vaccine failure has
continued to cause concern. The reasons for these possible
failures include the following:
a) challenge with virulent viruses before the development of
vaccinal immunity
b) interference with the development of immunity by the
maternal antibodies
c) improper use of the vaccine
d) the use of a non-protective vaccine strain.
Vaccinating alternate generations with different types of
vaccines can reduce the effects of interfering passive
antibodies. Early exposure to MDV can be significantly
prevented by improved hygiene and biosecurity measures.
Despite the success achieved by vaccines in controlling MD,
the continuous evolution of MDV strains towards greater
virulence leading to the emergence of vv and vv+ pathotypes
of MDV is threatening to pose problems in the future (45).
The development of more effective vaccines through
recombinant DNA technology (33), and the use of
immunomodulatory approaches to enhance the response to
vaccines should improve vaccination strategies in the future.
Selectio n fo r geneti c resistanc e
Genetic resistance to MD is well documented, and susceptible
and resistant lines can be developed by progeny testing,
selection from survivors of MD challenge, or blood typing.
Two distinct genetic loci that play a major role in controlling
resistance have been identified. The best characterised
association is the one between the chicken major
histocompatibility complex (MHC) and resistance to MD, the
most notable being the association with the B 2 1
allele. This
association develops early in life and is accompanied by
reduced numbers of infected T-cells. A second type of
resistance associated with non-MHC genes is provided by the
observation that RPL (Regional Poultry Laboratory) line 6 and
7 chickens, which are both homozygous for the same MHC Rev. sci. tech. Off. int. Epiz., 19 (2) 551
allele, differ markedly in MD susceptibility. Mapping of genes
associated with such resistance is in progress and evidence
suggests that the NK region within chromosome 1 contains a
resistance gene, which has been designated MDV1 (5). As
aditional tools for selection for genetic resistance become
available, the opportunities for genetic selection against MD
will be extended.
Hygiene measures
The use of vaccines should never be an excuse for poor
management or lack of biosecurity measures. Removal of used
litter and disinfection of buildings are important aspects of
disease control, especially in view of the possibility of
selection for pathogens with increased virulence.
Furthermore, placing chicks in an environment heavily
contaminated with virus, before solid immunity can be
developed, can lead to vaccination breaks. Strict biosecurity is
also necessary to prevent the introduction of new MDV strains
onto a farm.
The fluid from Olivia's leg had a LOT of aplastic lymphocytes and other inflammatory cells. It appears to be a peripheral nerve tumor. Probably Marek's. I was really hoping she may have been lucky enough to have developed a resistance since she is going to be 2 yrs old.
In less than 2 yrs, this horrible disease has killed all but one of my chickens.
Well...off to give her Metacam, feed her as much scratch/meal worms as she wants and give her some cuddles. Poor girl...
In less than 2 yrs, this horrible disease has killed all but one of my chickens.
Well...off to give her Metacam, feed her as much scratch/meal worms as she wants and give her some cuddles. Poor girl...
OMG!!!! You have sure suffered alot of birds. 2 years old with a tumor. My first few demises were around 2 years old before I knew why. Then I lost a whole batch of chicks one by one to paralysis and gasping.The fluid from Olivia's leg had a LOT of aplastic lymphocytes and other inflammatory cells. It appears to be a peripheral nerve tumor. Probably Marek's. I was really hoping she may have been lucky enough to have developed a resistance since she is going to be 2 yrs old.
In less than 2 yrs, this horrible disease has killed all but one of my chickens.
Well...off to give her Metacam, feed her as much scratch/meal worms as she wants and give her some cuddles. Poor girl...
Know that you are not alone.
The fluid from Olivia's leg had a LOT of aplastic lymphocytes and other inflammatory cells. It appears to be a peripheral nerve tumor. Probably Marek's. I was really hoping she may have been lucky enough to have developed a resistance since she is going to be 2 yrs old.
In less than 2 yrs, this horrible disease has killed all but one of my chickens.
Well...off to give her Metacam, feed her as much scratch/meal worms as she wants and give her some cuddles. Poor girl...
so sorry to hear about olivia's fluid biopsy and probable diagnosis. thinking of you and hoping today was a better day.
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