The disease is caused by a fungus, Aspergillus fumigatus.
Transmission
Transmission is by inhalation of fungus spores from contaminated litter
(e.g. wood shavings) or contaminated feed.
Hatcheries may also contribute to infection of chicks.
Species affected
Young chicks are very susceptible, older chickens are more resistant
to infection.
Turkey poults, pheasant chicks, quail chicks, ducklings, and goslings
may also become infected.
Clinical signs
Infected chicks are depressed and thirsty.
Gasping and rapid breathing ("pump handle breathing")
can be observed.
Mortality is variable, from 5 to 50%.
Gross lesions involve the lungs and airsacs primarily.
Yellow-white pin-point lesions can be found.
Sometimes all body cavities are filled with small yellow-green
granular fungus growth.
Diagnosis
The presence of Aspergilllus fumigatus can be identified microscopically
or sometimes even with the naked eye in the air passages of the lungs,
in the air sacs or in lesions of the abdominal cavity.
Treatment and control
There is no treatment for aspergillosis.
Affected chicks should be removed and destroyed.
Strict hygiene in breeder and hatchery management is necessary.
Choice of litter material is important so that no spore-bearing wood
shavings are used.
Main transmission is by infected premises, where day-old chicks will
become infected by the oral and respiratory routes.
Dander from feather follicles of MD-infected chickens can remain infectious
for more than a year.
Young chicks are particularly susceptible to horizontal transmission.
Susceptibility decreases rapidly after the first few days of age.
Species affected
The domestic fowl.
Clinical signs
MD eefected liver
Leg paralysis
Infected birds show weight loss. or may exhibit some form of paralysis.
Mortality varies from 5 to 50% in unvaccinated birds.
The classical form (paralysis) with leg nerve involvement causes a
bird to lie on its side with one leg stretched forward and the other
backward.
When the gizzard nerve is involved, the birds will have a very small
gizzard and intestines and will waste away.
Mortality usually occurs between 10 and 20 weeks of age.
Diagnosis
The presence of tumours in liver, spleen, kidneys, lungs, ovary, muscles,
or other tissues is indicative of MD, but they can also be indicative
of lymphoid leucosis.
However, nerve involvement, either grossly (swelling of leg, wing
or other nerves) or microscopically, is typical of MD.
Eye involvement can be visible as an irregular constriction of the
iris (ocular lymphomatosis).
Skin involvement (skin leucosis) often consists of tumours of feather
follicles or in between follicles.
Skin leucosis is a reason for broiler condemnation in certain parts
of the world.
A proper diagnosis to differentiate MD from LLrequires histological
examination.
Treatment and control
Intra mascular
Intra nasal
Vaccination of day-old chicks is an effective mean of control.
It has been demonstrated that MD vaccine only prevents the appearance
of Marek's disease tumours and paralysis, it does not prevent the birds
from becoming infected with MD -virus.
It is therefore of major importance to maintain high hygienic and
sanitary measures by good management to avoid early exposure of young
chickens.
Presence of pathogenic M.D. virus at the farm is the biggest etiologic
factor of M.D The infection is followed by a quick and heavy multiplication
of the virus in the defense organs of the body such as bursa, thymus,
spleen etc.
This explains why M.D. is an immunosuppressive disease. Then a stage
comes when multiplication of virus decreases and now we can see formation
of tumors and affection of the nerves.
Factors of 2nd order
Genetics
Several lines of chickens with genetic resistance to MD have been
selected and maintained experimentally.
Spencer et al (1976) found genetically resistant chickens were protected
by vaccination to a greater extent than more susceptible ones.
Breeding for genetic resistance may be a valuable adjunct to immunization
for control of MD.
Age
Prevention of early exposure of vaccinated birds with virulent M.D
virus (MDV) enhances the efficacy of the vaccine.
If one can achieve his, he will definitely emerge victorious over
M.D.
Factors of 3rd order
Sex
It is interesting to know that females are more sensitive to M.D.
than males. This is indicated by a shorter duration incubation period,
higher frequency of clinical manifestations and larger no.of females
with tumors.
Maternal Antibodies
The presence of maternal antibodies (MABs) significantly impedes the
multiplication of MDV during the first stage of disease.
The degree of this procection depends on the antibody titre. Maternal
antibodies also impede propagation of MD vaccine virus.
Factors of 4th order
Viral infections
Chicken anaemia agent (CAA) and Reo virus can predispose the birds
to or aggravate MD.
Bacterial infections
Mycoplasma synovie can act as a predisposing factor for MD
Factors of 5th order
Aflatoxin induced immunosuppression can make the birds prone to MD.
Sanitation and biosecurity play very important role in the occurrence
of Marek's disease.
EPZOOTIOLOGY
All strains of MDV develop in an infectious form in the cells of feather
follicles. Therefore, the no.of produced and released MD viruses increase
during the chicks, a young animal and layer's moult.
From the feather follicles, MDV reach the air and get settled in
the dust. In dust, the effectively of MDV is preserved for a very long
time.
The dust usually concentrates on the ceiling and walls but also in
the ventilation of the chicken house. A through mechanical removal and
an innocuous disposal (heating) of the infectious dust are important
measures against further infections.
Various insects which live in the litter as for ext. black lesser
mealworm is a carrier of MDV. If these insects (beetles) are eaten by
chickens, they might be infected.
The most significant way of MDV transmission is the inhalation of
infected dust. Any alternate ways of infection (mentioned below) which
are common with other viral diseases, are meaningless for MD.
Vertical spread (Vertical via the hatching eggs)
Genital spread (during the mating of a male and female)
Oral communication (through feed or drinking water)
PREVENTION
The occurrence of Marek's disease can be successfully prevented if
one carefully studies the following points:
Preventing the pathogen's introduction
MDV strains are never vertically transmitted (i.e. via the hatching
eggs). The only source for infection for chicks and chickens of all
age groups is dust containing the virus.
They get infected in an environment which is contaminated with MDV
Cleaning and disinfecting can decontaminate the chicken houses.
The interested readers can obtain the protocol of disaffection program
from our office. The introduction and spreading of MDVs in farms can
be effectively and continuously prevented by appropriate architectural
measures.
This method is used by the producers of specific pathogen free (S.P.F)
hatching eggs. SPF flocks are kept in positive pressurized houses having
filters to nullify possibility of entry of any microorganisms.
Proper vaccination
Faulty application of the vaccine such as dilution mistakes during
the preparation, faults in the technique of injection, too long times
of storage or too high ambient temperate of reconstituted vaccines.
In the modern hatchery practices possibility of such lapses is very
minimum. · Too low content of viruses in the vaccine. The protection
by inoculation depends on the dose of injected viruses.
Ventri's MD vaccine contains minimum 4000 to 5000 P.F. US/ dose as
against British pharmacopea (Vet), standards of 1500 PFU/close. A higher
content of viruses does not lead to any significant improved protection.
In case of severely affected farms, a booster dose of MD vaccine may
be tried on 18th day. There are some reports of encouraging outcome
with such practice of MD booster vaccination.
If an infection with virulent MDV occurs simultaneously with or a
few days after the vaccination, there can be no sufficient protection
from the vaccine. In our opinion, this applies to all available vaccines.
The older the chicks are at the time of infection by MDV, the lower
the rate of spread of field strain (pathogenic) is. This can be achieved
only with the help of accurate cleaning / disinfection and strict biosecurity
measures, for first 15 days post hatchery vaccination. ·
As it is known of other live virus vaccines, the contamination of
a vaccine can lead to damage to the inoculated chick by concurrently
present microorganisms. This explains the need of accurate sterilization
of injection appliances before being used.
The presence of high maternal antibodies can also impede the development
of immunity in the vaccinated chicks.
In short, occurrence of MD cases despite of vaccination can be attributed
to
Improper sanitation and poor biosecurity.
Early exposure to virulent MDV
High maternal antibody
Poor vaccination procedures
In 1982, two American scientists found that vaccination of 18-day-old
embryos accelerated development of protective immunity by several days
and proposed this technique for controlling detrimental effects of early
exposure to virulent MDV. This technique is named as: In ovo Mark's
vaccination". The in ovo method eliminated the need for manual post-hatch
inoculation of day old chicks and result in healthier chicks due to
earlier introduction of disease preventing vaccines and less stress
to the chicks. Tri-bio laboratories, U.S.A. (collaborator of Ventri
biologicals Divn) have already produce one such in ovo MD vaccine.
Prevention of other infections
clinically healthy chicken only can develop protective immunity after
the vaccination. This means that in order to have a successful program
to control MD., other pathogenic agents must be eliminated. Certain
infections which can make the bird susceptible to Mark's disease are
mentioned below:
Certain species of avian mycoplasma enchase the multiplication of
Marek's disease virus in cell cultures according to Dr. Kaleta Gieban,
an eminent European scientist.
Chicken Anaemia Agent (CAA)- Experimental dual infections with CAA
and subclinical doses of MDV caused enhancement of MDV antigen shedding
to feather follicles.
Nutritional Prophylakis
Aflatokins increase susceptibility of poultry to Marek's disease.
The mechanism is through depression of the cell-mediated immune response.
Certain vitamins like vitamin A, C, E, B6, H etc., are very essential
for the development of lymphoid (defense) organs of the body like bursa,
thymus, spleen, liver etc., one should always use the vitamins which
are procured from a dependable source only because the use of substandard
vitamins may lead to imunosuppression.
Environmental factors
According to a study undertaken in hot climates successively for two
years by Dr. Raghard Al-Khoja, the heat stress can affect the efficiency
of immunity build up against Marek's disease. He found that the chicks
hatched during summer (i.e March to June) are more susceptible to MDV
infection. So one should take extra care during summer to prevent MD
incidences.
Mark's disease vaccination is carried out during the 1st 24 hours
of a chick's life and its effectiveness is determined until the chicks
reach the age of at least six weeks. Therefore, chicks should be protected
from exposure to field (Pathogenic) MDV for atleast first 6 weeks are
even more crucial.
Only persons working on the farm and dressed in clean protective
clothing shall be admitted to the chicken houses.
THE SIGNIFIDACE OF MARK'S DISEASE
Prior to the use of vaccines, MD constituted a serious economical
threat to the poultry industry because of heavy mortality and losses.
Since vaccine does not mean full proof protection, losses still occur
but they are no longer as serious a problem.
Perhaps the greatest impact of MD is immunosuppression (impairment
of immune system) apparently caused by the damage to the bursa, thymus,
spleen, liver etc. Both humoral antibody and cell mediated immunity
can be depressed by MD. These are reflected by reduced antibody response
to a variety of vaccines and by alteration of T cell functions. MDV
infection could increase susceptibility to primary and secondary infections
with coccidia and reduced antibody response to M. sysnoviae.
In broilers, MD may exist in sub clinical form if not in clinical
form. This may lead to vaccine failure. That is why MD vaccination (at
least half dose) is recommended in day old broiler chicks.
A very resistant small virus known as CAA (Chicken Anaemia Virus)
or CIAV (Chicken Infectious Anaemia Virus) causes infectious Anaemia.
Transmission
The major mode of transmission of Infectious Anaemia is vertical transmission
from infected breeder hens.
Horizontal transmission from bird to bird or by infected equipment,
clothing, etc. is also possible.
Clinical sings and lesions
CAA causes a syndrome in young chicks up to approximately 3 weeks
of age.
Adult birds may get infected but will not develop clinical signs.
The disease is characterized by increased mortality and anaemia associated
with atrophy of the haematopoietic tissues in the bone marrow.
Subcutaneous and intramuscular haemorrhages can be found accompanied
with atrophy of the lymphoid system.
Affected birds may show focal skin lesions (also known as blue wing
disease).
Mortality rates vary from 20% to 70%.
Affected flocks will show poor growth reflected in economic losses.
Diagnosis
The diagnosis can be based on the clinical signs and pathological
findings in affected birds.
Blood serum testing for specific CM antibodies can be carried out
(IFT, VN, etc.) Virus isolation is also possible but it is time-consuming
and expensive.
Treatment and control
No treatment is available for Infectious Anaemia.
Maternally derived antibodies can offer protection.
The induction of high maternal immunity in the progency by vaccinating
breeders is the best approach to successful CM control.
The disease is caused by an avian adenovirus (for example the Tipton
strain) and is usually simultaneously accompanied by other immunosuppressive
diseases such as Infectious Bursal Disease or Infectious Anaemia.
There are 12 known serotypes of avian adenoviruses that may be involved
in the development of this disease.
Transmission
Egg transmission is an important factor.
Horizontal transmission from bird to bird by contact with droppings.
Once the bird becomes immune, the virus can no longer be isolated
from the droppings.
Species affected
Chickens, turkeys and pheasants and possibly other birds can be affected
by avian adenovirus.
Clinical signs
Chickens with inclusion body hepatitis are affected at usually 5 to
7 weeks of age.
The birds are listless, with ruffled feathers.
Mortality is usually quite severe, up to 25% in the first 10 days
of the disease.
Internal lesions
Affected chickens have mottled livers, many with pinpoint necrotic
and haemorrhagic spots.
Pale bone marrow and, in some cases in presence of Infectious Anaemia,
gangrenous dermatitis can be seen.
Kidneys are pale and swollen.
The spleen is usually quite small (atrophy).
If Gumboro disease (Infectious Bursal Disease) has been present in
the birds, even if sub-clinical, the Bursa of Fabricius will be very
small (atrophic).
Such chickens are immune-suppressed and usually have more severe cases
of inclusion body hepatitis and/or infectious anaemia.
Mature birds do not have clinical signs of adenovirus infection, they
only start showing antibodies in their blood.
Diagnosis
Typical mottled livers with pin-point lesions, pale bone marrow and
kidneys, small spleen and bursa are good indications of the disease.
Histological examination (intranuclear inclusion bodies) of liver
and/or virus isolation are helpful means of diagnosis.
Treatment and control
No treatment exists.
Antibiotics can be used to prevent secondary bacterial infection and
possible gangrenous dermatitis.
The best method of control is to ensure adequate immunity against
other immune suppressive diseases (e.g. Infectious Bursal Disease).
Breeder chickens may be vaccinated with live vaccine, followed by
inactivated oil-emulsion vaccine application before egg production begins.
This procedure ensures adequate maternal immunity against IBD disease
in the offspring which assists in preventing inclusion Body Hepatitis.
Several different serotypes of IB virus are known to exist.
Transmission
The virus is transmitted from bird to bird through the airborne route.
The virus can also be airborne between chicken houses and even from
farm to farm.
Species affected
Only chickens are susceptible to IB virus.
Clinical signs
In young chicks IB-virus infection causes a cheesy exudate in
the bifurcation of the bronchi, thereby causing asphyxia, preceded
by severe respiratory distress ("pump handle" breathing).
In older birds IB does not cause mortality.
Respiratory signs include wet rales, gurgling, and wheezing.
Egg production will decrease dramatically, deformed eggs with wrinkled
shells will often be laid.
Internal lesions
Mucus and redness in tracheas froth in airsacs in older chickens.
In young chicks a yellow cheesy plug at the tracheal bifurcation is
indicative of IB infection.
Diagnosis
There are three main factors to be considered in order to arrive at
a diagnosis
The clinical picture including post-mortem findings in
the flock.
lsolation of the virus In the laboratory.
Rising antibody titre when the serum is tested against
a known strain of bronchitis virus.
Treatment and control
There is no treatment for Infectious Bronchitis.
Secondary bacterial infections may be prevented by, or treated with
antibiotics.
Prevention by vaccination is the best method to control.
The disease is caused by a birna virus of serotype.
Virus strains can be divided in classical and variant strains.
The virus is very stable and is difficult to eradicate from an infected
farm.
Transmission
IBD virus is very infectious and spreads easily from bird to bird
by way of droppings.
Infected clothing and equipment are means of transmission between
farms.
Species affected
Chickens and turkeys appear to be natural hosts.
Clinical signs
Clinical lBD occurs usually between 4 and 8 weeks of age.
Affected birds are listless and depressed, pale and huddling.
Mortality varies usually new cases of IBD have a mortality rate
of about 5 to 40% but can be as high as 95% depending on the pathogenicity
of the strain invalued.
In subsequent infection on the same farm, mortality is lower and eventually,
with successive attacks, there is no mortality noted.
The sub-clinical form caused by the immunosuppressive effect of the
IBD virus is now of more economic importance in that the immune system
of the bird is damaged.
In broilers this form of the disease results in bad performance with
lower weight gains and higher feed conversion ratios.
Diagnosis
In acute cases the Bursa of Fabricius is enlarged and gelatinous,
sometimes even bloody.
Muscle haemorrhages and pale kidneys can be seen.
Infection by variant strains is usually accompanied by a fast bursal
atrophy (in 24-48 hours) without the typical signs of Gumboro disease.
Also in chronic cases the bursa is smaller than normal (atrophy). The
bursa destruction is apparent on histologic examination.
The lack of white blood cells (lymphocytes) results in a reduction
in the development of immunity and decreased resistance of the birds
to other infections.
Typical signs and lesions are diagnostic of IBD.
Histopathological examination, serology and/or virus isolation are
helpful tools. IBD can be confused with sulfonamide poisoning, aflatoxicosis,
and pale bird syndrome (vitamin E deficiency).
Treatment and control
No treatment is available for IBD.
Vaccination of parent breeders and/or young chicks is the best means
of control.
The induction of a high maternal immunity in the progeny of vaccinated
breeders is the most effective approach to successful IBD control.
The underlying cause of CRD is Mycoplasma gallisepticum (Mg). The
condition is frequently triggered by respiratory viruses such as NO
and 18 and subsequently complicated by bacterial invasion.
The main agents involved in the infection are Mycoplasma gallisepticum.
Stress caused by moving the birds, by de-beaking or other operations
or other unfavourable conditions e.g. cold or bad ventilation, make
the birds more susceptible.
Transmission
The main problem is that parent birds infected with Mycoplasma gallisepticum
can transmit the organism through the egg to their offspring.
In addition, infection can occur by contact or by airborne dust or
droplets. The incubation period varies from 4 days to 3 weeks.
Species affected
Chickens and turkeys.
Clinical signs
Young chickens (broiler chicks or layer pullets) will show respiratory
distress. The birds frequently show a lack of appetite, decreased weight
gain and increased feed conversion ratios.
In adult birds the most common symptoms are sneezing, coughing and
general signs of respiratory congestion. In laying birds a drop of egg
production between 20-30% can occur.
CRD does not normally cause an alarming number of deaths. The effect
is more of a chronic nature causing reduced weight gain and feed conversion
ratios in broilers and lower egg production in breeders and layers.
In this way the overall economic loss can be very great in broilers
but less dramatic in breeders and layers.
Internallesions
A reddish inflamed trachea and/or cheesy exudates in airsacs, especially
in complicated cases (e.g. with secondary E. coli infections) are observed.
In mild Mg infections the only lesion might be slight mucus in trachea
and a cloudy or light froth in the airsacs.
Turkeys with Mg infection usually have swollen sinuses under the eyes.
Diagnosis
Diagnosis of Mg infection can be made by blood testing of chickens,
post-mortem examination and ultimately by isolating the causative Mg
organism from tracheas or airsacs of affected birds.
Differential diagnosis
Respiratory virus infection (Newcastle disease or Infectious Bronchitis)
with secondary infection (E. coli, etc.) can give similar lesions.
Treatment
Treatment of Mg-infected chickens or turkeys with suitable antibiotics
or chemotherapeutics has been found to be of economic value.
However, control by medication or vaccination and eradication of Mg
infections has been by far the most effective method of combating the
disease.
Fertile eggs from infected birds can be treated with antibiotics
such as tylosin to eliminate the Mycoplasma gallisepticum organisms.
Methods used are the injection of fertile eggs or egg dipping.
Blood serum testing of breeder chickens for Mg antibodies has become
a routine to test flocks for a Mg infection.
