1. Marek's Disease
The virus was discovered in 1907
by Jozsef Marek, a Hungarian vet and there are non-pathogenic,
mildly virulent, virulent and very virulent strains.
This is a herpes virus which gravitates towards lymphoid
tissue (lymphoid tissue is spread throughout a chicken, unlike a
mammal where it is confined mostly to lymph nodes) and also causes
demyelination of peripheral nerves (leg and wing). Various strains
of the virus have been isolated and there are two types, one which
lives in the cell and one which is cell-free and lives in the
feather follicle. The virus replicates in the host chicken's
lymphoid tissue and is shed in feather dander.
Chickens from 6 weeks of age are affected, symptoms are most
frequently seen 12-24 weeks of age with the hormonal stress of
point of lay being a classic time for the signs to appear. Older
birds can sometimes be affected if stressors (changes in weather,
food, handling, environment) are not minimised. Females are more
susceptible than males. Affected birds go lame and this can be
mistaken for a sprain or injury, often with one leg forward and one
back. The lameness worsens despite anti-inflammatory drugs and the
bird uses one or both wings order to balance itself.
Mortality is variable and depends on which of the peripheral
nerves is affected but leads to progressive spastic paralysis of
the legs and wings with the bird remaining quite bright and still
eating. Sometimes, if the neck nerves are affected, the neck can
twist around. There is an acute form where birds may die suddenly
with no symptoms and tumours may be found in the liver, gonads,
spleen, kidneys, lungs, gizzard, heart, muscle and skin.
Fig 1: A White Plymouth Rock pullet in classic
Marek's disease pose
The virus can remain viable for at least one year in feather
dander and henhouse dust. The virus is ubiquitous in poultry
worldwide. Infection in chicks occurs by inhalation and two weeks
later, the virus is shed by the infected chick in feather dander
and by oral and nasal secretions. The virus is NOT passed on
through the egg. Infected and recovered birds continue to shed the
virus for life.
Affected chickens must be culled as their welfare is severely
compromised by this disease.
Lack of response to treatment for lameness,
clinical signs of paralysis and post mortem lesions.
Fig 2: A Welsummer pullet, struggling to
Fig 3: Marek's disease post mortem: left femoral
(leg) nerve is severely thickened in comparison to the normal one
on the right
Cull any affected birds. This increases the resistance to the
disease in the surviving birds.
Vaccination is feasible, especially if Silkies or Sebrights are
kept. These are very susceptible to clinical signs of Marek's and
there would be few of these breeds seen at exhibitions if
vaccination was not used. The vaccine is administered by injection
when chicks are ideally dayold or before 3 weeks old. The
vaccine is not effective in older birds.
In other breeds, using vaccine can hide the virus and so the
whole stock gets progressively more susceptible (weaker) without
any symptoms and if birds are sold without the recipient being told
of the vaccination, the birds can pass on the virus to unvaccinated
chicks, thereby bringing the disease to a flock which may have been
free of it before.
Good biosecurity is important, quarantine any new stock for 4
weeks. Rear chicks for 2-3 months away from adult feather dander if
adult birds have shown symptoms. Ask vendors if stock has been
vaccinated. Be prepared to vaccinate chicks at under 3 weeks.
Genetically resistant breeds include the Fayomi.
2. Other tumours
The avian leukosis/sarcoma group of viruses was discovered by
Ellerman and Bang in 1908 to cause erythroid leukosis - the first
virus shown to cause leukaemic disease. Subsequently, an avian
sarcoma virus was the first solid tumour shown by Rous (1911) to be
transmitted by a virus. These diseases have become widely used as
model systems of viral oncogenesis in biomedicine.
Other tumours in poultry (not Marek's disease, see above) are
caused by retroviruses and these include the avian leukosis/sarcoma
viruses. The genetic makeup of lymphoid leukosis is associated with
slow cell transformation and tumour development over several
months. Other avian oncoviruses cause rapid neoplastic tumour
development within a few weeks.
Any or all of the following: poor appetite, weak and
emaciated, diarrhoea, pale wattles, enlarged liver.
Lymphoid leukosis (most common): enlarged liver,
spleen, bursa, kidneys, ovary.
Erythroid leukosis (rare): moderately enlarged
liver and spleen, leukaemia, liquid cherry red bone marrow.
Myeloid leukosis (sporadic): enlarged liver,
spleen, kidneys, ovary, yellowish grey bone marrow.
Osteopetrosis (rare): thickening of long bones in
legs and wings.
There are two types of mechanism: lymphoid leukosis virus (most
common) slowly transforms cells into neoplastic ones and the
acutely transforming viruses do the damage faster, all of them
using and damaging genes and causing tumours which can include
fibrosarcoma, chondroma, endothelioma, haemangioma, nephroblastoma
and hepatocarcinoma - almost anywhere in the chicken as lymphoid
tissue is spread throughout the bird (unlike mammals which have
Lymphoid leukosis: incubation period from infection to the
developed disease and death is about 4 months. Losses occur from
5-9 months of age in egg-laying and breeding stock. Other leukosis
viruses affect adults sporadically.
The virus is ubiquitous in poultry worldwide and is passed down
through the egg as well as transmitted by direct or indirect
contact. Virus survival outside the body is only hours, so the
disease is not very contagious.
Birds affected by lymphoid leukosis die in
about four months but pass the disease through the egg before
symptoms are apparent. Less virulent strains of the virus do not
produce tumours but egg production is severely depressed and
There are virological tests available, plus post mortem
lesions and tumours are diagnostic.
Fig 4: The internal organs of a chicken affected by
No treatment or vaccines are available. Control is based on high
standards of hygiene and selection for resistance to the viruses by
culling affected birds.
Some breeds are resistant to tumour development. Good husbandry
with minimal stress will help prevent the disease transmission.
Fig 5 Osteopetrosis