specifically YOUNG LAYER chickens (layers have stuff coming out their butt where the infection is)
why is IBD so economically important?
dz causes increased susceptibility to other diseases and negative interference with effective vaccinations
how are birds infected with IBD?
fecal-oral route (bursa->butt->fecal oral)
what is mortality like with IBD? what factors is this dependent on?
Mortality rates vary (range 20-90%) with the virulence of the strain, the viral dose, existence of immunity, presence of concurrent disease and the ability to mount an effective immune response
what are the two forms of IBD?
(1) acute (not highlighted, but-- birds are prostrated, debilitated and dehydrated. They produce watery diarrhea. Most chicks are recumbent and have ruffled feathers) (2) subclinical (not in yellow, but- cause immunosuppression...so then suddenly young chickens start dying with a whole bunch of different things)
what is important to know about serotypes of IBD?
There are two distinct serotypes of the virus, but only serotype 1 viruses cause disease in poultry
what are antigenic subtypes of a serotypes are called what?
what should you know about the VARIANTS (subtypes of serotype 1)?
they are able to break through high levels of maternal antibodies
pathogenesis of ibr? (which cells does it attack?)
attacks the BURSA, the B-CELLS in secondary lymphoid tissue, and VV(very virulent) strains also deplete cells from the thymus, spleen and bone marrow
what are two big red flags for IBR?
Atrophied bursa AND ENLARGED KIDNEYS+ accumulation of urates(prolly bc of dehydration+immune complexes in glom) (bursa in the butt, urates from the huge kidney come out the butt)
common cause of mortality from IBR?
kidney failure (enlarges kidneys with lots of urates)
how do you dx IBR with necropsy?
CHANGES IN BURSA--> Swelling, edema, hemorrhage, the presence of a jelly serosa transudate, and eventually, bursal atrophy. Might also see pathological changes such as (and esp.) hemorrhages in skele mm, intestines, kidneys, and spleen
dx tests for determining if IBR?
IF or IHC, RT-PCR, viral isolation. SEROLOGICAL TESTS ARE ONLY USEFUL IF there is an unvaccinated flock
aside from dx (of an only unvx flock) what else can serological tests be used for in IBD?
to monitor vx responses
which type of flock would you particularly want to vx? why?
BREEDER FLOCKS--> high level of maternal antibodies that protect the chick for 4-7 weeks after hatching
what do you do if your chick's Ab levels against IBD are low?
vaccination with an attenuated virus is done at 1-2 weeks of age (1-2 vaccinate against poo)
is there a vx?
yes! (need to constantly change in develop tho, bc of bisegmented mutations)
what do you need to know about the vxs?
Constant vaccine adaptation is necessary to protect against the new variants that emerge
what is a good way to try to control IBD? what should be noted about this?
BIOSECURITY! however, Post outbreak hygiene measures may not be effective (NAKED VIRUS--> RESISTANT)
describe the "Neurolymphomatosis" syndrome, and what is it aka?
aka "classical mareks". there is asymmetrical paralysis with incoordination being an early sign. there is wing dropping and lowering of the head. If the vagus n is involved, there may also be dilation of the crop and gasping.
describe the ocular lymphomatosis of mareks
graying of the iris of 1 or both eyes because of lymphoblastoid cell infiltration. The pupil is irregular, eccentric and there is partial or total blindness (marek is an ecentric guy with grey, crazy eyes)
what is the viremia like?
MACROPHAGE ASSOCIATED VIREMA ( Macrophage Mareks)
how does the immune system respond to mareks?
there is IMMUNOSUPPRESSION because the lymphoid cells of the thymus, bursa, bone marrow, and spleen
which lymphoblastoid cells proliferate in mareks? What is the result of this?
***T*** LYMPHOBLASTOID CELLS. Lesions result from the infiltration and in situ proliferation of T cells
what should you know about the genome of mareks?
CONTAINS AN ONCOGENE (hence the lymphoid tumors)
what is the most constant gross finding in mareks?
Enlargement of one or more peripheral nerve trunks, most often unilateral. (marek is a dude with a lot of nerve)
Lymphomatous lesions are indistinguishable from what other disease? how do these lesions appear?
ddx of avian leukosis, they present as small, diffuse and transluscent nodules.
what is shedding like for mareks?
there are LIFE LONG CARRIERS AND SHEDDERS (herpes!) but there is NO IN OVO XMSSION
look at mareks vs avian leukosis table!!!
what type of diagnosis is necessary for mareks? what must you look at?
ETIOLOGICAL diagnosis. must look at the characteristics of the tumor CELL, not just the tumor.
mareks vs leukosis--> AGE mareks affects?
Marek’s can affect birds at any age, including <16 weeks of age! (marek dont care bout no age)
mareks vs leukosis--> distinct clinical signs of MAREKS?
frequent wing and leg paralysis
mareks vs leukosis--> what is incidence like for Mareks?
>5% in unvaccinated flocks
mareks vs leukosis--> distinct gross lesions of mareks?
mareks vs leukosis--> what is a specific type of tumor in the bursa in Mareks?
interfollicular (marek is obsessed with his hair follicles)
mareks vs leukosis--> does mareks have CNS involvement?
mareks vs leukosis--> where does lymphoid prolif occur in mareks?
skin and feather follicles (hence contageous dander)
mareks vs leukosis--> lymphoid cells looks like what, and are where, in mareks?
Pleomorphic lymphoid cells in nerves and tumors
mareks vs leukosis--> what kind of lymphomas do you see in mareks?
T-cell lymphoma (Marek likes to drink T)
how would you go about virus isolation for mareks?
need cell culture in chicken kidney, which you innoculate with the buffy coat to confirm serology (Merek is buff, but is destroying his kidneys to be that way, SEROusly)
is there a vx?
how does the vx work?
vx does NOT prevent transmission! Also, peripheral neurologic disease continues to occur but at reduced incidence (Vx only helps deter Marek, but its not like you can tell him what to do)
how do you admin the vx?
most common is IN OVO VX (nip it in the bud)
does mareks spread vertically?
what is one of the major ways that farmers can protect their livelihood from mareks, that isn't vx?
there are certian birds with genetic resistance!! can have a flock of these (Marek has special genes that protect him)
disease is sporadic in birds over 14 weeks of age with an incidence of 3% (retro cant be retro till it's old)
What are the methods of transmission? (general)
HORIZONTAL AND VERTICAL (genetic and congenital vertical)
explain the horizontal transmission of avian leukosis
inefficient bc requires long, prolonged contact
describe the vertical transmission of avian leukosis
TWO WAYS! (1) congenital..this is when ONLY FEMALES are involved, the egg is infected when it is in the repro tract by the infectious RNA form of the virus (2) genetic transmission..this is when MALES are also involved, this is where the viral DNA genome is integrated into the GAMETE DNA (provirus inserted into nuc of egg and sperm)
how do you know the rooster has no way of causing vertical congenital xmission?
congenital infection is via the RNA form, and sperm have no cytoplasm, and RNA viruses stay in the cytoplasm. So roosters can ONLY transmit vertically via genetic when the RNA virus is in its proviral form
describe a chick which has been vertically CONGENITALLY infected with avian leukosis
virus was not in proviral stage-- so not latent, so chronic viremia, tolerance, leukemia is common
describe a chick which has been vertically GENETICALLY infected with avian leukosis
the DNA of the chick holds the latent proviral form of the retrovirus, so it is usually latent with no viremia and no leukemia
if a chicken is infected with a exogenous(this means it's not in proviral form! vert.congenital. not horiz bc need chronic viremia) nondefective virus, when would you see tumors? which cells is this more likely to happen in, and why?
since nondefective, doesnt have V-oncogene, so when persistent viremia, and then the virus inserts itself to become proviral DNA, it inserts near a C-oncogene, disrupting it, causing the tumors. This is most likely to happen in LYMPHOID CELLS (they have a higher chance of being transformed) because they have a high rate of cell division and constitute 10% of all cells in the body)
what's going on with the infection of a chicken with a replication-defective avian leukosis virus?
rarer occurrence, they carry a V-oncogene but then they dont have all the genes they need to replicate, so they need to have a COINFECTION with a "helper" virus which will donate the needed genes to finish the replication
how does avian leukosis cause tumors?
(situation with a non-competant v-oncogene carrier virus with a helper virus coinfection is rare and super fatal). You need to have a replication-competent strain, which infects the chicken CONGENITALLY (because this means it wont be latent like the genetic infxn, and also it will have a high viremia, unlike the horizontal where it's only transient) and it infects and then INSERTS near a C-ONCOGENE-->tumors
main ddx for avian leukosis?
how do you dx?
how is a chicken made to be immunologically tolerant?
congenital infection (vertical)
which chickens can transmit the virus vertically and horizontally?
the immunologically tolerant chickens (which happened bc of vertical congenital infxn)
which kinda viremia does a horizontally, congenitally, and genetically infected chicken have?
what should you know about enviro contamination? (enveloped or naked?)
retro=enveloped. so usually enviro contamination not a huge deal. HOWEVER! large amounts of virus are shed in the meconium at hatching, resulting in heavy environmental contamination---> and the virus can manage to persist a little longer in the incubator. SO! you need to clean out your incubator after every batch of hatches, srsly. (My incubator has leukemia. What a weird problem)
is there a vx?
yeah, but it's "ehhhhh" effective
best control of avian leukosis?
keeping flocks of genetically resistant birds
Pages linking here (main versions and versions by same user)