Viro - Poultry 1

drraythe's version from 2015-08-30 22:34

Newcastle Dz ("Distemper of Poultry")

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Paramyxoviridae, RNA, enveloped (castle made of pearls)
What is exotic Newcastle dz aka?Also known as Velogenic Viscerotropic Newcastle dz (veloceraptors are very exotic)
What determines the severity of Newcastle dz?Severity varies w/ type (strain) of virus
Who is affected by Newcastle dz?POULTRY (ducks & geese usually have inapparent infections)
What is the mortality like in Newcastle dz?Up to 100% mortality in unvaccinated flocks & 10-20% mortality in vaccinated ones. (You’d be dead if a castle crushed you too, unless you have magical caste protecting vxs)
What are the CS of Newcastle?Respiratory, circulatory, gastrointestinal and/or nervous signs. (Might not all be present at the same time) (Castle big enough to hold ALL of the symptoms)
What factors are the types of CS dependent on?The set of signs depends on the age & immune status of the host & the virulence & tropism of the virus
*What does velogenic mean?Strain of high virulence
*What does mesogenic mean?Strain of moderate virulence
*What does lentogenic mean?Strain of low virulence
How long do maternal Abs protect the chick?For the 1st 4 wks (vx every 4 mo, Abs for 4wk)
Which Abs from the mother protect & in which ways? Where ARE the abs? (2)(1) blood.. Blocks viremia (but doesn’t prevent resp. infxn)
(2) IgA is important both in the respiratory & GI tract (Y blood? bc A = gut)
How do you dx Newcastle?Virus isolation, IF, Antibody detection is only diagnostic in unvaccinated flocks, Determination of virulence is essential!!!! (IF only I could be ISOlated in a castle made of pearls)
What is essential for you to do when you are trying to dx Newcastle?Determination of virulence is essential (NEED TO KNOW STRAIN)
How can Newcastle be spread? Via what?DIRECT & INDIRECT CONTACT, in ALL SECRETIONS & EXCRETIONS (a castle full of secretions & excretions sounds gross)
Which strain has a unique form of transmission (& what is that?)Lentogenic strains, transovarian transmission (slow virus....if you’re gonna infect an egg, its gonna take longer to infect a chicken....eggs take a while to become chickens)
Why should you be careful w/ CAGED birds?Caged birds imported from endemic areas are a risk for the introduction of velogenic strains
Is there a vx?Yes, of lentogenic strains & inactivated. (Yeah, an entire castle filled w/ slow vxs)
How often are hens (& which hens?) vaccinated?Laying hens are revaccinated every 4 mo (castle w/ 4 points bc 4 corners)
Zoonotic?Technically can give ppl conjunctivitis, but she didn't emphasize it

Infectious Bursal dz (IBD)

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Birnaviridae, RNA, naked
What should you know about this virus's structure?(Bi)SEGMENTED genome (Bursa Birna Bisegmented gumBoro)
What is IBD aka?Gumboro dz (Bursa Birna gumBoro)
Which type of birds does IBD affect? (Specific)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 dzs & negative interference w/ effective vaccinations
How are birds infected w/ IBD?Fecal-oral route (bursa->butt->fecal oral)
What is mortality like w/ IBD? What factors is this dependent on?Mortality rates vary (range 20-90%) w/ the virulence of the strain, the viral dose, existence of immunity, presence of concurrent dz & the ability to mount an effective immune response
What are the two forms of IBD?(1) Acute (not highlighted, but-- birds are prostrated, debilitated & dehydrated. They produce watery diarrhea. Most chicks are recumbent & have ruffled feathers)
(2) Subclinical (not in highlighted, but -- causes then suddenly young chickens start dying w/ 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 dz in poultry
What are antigenic subtypes of a serotypes are called what?Variants
What should you know about the VARIANTS (subtypes of serotype 1)?They are able to break through high levels of maternal antibodies
Pathogenesis of IBD? (Which cells does it attack?)Attacks the BURSA, the B-CELLS in secondary lymphoid tissue, & VV (very virulent) strains also deplete cells from the thymus, spleen & bone marrow
What are two big red flags for IBD?Atrophied bursa if <3 wks, Hemmoraged Bursa if >3 wks & 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 IBD?Kidney failure (enlarges kidneys w/ lots of urates)
How do you dx IBD w/ necropsy?CHANGES IN BURSA → Swelling, edema, hemorrhage, the presence of a jelly serosa transudate, & eventually, bursal atrophy. Might also see pathological changes such as (& esp.) hemorrhages in skele mm, intestines, kidneys & spleen
Dx tests for determining if IBD?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 w/ 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)

Marek's dz

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?HERPES (no specific number tho!!) DNA, enveloped. (Marek doesn’t have a phone number, bc then when he gives girls herpes they dont call him)
Microscopic giveaways?Intranuclear inclusion bodies (HERPES)
Where does this dz occur geographically?Worldwide, but thanks to vx, less occurrence, but still super important in the poultry industry
Where can you find the virus in the chicken? (For dx, & related to shedding)IN THE DANDER OF THE FEATHER FOLLICLES (Marek needs some head n shoulders)
In general, what are the signs like for Marek’s dz?Variable
What are the 4 syndromes of Marek’s, & how do they relate?They OVERLAP!
(1) Neurolymphomatosis (classical Marek’s)
(2) Acute Marek’s dz
(3) Ocular Lymphomatosis
(4) Cutaneous Marek’s
Describe the "Neurolymphomatosis" syndrome, & what is it aka?Aka "classical Marek’s". There is asymmetrical paralysis w/ incoordination being an early sign. There is wing dropping & lowering of the head. If the Vagus n is involved, there may also be dilation of the crop & gasping.
Describe the ocular lymphomatosis of Marek’sGraying of the iris of 1 or both eyes bc of lymphoblastoid cell infiltration. The pupil is irregular, eccentric & there is partial or total blindness (Marek is an eccentric guy w/ grey, crazy eyes)
What is the viremia like?MACROPHAGE ASSOCIATED VIREMA ( Macrophage Mareks)
How does the immune system respond to Marek’s?There is IMMUNOSUPPRESSION bc the lymphoid cells of the thymus, bursa, bone marrow, & spleen
Which lymphoblastoid cells proliferate in Marek’s? What is the result of this?***T*** LYMPHOBLASTOID CELLS. Lesions result from the infiltration & in situ proliferation of T cells
What should you know about the genome of Marek’s?CONTAINS AN ONCOGENE (hence the lymphoid tumors)
What is the most constant gross finding in Marek’s?Enlargement of one or more peripheral nerve trunks, most often unilateral. (Marek is a dude w/ a lot of nerve)
Lymphomatous lesions are indistinguishable from what other dz? How do these lesions appear?DDx of Avian Leukosis, they present as small, diffuse & transluscent nodules
What is shedding like for Marek’s?There are LIFE LONG CARRIERS & SHEDDERS (Herpes!) but there is NO IN OVO XMSSION
Look at Marek’s vs avian Leukosis table!!!Important!
What type of Dx is necessary for Marek’s? What must you look at?ETIOLOGICAL Dx. Must look at the characteristics of the tumor CELL, not just the tumor.
Marek’s vs Leukosis → AGE Marek’s affects?Marek’s can affect birds at any age, including <16 weeks of age! (Marek’s don’t care bout no age)
Marek’s vs Leukosis → distinct CS of MAREK’S?Frequent wing & leg paralysis
Marek’s vs Leukosis → what is incidence like for Marek’s?>5% in unvaccinated flocks
Marek’s vs Leukosis → distinct gross lesions of Marek’s?Enlarged nerves
Marek’s vs Leukosis → what is a specific type of tumor in the bursa in Marek’s?Interfollicular (Marek’s is obsessed w/ his hair follicles)
Marek’s vs Leukosis → does Marek’s have CNS involvement?Yes
Marek’s vs Leukosis → where does lymphoid prolif occur in Marek’s?Skin & feather follicles (hence contagious dander)
Marek’s vs Leukosis → lymphoid cells looks like what, & are where, in Marek’s?Pleomorphic lymphoid cells in nerves & tumors
Marek’s vs Leukosis → what kind of lymphomas do you see in Marek’s?T-cell lymphoma (Marek likes to drink T)
How would you go about virus isolation for Marek’s?Need cell culture in chicken kidney, which you inoculate w/ the buffy coat to confirm serology (Marek’s is buff, but is destroying his kidneys to be that way, SEROusly)
Is there a vx?Yes
How does the vx work?Vx does NOT prevent transmission! Also, peripheral neurologic dz continues to occur but at reduced incidence (Vx only helps deter Marek, but it’s 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 Marek’s spread vertically?No
What is one of the major ways that farmers can protect their livelihood from Marek’s, that isn't vx?There are certain birds w/ genetic resistance!! Can have a flock of these (Marek has special genes that protect him)

Avian Leukosis

Question Answer
Etiological agent? DNA or RNA? Enveloped or naked?Retroviridae, RNA, enveloped (blood cancer= retro)
How common is Avian Leukosis?Endemic in almost all flocks of chicken!
What age of birds does Avian Leukosis affect?Dz is sporadic in birds >14 weeks of age w/ an incidence of 3% (retro can’t be retro till it's old)
What are the methods of transmission? (General)HORIZONTAL & VERTICAL (genetic & congenital vertical)
Explain the horizontal transmission of Avian LeukosisInefficient bc requires long, prolonged contact
Describe the vertical transmission of Avian Leukosis2 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, & the viral DNA genome is integrated into the GAMETE DNA (provirus inserted into nuc of egg & sperm)
How do you know the rooster has no way of causing vertical congenital xmission?Congenital infection is via the RNA form, & sperm have no cytoplasm, & 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 w/ avian LeukosisVirus was not in proviral stage-- so not latent, so chronic viremia, tolerance, leukemia is common
Describe a chick which has been vertically GENETICALLY infected w/ avian LeukosisThe DNA of the chick holds the latent proviral form of the retrovirus, so it is usually latent w/ no viremia & no leukemia
If a chicken is infected w/ a exogenous(this means it's not in proviral form! vert. congenital. not horiz bc need chronic viremia) non-defective virus, when would you see tumors? Which cells is this more likely to happen in, & why?Since non-defective, doesnt have V-oncogene so 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) bc they have a high rate of cell division & constitute 10% of all cells in the body)
What’s going on w/ the infection of a chicken w/ 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 w/ a "helper" virus which will donate the needed genes to finish the replication
How does Avian Leukosis cause tumors?(Situation w/ a non-competent v-oncogene carrier virus w/ a helper virus coinfection is rare & super fatal). You need to have a replication-competent strain, which infects the chicken CONGENITALLY (bc this means it won’t be latent like the genetic infxn, & also it will have a high viremia, unlike the horizontal where it's only transient) & it infects & then INSERTS near a C-ONCOGENE → tumors
Main DDx for Avian Leukosis?Marek's dz
How do you dx?RETRO=SEROLOGY
How is a chicken made to be immunologically tolerant?Congenital infection (vertical)
Which chickens can transmit the virus vertically & horizontally?The immunologically tolerant chickens (which happened bc of vertical congenital infxn)
Which kinda viremia does a horizontally, congenitally, & genetically infected chicken have?Horizontal = Transient viremia
Congenitally = Chronic viremia
Genetically = None
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 → & 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