 Well, it's always exciting, right? First off, I wanted to thank everyone. I have had a wonderful time being here. It's been nice to live in Kentucky, but it's nice to be back home. So it's been very good, and you've all been very kind. So I had the wonderful privilege of starting out this rotation with Dr. Vitaly. And the first day, I saw three bird shop patients. I've never even heard this thing before. And so I was talking to him a little bit, and he said, how you should do bird shot, it'd be great. He's like, just do pictures and let everyone see because no one's gonna know what you're gonna be talking about. So they'll look at the picture and say, that looks good, but they still don't know what you're talking about. So he's like, it's a pretty safe topic to talk about. As far as Kentucky goes, Jim knows a little bit of all this. So Kentucky's known as the horse capital of the world. Their big thing was this last year, I guess in 2010, they had the world equestrian games there, first time ever outside of the United States. There are, it's fifth in the United States for number of horses, being 327,000, first is Texas. But it's number one for wealth of horses. Each year there's $1.7 billion worth of horses bought and sold within Kentucky. So it's a pretty place. So bird shot, what is it? It's this uncommon form of poster uveitis. And they'll say all pictures except for this one and one other one are patients from the Moran that you'll be seeing. It has this characteristic crinkled lesions. It also usually presents with phytritis, retinal vascularis, and sometimes if you do not have the lesions at first, which the lesions are, they can either come initially and then you begin having the symptoms or you can have lesions years after symptoms. People often think it's the retinal vascularis. So that sometimes is an issue that people work through is getting the right diagnosis, but it also has the inflammatory lesions of the RPE. Back in 1980 is when this term was coined, so it's a relatively new term. There were 13 patients and Ryan and mommy saw this and they decided that it looks like bird's eye, a shotgun in order to hit some papers. They called it bird shot. A little bit later, gas, he called it this vitiliginous choriditis because it looks like vitiligo of the cutaneous tissue. However, later I was seeing that that is not really the case. It's not vitiligo in the eye. So as far as it's prevalent in cases, it's only 0.6 to 1.5% of the UVIS, which I thought was really interesting that on my first day I saw three of these people. I guess that's Dr. Vitale's clinic for you. And it comprises six to 7.9% of the poster UVIS. Now, a lot of times people think it actually comes on quite a bit younger, young females or whatever, but in literature, the average age is really 53. It's more for middle age or younger age women and you see the range there. And it is more predominantly in European descent, which has a lot to do with its etiology of it being responsible for the HLA29A subtype. And we'll get into that little bit. And you can see it has a female prolection. So how do they present? They're usually a very healthy people. They don't ever have any symptoms or anything. They feel great, but then they begin having these visual symptoms and it's a little concerning. So they show up and really none of them really have any systemic disease for the most part. However, on presentation, you find out that 20% of these people usually do have some unknown idiopathic hypertension. And then over five years, it's found out that most people will have hypertension if they don't already have it. And that is the same as the Dutch population, which is interesting because of the HLA29 subtype. But also they have this cardiovascular diseases. Six in this research by Prim et al, five had coronary artery disease, two had CVA's and a few had CVO's. So other associations, or just sensory neural hearing loss, mildest plastic syndromes, sarcoid, which is on a differential in atopic diseases. So back to gas, he thought, remember, it was the vitiligus coroid, but Dr. Vitalli's text, believe this really, it was confused with idiopathic gutate. Just text him by. Well, no. Don't tell him that, but no. He, and going through with the literature, they believe that really what gas was seeing was this idiopathic gutate hypolynosis. They also usually show up with 20% of chitinium splenuses. Most of those are, of course, for basal cell. There was one case report of malinoma, melanoma, then psoriasis. Now all other things really are just coincidental. So they usually present with this gradual, painless vision loss, which the vision loss usually just occurs in one eye, what they notice, although it does affect both eyes. They're the photophobia, photopsia, and nictalopia. And then I thought it was something very interesting. A lot of them will have this subjective loss. So they might still see 20, 20, but if you're asking how their vision is, they believe it's really not that very good. So you go on to the ocular exam. There's really quiet end to your segment, a little bit of hypotony. You have some open angle, but that's usually just because of the chirochrysteroids. Very rare is the disease itself. And you have the granulomidus aspect. On the biomacroscopy, this mutton fat is really the posterior vitreous face. You only see that during periods of disease activity. So that's common go based upon if they're flaring or not. So on fundoscopy, you see bus through indirect, and you see these wonderful ovoid around spots. And they usually call this cream colored hypopigmented areas. And they're usually in a radial distribution away from the optic nerve head or the infratemporal direction. Like I said earlier, if you do not see these spots, they still have those symptoms. You cannot rule out bird shot because the spots don't always coincide at time of presentation. When that happens, they usually believe it is, or it gets misdiagnosed as idiopathic retinobascularitis. These spots, something to know is with all the different white dot syndromes, they have a wide range in the size ranging from 50 to 1500 microns, which tends to be a lot larger than a lot of the other white dot syndromes. So here you see in the posterior pole, you see some of these large white dots, peri-papillary. And usually you'll see through more pictures it comes down this inferior nasal quadrant and it follows the radial coroid arteries. And you can have plus minus macular involvement. So as far as the grading goes, you can have small, subtle, medium, or large and confluent sizes. And the other grading is less than 10, 10 to 50, or greater than 50. And the pigmentation is either minimal, medium, or severe. And what's thought is your degree of pigmentation has a lot to do with your prognosis. The more hypopigmented it is, the worse the symptoms as well as the disease severity. And the most common complication is macular demerit, whether it be cystoid or it's diffuse, and you can have sub-retinal. But for most people, you'll have some type of macular demerit within five years. You have the ERMs, the coir near vascularization, that ranges from six to 14% within five years and the cataract and everything. This optic atrophy, they believe, is due to ischemic anterior optic neuropathy. So this pathophysiology, it's not clearly understood right now what the true mechanism is. As I said earlier, the reason why I was stressing the Northern European descent is because of you find most of this HLA 29 within the Northern European population. It's found in a large percentage of the people. However, the 7% of us would have it anyway. And if you remember, I guess I cut off some of this, although this is pretty high specificity because of its rare prevalence in the population, you can't have a very good positive predictor value with this, 93%. So a lot of this is your clinical suspicion. 70% of the diagnosis comes from clinical. If they are A29 positive, it'll bump it up to 97%. But if they're A29 negative, then you go from 70% down to 8.5%. And what that bottom thing is says is that 5% to 15% of those bird shot don't have the HLA A29. So there was a lot of research done trying to figure out if this was the main cause of this disease. And they found out that there are two subtypes, well, there's actually 12 subtypes, but 0.2, which is what we usually see in the European descent, and 0.1, in three studies, they found everyone was, well, none of them were 29.1. If they were any HLA A29 positive, it was all this 0.2. So they began to think maybe this is what confers to disease pathology. When they sequenced it out and there's one little substitution that changes the extracellular binding site of this. And so they thought that this 29.1 offered some type of protection. However, later studies show that even A29.1 can have bird shot. So then they went on to believe a little bit more that it wasn't this specific area, but it was the areas around it. And that's why they thought it was the satellites. And then they thought, well, maybe that can't be it also. Maybe there's some major history of compatibility reasons behind it. So this is reaching far back into my recesses of immunology, it was even just two years ago. So the major history of compatibility complex, it presents antigens, and that stimulates this autoimmune system. And there was research found that in people who had some type of ocular inflammation, the serum level of S-antigen and this binding protein increased quite a bit. And then they also found that these two antigens are able to be picked up by MHC1 and then presented. And they believe that this is sort of the mechanism on which this process begins. And when you inject S-antigen to mice, they go on and have the exact same presentation as bird shot. The MHC1 also initiates not just the adaptive immune system but also innate by activating these other CD1 or CD8 relinked immunology cells. So then they also, there were a few cases that four of 11 people had Lyme disease. And so they wondered if there was some correlation between Lyme disease and bird shot. Probably not. Same with Q fever, the same thing happened. And then also not too long ago, there was this report out by maybe the pineal gland gets inflamed and when it gets inflamed because it's the same embryologic origin, it expresses S-antigen and the other IRBP and then that causes bird shot. So as you can see, there's still no real understanding of what causes bird shot, but that it's autoimmune. The pathology, nothing all that you would not expect can be granulomatous, which is why sarcoid and TB become the differential, but a lot of them believe as we begin to see that not only is the retina affected but also the coroid, that the coroid they believe lags behind and becomes a secondary response. So the different ways to sort of separate this out either by type for differential or by white dots present or not. So if you did it by type, here's the list. And if you did it by a white dots present or not, these are the different white dots syndromes. And so these are the things you gotta start looking at. First we have to do is rule out infectious. So if you were to do the diagnostic criteria, you'll see here a lot of this is just clinical. And then if you want to, you can get it checked, but most people do not check the HLA-829. And then if you have any KPs or posterior snicky eye, you rule it out. So how do you go about working this up? Like I said earlier, the biggest thing is to quickly rule out those infectious ones. So syphilis and tuberculosis. And then these other ones, the non-infectious, you gotta do a little bit more of intensive work up. Imaging, there's lots of stuff for imaging. You could have had 30 minutes or more just talking about imaging. But FAA really isn't all that reliable. It can show and it cannot. It depends. ICG is a lot better in that it does show some of these coroidal spots, which you don't usually, you don't see in FAA, but they don't coincide. The spots that you see on FAA and ICG. And that led to sort of the idea that they are two separately involved processes. In different locations. And as you know, as I said earlier, macrodema is a common complication. And so you'll get OCT with that. Autofluorescence, you do see a whole lot more of the hypo-autofluorescent spots than you would on ICG or FAA, ERG, you can see. And then interestingly enough, they still use the visual field to follow pH patients on a long-term basis to see how it's progressing. So like with most autoimmune things, you hit them hard, try to get things under control with steroids, but you try to get them off of steroids or on a low maintenance dose of five milligrams per gig per day or less. Which for most people doesn't have very much effect. Most people cannot keep it under control with that little of steroids on board. So then you move to the other immune modulatory therapies, cyclosporin. Most cases, they started out high doses of 10 milligrams per gig per day, but they found that you have a lot of renal complications. And the literature today supports starting really low with cyclosporin and maintaining them on that. And if you combine it with another immune modulator, then it works quite well and it keeps it at bay. So I thought it was interesting, there's current research on antidellucan-17, which is the, an illucan-17 is supposed to be the auto regulator of your immune system. And they are currently developing drugs to target this to see if you can knock that out. So now it comes to birdshot or not, birdshot or not. And so this tuberculosis picture is one of the ones that is not a Moran, everything else is a Moran patient. And all the different birdshot pictures are different patients with birdshot. So hopefully you'll get an appreciation of the different ways it can present. So both birdshot and TB will have panuviitis and cream-colored lesions, as you can see. The difference is TB is usually not ovoid and the degrees vary of retinal pigment epithelial and TB patients. And then you also have the systemic findings. Oops, wrong way. For another white dot, a syphilis. However, the syphilis, you know, you do your normal workout for syphilis, but they also are non-ovoid and they also have varying, varying RPE. So for ocular histoplasmosis, the big thing which you do not have for the most part in birdshot is this peripapillary hyperpigmentation. And then also for a histo, you usually have very well demarcated sort of punched out lesions, which you don't see very well in this picture. But if you do have peripheral or histo lesions, they're very circumscribed, whereas birdshot's very feathery looking. And the vitreous in histo is usually pretty quiet where you have some underlying vitreous in birdshot. So Ducan syndrome is done by a nematode that gets in the back of the retina and crawls in the retina by the RPE layer. Sometimes you can see the nematodes, but you also often see RPE tracks. And also you have these gray-white lesions. It's a lot more white than the cream color to birdshot. And diffuse or Ducan usually does have pretty significant vitritis. So now non-infectious, white dots, sarcoid. We already talked about the workup of sarcoid. You do a systemic, see what their Elysa's own level is, their ACE, chest X-ray. But you'll see one thing is that sarcoid, they tend to have more of what they call candle-wax spots, which I can't really appreciate the difference between the candle-wax spots and the birdshot, but that's what they have in literature. Other than that, they're usually pretty indistinguishable, so you have to do the systemic workup. VKH, big thing for VKH, you have to have an exudative RD, as well as the crudal inflammation is gonna be a lot more, you'll see here the way with birdshot. Also, VKH, they usually present with sensory neural hearing loss, meningiol symptoms, and poliosis. Sympathetic ophthalmia, you have to have some usually inciting event or trauma to the eye to expose the antigens. You also have Daelin Fuchs nodules, and they usually have a lot more discrete images or lesions than the birdshot. They just have a cloudy media here with your botrytis currently. So for multifocal chlorideis panuviatus, the difference here is that it's multiple bilateral post-ecrotorial lesions of only 50 to 200, whereas with birdshot, you can get up to 1,500, and you'll have anterior segment inflammation. Mudes, younger females, usually only unilateral, goes away after seven weeks, and this is in the outer retina, the RPE layer, no chloride involvement. Ampii, you have bilateral, it's asymmetric, more in the posterior pole than the infernasal area, and more of a plaque-like staining quality. So now for the sort of masquerading ones of white dots absent is interlocutor lymphoma, but you can have this sort of leopard-like lesions in lymphoma. So here's one intraocular lymphoma patient we have here, and then also, though, you can have this, the real white dot absent presentation lymphoma, and you can't see here, if you had OCT, this is very highly elevated. So just another picture of birdshot, just to hopefully ingrain it in your minds. Like I said, the lesions aren't always here. Sometimes they are present, other times they're not. So if you have a patient who goes for a long time, also know what it is, it could be birdshot. Here's a picture of a red-free, it just highlights the lesions a little bit better, same eye. And I wanted to thank Dr. Vitale. He did help quite a bit. You know, this is a younger version of him with less hair. But he was very kind and he gave me his before-press copy of his recent edition. So if you want to read 60 pages on birdshot with 178 references in it, which I did not read all references, he'd be more than willing probably to let you read it. And there it is, but I appreciate your time. Any questions? Thanks.