Lecture: Ocular Toxoplasmosis

Ocular toxoplasmosis, caused by the protozoan T. gondii parasite, is one of the most common causes of posterior uveitis worldwide, although the risk of infection and subsequent ocular involvement vary in different parts of the world. In this webinar, we describe the clinical features and course of ocular toxoplasmosis, as well as current approaches to the diagnosis and treatment of this infectious disease.

Lecturer: Dr. João M. Furtado, Assistant Professor of Ophthalmology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil


DR FURTADO: Good afternoon, everybody. My name is Dr. Furtado, and I’m based in Ribeirao Preto, Sao Paulo, Brazil. Today we are going to talk about ocular taxoplasmosis, I have no conflicts of interest, and we’re gonna divide the presentation in four main areas. First we’re gonna talk about an introduction, a little bit of parasitology and prevalence of the disease. Then we’re gonna focus on ocular manifestations, which is probably the biggest part of the presentation, followed by treatment and outcomes, and we’re gonna wrap it up with conclusions, and then later I’ll be happy to answer any questions you have. The toxoplasma gondii is an obligate intracellular parasite. And in theory, it can infect every nucleated cell. A cell should be nucleated in order to be infected by the parasite. Its definite host is a feline, and it has three forms. The oocyst, as you can see in the bottom left, the tachyzoite — tachy means fast — and the presence of these in the blood will define acute infection, or if this version of the parasite is found in the eye, it will determine active lesions. And because of the immunological system and the drugs, the tachyzoite might turn into bradyzoite, and become surrounded by a wall and a cyst. The toxoplasmosis has a big prevalence, compared with most other infectious disease. So it’s estimated at around 30% of the population is infected. And the prevalence varies a lot from region to region, so some regions — and the biggest example for us is Latin America. We might have up to 70% to 80% of the total population infected. And in this area as well, the disease is more aggressive. The disease — well, the toxoplasmosis creating eye damage, which means the ocular toxoplasmosis, is one of the most common causes of posterior uveitis in the world, and the most common uveitis in some regions of the world, like Latin America, as another example. In the following slide, I’ll show you a graph to make it more clear, but a person can get infected by eating undercooked meat containing tissue cysts, or by drinking water or eating contaminated fruits or vegetables contaminated with oocysts of the parasite. Also when pregnant women get infected and transmitted to the fetus, it’s very rare, but it’s also possible to get it through organ transplants. When we have an outbreak, which means a large number of people getting infected in the same area at the same time, we usually think — although sometimes it’s hard to track down — but we usually think it’s related to water sources. And when we see a patient with toxoplasmosis at the clinic, it’s very hard, almost impossible, to identify how the person got infected, or what’s the parasite source in this case. So here is a very good chart made by CDC, showing that the cat will release oocysts, in the environment. So a cat or any feline — it’s the only type of animal that will do that. A livestock animal might get infected, and a human can eat this meat, infected, and get the disease as well. Another option of infection is the human being infected directly through the oocysts released by cats. By drinking water, contaminated water, or by washing vegetables and fruits with this water. So these are two ways of being orally infected. And as I mentioned, once a woman is infected during the pregnancy, the baby can get the disease as well. Just to mention that we are currently having the biggest outbreak in history. It’s happening in Brazil, in the South part of Brazil. We have more than 600 confirmed cases of acute infection, all in the same city, and more than 500 still under investigation. We still don’t have data on ocular lesions in these cases. But potentially it’s sight-threatening, and as I mentioned before, in these cases, we tend to believe that the water plays a bigger role than the meat. And the water could be either built reservoirs, or the aquifer, the groundwater. So why are we talking about a parasite presentation related to ophthalmology? It is actually a very interesting topic for ophthalmologists and those who like or who see patients with uveitis. And basically because the parasite has a specific tropism for the eye, and being even more specific for the retina. And also because of the burden of disease, in terms of blindness and visual impairment. And when we talk about burden, one concept which is interesting, but not very familiar to many ophthalmologists, is called DALY, disability adjusted life years. It’s a measure of overall disease burden. It expresses years lived with disability, plus the years of life lost. Thinking about ophthalmology, nobody is gonna die because of an ocular lesion, but people might get visually impaired or blind due to the disease, and not to mention the congenital impact of transmission, when a woman gets infected during pregnancy. So here sometimes we’re gonna talk about congenital, sometimes we’re gonna talk about acquired, although many aspects of the eye lesions are common to these two types. So the congenital disease happens when, as I mentioned, a woman gets infected during pregnancy. And this is a graph — it’s a very nice graph — for a very important paper published in 2004. And it shows that it is easier to get infected at the end of the pregnancy, but on the other hand, infections — I mean, the fetus, the baby getting infected — but if the infection happens at the beginning of the pregnancy, it is devastating for the child. It can cause multiple clinical symptoms, perinatal death, or stillbirth. But the potential outcomes for the congenital disease is miscarriage, malformation, and ocular disease, among others. Talking about now the acute infections, the disease is mostly asymptomatic in healthy individuals. Here in this red arrow — it is very uncommon to have more severe presentations like myocarditis, polymyositis, and pneumonia. This is very uncommon. It’s very hard to define the source of infection. Talking about meat versus water, in terms of oral infection. And it is not common to have one person with acute toxoplasmosis infection and ocular manifestations at the same time. After the person recovers from acute infection, most individuals remain asymptomatic throughout their lives. And the parasite gets hidden inside the host body. So I’ll detail more later, but no drug is able to remove the parasite from the host. And just a tiny part of the infected individuals, which vary from 2% to 10%, based on previous papers, just a reduced part of them will develop late ocular manifestations of the disease. Not necessarily associated with acute infection, but they more often would happen later in life. Focusing now on the ocular manifestations, I live in an area where toxoplasmosis is very prevalent. But what we usually see is a white focal retinal lesion, pointed in red here in this image. With an intense overlying vitritis. The vitritis can be diffuse, but it’s almost 100% of the cases. It will be more intense next to the lesion. The disease tends to be self-limited if the person is immunocompetent. And when we have hyperpigmented scar, which is usually next to the active lesion, it is easier for us to think about toxoplasmosis. But not necessarily we will see that. And having a scar means that the person had an active ocular episode in the past. Which also means that the acute infection is not happening right now. So the person got infected. We don’t know when. And he is having late manifestation. Another very common way of describing the disease — and it’s very common to see in books about uveitis — is the term “headlight in the fog”. And that’s an example of it. This image shows that. So we can see this whitish lesion. It’s in the retina. But we cannot see clearly the limits of it. And the image we have is very blurry, because this big lesion is releasing inflammatory cells to the vitreous, so we cannot photograph or see the fundus through the medical examination. So that’s an example of the headlights in the fog. And we also read in books that it’s a full thickness retinal lesion, which obviously, just by checking the fundus, we will not be able to see that, but with the development of OCT, we can see it clearly. So that’s an example. So this image and this one are both from the same patient, from the same lesion. As we can see here, comparing to the normal retina, we can see and define retinal layers, which is not possible (audio breaking up) what a typical toxoplasmosis lesion would look like. Although it’s basically a retinal issue, as I mentioned. Also, inflammatory reaction, in the anterior chamber, as you can see here. This is keratic precipitates, seen here like a triangle. So this is suggestive of granulomatous uveitis in general. The disease can cause permanent visual impairment. Because the retinal tissue, as you know, does not regenerate. Because of the recurrences, and because of the associated complications. This is an example of one of the patients I saw in the clinic. This whitish lesion, the active lesion — once that is gone, there are no longer tachyzoites, but this scar in a very specific part of the retina caused damage in visual acuity. So other than this scar, there are no photoreceptors in the affected area. (audio breaking up) so these cases… Because the macula would be affected. So this is a normal eye. And this is… (no audio) not sure what happened here, if I lost connection. So I’m not sure if I lost connection to you guys. I was just talking… About congenital…

>> We lost your connection. Your Wi-Fi is a bit unstable. Is there a place that we can move, which is better? Which has better Wi-Fi?

DR FURTADO: Oh, sorry. I’m happy to go back to the previous slides, and present it to you.

>> Yeah, I think the last five minutes, it was difficult, Dr. Furtado.

DR FURTADO: So I could go back, and I’ll…

>> Your Wi-Fi is still an issue. Is there a place that you can move, so that you can get a better signal?

DR FURTADO: I’m not sure. What I could do, I could use the desktop, but it would take me a few minutes to turn it on. And it’s placed in a room where (audio breaking up) if we just stop for a few minutes… And resume it later… What do you think?

>> If it is one or two minutes, I think we prefer that. This is getting very difficult. If you move your laptop to a different place, maybe it will help?

DR FURTADO: Yeah, I’ll be in the same room, and I’ll move a little bit and see if it works. Just let me know, and then we can try a different thing.

>> Or you can start the desktop. That may help.

DR FURTADO: Okay. Let me do that. I have to change the headset. And just let me know if it’s working or not. I’ll do that soon.

>> Okay, Dr. Furtado.

DR FURTADO: Yeah, I’m sorry for that. We just tested, and it was working nicely.

>> Yeah, you never know. The internet. Do you need any help, Dr. Furtado? You’re able to open the link? Do you need any help?

DR FURTADO: Can you hear me?

>> I can hear you, but it’s not that clear.

DR FURTADO: Can you hear me now?

>> I can hear you. The loudness is a bit low. But I can hear you.

DR FURTADO: Another issue here. The camera is not working.

>> That’s fine. We can use this camera. Can you use the other headset? Or it’s not possible to use the other headset?

DR FURTADO: It’s not possible. I can speak louder. Is that okay? So just let me know. Where should I get started again? Is it… Is it a good slide to get started?

>> We don’t see any slide, Dr. Furtado.


>> It’s stuck there. It’s not moving. Do you want me to share the PowerPoint from my side? I can do that.

DR FURTADO: Can you see now?

>> No, we don’t see anything.

DR FURTADO: I’ll try it again.

>> Okay, sure. Yeah, we see now.

DR FURTADO: Okay, yeah. So just let me know where should I get started again.

>> Just three or four slides before this.

DR FURTADO: Okay. So I was just mentioning… That we recently had an outbreak in the South part of the country, called Santa Maria. We have more than 1,000 cases under investigation. And although we have no data on eye lesions yet, the groundwater, or the built reservoir, source of potential infections here. So why are we talking about a parasite in a talk in ophthalmology? So first, the parasite has a tropism for the eye, more specifically the retina. And also because of the burden of the disease, and by burden, I mean blindness and visual impairment. One way of calculating is disability adjusted life years, in this case blindness or visual impairment. And it doesn’t happen in eye disease, but if you consider congenital infection, that’s a big burden. We’re gonna talk about congenital and acquired disease. So the congenital disease, as I mentioned, happens when a woman gets infected… And it’s easier to transmit the parasite to the fetus at the end of the pregnancy. But if infection occurs in the beginning, especially in the first trimester, it could be devastating, in terms of clinically apparent lesions in multiple organs. Or even perinatal death. The potential outcomes for the congenital disease are multiple, but just to name a few, miscarriage, malformation, microcephaly, and ocular disease, as you can see here in this image. The acute infection — so when a person gets infected by the parasite, it’s often asymptomatic in healthy individuals. A person might notice lymphadenomegaly, as you might notice here in red. It’s not very common, especially in healthy individuals, but myocarditis and polymyositis and pneumonia might happen as well. It’s hard to consider infection in meat versus water, and it’s not very often to have ocular toxoplasmosis concomitant to acute infection. After recovery, most individuals remain asymptomatic throughout their lives. The parasite remains hidden inside the host body, and part of the infected individuals, which is — depending on the articles — will tell us from 2% to 10%. They will develop late ocular manifestations of the disease. And talking about the ocular manifestations, which is the biggest part of the presentation. What we can see, when we suspect toxoplasmosis, is when we see a white focal retinal lesion, pointed here in red. With an intense overlying vitritis. And the disease, if the person is healthy, this is an immunocompetent person, the disease is usually self-limited. Not exclusively, but if we see a hyperpigmented scar next to the lesion, next to the active lesion, it will become more easy to suspect toxoplasmosis. And having a scar means this person had an active ocular episode in the past, which also means that the person is not having the acute infection at that moment. The books tell us about a name, “headlight in the fog”, to describe the lesion. And in this image, you can see an example of it. So this whitish lesion is the active toxoplasmosis lesion. But with this intense vitritis, we cannot see clearly parts of the retina and other parts of the fundus, because of the intense inflammatory reaction caused by the infection. And we might also read about — that toxoplasmosis is a full thickness retinal lesion, which obviously we cannot see just by checking the fundus, but with the development of the OCT, we can see that the lesion might affect all layers of the retina, and we kind of lose the definition of the different layers. This aspect here of like dust is the inflammatory reaction being released by the lesion into the vitreous. I mentioned that the disease is mainly a retinitis, but in cases where the inflammatory reaction is intense, the anterior segment might be affected as well, and this is an example of what we can see in such cases. And the disease can cause permanent visual impairment, because the retinal tissue obviously does not regenerate, because of the recurrences, and because of the associated complications. I’m showing you an example of an active episode of ocular toxoplasmosis. So active means there are tachyzoites in this lesion, and once we treat this patient, there is a formation of a retinal scar, and in this scar, there’s no photoreceptor. So when the light hits the macula — in this case, the macula — the person will have difficulty to see it. Mentioning the congenital ocular toxoplasmosis, one problem is the central retina is more often affected, when we compare to acquired cases. And centrally, obviously, means a higher burden of disease, in terms of visual acuity. I’m showing you here a normal example of fundus of a healthy person, highlighting the macula. And here what we can see is that the person barely has retinal tissue in the macula, right? And when we analyze it through an OCT, we can see that outside the scar, we have normal retina, and then the scar here — we can see that the person barely has retinal tissue here. Unfortunately. About the congenital infection, it’s also important to point that sometimes the person has — once he or she is born — we will have the lesions already, either active or scars, but once the person is congenitally infected, he or she may develop late ocular manifestations. So that’s an example of what I’m showing here. So this is a 15-year-old girl who got congenitally infected, and 15 years after her birth, she developed her first ocular episode. This is not very common, but that’s possible. And that’s another example of a lady who was born with a congenital scar, due to toxoplasmosis, and now she’s having an active episode here, as I’m pointing. That’s possible as well. So there’s the congenital scar, and the reactivation, the active lesion. So how do we do the diagnosis? In most cases, unfortunately, the diagnosis is presumed. Clinical aspects that might be toxoplasmosis, and that’s an example. Right? An active lesion next to a scar. In this case, it’s easy to think about toxoplasmosis. Plus a positive serology. In a very limited number of cases, because it’s invasive, and because not often we will have the lab and the logistics available for that, but we can do the PCR, with intraocular fluids, to check — to look for parasite DNA. And this can be performed in the anterior chamber or the vitreous chamber. Talking about the serology, there are multiple IgE/IgA, but what we usually do in the workup is the IgG. That if positive, it indicates infection. Not necessarily acute infection. And the person remains with the IgG positive, throughout his life. And the IgM, when it’s positive, it suggests acute infection. And its titers decrease after months of acute infection. Months or years. Usually months. Especially when someone is infected during pregnancy, it is important to check the IgG avidity. And high avidity rules out recent infection. And most patients we see in the clinic with retinal lesions, they are IgG positive, IgM negative, which means they got infected in the past. We don’t know when. And now they are having ocular issues. This case highlights an example of when the PCR of the aqueous humor helped us in the diagnosis. So this is an HIV positive person with a low CD4 count, below 50, which is very low. And in this case, as I’m gonna mention, the disease becomes less typical, so it’s harder to make the diagnosis. And this person was treated for CMV with no response. And then after the positive PCR for toxoplasmosis, it got treated properly, and he recovered his vision. The previous images I’ve showed you are considered typical cases, or cases which are more easily identified as presumed toxoplasmosis. But not always that’s the case. Right? So when we see a person with a bilateral active disease, this is very uncommon. And although it might be toxoplasmosis, we have to investigate other potential diseases. Again, not very common, but rough spots can be seen, associated with toxoplasmosis. So we can see here in these blue arrows — and potentially in this case, the location of the disease next to the optic disc was the cause of those rough spots. Again, not very common, but we might have scleritis associated with ocular toxoplasmosis. And in this case specifically, the lesion the patient had was very close to the place where he was having this affected scleral area. In immunosuppressed individuals, lesions tend to be multiple, bigger, and bilateral. Which is very challenging, to make the diagnosis. That’s an example of an extensive ocular lesion due to toxoplasma, and in this case, associated with neurological manifestations of the disease as well. Very uncommon. The differential diagnosis of ocular toxoplasmosis — so we should think about toxoplasmosis every time we have a focal retinitis, and we should try to exclude every disease that might cause — might be the cause of focal retinitis. So I listed some, but we have a larger group of diseases. But the image I’m showing here is a patient with ocular syphilis. But other diseases, such as ocular tuberculosis, cat scratch disease, toxocariasis, or masquerade syndromes can cause the disease as well. Now we’re gonna focus on the treatment of the acquired disease. And the principle and the goal of the antimicrobial treatment is to limit the parasite multiplication during active retinitis, during the active ocular episode. And it is important to mention that no drug is able to eliminate the parasite from the host, which means the person is at risk of having recurrences over time. There is a debate on when should we treat. In places where the disease is more frequent and more aggressive, and again, the example is Latin America, most doctors treat every time we see an active lesion. In selected cases, in places where the disease is not frequent, and not very aggressive, having an example — the United States and Europe — some people tend to just follow the patients over time, if the lesions are small, and are far away from the macula. In this example I’m showing you here, it’s pretty easy to consider treatment, no matter where you are, because the lesion is pretty close to the macula. But in small lesions, and the patient with good visual acuity, and a mild vitritis, depending on the place you are, people might tend just to observe. The classic treatment is a combination of sulfadiazine, pyrimethamine, and oral steroids. The steroids vary in the size and the degree of inflammatory reaction, but for an adult, most people start with 40 milligrams. The most used alternative is a combination with sulfamethoxazole and trimethoprim, two times daily, combined, again, with oral steroids. And these two regimens are the most frequent ones. Some people might use also clindamycin and azithromycin, as alternatives, but they are not used very frequently. One question people have is: What’s the duration of the treatment? We should treat until the lesion is no longer active. Which is usually from 40 to 60 days after the treatment was initiated. So treat until we see a scar. That’s the main thing. But usually 45 days. Right? Here, an example — the same patient followed over time. Here we have an active lesion. We cannot see very clearly the fundus, because of the vitritis. And then we started treatment, it’s still active, and then there’s a formation of scar. So in this moment, we should stop medication. So what I usually do in the clinic — so when I suspect ocular toxoplasmosis, if the case is very clear to me, I already prescribed the drugs, and then I do the workup, the IgG, IgM, and other exams I want to order. And after 15 days, I like to see the patient, to reevaluate — see if it’s getting better or not. To check serology and to talk about potential side effects and change the medication if needed. Right? And then if everything is going well, I’ll reduce the steroid doses, and I’ll see the patient again, 30 days from this evaluation. Which means 45 days to the diagnosis. And if the disease is no longer active, I’ll stop all medications. And as I mentioned, everybody is at risk of having recurrences. So during the first year, I will see this patient more often. Like every 4 or 6 months. And then annually, if everything is okay. I mentioned the oral treatment, but for a limited number of patients, we can try, in cases where the patient for any reason cannot use oral medications, there are some articles in the literature describing the intravitreal injections of antibiotics plus steroids. As you can see here in this screen, the use of clindamycin, injected clindamycin, and here injected sulfamethoxazole and trimethoprim, combined with dexamethasone. We use it for just a limited number of patients, but it’s an alternative when a person cannot use oral medications for any reason. We don’t have a lot of treatment-related complications. The most common one is allergic reactions. And the patient might complain of rash, itching, and in this case, we should suspend medication, and try to find an alternative. And although rare — and will cause a big burden — is blood disorders like aplastic anemia. That’s rare, but it could be fatal. So we should take a look at the blood count. In cases that we are using these antibiotics mentioned. So here are different patients with skin reactions, due to sulfadiazine. The treatment varies depending on the place you are, but usually what people in France and Brazil do — these are two countries with an increased burden of the disease — so once the congenital disease is diagnosed, usually the baby gets treated for a year. Even if he or she doesn’t have ocular lesions. And when the ocular lesion is active, we’re gonna associate oral steroids. But no matter how the ocular involvement is, usually these babies get treated for a year. I mentioned a few times — we’re gonna talk with deeper details about recurrences. Who is at risk of getting a new ocular lesion? In theory, everybody infected is at risk, as I mentioned. So the parasite doesn’t get rid of — so the host doesn’t get rid of the parasite. Not even using these drugs. Right? That can happen in immunocompetent and immunosuppressed individuals. And statistically, by checking case series, we see that the closer we are from the last episode, we are in a higher chance of having a recurrence. As you can see in this article, I’ve highlighted here. So in the first one or two years of the last episode, we are in a higher chance. I’ll show you an example of a patient I saw. A 20-year-old healthy male. And he brought this image to me, saying he had an episode of ocular toxoplasmosis in 2007. And we were in 2014. And he was complaining about his vision. And we documented this lesion at that time. And then one year later, we saw the old scar and the newer scar. And he didn’t have any other recurrences so far. Example two. So that’s a lady with — so every lesion you see is one scar from a previous active episode. Right? So it’s even hard to count, because they kind of group. But we have maybe more than 10 lesions. So 10 ocular episodes. And the whitish lesion here is the active episode. As you can see here, we barely have retinal tissue in the macula. In the right eye. And we are concerned about having the same problem at the left eye. So in these cases, for any reason, she’s an immunocompetent lady, but for any reason, it could be — the parasite is more aggressive, or any problem, host-related problem, for any reason, she’s having more recurrences than an average person. And in this case we have the following question: Is there anything we can do to reduce the risk of recurrence? We didn’t have much in the last decade, but this very important article published in 2002 tested. So people with toxoplasmosis, they got treated accordingly, and once there was a formation of a scar, they were divided into a group that didn’t do anything, and they were just followed, and a group that used sulfamethoxazole and trimethoprim in a lower dose. Instead of a full dose, they took the tablets every other day. And this group of investigators, they showed that the group that used these drugs in a lower dose had a smaller number of recurrences. So about 12 years later, a different group used the same idea, but created a placebo group, and compared the same thing. And they saw the same feature. So the group that used a lower dose of sulfamethoxazole or trimethoprim got less recurrences than the group that took the placebo. And the same group followed these patients over a three-year period, and they kept seeing the same pattern of a protection, of these groups that used the drug. So right now, in cases where we have a patient who already lost his or her vision in one of the eyes, and is having a high number of recurrences, and they are good candidates to receive a low dose sulfamethoxazole/trimethoprim for one year. I don’t recommend to do that for everybody, but for these selected cases — and the good candidates are candidates who lost vision in one eye, are having recurrences in the other one — these are good candidates for a prophylactic dose of sulfamethoxazole/trimethoprim. We have multiple potential complications of toxoplasmosis. And I named a few. And this image is showing a vascular occlusion due to the parasite. But we can also have retinal detachment, choroidal neovascularization, ocular hypertension leading to glaucoma, macular edema, optical atrophy, and cataract, among others. The prognosis is usually good if we consider that more than 90% of the infected people won’t have ocular lesions. But if we see a referral service, we have a uveitis clinic, and we see this patient — so this is not what is happening in a population-based study, but seeing patients who are seeking for help to treat their ocular problem. So these attendings — I gave an example in the hospital where I’m based — one out of four eyes are legally blind. This causes a high burden in the area. We have a few conclusions about the disease. Toxoplasmosis is asymptomatic in most cases. Not everybody. Most people won’t get eye disease. Ocular toxoplasmosis is one of the most common causes of posterior uveitis, worldwide. It can cause permanent visual impairment. And in most cases, we do the presumed diagnosis. We don’t isolate the parasite DNA. And the presumed diagnosis will be easier when we see a focal retinitis, and the person should have a positive serology. And the diagnosis is very challenging in atypical manifestations. Not necessarily, but more frequently in immunocompromised individuals. And as I mentioned, since drugs only act on the tachyzoites, which means the active lesions, every infected person is at risk of having recurrences. And unfortunately, we never know when they will happen, who will have recurrences, and in what part of the eye. This is what I wanted to present to you. And I apologize for the internet issues we had. And now I’m happy to answer any potential questions. And after the presentation, I’m also happy to answer any other questions through email. And you have my email listed here. So I’m gonna answer to everybody. So the first question… What lab investigations do you prefer? I prefer IgG and IgM. Do you have screening in pregnancy? In endemic areas, such as Brazil, it is mandatory. So every pregnant woman will get tested. So I recommend that in endemic areas, it should be performed. Again, IgG and IgM. And in case we have the IgG, in case we are not sure if the pregnant woman got infected during pregnancy, we can do the IgG avidity. Next question is: Why ocular toxoplasmosis mostly occurs at the macula. This happens in congenital infection, not… Sorry. This would happen in congenital infection, and the theory we have is that since intrauterus, the vascularity of the retina starts from the optic disc to the peripheral parts of it, one theory is that the disease is more often located at the macula, because it’s impossible to have peripheral lesions if we don’t have peripheral vascular tissue at that moment. Another question: Do you usually do serology in every case? Yes, I do IgG/IgM in every case. And when the patient returns, if we are treating him or her for toxoplasmosis, and the IgG turns out to be negative, we should think about a different cause of uveitis. Right? Because obviously in order to have ocular toxoplasmosis, the person should have positive serology. How does toxoplasmosis cause cataract? So cataract is a feature seen in every case of intraocular inflammation. Or uveitis. The same thing for that. So the uveitis in general, regardless of the cause, can cause cataract. Alternatives, if we don’t have pyrimethamine, I suggest sulfamethoxazole and trimethoprim as the first option. About the oral steroids… So it’s hard to measure. What causes the most damage in the retina. Is it the parasite? Or the inflammatory reaction? So in cases of an intense inflammatory reaction, we believe that the steroids would help to reduce inflammation and reduce the involvement of the retina. Right? And it varies, the doses you can have, depending on the degree of inflammation. What is your preferred antibiotics for active retinitis? It varies according to the person. So if we do a survey, people might respond differently. But I prefer sulfamethoxazole and trimethoprim, because it’s much easier to obtain at the pharmacy. At least here in Brazil. And it is less tablets per day. So two tablets a day would work. So if you use sulfadiazine, it’s multiple tablets, multiple times a day. So that’s the main reason I prefer sulfamethoxazole, combined with trimethoprim. Do you give steroids same day as antibiotics? And what dosage? Yes, at the same day — we just have to orient the patients, that they should not take steroids without using antibiotics. Right? But we can start at the same day. The dosage varies, according to degree of inflammation. But in general, for a healthy adult, like weighing 60 to 70 kilograms, usually I start with 40 milligrams. That’s what I do most often. When do you introduce steroids for acute acquired cases? So I think in this case, the person is asking about acute cases with ocular involvement. Usually at the moment of the diagnosis. So I prescribe antibiotics and steroids at the same time. So usually they start at the same day. Can we differ toxoplasmosis from toxocara? That’s a very good question. Sometimes it’s hard to differentiate. In areas where the prevalence of toxoplasmosis is higher than the prevalence of toxocara, if you consider that the patient is having toxoplasmosis, you’ll have a higher chance of getting it right. But usually cases of toxocara will have granuloma under the retina. And the toxoplasmosis — usually the problem is within the retina, as in some images I showed you. Usually in toxoplasmosis, the vitritis is more located overlying the lesion, and in toxocara, that’s not the case. The vitritis might get diffused. But that’s a good question, and it’s not that easy to differentiate in some cases. Another aspect of toxocara — we see it more often in children and adolescents, because of the way we might get infected. While in toxoplasmosis, the disease is more spread between age groups. Another question: How we prevent recurrence? It’s by using a low dose of antibiotics, and the only ones that were tested is the combination of sulfamethoxazole and trimethoprim. And instead of using one tablet two times a day, we use it one every other day. And the principle for that, since no drugs are able to eliminate the parasite from the host, the principle for that is that, between recurrences, if we have a low dose of antibiotics, even before the patient starts complaining about his vision, and even before we see an active lesion, the person has a certain level of antibiotics circulating in their blood. That’s the principle. What is the dose and presentation of steroids? So usually oral steroids, 40 milligrams. If we have associated anterior uveitis, we can use steroid drops as well. Which do you prefer on steroid regimens? Single dose or divided dose? Usually single daily dose. So, for example, 40 milligrams will be two tablets of 20, taken in the morning. As an example. What antibiotics will you use if you can’t get sulfamethoxazole and trimethoprim? I would try sulfadiazine and pyrimethamine. As an option, we could do clindamycin alone, or in combination with pyrimethamine Do you see ocular cysticercosis? What’s the differentiation? I don’t see it very often. The cysts can be in the retina or at the vitreous. It’s not very common. Or even at the anterior chamber. Again, not very common. While the toxoplasmosis is mainly in the retina. So the main tissue affected is the toxoplasmosis. And that aspect, that headlight in the fog, is something that will help you to think more of toxoplasmosis than cysticercosis. So we see the vitreous has inflammation, but this inflammation is located more next to the lesion. That will help you more frequently. What’s the role of sub-Tenon’s steroids? The advantage in general is that its effect will last for two or three months. But I don’t suggest you to use in cases of active ocular lesions. I never had a case like that, but by seeing in conferences, I saw some cases that people injected sub-Tenon’s steroids, and the person discontinued the antibiotic for any reason, like they could not get the medication or had an allergic reaction, so the patient wasn’t using antibiotics, but the sub-Tenon’s steroids was there, so it caused a very big and severe lesion. So I would not use sub-Tenon’s steroids in ocular toxoplasmosis, as a general recommendation. What is the follow-up of newborns with congenital toxoplasmosis with no ocular findings? That’s a very good question as well. I would see them once they are born. And we would see no ocular lesions in this case. I would reinforce them to get treated, even without ocular lesions. And I would see them… Well, at birth, and then at three or four months, and then three months later, which would be like six months of age, and then at 12 months of age, and then once a year, ’til they could start… ’til they would be more able to tell us if they’re having any major problems. So more frequently, ’til they get one year of age, and then once a year, ’til they get, like, six years or so, and then every three years or so, but always reinforcing that any decrease of visual acuity, they had to come earlier. Is macular OCT needed in case of all toxoplasmosis lesions? No. Like, considering a patient where the old lesion is away from the macula, if the patient has a good visual acuity, and by checking the fundus, you see the macula is looking good, no. But if you are suspecting of a membrane, or a macular edema, yes, I would do that. But without anything you would consider that — I would not do it. Is it common to have recurrence after cataract surgery? That’s a very good question as well. The scientific literature does not show that, but some people, just in case, prefer to start the prophylactic treatment before conducting the surgery. But the scientific literature does not show that having a cataract surgery will increase the risk of recurrence. For PCR, which fluid do you usually use? Aqueous or vitreous? If you can do the vitreous, it’s better, considering that the lesion is at the retina. And you can get more material at the vitreous. But it’s definitely more invasive. So I usually do the aqueous for PCR. And in this case, the more inflammation you get, the better. The higher is the chance of getting a positive PCR. Right? So usually I do the aqueous, because it’s less invasive, and you don’t even have to go to the OR for that. What’s the intravitreal regimen you recommend for active choroiditis? It’s very uncommon for me to do that. Every time I do it, I just check what is written in the literature. So at the top of my head, I don’t know the right doses. But I would suggest you look at the references I mentioned in the presentation. But it’s not that common. It’s something that we do… Let’s say twice a year, for that. In a service that we see 200 cases a year. Okay, I think I got all the questions answered. As I mentioned, if you have any other question, feel free to email me. So my email is [email protected]. I would like to thank you again for the opportunity, and I would like to apologize for the poor connection in the first half of the presentation. Thank you very much.

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November 22, 2018

Last Updated: October 31, 2022

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