Case guesses:
Håkon writes:
Hello again from sunny Athens Ga, 88 and sunny here. Given the questions about contact with cats or undercooked meat my guess for this weeks two cases are both Toxoplasma Gondii. Given the cat questions for the first and the HIV positive status for the second patient this was the parasite that came to mind first. Second to this was GAE (Granulomatous Amoebic Encephalitis) – from the amoebae: A. castellanii. Less likely though so I settled for toxo. Sulfadiazine for treatment I assume?
Thanks again for another great episode.
Håkon
Owain writes:
Dear TWIP team,
I think both of these patients have quite different manifestations of toxoplasmosis!
I like the use of both cases to illustrate the broad disease spectrum – very helpful!
Hope you’re all well,
Owain
Justin writes:
Hello TWiP presenters,
It is 14C and rainy here in Ontario Canada, a nice change from the smoky weather we have been having lately due to wildfires.
My guess for the double case from TWiP #217 is toxoplasmosis due to the flu-like symptoms and eye disease of the older patient, and the headache of the immunocompromised patient.
Thank you for the lovely podcast,
Justin
Loren writes:
Greetings to my esteemed teachers of the Microbe TV universe.
My diagnosis is Toxoplasma gondii for both patients. I would have been clueless without the hint about the same diagnosis fitting both patients. I did not use Chat GPT (boring) but did go down quite a few search engine rabbit holes that finally led me to the fine NIH web site (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7157559/). I learned much about toxoplasmosis, in particular how common the infection rate is both worldwide and in the USA. Also about the reversible differentiation from the bradyzoite (chronic infection, usually suppressed by healthy immune system, not really treatable) to the tachyzoite (active infection, new or reactivated, drugs exist for treatment) stages in the infected host.
The first gentleman (60s, HIV negative, works in IT for bank, got all the right prophylaxis and treatment for COVID) is suffering from a reactivation of a dormant infection with Toxoplasma gondii in addition to his PASC or possibly creating all the symptoms that might otherwise be interpreted as PASC. The initial infection was likely immediately prior to the incident he reports from several years prior, with symptoms of fever, sore throat, tender lymph nodes for a few weeks and then ongoing sleep disturbance and fatigue for many months, which eventually went away. To be explicit, the symptoms went away, but T. gondii never goes away, it just lies in wait. Presumably in his case it is encysted in the brain and CNS. I am fabricating a story to go along with this, with a guy in his late 50s who has heretofore led a structured life deciding to do something a little bit out of the ordinary, like take up with a new partner (who has cats), travel, go out to eat, and generally live it up in comparison to his previous habits. Maybe he just took up gardening. My fanciful story is just to explain a change of environment that exposed him to T. gondii when he previously had not been so exposed. Pardon my digression.
The episode of COVID in September 2022 somehow woke up the dormant T. gondii, presumably because the immunological resources previously used to suppress it were distracted and spread thin by the coronavirus infection. Also Daniel mentions in passing that this gentleman is a remote worker, providing IT support via Zoom and other platforms. Maybe he was given this assignment as a reasonable accommodation to an immune-compromised condition not otherwise mentioned. Or maybe he is immune-compromised but without that being diagnosed, and his working remotely is just a coincidence. I hate to disregard this bit of personal information (or any other) in case it is relevant. I understand that those of us in our 60s do experience a decline in immune system vigor, so the age of the patient may be relevant. However it momentarily escaped immune suppression, T. gondii took the opportunity to work on trying to complete its life cycle, with quiescent bradyzoites morphing into active tachyzoites, reproducing the symptoms of sleep disturbance and fatigue experienced in a previous illness. The eye was either newly infected or the reactivation of a previously dormant cyst created the symptoms of elevated intraocular pressure and vision abnormalities, and persistent fatigue resulted from the body’s ongoing efforts to fight off the infection, diverting resources from the more desirable zest for life and energy for having fun of all kinds. A blood test for antibodies can distinguish between an active infection and a previous infection presently dormant, so his test could have confirmed an infection recently active. I wasn’t sure what was meant by URI symptoms, but assuming it’s “upper respiratory infection,” I don’t know how to fit that into this case.
Patient 2, the gentleman in his 30s (went to ER for left arm weakness) was probably previously unaware of his HIV status and not under any sort of regular medical care. If so, he really had a lot to take in. The COVID infection must have been the last straw for his immune system, and a previous latent T. Gondii infection reactivated with a vengeance. Complications from T. Gondii infections are very common and well-known in persons living with HIV. Interferon gamma (IFNγ) and its production by CD8+ T-cells are essential for controlling the proliferation of T. gondii tachyzoites. The high “viral load” (relating to the HIV, I understand that the terminology is somewhat problematic) and extremely low T-cell count would likely have led to the patient being started on antiretroviral therapy without delay, as Daniel mentioned that the patient had already commenced some sort of therapy. The finding of a lesion in the right side of the brain upon CAT scan, inconsistent with stroke but consistent with a common infection seen in HIV-positive persons would have led to the referral of this patient to a pre-eminent academic center for the diagnosis and treatment of infectious disease. His headache symptoms could be explained by the observed lesion, presumably reactivated, and the left arm weakness, preceded by the headache, could also be caused by the observed lesion in the right side of the brain.
Wishing both patients good outcomes and glad they are in good hands.
I never miss an episode, but often listen later, trying to find nooks and crannies of time while driving or performing other necessary but tedious chores.
Best regards,
Loren
Kimona writes:
TWiP 217
Greetings again from Vermont!
A man in his 60s who has had ‘no cat exposures’ – is pure poppycock! But perhaps I state this in an effort to make both these men’s diagnosis conform to toxoplasmosis. Its like maneuvering that puzzle piece into a slot where you know it may not belong….
Toxo is my best guess for these two men presenting with CNS involvement and no mention of travel, hiking, lake swimming, poor sanitation, animals, or unusual diet, and residing in the Northeastern US. This protozoan is ubiquitously found throughout the world. It can be acquired from ‘cat feces exposure’ (the definitive host) but also from eating undercooked contaminated pork, beef, or lamb (intermediate hosts) and can persist asymptomatically in a healthy person for long periods of time – until perhaps the immune system is weakened.
Patient #2 is HIV+ with a very low T cell count and susceptible to opportunistic infections or reactivation of a dormant state. The hypodense lesion on head CT can certainly represent CNS toxoplasmosis which would produce encephalitis, headache and then focal neurological deficits such as his left arm weakness.
Patient #1 is perhaps not as straight forward….. a recent Covid illness, cold agglutinins, and an eye problem. The cold agglutinins could indicate an autoimmune hemolytic anemia following his SARS-CoV-2 infection, leading to further immunodeficiency. His illness a few years prior could have been acute toxoplasmosis, which clinically can mimic mononucleosis. But even a true EBV infection can in rare cases take on a chronic active state and induce a progressive immunodeficiency involving both B and/or T cells….Who knows… T. gondii may have lain dormant in this man since exposure in childhood (playing in the sandbox where the neighbor’s cat would visit) and is now reactivated due to his weakened immune system. His eye ailment may be uveitis or retinochoroiditis as seen in ocular toxoplasmosis.
Diagnosis can be made by PCR or detecting IgG or IgM antibodies on serology – IgM being more indicative of an acute infection.
Treatment of toxoplasmosis in immunodeficient patients uses a combination therapy with pyrimethamine and sulfadiazine for both neurologic and/or ocular disease. In a healthy individual, treatment is often not required.
However, IF these two patients have disease caused by two different parasites, then I would also consider a tick borne infection such as Babesiosis, for Patient #1. B. microti has become more prevalent in the Northeast and can exist in a carriage state for long periods and then undergo reactivation, similar to t. gondii. Several articles also describe the importance of CD4 T cells in the clearance of babesia from within red blood cells. Not sure it would explain his eye ailment though….?
As always, in eager anticipation and sincere appreciation, Kimona
Paul writes:
Hello from Petoskey, Michigan: 30 miles from the University of Michigan Biological Station where I recently learned Dr. Deplamier spent educational time in the 1960s.
These two cases are examples of Toxoplasmosis in an immunocompetent and immunocompromised host.
Case 1: Toxoplasmosis with ocular involvement. The test suggesting the diagnosis was likely IgM serology to indicate recent infection. Most cases resolve spontaneously in the immunocompetent. Treatment of a symptomatic case with ocular involvement would be Pyrimethamine with Sulfadiazine and Leucovorin. Differential diagnosis of parasitic diseases with ocular involvement in the U.S. would include Toxocariasis and Acanthamoeba which have clinical stories quite different from this case.
Case 2: Cerebral Toxoplasmosis in a patient with HIV with CD4 count < 50. Differential diagnosis is complicated including TB brain abscess, cryptococcosis, amebic brain abscess, neurocystercircosis, nocardiosis, invasive aspergillosis, and lymphoma or other malignancy.
Diagnosis in HIV disease is complicated: serology may be negative in the immunocompromised. Performing a spinal tap for cerebrospinal fluid for diagnostic studies in a patient with a brain mass risks the catastrophic complication of brain herniation. Brain biopsy is invasive and risky. Treating for 14 days with Pyrimethamine/Sulfadiazine/Leucovorin, observing the response and doing invasive testing if there is no response appears to be the safest strategy. Anti-retroviral treatment should be started after initial anti-parasitic treatment.
Dr. Paul Blanchard
Letters
Obadah writes:
Hi Vincent,
I’m a regular listener to TWIV, and really love the way you explain things clearly.
Anyway, the reason I’m contacting you is because our family has recently got scabies and it took us 5 long months to get to the right diagnosis!
I feel this is a disease that both parents and physicians should be educated on.
The main issue was every doctor seemed to confuse it with Allergy/eczema and even when I suggested Scabies after googling our symptoms, the doctors always look between the finger and wrist then rules it out.
Well in our particular case there was nothing between the fingers until 5 months in, and even then it was only 1 out of 4 infected family members that displayed this.
It was only after I got me a cheap amazon usb microscope and my wife (non medical) mastered the art of skin scraping that we got photo and video evidence to show the doctors so they won’t go back to eczema crap.
By the way during that last month were some doctors were saying it might be scabies no, but no one here in Ontario Canada would dare to prescribe ivermectin in addition to the Permethrin cream, I guess the whole ivermectin covid crap harmed the wrong people.
We did two applications of permethrin cream all of us 2 weeks apart and the leaflet tells you that the itchiness could persist up to 6 weeks so we went back to our normal lives, and then 4 weeks from the second application we managed to see live mite all over our bodies and that’s when we found a new family doctor and showed him the evidence that we got oral ivermectin and took it a week on top of yet another permethrin application.
So far we seem to be doing well and no sign of new mites, still have a second dose of ivermectin 14 days from the first one and hoping for the best.
Sorry for the rambling and ranting and appreciate you reading all that.
Best Regards,
Obadah
Jillian writes:
Hello!
I just wanted to reach out as listening to the latest episode of TWIP I noticed that my guess was skipped and sadly I realized that I’d accidentally switched case number 212 with 121!!
With that in mind I wanted to quickly send along my response to the 1 “cent” question regarding the pronunciation of centimetre for your interest.
I have to say this was almost as interesting as the case study, as Actually I’d never heard it pronounced as “sonti”meter before, in fact a previous episode had found me on google, searching for a blemish-specific measurement that I was unaware of!
In discussing with my friends though, we suspect the pronunciation is connected not to Canadian English at large (What aboot t’em colours, eh?), but rather could suggest a Quebecois-specific linkage, afterall “cent” is pronounced “sont” when it is 100 en francais.
It also seems like there might be some connection to French as being seen as a “more elite” language at some of the long established medical schools
https://www.diagnosticimaging.com/view/radiology-grammar-police-centimeter-or-sontimeter/ https://linguaphiles.livejournal.com/2351091.html
Hope you found that as interesting as i did! All the best
(And I’m glad I guessed right on the case as well!)
Jillian
Joshua writes:
Dear Doctors Despommier, Griffin, Naula and Racaniello,
I trust that you, your loved ones, and all my fellow listeners, are enjoying the festive season. Nowadays, however, thanks to your addictive podcast to which I have been glued during the Christmas holidays, I view the egg nog, the turkey, the ham, and even the plum pudding with some alarm – what pesky parasites perhaps proliferate within these and other delicious delights? It is a warm 27°C this afternoon here in Launceston, Tasmania, on this, the last day of 2022. I must confess I await 2023 with trepidation bordering on dread after all the world has been through during the first three years of the twenty-twenties…
But on to the case! Initially, I thought that the young boy, malnourished but with protruding abdomen, was the victim of an infestation with a mass of Ascaris lumbricoides worms. Such a bolus can lead to death if it causes blockage or perforation of the intestines, which could have been the cause of the tragic demise of his older brother. In areas where ascariasis is common, mass deworming campaigns should be carried out, but I do not know if the region around Jinja in Uganda has benefitted from such periodic treatments.
However, when I thought to look up the meaning of the “ascites” suffered by the lad, I found that it refers to a fluid build-up in the abdomen, which is caused, not by ascariasis, but by schistosomiasis – and that dovetails with the reference to the boy and his brother having lived by the shores of Lake Victoria. Therefore, I must change my diagnosis to an infection by the parasitic helminth Schistosoma mansoni, whose malign effects can lead to death in various ways, as happened to the boy’s brother. Again, a mass annual administration of praziquantel to all residing in endemic areas is highly recommended, but I do not know if that is done in Uganda. The drug must be given twice, some weeks apart, as it kills only the adult worms.
Now for some peculiar Christmas presents – parasitic, but not infectious – for the TWiP team to enjoy!
For Dr Despommier, I will mention that Tasmania used to have a severe problem with hydatids caused by Echinococcus granulosus. “In 1966 over half of adult sheep had hydatid cysts, and more than 1 in 8 rural dogs had adult worms. In the 1950s Tasmanian surgeons operated for human hydatid disease about once every week” and “Hydatids caused the death of a Tasmanian child every few years until 1968.” However, government action commenced in 1965, testing and quarantining infected dogs and sheep, and “the last new human case was diagnosed in 1976.” Thanks to this eradication campaign, Tasmania was declared free of hydatids in 1996.
(Source: https://www.utas.edu.au/library/companion_to_tasmanian_history/H/Hydatids.htm)
Next, I must thank Dr Griffin for alerting me, via a mention some years ago on TWiP 129, to a very rare endemic Tasmanian helminthic disease of which I had never heard, parasitic myositis caused by Haycocknema perplexum. Years ago, a visiting friend of my mother made the adventurous food choice of a rare possum steak that looked like quivering meat jelly – hopefully the marsupial meal did not conceal nematodes awaiting their own feast of fresh flesh. Doubtless, in his time in Colorado, he treated cases of Rocky Mountain Spotted Fever – but has he ever heard of its Tasmanian equivalent, Flinders Island Spotted Fever? It is caused by the bacteria Rickettsia honei, transmitted by tick bites; the ticks are parasitic on native reptiles.
For Dr Naula, I will make reference to the well-known devil facial tumour disease (DFTD), a transmissible cancer, first identified in 1996, that has gravely reduced the numbers of the Tasmanian devil (Sarcophilus harrisii), leading to it being listed as an endangered species. It is the largest remaining carnivorous marsupial, as the Tasmanian tiger (Thylacinus cynocephalus) became extinct in 1936. On display in the local museum is a very sad silent movie of the last thylacine pacing in its cage at the old Hobart Zoo; at a local zoo, I have seen the Tasmanian devils being fed (they chomp through kangaroo bones like butter), and I hope they will not go the same way. I haven’t yet listened to the discussion of this disease on TWiV 371, but will soon do so!
Lastly, for Dr Racaniello the poliovirus expert, I will mention the Tasmanian infantile paralysis epidemic of 1937 to 1938. This was the second-worst per capita epidemic of polio ever recorded (only surpassed by the 1924 Icelandic outbreak), with a case rate of 421 cases per 100,000 people. (Anne Killalea, The Great Scourge, Sandy Bay: Tasmanian Historical Research Association, 1995.) What is now a local school for children with special needs was established in the aftermath of that epidemic as the Home for Crippled Children. I know a retired nurse who was born ten years later, but still remembers her mother being very anxious about letting her visit the neighbourhood playground, such was the fear, even in the nineteen-fifties, of catching poliomyelitis.
May I finally thank him for the fascinating interview on TWiV 962 with Dr Chiara Mingarelli about black holes and related topics – my honours degree was in astronomy, and I have always retained my childhood fascination with outer space.
Yours sincerely,
Joshua.