I will venture into a guess, given that I’m a TWiP-trained electronics engineer. I grew up in Venezuela where I contracted Ascaris lumbricoides, head lice, amoebiasis and even cutaneous larva migrans from playing in a sand pile contaminated with cat feces. I cannot believe that I, growing as a middle class boy in Venezuela, got more parasites than the patient, who is a refugee from Africa and had a dramatic journey. I can only suppose he had been given a course of Albendazole at some point and so my guess would be neurocysticercosis: after the cyst is killed by Albendazole, the inflammatory reaction sets in, and would be consistent with the neurological symptoms. He would have ingested the eggs of Taenia solium at some point in his journey, probably from soil contaminated by a pig farm.
Dear Twip, Twipp and Twippy
For my main guess I’d have to go with African Trypanosomiasis caused by Trypanasoma brucei gambiense. This nasty critter can be obtained from the bite of a Tsetse fly which is endemic to central and western Africa. The trypomastigotes then spread throughout the body (including the lymph nodes which leads to the lymphadenopathy) and divide by binary fission. The offspring sometimes have differing surface glycoproteins. As a result, your immune system makes IgM and IgG for whatever is prominent initially, but a few trypomastigotes survive the onslaught and repopulate (leading to the recurrent fever.) You are left with a chronic infection where you make tons of different antibodies desperately seeking to eradicate this unwelcome pest (which leads to the elevated ESR and antibodies). The constant battle between your immune system and this foreign invader releases tons of cytokines which lead to an anemia of chronic disease (which may be normochromic and microcytic.) I would get a blood smear to confirm this diagnosis.
My active alternative diagnoses are:
Trypanosoma brucei rhodesiense: Very unlikely due to the fact that it is usually fatal within a few months while gambiense can result in a chronic infection.
Plasmodium falciparum: Would be a nice trick since we just had a Twip on cerebral malaria. It fits somewhat well (the relapsing fevers and neurological symptoms), but would most likely have been checked for before he got to Canada.
Toxoplasmosis: The patient is HIV negative, but I don’t recall a white count. It is unlikely that immunodeficiency would be missed and toxo has a pretty distinct lesion of MRI.
Neurocystercicosis: I would consider him lucky if he was able to find a pig to eat while running away! Unfortunately, almost nothing fits with this diagnosis except the neurological involvement.
Thank you for all the good work and I hope that this patient did well!
MD Candidate at Hofstra Northwell SOM 2018
Dr. Wink writes:
RE: Loopy African expatriot
I’m guessing T. b. gambiense infection (West African sleeping sickness), Eh?
Dear TWiP Trio (And Guests)
After doing some serious internet research and discussion with my parasitically-literate girlfriend Megan, we would like to hazard a guess to the case of the refugee from the Democratic Republic of the Congo. We believe he has contracted a case of African trypanosomiasis (AKA Sleeping sickness) caused by a Trypanosoma brucei species, most likely T. brucei gambiense.
We have come to this conclusion for a multitude of reasons:
- No eosinophilia in T. brucei infections
- On and off fever, anemia are typical symptoms
- The patient had an erratic sleep cycle
- The mental symptoms (mood swings, depression, hallucinations, delusions) are symptoms of this parasite (but also exacerbated due to stress/PTSD
- More than 80% of sleeping sickness cases originate in the DRC
- There is evidence of autoantibody formation with African trypanosomiasis
- The 1-3 year incubation period is consistent with that of African trypanosomiasis
- The enlarged axillary/inguinal lymph nodes (or Winterbottom’s sign in the neck) are suggestive of cerebral infection due to African trypanosomiasis
- The malaria drugs as well as the ivermectin should be ineffective against Trypanosome brucei
- Lower back pain may be the bite zone from the tsetse fly, or the parasite itself in the spinal cord
Performing a lumbar puncture to collect cerebrospinal fluid should reveal trypomastigotes. Treatment should include i.v. eflornithine and/or nifurtimox to cure 2nd-stage infection, while 1st can be cured with pentamidine.
Thank you once more for your many informative podcasts.
I’m a TWiP-educated parasitology hobbyist. I have a bachelor’s degree in chemistry and I hope to apply for an MD/PhD program in August, in immunology.
My guess is: T.b. gambiense. Or possibly another subspecies in the Tryanosoma brucei species (eg T.b.rhodiense).
I think the man (or his central nervous system, most of the time) is a great reservoir for trypomastigotes. Ivermectin is known to have difficulty crossing the blood-brain barrier (especially in mammals), so it isn’t likely ivermectin treated the advanced stage West African sleeping sickness in his brain. The periodic fever is a manifestation of the life cycle of the parasites and the patient’s immune response to the parasite. Periodically, the trypanosoma in his brain, I suppose, reach a certain parasitic-load so as to break free of the brain cells where it is safe from antibodies and macrophages and the like. His body would appear to have developed an immune response to trypanosomes circulating in his bloodstream (if these parasites somehow result in more oxygen free radicals in his blood and anemia, then the p-ANCA antibodies his neutrophils are synthesizing are in response to this elevated oxygen free radical concentration).
To find out, you could examine his CSF under a microscope, or his blood shortly before he experiences a fever (though I’m not sure how you would anticipate it), or you could treat with Melarsoprol and see if that helps or not.
How did I do? What do you all think?? Thank you for your podcast!
Dear TWIP Trifecta,
Here I am, and many apologies for being AWOL for TWIP 102. The long march of spring school holidays is upon me, severely cramping my style. I hope this finds you well. The yo-yo-ing weather finds it pretty warm today in lower Manhattan, currently 52 degrees F/11 degrees C.
It is remarkable, first of all that your guest, Dr. Libman’s patient managed to survive to the point where he would have to deal with a parasite and how horrible, on the other side, to be brought so low by one after making it through so much. We don’t know the outcome but I do hope he managed to get some relief.
My guess at a diagnosis for the 42 year old patient originally from the Democratic Republic of Congo is that he is harboring Trypanosome brueci gambiense and is suffering from West African trypanosomiasis.
The symptoms of West African trypanosomiasis are very similar to those that the patient experiences: substantial cognitive problems including depression and psychosis, highly disordered sleep patterns and exhaustion, intermittent fever, and some anemia. West African trypanosomiasis can also take an extended period of time (years) to make itself manifest, unlike the East African form of the disease, which progresses extremely quickly. (This parasite has complicated and shifting methods to getting around the human immune system, which may account for some of the cyclical aspects of the patient’s symptoms, in addition to the parasite being so hidden for so long.) The slow progress of the disease explains why the patient’s problems were thought initially to be more psychiatric in origin.
One clue we were offered is that the gentleman had an “injury” to his back, though we don’t know what sort of injury it was. Is it possible that this injury was the wound from the tsetse fly bite? I have seen many descriptions of these bites as being very painful and if he was bitten while he was in hiding, it could easily have gotten infected.
I am, of course, very interested to hear what exactly the patient’s lumbar puncture revealed. I read about a very similar case in which a young woman arrived in the Netherlands from Angola with very similar symptoms and a definitive diagnosis was only able to be made after at least two lumbar punctures. (Like the patient, her scans revealed somewhat vague abnormalities.)
I did look into other parasitic infections of the central nervous system, but trypanosomiasis seemed like the best fit. One thing I was wondering is whether the patient’s life of extreme stress and near starvation before he arrived in Canada may have slowed the progress of the disease, so that it wasn’t until he arrived in a “safe” place that he recovered enough for the disease to really hit its stride.
As always I look forward so much to your podcasts.
Thank you so much for everything and all best wishes,
I am going to go for schistosomiasis for the 42 yo man who was forced to live in the jungle of the DRC. I will go further and say S. mansioni with a nod to a S. guineensis, which is a new one for me.
I encountered S. japonicum as a medical officer in the US Navy. A rectal biopsy showed an incidental finding of S. japonicum mostly calcified eggs in a man who was a prisoner of war in WW II in the Pacific. The schistosomias was not a clinical issue. That finding stimulated a short term of research in schistosomias and its interaction with viral hepatitis. I still remember the mice waiting to have their tails dipped into the water tank housing the infected snails. At that time the Navy had a medical research unit in Egypt—that was a different era.
I have one question related to the lady from India with echinococcosis probably from dog exposure. I am a “dog person” and unabashed anthropomorphizer. I have an acquaintance who is into the current fashion of feeding dogs only raw meat of uncertain origin. I would think that is a risk for echinococcus infection in the dog and pet owner. This meat is sold by some pet suppliers. What is your opinion?
Weather in Alabama is windy, 11 C after 3.5 inches of rain and tornado warnings last night.
Keep up the good work,
Greetings TWIP Trio from Creighton University in Omaha, NE!
The weather here is unusually mild for February with a current high of 8 C
I’m teaching Parasitology this semester and I enjoy playing the case studies while the students are in the lab. I like to have them guess the answer. So far, they’re doing fairly well. So keep those case studies coming!
Last week, I had them listen to TWIP 102 and asked them a few questions about the paper regarding eosinophils supporting Trichinella growth. I also had each of them formulate a question for you. I won’t overwhelm you with all 16 questions, but here are two I found particularly interesting:
- How does the parasite react/adapt to low nutrient/low glucose situations within the host? Does it die or does its behavior change?
- I would like to ask the TWIP trio if a larger increase in cellular oxygen availability would outcompete the increase of glycogen storage to prevent the transformation from aerobic to anaerobic cycles in the muscle cells? If the worm is unable to rely on the increase of glycogen storage within the muscle cell would it then die?
Thanks again for your time and dedication to TWIP! We really appreciate your work.
P.S. One of the students asked me if you guys get paid for doing TWIP. I just laughed 😉
Hope I’m not late for my diagnosis guess. Based on the set of symptoms presented as Dickson pointed I would first rule out a TB condition as a possible co-infection. Prefer a GeneXpert assay and a sputum culture as a screening test. Considering that we are looking only at parasitic possibility for now am ignoring other set of microbes.
In India I can affirm that a person will come to clinic only if that person is really suffering and is especially the case if they have poor economic conditions. So I believe that the patient in question has frequent haemoptysis.
I would suggest a sputum wet mount. Though lung biopsy is recommended in some cases, it doesn’t seem necessary at this point. The case appears to me like that of P westermani. I maybe wrong. Treat with Praziquantel.
Keep Twiping.. Won’t miss the TWiX show for any reason.
Varun C N
Department of Neuromicrobiology
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