Dear esteemed TWIP-Triumvirate,
My brief diagnosis to the illness of the guys who were desperate to baptise in Lake Victoria is Schistosomiasis, most likely caused by Schistosoma mansoni.
Many hints given in the episode aim at it: the rash with (Katayama-?)fever and shortness of breath weeks after returning home, (caused by the nodules in the lungs?), the elevated white blood cell count, notably the abnormal high amount of eosinophils.
In particular staying for hours waist deep in the water of an African lake – notice the healthy one who didn´t go into the lake – and not recognizing the village´s poor sanitation habits appear very inapt to me. And I will abandon any further (i.e. non-scientific) comment on the enterprise of baptising native people in some kind of crash course…
Many greetings from Wiesbaden, Germany,
(still science teacher at a german secondary school)
I found the note in Dickson´s ‘Parasitic Diseases’ extremely interesting that the Schistosomiasis’ symptom of blood in the urine in (ancient and modern!) Egypt was seen as a male version of menstruation and considered as a rite of passage for boys.
Dear Day TWiPPers,
Thank you once again for an informative episode of This Week in Parasitism.
After careful research, I would like to guess that the patient in TWiP has contracted schistosomiasis from a Schistosome species, most likely S. mansioni. This parasite has been found to be quite prevalent in Lake Victoria, and the rash, fever, and shortness of breath can all be symptom of schistosomiasis:
The rash is known as “swimmer’s itch” – although it is odd that the rash developed weeks after the man returned – typically swimmer’s itch occurs within hours of infection and does not last for more than a week but there are always exceptions.
The fever, known as Katayama fever, is a systemic immune response to the schistosomula as they circulate in the bloodstream to the liver through the lungs. The nodules in the man’s lungs could potentially be an immune response to the schistosomula within the lung tissue itself.
The fact that a fourth friend who did not go in the water did not show any symptoms point to a waterborne illness, however he did not eat much food either, which those who became ill did – however, i believe this is a red herring or an additional parasite could have been introduced in the consumption of local African dishes.
However, I believe that the rash, fever, and difficulty breathing are due to schistosomiasis. Keep up the well-researched and fascinating podcasts
Dear heralds of parasitic tidings,
Uplifted by the success of my first diagnosis, I will try to find out the pathogenic origin of the case of TWIP 105’s young man baptizing in Kenya. This time, there were lots and lots of possible sources of parasitic infection, and it almost seemed as if the missionary was intent on returning home with an infection of some sort. As my previous email was quite long, I will try to be brief this time.
To begin with, I used Dr Griffin’s CHINA mnemonic as a first selection for eosinophilia. Given the infectious nature of the pathogen (3 out of 4 friends showed comparable symptoms), connective tissue disease, idiopathic eosinophilia and neoplasia could be excluded. Allergies, the original diagnosis of the US doctor, might be a reason, but seems very unlikely given their recent travels.
A simple search on “parasites Lake Victoria Kenya” returned a number of hits suggesting that the idyllic shores of Lake Victoria are second to none when it comes to parasitic infections. As the majority of the hapless missionaries were infected, I guessed it would be a very common infection.
Common protozoans easily found on the local markets included entamoeba histolytica, giardia lamblia and balantidium coli, but these do not cause eosinophilia.
This narrowed the list down to Ascaris lumbricoides, hookworms and trichuris trichiura commonly infesting local food.
The other major parasites very prominently present in Lake Victoria are Schistosoma mansoni and Schistosoma haematobium, causing bilharzia.
Trichuris does not seem to fit the symptoms well at all.
Both Ascaris and hookworms (Ancylostoma duodenale and Necator Americanus) can cause Loeffler’s syndrome, with eosinophilic pneumonia.
Still, given the combination of rash, the fever and the lung nodules, I bet on Schistosoma. Drug of choice would be praziquantel.
I wonder why our guy even bothered taking malarone, while he threw all caution overboard when it concerned other parasites. It is ironic that their aquatic activity was baptism; if in one way or another the local population had escaped infection so far, I hope God’s blessing protected them while they were being baptized.
Greetings from a hot and humid Jinotepe (28 C at 8 PM).
Hello, TWiP team!
First, I’d like to follow up on episode 105 and mention the possibility that infected brine shrimp might exhibit gregarious activity. I’m uncertain if that’s known to be the case, but it certainly wouldn’t be the first time a parasite altered a creature’s behavior.
Now for the case study. Young male with travel history presenting with transient rash (which I would like to know more about, but I’m going to venture a guess that it wasn’t purulent, and was localized, probably to regions that had contact with water), fever, and shortness of breath. Exam shows lung nodules and eosinophilia.
The nodules, shortness of breath, fever, nodules, and travel history make me at once suspicious for Tuberculosis, but the incubation period seems rather short, the patient lacks the characteristic cough, and I would hardly expect eosinophils to predominate. Additionally, the other two baptisers falling ill with similar complaints suggests a shared infectious organism, with a shared exposure history. Such a high R0 in such a short period seems uncharacteristic of Tuberculosis.
Going with the eosinophilia, shortness of breath, and travel history, I would suspect hookworm, but he lacks some things we might expect, such as diarrhea, rash to the soles of his feet, and abdominal pain. Those seem like weak pertinent negatives, though, and it would be prudent to seek a stool sample.
My expectation, weighted most heavily by his (and his friends) all-day exposure to fresh water in an endemic area with recent run-off from populated areas, is schistosomiasis. The signs and symptoms fit reasonably well, also. A stool sample should nail the diagnosis, and indicate treatment with Praziquantel.
Thanks so much for the countless hours of edutainment!
My name is Christina and a graduate student in the infectious diseases program. I work with an avian virus but our graduate coordinator always invites us to branch out of our research focus and learn about other infectious agents. I’ve found the case studies on TWiP to be very entertaining and has revived my interest in parasites 🙂
And so, here’s my guess: I believe the patient has schistosomiasis. Schistosomiasis is found throughout the world and is common where there is poor sanitation. Consistent with the patient’s exposure to freshwater, this parasite is contracted in freshwater contaminated with Schistosoma cercariae. The cercariae are released by infected snails and swim around until they find a host and penetrate through the skin. After which, the parasites enter the circulation and pass through the heart, lungs, and then to the liver. Like in our patient, the parasite can cause widespread nodules in the lung. Acute schistosomiasis can present as rash, fever, cough, and shortness of breath, which occurs between 4-6 weeks after exposure. Eosinophilia is also consistent with a schisto infection. And so, it appears that our patient is experiencing acute schisto. A Google scholar search for schistosomes in Kenya led me to a paper that said that prevalence of Schistosoma mansoni in schoolchildren is 60.5% in an area around Lake Victoria and so our patient’s chances of exposure is probably high.
Thank you for all that you do and keep Twipping!
A fan from UGA
Lung fluke, Paragonimus sp
At first thought leptospirosis, but pulmonary hemorrhage wouldn’t look like nodules on CT
Dear TWIP Trifecta
How are you? Spring is creeping up on Lower Manhattan. Today it is murky, but 61 degrees F (16 C). I am very curious about this case and not sure if I have got a correct diagnosis, but here is an attempt.
In light of the patient’s long immersion while performing Baptisms in the waters of Lake Victoria in Kenya, I believe he may have Schistosomiasis. It makes sense that his initial doctor didn’t recognize his symptoms because there are not many cases in the United States, though one source suggests that 85% of the cases are in Africa, so given the patient’s travels and behavior, it may have been worth looking into diseases endemic where he had been traveling.
The patient’s symptoms are consistent with Schistosomiasis: he has a rash, some fever, and nodules in his lungs (which brings about his shortness of breath) and his extremely elevated eosinophils are all strong indications that he is hosting this helminthic infection. The timeline is also consistent with schistosomiasis. The patient (and the friends of his who went in to the water with him) didn’t start to present symptoms until several weeks after their exposure to the water in Lake Victoria, and the fact that they returned before exhibiting symptoms may have led to their later diagnosis.
Does the later diagnosis mean that the travelers might sustain greater damage or will they all recover just as easily as they would have had they been diagnosed earlier? There are long lists of potential complications from schistosomiasis, including squamous cell bladder cancer, neuron schistosomiasis, infertility, and renal failure. Are these men at all more likely to find themselves with long term sicknesses?
As far as a differential diagnosis goes, and perhaps what the patient’s first doctor suggested, these symptoms are so general that they could indicate an autoimmune disease or an inflammatory disease and perhaps the first doctor didn’t connect the symptoms to the patient’s travel since he had returned to the United States quite a number of weeks before his symptoms developed.
I am sorry to be writing in haste. I am struggling with a schedule in upheaval, but I am very eager to hear the answer to this mystery.
As always, thank you so much for everything you do.
Sounds like Schistosomiasis to me.
Lake Victoria not the best for swimming or wading near the shore.
Used to need to pay someone to ingloriously carry us out to the canoes. The rash does seem a little delayed to me.
Temp is still about 27ºC as usual here.
Sorry no time today for a fuller DD.
Loved your story about eflornithine and the search to find a commercially viable way to keep it available for Trypanosomiasis. Those jewels make it worth coming back.
Allan in Kona
The water in the African Rift Lakes is not brackish, but it is hard:
A quick and easy way to add minerals to aquarium water for African Rift Lake cichlids is to use Kosher salt and Epsom salt — 1 tsp of each per 5 gallons. Calcium carbonate gravel also increases the hardness (and alkalinity).
For the TWiP #105 case study, the fish consumed from Lake Victoria might not have been a cichlid, but that reminder of colonial mismanagement, the Nile Perch:
And if it was a cichlid, it quite likely was an introduced tilapia:
# # #
When fish eat brine shrimp infested with cestodes, will / can the fish become victims of the parasites?
# # #
TWiP’s been especially great since the introduction of Dr.Griffin.
From a former Alaskan with hunter/fisher patients, the minute you said Alaska I said, “beaver fever!” otherwise known as Giardiasis.
I think this is correct because this is the only parasite I’ve ever heard Alaskans getting and it is KNOWN to come from drinking from natural streams, which carry the parasites from wild animals.
I have known several people with this disease, and I’m not a parasite expert, but from the symptoms including muscle pain, 30% eosinophils, and stories from hunters, I’m hoping I might be right.
Thanks, I love the show!
Center for Life in Extreme Environments
Department of Biology
Portland State University
I am an American studying medicine in the Philippines. It is an ongoing adventure; this is not the place for someone with OCD tendencies. I had a micro teacher in undergrad medical micro in Berkeley who required us to listen to the older podcasts as part of the curriculum and we would discuss it in class. So I have returned to TWIP when I found I was having a hard time paying attention in lecture. I am very thankful for the podcasts because they bring these bugs to life and it’s more fun this way.
I’ll have a go at this case, since it’s like a mini review for finals.
History revealed the patient ate bear meat made me think of Trichinella spiralis. Normally the example used is pork, but I remember a black bear on a life cycle image from the CDC.
Ingested “encysted” larvae mature into adults, which mate and produce “live” larvae, which burrow out of the intestine, enter the blood system through the mesenteric vessels, and jump out and encyst in muscle tissue. This activates the immune system, causing inflammation, edema, increased WBC, fever, and myalgia. PE finding of bilateral periorbital swelling is consistent with Trichinella. Elevated muscle enzymes lactate dehydrogenase (LDH) and creatine kinase (CK) suggesting muscle injury or myopathy support the diagnosis.
According to the Katzung textbook the migration lasts 1 month and has a predilection for “highly active” muscle tissues including the diaphragm, tongue, masseter, intercostals, and extraocular muscles. I guess “highly active” because of the increase in blood flow. I guess we could do a muscle biopsy? I do not know if there would be enough muscle left over if a biopsy was done on the extraocular muscles.
Treat with steroids and mebendazole or albendazole. How do doctors decide between mebendazole or albendazole? Is it based on the patient or whatever is available?
Other parasites to consider:
Diphyllobothrium latum or Schistosomiasis: from drinking the river water or ingesting the salmon…which is caught in freshwater rivers.
Borrelia burgdorferi from deer ticks while walking around the woods hunting bear.
Dermatomyositis, which occurs in children or adults, may be caused by autoimmune response, presenting with bilateral proximal muscle weakness, skin rash of the upper eyelids, and periorbital edema.
Liver Cirrhosis secondary to Alcoholic Liver Disease or hepatitis, which can cause myalgia, diarrhea, and edema.
Poor nutrition can cause muscle pain and edema, though if it is June, wouldn’t there be vegetables available? I lived in Alaska when I was small and we had peas in the backyard.
Coliform bacteria: maybe the water source was contaminated somehow so both husband and wife became infected. That’s how I get my monthly diarrhea.
I personally don’t mind the side-comments, since for me it’s funny to listen to.
Thank you for sharing and teaching microbiology!
Hello Drs TWIP,
Thank you for the fantastic show, I love them all. I particularly love the new case reports, even though I never write in, I do enjoy thinking about them. I really enjoyed Michael Libman’s case of trypanosomiasis, he was a great guest and you should definitely get him back soon.
I am writing in now with some comments on your conversation on gene drives.
First off, I would like to respond to Chandran’s letter about gene drives. Chadran stated that Vincent’s concern that the cas gene could acquire a mutation and thus evolve around the gene drive system was a non-issue as the broken gene would just be replaced in subsequent generations by cas genes from the other parent. He is absolutely right about this, but the entire conversation misses the fact that most gene silencing does not happen by mutations in protein coding sequence, but in regulatory sequence. In the simplest case, if the gene drive locus did not include the promoter upstream of cas, a mutation to that promoter would silence the entire locus irrespective of how many times a functional cas sequence was swapped in by the CRISPR system. It would be easy enough to include the upstream promoter (as they did in the paper you discussed) in the cas sequence. However, there are many other repressive mechanisms that could do the same thing, for example acquiring some nearby runs of CGs could lead the whole region (both alleles) to be methylated and permanently silenced.
This leads me to the next point that came from the same letter: should we intentionally make a few species of mosquitoes extinct? My personal opinion is no, I don’t think that we are smart enough to know all of the ecological consequences of that action, and one needs only glance at Australia to see that our prior history of intentional ecological tampering for the greater good is not a great one. However, regardless of that, I personally feel that it would be impossible in this case: Anopheles gambiae has a population size in the billions spread across several continents with a very short generation time. A sterility gene drive is just about as powerful of a selective pressure possible, do we really think that that could possibly work? Even if evolving around the gene drive is a low probability event, we are talking billions of possible chances for it to happen. I think this would be a really interesting topic for you to discuss with Nels on TWiEVO.
On the other hand, the gene drive in the paper you discussed just targets malaria, that could possibly give the mosquito a selective advantage and thus actually work (although then there is pressure for the parasite to evolve quickly). Maybe we should do both? We could make the population crash and then release a second gene drive that makes the few remaining mosquitoes immune to Plasmodium. That would have a decent chance of actually getting rid of the malaria parasite completely, particularly if we combined it with a very well funded effort to treat everyone with latent malaria.
Also, Vincent, I wouldn’t be so certain that these mosquitoes will never be released. The burden of malaria is enormous, and I think people would consider it. If some random lab did it it would be a disaster, but if a UN panel of malaria endemic countries was convened and they voted to release the mosquitoes, I actually think it could happen. Malaria is just such a huge deal in so much of the world.
The weather here at Stanford is 18C, 63% humidity and overcast. We are finally getting a god series of storms in California and we actually have a flash flood warning, plus we are supposed to get 4ft of snow in the mountains this weekend, which is exciting. It is a strange winter though, because we are finally getting a lot of precipitation, but the snow line is very high, so we aren’t getting the huge build up of snow at lower elevations that usually makes for a good summer water supply.
Sorry for the very long email, but thank you for covering this very interesting topic and for running such great set of podcasts. Also, congratulations on the new website Vincent, I really like it a lot.
All the best,
Michael D. Dacre
Research Professional, Hunter Fraser Lab
Toxoplasma gondii Infection: Relationship With Aggression in Psychiatric Subjects
Emil F. Coccaro, MDa,*; Royce Lee, MDa; Maureen W. Groer, PhDb; Adem Can, PhDc; Mary Coussons-Read, PhDd; and Teodor T. Postolache, MDc,e
Objective: Toxoplasma gondii (T. gondii), a protozoan parasite that persists in host tissues, including brain, has been associated with several psychiatric disorders and with suicidal behavior. We sought to test the hypothesis that latent T. gondii infection, as manifest by circulating immunoglobulin G (IgG) antibodies to T. gondii, is associated with both categorical and dimensional measures of aggression.
Method: IgG antibodies to T. gondii were collected between 1991 and 2008 from 358 adult subjects with DSM-5 intermittent explosive disorder (IED), non-IED psychiatric disorders (psychiatric controls), or no evidence of any psychiatric diagnosis (healthy controls). Assessments of aggression, anger, and impulsivity, as well as state/trait anger, depression, and anxiety were completed. T. gondii seropositive status (IgG > 12 IU) was the primary outcome measure for this study.
Results: T. gondii seropositive status (IgG > 12 IU) was associated with higher aggression (P = .022) and impulsivity (P = .05) scores. When both aggression and impulsivity scores were controlled for, however, only aggression scores were higher in seropositive subjects (P = .011). In addition, T. gondii seropositive status and marginal mean ± SE aggression scores increased from healthy controls (9.1% and −0.66 ± 0.05) to psychiatric controls (16.7% and −0.27 ± 0.05) to subjects with IED (21.8% and 1.15 ± 0.06; P ≤ .05). These findings were not accounted for by the presence of other syndromal/personality disorders or by states or traits related to depressed or anxious moods.
Conclusions: These data are consistent with previous studies suggesting a relationship between T. gondii and self-directed aggression (ie, suicidal behavior) and further add to the biological complexity of impulsive aggression both from a categorical and a dimensional perspective.