Kevin writes:

RE: mitochondrial DNA (mtDNA) discussed Episode TWiP 171

The hair of the dog(matism) that bit me.

Your discussion of Amoebophrya and the dinoflagellates during TWiP 171 implied that transmission of mtDNA was exclusively maternal. Though not usually a big fan of Father’s Day, in deference to this seasonal potlatch I would like to raise a quibble (not a snippet) regarding this dogmatic statement (which, generally I agree with.) I think a nod to paternal leakage (such degrading nomenclature) is in order here. Paternal mtDNA transmission/inheritance is not uncommon among certain mussels. So that I am not accused of beating a dead mitochondria, I will leave off (almost) with Nature magazine NEWS AND VIEWS 14 January 2019 “Mitochondrial DNA can be inherited from fathers, not just mothers.” As the adage goes, “shit happens”. The TWiP team are always first to point out the exceptions to the rules, and for that I am grateful.

Kevin Carney



As a demonstrate of my long term interest in mitochondria, I direct your attention to my letter to Science dated 29 July 1988:

Mitochondria in Sperm

In Jean L. Marx’s article “Multiplying genes by leaps and bounds” (Research News, 10 June, p. 1408), the indefatigable long-distance swimmers, the spermatozoa, are described as bereft of mitochondrial DNA. Please reassure my gametes that this is incorrect.  


University of Illinois Hospitals and Clinics,

Chicago, IL

Response: Carney’s gametes can be reassured that they do have mitochondria. I regret it if my error caused them any concern.-JEAN L. MARX  SCIENCE, VOL. 24I

Suellen writes:

Thanks to Dickson Despommier for totally setting off my Hypochondria Detector with his story of the dressage riders in Massachusetts who all got toxoplasmosis from their indoor arena!

I board at a barn in Canton, GA where we have an indoor arena, and when I first moved my horses there 5 years ago, the arena was in pretty rough shape. Of course, I didn’t know that at the time, but after I got pneumonia TWICE in two years my husband started suggesting that maybe the dust in the arena was making me sick. I of course pooh-poohed that idea, but two years ago we got new footing in the arena and lo and behold! No more pneumonia, way less dust in the air. The old owner had never cleaned up the manure in the arena, which I now know is both bad for the footing and for the lungs of both horses and riders! The new owners keep the arena pretty pristine, so yay for that.

But, still, that Hypochondriac Warning System is buzzing in my head. Could I have contracted toxo during those bad years? Could my horse? Could my fellow riders? Yikes! How would I know? Before I embarrass myself with both my own doctor and my horses’ veterinarian, I’d like to get some more info from Drs. Griffin and Despommier. Not a diagnosis, naturally, but at least maybe discuss what the risk is of aspirating and inhaling cat/dog/horse feces — how likely is it that someone would contract toxo from such aspiration? I’ve never heard of it happening except in Dickson’s anecdote, but now I’m worried.

Until I know better, my dressage costume will be helmet, boots, gloves, mask, and maybe respirator. 🙂

Love your show.


in Roswell, GA

where it is already over 90 degrees this week!
PS Hey, after sending this I realized you guys don’t really know me that well and I might sound a bit hysterical in that email. I’m not. My question is a valid one — what is the risk of contracting something like toxo from aspirating feces? But most of the rest is hyperbole. I promise I’m not wearing a mask and respirator when I ride (it’s too hot here!) and I’m not totally freaked out. 🙂 Just my usual over-the-top way of communicating.

Case guesses:

Ben writes:

Dear metacyclic TWiPomastigotes

To borrow one of Dickson’s commonly used terms, this lesion sounds pathognomonic for cutaneous Leishmaniasis. I would guess L. panamensis because of the location, although it isn’t clear to me how well the distribution of these parasites corresponds with the countries they are named after. The mother definitely should be concerned about this ulcer, because L. panamensis has the capacity to cause mucocutaneous Leishmaniasis. Diagnosis in this location I assume would be by microscopy. I would guess that the best drug for treatment of the child would be paromomycin, either orally or injected but not topical, due to the ability of L. panamensis to cause mucocutaneous disease.

Something that has always confused me about the pathology of Leishmania is that the parasites are only found at the border of the lesion. As I understand it, the parasite infects the cells at the site of the sand fly bite, infecting cells and radiating outwards to find more permissive cells. If that is the case, what kind of cells do you find in the centre of the lesion? Do you only find cells that Leishmania cannot infect? If you find cells that Leishmania can infect, what advantage might the parasite get from replicating only at the border of the lesion?

I’ve taken a weekend twip across the English Channel and am currently in surprisingly sunny London where it is 22oC.

May your successful system continue to attract parasites like myself 🙂



Paper suggestion:

The authors show that an increase of erythrocyte cholesterol content inhibits the ability of P. falciparum merozoites to invade them, but serum hypercholesterolaemia does not alter invasion

Ben Liffner

PhD Candidate – Malaria Biology Lab (Wilson Lab)

Research Centre for Infectious Diseases

School of Biological Sciences

The University of Adelaide

Larry writes:


This is my first guess on a case. Not sure whether this is cheating, but I took a “painless” shortcut. The description of the boy’s leg lesion as “painless” seemed like a giveaway. I searched Parasitic Diseases, and found “painless” in two sections. In African trypanosmiasis, large painless chancres are discussed, but this doesn’t seem like a good fit for the boy in Panama, both because of geography and because his lesion was described as craterform, with a hard nodular border.

The other painless lesion discussed in PD occurs in cutaneous leishmaniasis. This lesion is described as a large ulcer with a raised, hardened edge. Exactly like the description of the boy’s lesion. Leishmania is endemic to the region where the boy lives, and he probably is exposed to sandflies at the times of day they are active.

PD cautions “that there are many other dermatological conditions that might be mistaken for cutaneous leishmaniasis.” If nucleic-acid amplification testing is possible in this very remote location, then that’s the best diagnostic approach, but it also might be possible to see the amastigotes by microscopy of a scraping of the healthy tissue adjacent to the lesion.

If Leishmania is present, treatment might be appropriate even though cutaneous leishmaniasis lesions normally heal spontaneously. Without treatment, there’s a chance that mucocutaneous leishmaniasis can develop. Because the lesion has been around for at least a few months, I wonder whether the boy is somewhat immunosuppressed, perhaps from malnutrition or another infectious disease? This would increase his risk for developing MCL.

Because the lesion was described as 2 – 3 cm, I think it can be treated by intralesional injection of pentavalent antimony, if the boy can be persuaded to tolerate the procedure.

I’m a little concerned that I’m guessing an organism that is referred to in the first word of the TWiP 171 program notes, but the description certainly seems to fit. Thank you, TWiP team, for setting the standard for excellence in science podcasting.



Kendra writes:

Hello TWIP Professors,

My guess for TWIP 171 is Cutaneous Leishmaniasis. Cutaneous Leishmaniasis is transmitted by sand flies. While feeding a sand fly injects the Leishmania species parasite into the host. The specific species of Leishmania should be identified prior to treatment. A treatment decision should only be made after species identification to prevent toxicity. The species can be diagnosed by nucleic acid amplification testing.  There are several different treatment options such as cryotherapy, liposomal amphotericin B, miltefosine, and azoles.

Differential- leprosy, paracoccidioidomycosis, blastomycosis, histoplasmosis, sarcoidosis, cutaneous tuberculosis, squamous cell carcinoma of the skin, basal cell carcinoma.




Parasitic Diseases 6th edition

Chris writes:

Greetings TWIPsters,

The persistent craterform lesion described in this case immediately brings to mind cutaneous leishmaniasis. The lesion is also non-tender, which is expected for the infection sight, unless it happens to be near a joint or has become painful with secondary bacterial infection. A confirmatory diagnosis could be made by scraping a sample from the margin of the lesion, which would contain live parasites, and either culturing the parasites or testing with PCR. Given the location and available resources, however, the diagnosis may be clear enough not to require confirmation.

Dogs serve as a common reservoir, so it’s likely the patient acquired this infection from a sandfly that previous fed on an infected dog.

Treatment seems to depend heavily on the clinician’s assessment of the case. Drug therapy can be used (including pentavalent antimony, amphotericin B, and miltefosine) but the infection often resolves without intervention and managing the lesion is all that’s necessary.

Looking forward to hearing some more details on how treatment is approached. Best,


Athens, GA

Courtney writes:

Greetings from Omaha, Nebraska.

I have a question regarding the possibilities of a cornea transplant in a young child: would it be worth it if a child is in a developing country with limited medical care? I am not a medical person so forgive me if I’m wrong, but wouldn’t the child need to be on immunosuppressants?  Or would the eyes still be considered “immune privileged” after the attack from the parasite?

My guess for this week: subcutaneous leshmaniasis.  I utilized Parasitic Diseases 7th edition. There is a terrific table in the appendix  (page 578) that list symptoms and common diseases associated with it. There were only 3 listed under ulcer 1) Leshmaniasis, 2) Dracunculus (Guinea worm) 3) Trypanosomiasis.

Trypanosomiasis has many symptoms that were not listed. Granted, some of these symptoms may take weeks to months to appear depending upon the subspecies.

Diagnosis for Dracunculus is done via finding the guinea worm and that was not mentioned in the podcast. So this is a possibility.

However, I go with Leshmaniasis because it is a “clean” ulcer and not painful. Daniel or Dickson did some fishing and asked if there were insects present  and Leshmaniasis is spread via sand fly (whereas Dracunculus is done via crustacean). Daniel also mentions travelling by boat, which is how he gets to some villages in Panama.

Anyways, I admire all three of you and I hope I’m half as productive as all three of ya’ll.


Kevin writes:

Rural Panamanian child with a painless, solitary lower leg ulceration of several months duration. Ulcer base is firm and ‘clean’, ulcer border is indurated and elevated. Child is otherwise well appearing.

I remember an old dermatology text that stressed an anatomic approach to dermatologic diagnosis. The endpapers of this text had a front and back illustration of a person festooned with various lesions. It was an attempt to make sense of the often confounding nature of skin disease diagnosis. I recalled this ‘geographic’ approach to diagnosis when I first listened to case 171. My attempts to find well-documented reports on lesion localization (or ulcer site preference) in American tegumentary leishmaniasis (or do you say New World cutaneous leishmaniasis) were not very successful. More on that later. The solitary nature of our patient’s lesion, the size, appearance, Central American location, and natural history are all typical of cutaneous leishmaniasis. Leg ulcers, common in the United States, are usually seen in adults and often due to venous stasis or arterial disease. A laundry list differential that do not really fit our case may include yaws (not reported from Panama since the 80s), myiasis, chagoma, cutaneous amoebiasis, pyoderma gangrenosum, necrobiosis lipoidica, carcinoma and Beçhet’s disease.

In Old World cutaneous leishmaniasis 48% of lesions were located on the head and neck with only 0.4% located on the legs (Askoy 2016). A case series of 43 adult patients in Brazil (Saldanha 2017) reports lower limb lesions in 86% of studied patients. Schubach (2015) in a case series of 151 Brazilian patients showed that 70% of lesions were solitary and 26% had lesions on the legs/feet. Torres-Guerrero (2017) reported that in a Guatamalan case series, most (43%) of ulcers were on the upper extremities. The Gonzalez 2018 case series (primarily Panamian patients) also notes that 60% of ulcers were found on the upper extremities. I apologize for veering off on this lesion site localization tangent, a largely useless exercise at best. However, I do remember a recent TWiP (? Surf n’ Perf TWiP 163) where there was a brief discussion of the feeble aerodynamic capabilities of the sandfly, resulting in more bites on the lower extremities.

Diagnosis here is best achieved with NAAT. Other modes of diagnosis: culture, histopathology, touch preps. Though lesions may resolve after several months, some remain chronic. Treatment of solitary lesions is usually local with the use of cryotherapy, topical paromomycin or intralesional pentavalent antimony. Skin lesions (especially facial) are socially stigmatizing which is another reason for treatment (in addition to prevention of scarring due to chronic lesions). Systemic treatment is reserved for patients at risk for development of mucocutaneous leishmaniasis. According to Dutari 2014, Leishmania Viannia braziliensis, the principal cause of mucocutaneous leishmaniasis (MCL), has not been isolated from infections in Panama. I was unable to find incidence rates/occurrence rates of MCL in Panama and would appreciate the TWiP-hosts comments on MCL in Panama.

Thanks for a great podcast.


Pediatric Cutaneous Leishmaniasis in an Endemic Region in Turkey: A Retrospective Analysis of 8786 Cases during 1998-2014, Mustafa Aksoy, et al, PLoS Negl Trop Dis. 2016 Jul; 10(7): e0004835. OPEN ACCESS

Case series of 8700 children…CL most frequent in the 6-10 year old group. Females affected more than males. Lesion localization: 0-5 y/o group: head and neck. 11-15 y/o group: fewer head and neck lesions, generalized lesions more frequent. Overall, the head and neck were affected in 48% of cases. The upper extremity in 7.3%, and lower extremity in 0.4% of cases…

Excellent 4 page CDC guide on the diagnosis of leishmaniasis

Cutaneous Manifestations of Human and Murine Leishmaniasis, Scorza BM, et al. Int J Mol Sci. 2017;18(6):1296. Published 2017 Jun 18. doi:10.3390/ijms18061296   Good table of the many leishmania species and their respective disease associations.

“LCL symptoms develop an estimated 2–8 weeks after the bite of an infected sand fly, depending on the infecting species. After the asymptomatic incubation period, a single or small number of nodular or papular lesions develop at the site of parasite deposition by the sand fly. Lymphadenopathy can develop as the earliest indication of disease caused by some species (notably L. (V.) braziliensis), and can precede lesion formation. The lesions may progress into well-delimited ulcers with raised edges. LCL can present with open lesions (wet lesions), which are subject to superficial secondary infection by bacterial or fungal species, with Staphylococcal species being most common. For reasons that are still under debate, lesion ulceration has been associated lesion healing. Indeed, patients infected with L. (V.) braziliensis who were treated before ulceration had a higher treatment fail rate compared to those treated after ulceration (75% vs. 25.8%). Lesions are capable of self-healing without treatment in many cases. However, resolution can take several months to years, and results in formation of a depressed, hypopigmented scar.”

PD7: permanent immunity to reinfection with cutaneous leishmaniasis is the ‘rule’. PD7 lists 15 species of sandfly that transmit disease

Characterization of the Histopathologic Features in Patients in the Early and Late Phases of Cutaneous Leishmaniasis, Maíra G. Saldanha et al, Am J Trop Med Hyg. 2017 Mar 8; 96(3): 645–652.

Case series of 43 adult patients. Lesion site was lower extremity in 86%, upper extremity in 1%.

The clinical progression of disease is described as: initial lymphadenopathy followed by bite site desqumation, nodule development and finally ulcer development.

American Cutaneous Leishmaniasis in Panama: A historical review of entomological studies on anthropophilic Lutzomyia sand fly species, Larissa Dutari et al, Parasites & Vectors · May 2014

“Leishmania transmission cycles: Many more studies have been undertaken on the vectors of ACL in Panama than on Leishmania parasites. To date, seven Leishmania species have been reported in the country, but only three have been isolated from humans: Leishmania (Viannia) panamensis, Le. (Viannia) colombiensis and Le. (Leishmania) amozanensis, with the former being by far the most predominant disease agent.”

American tegumentary leishmaniasis: correlations among immunological, histopathological and clinical parameters., Martins AL, et al., An Bras Dermatol. 2014;89(1):52–58.

Cutaneous leishmaniasis: an overview, Hepburn NC. J Postgrad Med. 2003;49:50–54. OPEN ACCESS

Retrospective study of 151 patients with cutaneous leishmaniasis treated with meglumine antimoniate, Armando de Oliveira Schubach et al, Rev. Soc. Bras. Med. Trop. vol.38 no.3 Uberaba May/June 2005 OPEN ACCESS

151 cases, mean age 16 years, 70% had one lesion, 14%: one or more lesions, 16%: 3 or more lesions. 26% had active lesions on the feet or legs.


“…caused by L. panamensis, L. braziliensis and L. colombiensis. Sloth species (Choloepus hoffmani and Bradypus griseus) are the primary reservoir host of L. panamensis. In areas of Panama, 19.3% of C. hoffmani were found to be infected. The parasite was present in skin, blood, bone marrow, liver and spleen.”

Leishmaniasis: a review, Edoardo Torres-Guerrero et al, F1000Research 2017, 6(F1000 Faculty Rev):750 ( OPEN ACCESS

“Pure CL was first described in the Old World by Lewis and Cunningham in 1876. It is caused by L. tropica17. In the Mexican Southwest and at its border with Guatemala, the causal agent is L. mexicana2. It occurs in areas of the body exposed to insect bites; in decreasing order of frequency, the most involved regions are the ears (areas usually involved are the helix and anti-helix), nose, upper lip, cheeks, legs, hands and forearms, and ankles17. It is striking that in Guatemala the most affected sites are the upper limbs (up to 43% of cases).”

GONZALEZ, Kadir et al . Histopathological characteristics of cutaneous lesions caused by Leishmania Viannia panamensis in Panama. Rev. Inst. Med. trop. S. Paulo,  São Paulo ,  v. 60, e8,  2018 OPEN ACCESS

“Cutaneous lesions of 49 CL-suspected patients were analyzed using molecular and histopathological methods. Of the patients studied, 73% were male and 27% female. Most of the patients (96%) came from the province of Panama. The age range was 23 to 71 years with an average of 41 years old. Evolution time of lesions varied from 10 to 90 days with an average of 30 days. The number of lesions ranged from 1 to 8 with an average of 2 lesions per patient, mostly located in the upper limbs (60%). Out of the total samples, 94% (46/49) were positive by PCR (Viannia, Hsp-70). Positive PCR Hsp-70 samples (78%, 36/46) were characterized as L. (V.) panamensis by PCR-RFLP analysis.”


While we are, broadly, or at least superficially, on the topic of dermatology, I would like to include a quotation from an old dermatology text. A co-author of the text is Robert Willan (1757-1812), regarded as the founder of the discipline of dermatology. He was influenced by Linnaeus and attempted a taxonomic classification of skin diseases, a curious and largely abandoned system. The book [A Practical Synopsis of Cutaneous Disease according to the arrangement of Dr Willan, Thomas Bateman, Robert Willan, Anthony Todd Thomson, 8th Edition, London: Longman, 1836] is available free on Google Books. What I find particularly amusing about 18th century English medical writing is the manner in which the authors freely trash other physicians, quacks, pharmacists, etc. An example of such trolling avant la lettre is quoted below:

“M. Alibert, with loud pretensions to superior skill, and much vaunting of the services which he has rendered in this department of medicine, has, in fact, contributed nothing to the elucidation of the obscurity in which it is veiled. The merit of his publication belongs principally to the artists, whom he has had the good fortune to employ : for he has adopted the ancient confusion of terms, without a single definition to fix their acceptation ; and he has not scrupled to borrow the nomenclature of the vulgar, in its most vague and indeterminate sense.”

Christopher writes:

Hello hosts,

For this weeks case I would say that the l cutaneous leishmaniasis, which would’ve been transmitted by the bite of a sand fly. You can identify this parasite using a light microscope, in which you would want to scrap the edge of the lesion with a scalpel to obtain the parasite. According to Parasitic disease 7, this lesion could probably just be left alone and will heal itself in time. And because its only on his leg the scar probably won’t impact his life too much.

Minor oceanography misunderstanding:

Iron does not control plankton blooms on the coast, but Iron does control plankton  in more oligiotrophic ecosystems such as the southern ocean and  ocean gyres. These systems are known as high nutrient low chlorophyll regions (HNLC) as there have high abundance of what is normally the limiting nutrient (mainly nitrogen) but are limited by iron. There were some really cool experiments done in the 1990’s where they proved this ( definitely worth the read. In general the coasts systems are limited by nitrogen, which since the invention of fertilizer, and the massive amounts of run off due to the excessive use of fertilizer, have created numerous dead zones in our ocean such as the massive dead zone in the gulf of Mexico. So just a minor correction to Dickson’s statement last episode.

parasitology heroes:

I  think I speak for all TWIP listeners when I say that 3 parasitology heroes that very much deserve to be added to the hero section of the new book are Vincent Racaniello, Dickson Despommier, and Daniel Griffin for their countless hours and efforts in educating the public about parasites, helping create and spread the most up to date, inclusive and informative FREE textbook on human parasite, and their own numerous contributions to the field. These three heroes have greatly contributed to the field by producing 171 lectures on current literature, educating tens of  THOUSANDS of people all over the planet and for their notable individual contributions, Dickson and his research, Vincent in starting the podcast and pushing it forward and Daniel for helping people all over the planet and his research, as well as the websites all three of them maintain with important information and the outreach events they also participate in (I Could go on for hours about the countless  contributions but I am trying to keep this email shorter). in terms of parasitology education these three have probably taught more people about parasitology than any other parasitologist ever, and for that alone I believe all three deserve the title of parasitology heroes.

Lastly, attached below is a  cool video of cercaria I pulled from a snail this week that I thought you all would enjoy.

Thanks for the great show.

Warm regards,

Christopher Brianik

School of Marine and Atmospheric Sciences,

Stony Brook University, Stony Brook, NY

Taylor writes:

Dear Leishmaniacs,

Long time listener, first time answer-er. I’ll start with a big thank you for putting on this amazing podcast and writing a wonderful (and open access) textbook.

I imagine you will get a lot of answers along the same line as mine, so I will be brief. I believe the child has cutaneous leishmaniasis caused by a Leishmania parasite, possibly Leishimania panamensis or less likely Leishmania colombiensis. Diagnosis should be made by microscopic examination of infected tissues and then biochemical/molecular testing for specific species identification.

On a side note (not necessary to read on the podcast), when I listen to TWIP I try to imagine myself seeing the patient in clinic without knowing a parasite is the culprit. With that in mind, I try to come up with a non-parasitic Ddx.

My non-parasitic Ddx from most likely to least:

Mucocutaneous Paracoccidioidomycosis – caused by Paracoccidioides brasiliensis can have skin ulcerations and endemic in Panama (I think) but this is TWIP…

Cutaneous Sporotrichosis – caused by Sporothrix schenckii sensu lato. Again can cause skin ulcerations and seems endemic in Panama but this is TWIP…

“Tropical ulcer” – usually polymicrobial with Fusobacterium ulcerans. Common but typically painful and demonstrates undermined border, this case does not.

Buruli ulcer – caused by Mycobacterium ulcerans. Often in children, often in the lower extremity. I don’t see the Americas represented on the list of actively reporting countries by the WHO.

Bejel, Yaws, and Pinta – caused by endemic subspecies of Treponema pallidum. Primary stage is nodular but secondary stage can have painless ulcerations, but I would expect them to be more widespread than in this case. Also in Panama, I would expect Pinta but that one shouldn’t ulcerate from what I’ve read.

There are other causes of painless ulcers that are not infectious in origin but those are boring, so I won’t list them. Also, I wouldn’t expect most of them in a child this young. I’d love to know if Dr. Griffin has other ID etiologies on his Ddx that I missed!

Kind regards,


Chicago, IL

Cecelia writes:

Dear Doctors,

  I believe Dr Griffin’s patient suffers from Cutaneous Leishmaniasis.

   When the patient was seen previously in the clinic, he probably had the red papule where he was bitten by the fly.

The fly vector would have introduced the promastigote stage of the parasite. After the promastigote stage becomes the amastigote, the ulcer forms.

  The ulcer has a raised border where the parasites are found.

  In your book you describe several methods used for diagnosis including NAAT, histology, and culture. I’m curious how the diagnosis is made in such a remote location.

  Your previous description of the living conditions in that area would account for the presence of the reservoir host, dogs or rodents,as well as the sand fly vector.

  I would like to thank you for making your book, as well as the articles you feature each episode available to us.

  I have really learned a lot from TWIP as well as your other podcasts. I look forward to each new episode!


Cecelia from St. Petersburg, Fl.

Justin writes:

The Washington Post: She went to the hospital for an infection. Doctors found four bees living in her eye, eating her tears..

William writes:

I would like to share my story about schistosomiasis. I have discovered schistosomiasis haematobium is being spread sexually.

All the best,


Christine writes:

Hello Dr. Despommiers & Dr. Racaniello!

I sent an email before but I’m pretty sure I sent it to some wrong email address lol

Like some of your dedicated listeners I have no degrees in any of the subjects you discuss but I do have a strong passion for learning about parasites, viruses and bacteria. Actually I just love learning, whether its diseases, all subjects regarding space, history or nature.

I discovered my interest when I started watching Monsters Inside Me and I thought it was pretty neat that Dickson was the consultant for the show that got my passion started! I work as a receptionist and since I found TWIP I have been listening to you guys every day, 8 hours a day while I’m working and when I get home and start making dinner and cleaning I pick up where I left off at work. My boyfriend is pretty good about my obsession although I’m not allowed to listen to you guys while we’re eating dinner L.

I haven’t got too far into TWIV & TWIM as I am totally digging TWIP right now! You guys are really great together and I find myself chuckling quite often. I find you both very entertaining as well as informative.

My personal favorite parasite is the “zombie” parasites who commandeer the host to complete their life cycle. It seriously creeps me out but equally fascinates me! I am hoping there’s an episode or two or three dedicated to these amazing creatures!

I don’t have any clever questions or comments to make, I just wanted to email you guys and send my love for both of you and the shows! Keep it up, this is soul candy for me and you make my work life so much more enjoyable! <3

Love, Peace and Chicken Grease!

From Edmonton, Canada

Jim writes:

Dear TWIPtosporidia Academedicus:

Today is a coolish day here in Vancouver but the sun is shining.  It is great to be getting back to your podcasts after a while away.

Are you planning to do a paper or a program on parasites and climate change?  I know you were thinking of inviting Peter Hotez. Maybe that would be an interesting topic.

The TWIx podcasts are always in the zone.

Take care,


Chris writes:

Dear professors,

I received my signed copy of PD6 in the mail and have been enjoying it thoroughly! I find myself reaching for it whenever I need a quick reference or a refresher on a life cycle. I even referenced it for this case, which, given the available information, has myriad possible causes.

Going right into it, the patient is suffering from unilateral vision impairment and retinal retraction, possibly due to a visible granuloma. Ocular larva migrans caused by Toxocara canis seems immediately likely, and the presence of a granuloma supports this. Diagnosis could be made by ELISA against T. canis E/S antigens in the aqueous humor of the eye. The related ascarid Baylisascaris procyonis can’t be ruled out either, and Panama is home to a fascinating diversity of procyonids.

Other nematodes with possible eye involvement are Dirofilaria immitis and zoonotic species of Onchocerca, all of which may reach the eye by ectoptic migration and induce the reaction seen in this patient. Though these are much less common than OLM caused by T. canis.

Some tapeworms are responsible for eye pathology, at least one of which (Spirometra) is noted to induce local granuloma formation.

If I had to choose one likeliest cause based on the case notes, it would be T. canis. In the best cases, treatment involves corticosteroid and anthelmintic therapy, and in more severe cases, surgery. I’m very interested to hear more details and possibilities.



(Athens, GA)

Anne writes:


How I got infected by a botfly: