Case Guesses:

Alexander writes:

Hello all,

I was kind of saddened hearing about how some people might be under-trained, leaving them with fewer job opportunities, as while I was learning about forestry, my professor always stressed the importance of having something to fall back on when newer techniques don’t work, I remember hearing that with the old aerial photography you could actually count each individual tree and learning how to measure structures from the same photography, while now you are more limited by the pixels in the image. I still have a yard stick that I can use to measure diameters and heights of trees without having to use any specialized tools.

For this case though, given the possibility for a babesia infection I wanted to keep that in mind that it can produce rings in 1-10% of the red blood cells that is described in Parasitic Diseases pg. 176, however pretty much any time you all mention babesia, the Maltese cross comes up, so I wanted to put that one on the back burner. I also thought about Plasmodium vivax or P. ovale given the history in India, given that fever, abdominal pain, diarrhea, and vomiting are present. In Parasitic Diseases pg. 113, I read that usually only about 2% of red blood cells are parasitized and there is no eosinophilia.

Given what I was able to at least narrow it down to P. vivax/ovale, which I guess can be can be differentiated by Schüffner’s dots or James’s dots, is there a difference?

I would suggest chloroquine as a treatment.

Hannah writes:

Dear TWiP hosts,

When you mentioned intracellular ring forms, I immediately thought of malaria. The fever and gastrointestinal symptoms fit that diagnosis, but some other aspects of the case don’t add up. P. vivax and ovale can both relapse and are found in Nepal, but according to Parasitic Diseases, “Usually only about 2% of red blood cells are parasitized with P. vivax and P. ovale infections”. I had a feeling I was missing something.

Remembering that there was also a North American parasite with ring forms in the blood, I searched the textbook and found it: Babesia. Infection with Babesia spp. can result in headaches, fever, and gastrointestinal symptoms, and it is more severe in people with suppressed immune systems. 1-10% of red cells are typically parasitised, so that fits, and Babesia spp. are known to be vectored by ticks on Long Island. A co-infection with Ehrlichia, which is vectored by the same ticks, would explain the high white count and confusion. It can also cause flu-like symptoms like fever, headaches, vomiting, diarrhoea, and lack of appetite, and the timing (a very recent camping trip) fits too: ehrlichiosis tends to show up within a couple of weeks of infection.

This will probably be the last email I write to you from Berlin (where it is 22°C tonight, but daytime temperatures have been over 30°C, even climbing to 37°C earlier this week). By the time the next episode airs, I will be in Ottawa, where I will soon be starting a PhD at Carleton University looking at how cold stress impacts insect physiology. I won’t be working with any parasites, unfortunately, but I do find insect parasites (both parasites that ARE insects and parasites OF insects) really neat. Here’s a paper about flies that live in termite soldiers’ heads and emerge through their hind ends: and I think you’d enjoy talking about strepsipterans (twisted-wing parasites) and the Acroceridae (spider flies) as well 🙂

Before I sign off, an anecdote from when I was an undergrad: in a parasitology course that I took, the professor acquired some dead hedgehogs and fish, just ordinary wild animals with no known history of disease, and told us to dissect them and look for parasites. What really stayed with me was her confidence that we WOULD find parasites, and of course we did.

All the best,


Jessica writes:

Hello TWIP Professors,

My guess for case study 156 is Babesiosis, acquired during the camping trip earlier in the month.

My true reason for writing though is to suggest the topic of Cyclospora cayetanensis? There have already been several large recalls from major food manufacturers and a recall from a large food service chain. The current outbreaks/ recalls open up a lot of questions, with not a lot of answers. I’ve been eagerly tuning in every week waiting for you guys to discuss.

The weather in Chicago this evening is about as ideal as weather could be I’m very happy to report.

Thanks for a great podcast,


Kevin writes:

Chicago Weather–High summer, hot sun. Dry. Dogs panting.

Acutely ill elderly (late 70s) woman with a febrile illness plus anorexia, nausea, vomiting, diarrhea and dehydration. The time course is important in order to consider incubation periods of illness: patient went camping approximately 3 weeks prior to the onset of her illness.

Pre-existing illnesses relevant to her present illness:

-cirrhosis with portal hypertension and varices (cirrhosis is also regarded as an immunocompromised state)

-glucocorticoid immunosuppression: prednisone high daily dose.

-immune thrombocytopenic purpura (ITP)

-history of self-limited jaundice in Nepal 13 years ago

-could view chronic thrombocytopenia as a partial immune deficiency due to the recognized role of the platelet in immune function.

Infection risks:


-foreign travel

-foreign birth

-camping in known tick infested location (high-risk activity, high-risk geography, high-risk season)

-age > 65 y/o (age-related decline in innate and adaptive immunity)

Highly relevant data:

-microscopy showing <4% intra-erythrocytic inclusion bodies, specifically ‘ring forms.’

Despite the patient’s complicated past medical history and comorbidities, intra-erythrocytic ring forms point to two diagnoses, both being infection by members of the protozoan phylum Apicomplexa: malaria and babesia. The 2018 CDC yellow book states that there is no malaria transmission risk in Kathmandu, hence malarial ring forms can be dismissed as a possible diagnosis. Additionally the history strongly suggests a recently acquired infection, which leaves the culprit organism as Babesia spp. There are as many as 60 Babesia species, though the most commonly acquired type in US disease is B. microti. It is transmitted by the colloquially named ‘blacklegged’ or ‘deer’ tick : Ixodes scapularis. This tick also transmits the spirochete Borrelia burgdorfi (Lyme disease) and the rickettsial organism Anaplasma (formerly Ehrlichia) phagocytophilum (NOTE that Anaplasma may be associated with ‘morula’ intra-erythrocytic inclusions). Though not a diagnostic possibility here, it should be noted that there are rare non-infectious intra-erythrocytic inclusions called Cabot Rings which are ring-like structures that can be seen in erythrocytes in megaloblastic anemia or other severe anemias and lead poisoning. Other potentially distracting RBC inclusion bodies are well illustrated in an reference below.

The incubation period for babesiosis is between 5-30 days, which is consistent with our patient’s illness. Diagnosis is via immunofluorence assay (IFA) for Babesia IgM and PCR for the 18S rRNA gene. Treatment for Babesia in the immunocompetent patient is atavaquone and azithromycin;  immunocompromised patients or in those with more severe disease require IV clindamycin combined with either oral quinine or IV quinidine. Co-infection with Borrelia and anaplasma is a distinct possibility and in view of patient’s age, immunosuppression and co-existing illnesses, empiric therapy for these infections would probably be prudent (notwithstanding her relatively low level Babesia parasitemia).  Some feared complications of babesiosis- a review of 34 cases of babesiosis who were hospitalized in Long Island states that acute respiratory failure is the most common complication (7/34 cases), followed by disseminated intravascular coagulation (DIC) (6/34 cases) [REF] An uncommon but very severe complication is acquired hemophagocytic lymphohistiocytosis (HLH) which is an excessive inflammation, hypercytokinemia, abnormal immune activation and tissue destruction. I could not find any information that implicated prednisone or ITP as being unique risk factors for Babesia complications or severe disease. Though not applicable to our case, splenectomized patients are at high risk for aggressive disease, high parasitemias and increased mortality. An interesting association I encountered while researching this case is that a Babesia infection can be associated with inducing immune thrombocytopenic purpura (in persons with no prior ITP history). Finally, the leukocytosis is concerning, especially in light of the fact that leukopenia is frequently seen in babesiosis and high dose prednisone is typically associated with lower or moderated WBC counts. However, in a 1998 NY State review of 139 Babesia cases, a white count above 5000 cells/ml was a negative prognostic factor [REF]. The WBC elevation also again raises the possibility of dual infection with borrelia and babesia, (where leukocytosis has been described [REF]). The high white count must also stimulate a heightened vigilance for sepsis, abscess, spontaneous bacterial peritonitis and other bacterial infections, and hematological problems such as incipient leukemoid reactions or early stage CLL etc.

Incidental info/ red herrings:  

Her episode of jaundice 13 years ago could have been due to hepatitis E (hyperendemic in Nepal). She should of course be tested for HCV and HBV. Autoimmune etiologies of her cirrhosis should also be considered. I don’t consider any of this directly relevant to her acute illness (other than contributing to a ‘burden of pathology’ in the elderly). I regard the 2 glasses of scotch as incidental (and not a cause of her cirrhosis), of course a standard alcohol history should be obtained, but a regrettable rush to judgement should be avoided. The symptoms of nausea and vomiting are likely constitutional symptoms associated with her primary illness (babesisos) and should not lead us into an intestinal diagnostic morass. GI symptoms are less common in Babesiosis but have been described in a 1977 review [REF].

Finally, as an offshoot of the Ixodid tick discussion above, I would like to put in a plug  for the inclusion of a brief mention of tick borne encephalitis virus in Chapter 39 for your revisions to Parasitic Diseases. I became acquainted with this disease while discussing ticks with some Latvian artists, who I believe had been vaccinated for it. The ‘east’ still has its mysteries….

What a long, strange TWiP it’s been……thanks


Hepatitis E in Nepal.Kathmandu Univ Med J (KUMJ). 2006 Oct-Dec;4(4):530-44. Shrestha SM

Immune Dysfunction in Cirrhosis J Clin Transl Hepatol. 2017 Mar 28; 5(1): 50–58.  Mohd Talha Noor* and Piyush Manoria

Hematologic manifestations of babesiosis Ann Clin Microbiol Antimicrob. 2017; 16: 6. Tamer Akel1 and Neville Mobarakai2

Severe babesiosis in Long Island: review of 34 cases and their complications.Clin Infect Dis. 2001 Apr 15;32(8):1117-25. Epub 2001 Mar 26. Hatcher JC1, Greenberg PD, Antique J, Jimenez-Lucho VE.

Human babesiosis in New York State: Review of 139 hospitalized cases and analysis of prognostic factors.

White DJ, Talarico J, Chang HG, Birkhead GS, Heimberger T, Morse DL

Arch Intern Med. 1998 Oct 26; 158(19):2149-54

“…the presence of parasitemia values greater than 0.04, alkaline phosphatase valued higher than 125 U/L, or white blood cell counts higher than 5 x 109 /L should help alert the health care provider to those patients who may require special attention becasue of the higher risk for death.”

Babesiosis-associated immune thrombocytopenia Stem Cell Investig. 2017; 4: 1. Roshni Narurkar, Aleksandra Mamorska-Dyga, Anup Agarwal, John C. Nelson, and Delong Liu

The tail wags the dog. Here a babesiosis patient develops ITP

“Two Cases of Co-Infection with Babesiosis and Lyme Disease,”The Medicine Forum: Vol. 13 , Article 15DeCicco, MD, Anthony; Peiris, MD, B. Niluk; Kelly, MD, Cecilia; Latreille, MD, Michael; and Jungkind, PhD, Donald (2012)

Diagnosis and management of human babesiosis Trop Parasitol. 2015 Jul-Dec; 5(2): 88–93 Subhash Chandra Parija, Dinoop KP,1 and Hrudya Venugopal2 (open access)

Human Babesiosis N Engl J Med 2012; 366:2397-2407 Edouard Vannier, Ph.D., and Peter J. Krause, M.D.

Human Babesiosis Infect Dis Clin North Am. 2008 Sep; 22(3): 469–ix. Edouard Vannier, PhD,et al  (open access)- more comprehensive than the Vannier review in the NEJM 2012. “Leukocyte counts are generally normal to slightly decreased, with a left-shift.”

Babesiosis in Immunocompetent Patients, Europe Emerging Infectious Diseases • • Vol. 17, No. 1, January 2011 Martin Martinot, (open access)

Human babesiosis on Nantucket Island: clinical features. Ruebush TK, 2nd, Cassaday PB, Marsh HJ, et al.  Ann Intern Med. 1977;86:6–9.  Very beautiful discussion of RBC inclusion bodies with excellent illustrations and several clear photographs of Cabot rings.

Inclusion Bodies in Tick-Borne Diseases Diagnosed in Patients from Northern Wisconsin Clin Med Res. 2009 Jun; 7(1-2): 45–47. Mrinal M. Patnaik, MD

Alexandra writes:

Dear TWiP team,

Here goes my first case diagnosis!

When I first heard the case in episode #156, I thought the woman was infected with Plasmodium vivax, one of the causative agents of malaria. Vivax parasites can remain dormant in the liver for years before being released into the blood and causing symptoms, so she could have been infected while in Nepal in 2017.

Another possible diagnosis is babesiosis caused by infection with Babesia parasites. Babesia spp. are related to Plasmodium (both are Apicomplexans) but are transmitted by ticks instead of mosquitoes. B. microti is the most common species in the U.S. and is especially prevalent in the northeast, so the woman could have been infected during her recent camping trip on Long Island. B. microti parasites are transmitted by the nymph stage of the Ixodes scapularis tick, which is about the size of a poppy seed, so she might be unaware that she was bitten.

The woman’s symptoms of fever, diarrhea, nausea, vomiting, and appetite loss could result from infection with either P. vivax or B. microti. Both of these infections are generally associated with normal or low WBC counts, but this woman’s high WBC count could be attributed to the fact that she is on prednisone.

While P. vivax is present in some parts of Nepal, it is not in Kathmandu, which is the area she reports visiting. For this reason, I believe the most likely diagnosis is B. microti. Based on PD 6th edition, most people with Babesia infection have 1-10% parasitized RBCs, and her level of less than 4% fits in that range. Many people with Babesia infections are asymptomatic, but this woman’s clinical manifestations could be due to her immunosuppressed status as a result of taking prednisone.

To confirm the diagnosis, I would re-examine the blood smear and look for tetrads of merozoites forming the “Maltese Cross” that is characteristic of Babesia and helps distinguish it from Plasmodium. I would also run PCRs for both Babesia and Plasmodium.

The woman should immediately be started on treatment for severe babesiosis, which according to PD 6th edition is intravenous clindamycin + oral quinine or intravenous quinidine. Conveniently, these drugs are also effective against malaria.

Thanks for the great podcast!


Post-bac fellow at NIH

Kendra writes:

Hello all!

The weather in Casper, Wyoming is sunny and 99F with much cooler weather predicted for the next couple of weeks.

My guess for case study 156 is Babesia microti. It is probable that the woman in her late 70s was bitten by a tick during her 3 day camping trip with family in Long Island. The parasite is commonly found in the Northeastern part of the United States, particularly in Suffolk County (eastern Long Island).  B. microti is spread by Ixodes scapularis ticks. The young nymph stage of this tick is very tiny and a bite by this tick may go unnoticed. The incubation period is 1-4 weeks which follows the timeline presented. Symptoms vary and are more severe in immunocompromised individuals. Mild symptoms of a Babesia infection are fever, loss of appetite, nausea, and fatigue. More severe symptoms are jaundice, enlarged spleen, enlarged liver, renal failure and organ dysfunction.

I did suspect Plasmodium falciparium as a possible diagnosis due to intracellular rings found on the blood smear. However, I did find that in areas where P. faliciparium and B. microti are found together, B. microti is often misdiagnosed as P. faliciparium as the pleomorphic rings found in a B. microti  bloodsmear may be confused with the intracellular rings of  P. falciparum.  Upon viewing a bloodsmear positive for B. microti, it is typically found that 1-10% of red blood cells will be infected  and there will also be extracellular rings present (which are not found in P. faliciparium). I did initially suspect schistosomiasis as well due to the cirrhotic liver. However, the podcast did state that she has a past history of cirrhotic fatty liver and a history of drinking a large amount of alcohol in one sitting.

microti can be diagnosed with a Wright or Giemsa-stained thin blood smear and/or by PCR. The treatment of choice is atovaquone/azithromycin. In addition, I would perform PCR assays to rule out a coinfection of erlichiosis and/or anaplasmosis. I suspect her symptoms of diarrhea and confusion are due to a coinfection.

Best wishes,

Kendra David


Parasitic Diseases Sixth Edition – Despommier, Griffin, Gwadz, Hotez, Knirsch

David writes:

Dear Hosts,

After taking a few weeks off of guessing the case study diagnoses, I think I will venture a guess thing time around. I believe the woman from Nepal in her late 70’s is suffering from complications due to Plasmodium vivax malaria. This form of malaria produces an interesting life cycle stage known as the “hypnozoite” which can stay dormant in the liver long after the initial infection. The patient’s fever, jaundice, nausea, and diarrhea are consistent with the malaria diagnosis. Unfortunately, her apparent intense drinking is doing her damaged, cirrhotic liver no favors, and may have kickstarted the reactivation of the parasite into her system. The low percentage of ring stages in her blood smear are also consistent with the low number of circulating infected erythrocytes characteristic of P. vivax infection. I hope this woman receives the proper care she needs to recover.

Thanks again for the informative and entertaining podcasts.


David P.

Chris writes:

Hello TWIP team,

There’s a lot going on in this case, but best lead immediately seems to be parasitemia observed by blood smear. The intracellular ring forms bring to mind a couple of apicomplexans; Plasmodium and Babesia. If this were a case of malaria, I would expect at least to see a recurring fever, but this is not reported. Malaria transmission does still occur in Nepal, but not in Kathmandu, so I feel comfortable excluding this from a differential.

Babesia, however, is a tick-borne parasite endemic to Long Island, where this patient was recently camping. The potential for transmission is very much present, and onset of symptoms agree with the incubation period (1-4 weeks being most common). The symptoms themselves are mostly consistent with babesiosis, including nausea, vomiting, and anorexia. Other gastrointestinal symptoms are not typical of this infection and may be due to stress or unrelated causes.

Giemsa-stained blood smears should be diagnostic. Babesia microti is the most common species in this area and is transmitted by the deer tick, typically the nymph, which is small enough that it could easily avoid detection. Combination drug treatment is recommended, but I’ll spare everyone the trouble by not listing them all here.

Another interesting case and I hope I approached it from the correct angle.


Athens, GA

Regular email:

Jean writes: [re:TWiP 149]

I am a Physician Assistant and graduate of the Bangkok school of tropical medicine. I used to practice on the small Hawaiian Island of Lana’i. I now live in “exotic Central Wisconsin” but am lucky enough to still have a place in Lana’i City. About 3 years ago I first started noticing the large African snails in my garden. I was aware that they were a vector of A. Cantonensis, as are many Hawaiian residents. I write because I have been advised by the locals to “just smash ’em”. I am concerned because this merely perpetuates the life cycle, when the rats eat the smashed snails. I have been dropping the snails in a bleach solution which I assume kills the worms. Please spread the word, “don’t smash ’em, bleach ’em”. Thanks, and “I’ll pass on the salad”.

Robert writes:

Greetings TWIP hosts!

I subscribe to the AVMA veterinary medicine update and this just came by:

Rat lungworm is prevalent in snails and slugs throughout Hawaii and will become more widely distributed at higher elevations as the climate warms, a study finds. Researchers at the University of Hawaii at Manoa say people should wash produce thoroughly, inspect and clean greens one leaf at a time and plant native plants.

It makes you reevaluate your place in the world …

Here’s the study:

and the “Maui Now” article:

Anthony writes:

Mention of Level 1 health care practitioners in TWiP 156. That brought to mind a short newspaper article that I read perhaps in ’65 about China’s Barefoot Doctors.  Googling that, I learned they were preceded by an avant garde of parasite fighters.

Octávio writes:

Dear Professors,

A few weeks ago, I was delighted to hear about Charles Donovan, for he is one of my favorite characters in the “History of Biology”.

I do not want to seem to have the hubris to correct Professor Despommier, but I would like to ask permission just to add a couple of notes to the story that was told.

The first “modern” record of a cutaneous lesions caused by Leishmania was made by Cunningham in 1885, who described the presence of “bodies” inside what would probably be macrophages. He thought that those could be spores of Mycetozoa, an Amoeboid somewhat similar to fungi.

Four years later, in 1898, a medical officer of the Czar’s Army named Piotr Fokich Borovsky observed in microscope preparations of “Sart Boil” (one of the many names given to cutaneous Leishmaniasis at that time), many particles with 1,5 micrometers in diameter, which contained one nucleus and a “process” that pointed to the periphery of the body. He correctly identified the organism not as  Bacteria but as a Protozoan and produced a correct description of its morphology, including the Kinetoplast and published it in that same year of 1898, five years before the articles of Donovan, Leishman and Ross.

But, as the article was printed in a Medical Military Journal, with little circulation and written in Cyrillic, it fell into oblivion, and the rest of the scientific community maintained the belief that these Bagdad Boils, Allepo or Balhk Sores, were caused by some kind of bacteria or fungi.

At the end of that XIX century there was an urge to find the reason behind the problems that afflicted the villagers from Garo Hills, east from the Brahmaputra River in the Assam province of India. There, more than 123 thousand people died, what resulted in intense depopulation and lack of workers to the tea plantations. This interest, driven by economy reasons, because the tea production was of uttermost importance to the British Crown, left to the suspicion that the culprit was an intestinal parasite identified by Otto Wurcher, a German ascendancy, born in Porto (Portugal), medical doctor, who went to live in Salvador, Brasil. He identified the parasite Acylostoma duodenale, which was the first suspect to cause the very high mortality rates in that region of Assam, as reported by George M. Giles in 1889 in A Report of An Investigation Into the Causes of the Diseases Known in Assam as Kala-Azar and Beri-Beri.

Dobson disputed the theory, arguing that Kala Azar afflicted people that had anaemia but also splenomegaly, and that was not found in cases of Ancilostomosis, indicating it might be some form of Malaria.

The discussions between “Malariophiles” and the proponents of other causes continued until the story told by Professor Despommier, where William Boog Leishman performs the autopsy of an Irish soldier who died after spending seven months in the Royal Victoria Hospital at Southampton, England, in consequence of falling ill during his commission in Dum-Dum (near Calcutta, India).

As before him, Borowsky also did, in that year of 1903 he described the larger mass of chromatin, of the nucleus, “and a smaller one, in the shape of a small rod, perpendicular to the circumference of the larger mass”, but concluded no more. Only 3 years later, while examining a dead rat infected with African Trypanosomes, he noticed the similarity between those and the bodies in the soldier’s spleen, and though those were also “degenerate trypanosomes”.

Donovan, nevertheless, considered those were not artifacts nor degenerated trypanosomes, for he observed smears from a fresh spleen biopsy from an Indian boy who had “irregular fevers”. After consulting with Charles Louis Laverain (Nobel in 1907) and Félix Étienne Mesnil, he wrote that those bodies must be a third entity still unknown. The French scientists concurred and even proposed the name Piroplasma donovani, but Ronald Ross criticized the French’s conclusions, made another description of the entity and proposed the creation of a new Genera (Leishmania), in the Sporozoa Class, and the name Leishmania donovani for the newly identified agent, the “Salomonic solution” recounted by Professor Despommier.

Donovan did correctly identified the agent first (or second, after Borowsky), than Leishman, but he also made another tremendous contribution; he observed that in 93% of the moderate and severe cases, the parasite was found in the monocytes and in the polymorphonucleate leucocytes, becoming evident that the spleen punction, which was an highly risky procedure at the time, was not necessary to have a diagnostic.

This was supposed to be just a small addendum to the story of Donovan, so, please forgive me the “too many words”. Edit, cut and paste, or don’t even bother to read this in the podcast, just add the curious fact of Borowsky, a proof that it is not only needed to publish not to die, but it is also necessary to do it in the “proper” journals, and the contribution of Charles Donovan to the diagnosis of Leishmaniasis.


always grateful Fan,


Veterinarian, MSc, Portugal

Katherine writes:


I am a listener, (along with my 83+ year old parents, just so you are aware of the age range of your audience!)— and wanted to comment after a recent episode alluded to poetry and parasites and immunosuppression..

Back in medical school at Cornell in the early 1990s, we had a wonderful parasitology course taught by Dr. Warren Johnson. One of my colleagues, Mike Hurwitz, created a limerick that I still remember to this day and thought I would share for Dickson.


Ode to the schistosome

Ode to never being alone

To be with my gal

In the gynecoforic canal

In copula, wherever we roam.


A small part of a lifecycle that was etched into memory via poetry/song.

On a different note—

Rituxan is s medication used by many providers to treat numerous conditions,

from cancer to ITP and many other dermatologic, rheumatologic and neurologic issues.

It may have been part of the cocktail that was used in the patient you presented with disseminated strongyloides.

A b-cell depleting agent, it is known to cause reactivation of hepatitis B virus —that can be clinically fatal in some situations.

I was wondering if you were aware of how Rituxans use may impact both serological testing results for microbial or parasitic infections, OR clinical reactivation of other non- HBV infections?

Immunosuppression is changing rapidly and often we are finding out after the fact, how and what are immune cells are doing for us.

Thanks for the great shows.


Lela writes:

Dear Professors Twip,

We are getting ready to go to the beach for the last week before elementary school starts here (NC). I’ve never learned how to sail, but we all enjoying taking kayaks, canoes, etc into the marsh. My brother has been catching lots of flounder this year and my son is super excited to go with him.

I didn’t have time to make a case diagnosis with rushing around getting ready for vacation this week, but I learned something interesting that I wanted to share – the evolution of the underground London mosquito, Culex pipiens f. molestus. Supposedly mosquitoes may have evolved to live underground and bite people instead of birds ( Do you think this is a new species and that creation of a new species can commonly occur quickly?

I am a postdoc and recently applied for a K99. My score was not favorable and I’m out of the application timeline. I’m been considering going into industry pretty carefully. Do you have any advice on switching scientific paths?



Anthony writes:

World Mosquito Day, observed annually on 20 August, is a commemoration of British doctor Sir Ronald Ross’s discovery in 1897 that female mosquitoes transmit malaria between humans.

On his discovery, he declared that 20 August should be, from then on, known as World Mosquito Day.

Connor writes:

Hello Docs,

Just wanted to check to see if any of the regulars on the TWIχ series are attending ASTMH Annual Conference?

The podcasts are all recommended listening for multiple of the Tulane School of Public Health and Tropical Medicine courses. My classmates and I would be delighted to meet anyone that opts to go to the conference.

Thanks for all you do in science education,

Connor E. Dunn

Tulane University School of Public Health and Tropical Medicine

MPH Tropical Medicine candidate