Chris writes:

Hi twip team! 

Snorkeling with the Cichlids and invasive Nile perch in Lake Victoria has always been a dream of mine, however thanks to TWIP, I learned that one should not enter the waters from the shore as this is where the cercariae of Schistosoma haematobium and mansoni live. Instead, I should enter from a safer, deeper distance where my only concern would be hungry crocodiles and territorial hippos.

These critters, newly emerged from their Bulinis and Biomphalaria snail hosts, swim to the top of the water column and seek exposed skin to bore into. Once inside the host, they will embark on the scenic route before ending up at their final destination, first visiting the lungs, the heart, the liver, and then the veins, undergoing a complex transformation into fully-fledged schistosomes along the way. Once two adult flukes find each other, they will embrace in a lifelong cuddle session, they then will travel to either the venous plexus of the bladder or the mesentery, and finally, settle down and produce eggs. These eggs will then have to find their way out of the venules and into the external environment.

In a process that I’m not sure I fully understand, the eggs are transported across the walls of venules and into the lumen of either the bladder or the colon, depending on the schistosome species. I simply remember that haematobium has heme in the word, which is blood, and it reminds me of bloody urine so I know that one goes to the bladder. 

Some models I read posit that the eggs are “carried” across the different layers of tissue by the immune system while others say the eggs somehow dissolve their way through. Maybe the 7th edition of Parasitic Diseases has the answers, but alas, I do not have a hard copy 🙂 One thing is for sure, lots of fibrosis of tissue accompanies this process, especially if the eggs get stuck and the immune system endlessly tries to wall them off. 

At some point, too many eggs end up deposited in the small portal venules of the liver, which leads to cirrhosis and portal hypertension. This is exactly what I believe our patient is suffering from. For treatment, a short course of praziquantel should kill off the adult parasites, as well as some safety counseling to prevent future infections. This could include vigorously toweling off immediately after a swim as Dr. Griffin often states. Unfortunately, the damage to the liver is far more complicated to treat, and liver transplantation may be needed. 

Hopefully, I didn’t just write all of that just to get it wildly wrong, like my Tunga Penetrans guess the last episode. That was a good learning experience, however, since I assumed a negative skin biopsy should have ruled out leishmania. A lesson to double-check and question everything! 

Thank you for all you do! 

— 

Christopher Hernandez

David Geffen School of Medicine, MS2 

MPH 2020

Infectious Diseases and Vaccinology 

University of California, Berkeley

Owain writes:

Dear TWIP team,

I haven’t guessed in a while, and feel bad that you didn’t have many guesses in a recent episode! I have finally caught up with my backlog and am up to date, so my guess for this case is that the ascites is due to schistosomiasis, acquired when he entered the water of Lake Victoria. There may also be some hepatosplenomegaly contributing to his abdominal distension.

Hope you all had a great Christmas and New Year!

All the best,

Owain

Sara writes:

Hello Drs. Despommier, Griffin, Naula, and Racaniello and Happy New Year to all who celebrate it! 

It’s 6 degrees C (42 F) and drizzling outside. I’m hurrying to send this guess because I submitted my last guess just a few hours after you recorded the last episode which was very sad for me as I’d love to win a book someday!! 

Swimming Lake Victoria and ascites made me immediately think of Schistosoma species, particularly S. mansoni. I considered severe protein malnutrition (Kwashiorkor) from an intestinal nematode, the liver flukes Fasciola hepatica, Opisthorchis, and Clonorchis, and peritoneal tuberculosis but the liver flukes would not cause portal hypertension and the geography is wrong. Mycobacterial infection would not earn this case a spot on this podcast (Although I’d love to see you make a This Week in Mycobacteria podcast discussing NTM, TB and lookalikes!!!). 

I suspect this patient has periportal fibrosis and granulomatous inflammation resulting in portal hypertension from the body’s own immune response to Schistosoma mansoni eggs deposited in this youth’s liver. The result is clinically significant portal hypertension with its associated ills (portocaval shunting, gastroesophageal varices and risk of bleeding, splenomegaly, hepatomegaly) not to mention chronic malnutrition (leading to even lower albumin in his vasculature further exacerbating the ascites through decreased intravascular oncotic pressure) and halted growth/development.

A diagnostic paracentesis would likely show an elevated serum-to-ascites albumin gradient which in this patient would point to portal hypertension from some process. But to get at the cause, would require finding the large S. mansoni eggs and their single spike possibly in the patient’s stool sample (Though as Dr. Shauna Gunaratne taught us last episode, a rectal snip might also yield the same result). 

If S. mansoni eggs were found, I’d give praziquantel and hope to reverse his portal hypertension to any extent possible. I’d follow up with stool samples to confirm eradication. 

If there is time, I have two questions for you experts:

If this patient has a high burden of eggs could treating him trigger a dangerous immune response and temporarily worsen his illness? (I’m thinking of the neuroimmune response when a patient with high burden of filarial worms, esp loa loa and onchocerca is treated with DEC)

I know swimmer’s itch can be caused by duck schistosoma species that remain confined to the skin (similarly to cutaneous larva migrans) — why is it that duck schistosoma cercariae cannot circulate and become adults in humans?

As always with gratitude, 

Sara

Druti writes:

Dear twip Quadfecta, 

A 14 year old boy who is malnourished and has developed ascites over the years is a very grim situation in African and Asian countries (including ours). He can have any nematode infection like round worm, hook worm which can lead to anaemia and protein losing enteropathy. 

Dr Shauna also mentioned a really impressive abdomen which may be seen due to hepatosplenic disease. Hepatosplenic disease in Africa opens a Pandora’s box of differentials like chronic malaria, Visceral leishmaniasis, Abdominal tuberculosis, Splenic abscess (due to Salmonella), leukaemias and hemoglobinopathies. But  as the patient does not have any fever,  most of the above mentioned differentials can be ruled out.But when I googled lake victoria, most of the articles were written specifically about one infection “Schistosomiasis” due to  Schistosoma mansoni. 

Based on host, environment, agent and disease, I am narrowing my guess down to Schistosomiasis. The Patient may have acquired it by swimming in the lake.  Contamination of lakes with faeces is an important epidemiological factor for the continuing Schistosoma cycle. Disease is because of the eggs causing intense inflammatory reactions leading to development of  pseudopolyps in the intestine, resulting in blood and protein loss, eventually to the development of  ascites .

Schistosoma eggs can cause intense periportal fibrosis in the liver called Symmers fibrosis, progressing to Portal hypertension, Splenomegaly and esophageal varices.

Diagnosis can be made with stool microscopy wherein you can see eggs with a lateral spine, characteristic S. mansoni. Serology: how much of it is useful I don’t know. Radiological investigation can be done to look for various organ involvements.

Treatment with a single dose of Praziquantel and Oxamniquine is effective to stop further shedding of eggs. Adding Oxamniquine with Praziquantel has shown good improvement in patients with hepatosplenic disease and schistosomal polyposis. 

 Whether repeat dosing is required or not, can be decided on clinical outcome post treatment (if patient is not improving) and repeat stool examination findings.

As always, Prevention is better than cure. 

Safe drinking water, safe recreational sites, adequate sanitary facilities, reduction of animal reservoirs as usually mentioned by Dr Depommier are some of the preventive measures. In India, we have a national programme “Swach Bharat abhiyan” ( Clean India initiative) which focuses on providing sanitary facilities in rural India. It is a good step towards limiting the spread of easily preventable infectious diseases in a developing country.

Thanks for the edutainment 

Dr Dhruti Sheth

M.B.B.S. , 3rd year DNB Microbiology,

Breach Candy Hospital 

Mumbai 

Dr Minipriya Rajmohan

M.B.B.S., 1st year DNB Microbiology

Breach Candy Hospital, 

Mumbai 

Gina writes:

Dear Vinny and the TWiPs,

Is it  Ascaris Lumbricoides ? 

I’m a little stumped but I understand you can get it from swimming in a lake. 

Welcome back Daniel, have a good trip Christina, and thanks for everything, Dickson and Vincent. 

C. gina   🐐

Michelle and Alexander from the First Vienna Parasitology Passion Club write:

Dear Schistosomu-Ladies and Schistosomu-Gentlemen,

We are very excited to have won a copy of Parasitic Diseases. The book will be made available to all current and future trainees at our division for Infectious Diseases and Tropical Medicine in Favoriten, Vienna.

A 14 year old boy presents with a distended abdomen and ascites. He also appears to be malnourished and his brother died from the same diagnosis one year prior. He grew up close to lake Victoria. He doesn’t have any b-symptoms, he is HIV negative and has no history of exposure to TB. 

The differential diagnosis for ascites is generally quite broad; taking into account the epidemiology, two different mechanisms can be differentiated: protein deficiency secondary to malabsorption, and portal hypertension as a consequence of liver disease. In the absence of other edema and with changes in portal flow on point of care ultrasound, the second mechanisms would seem more likely. Furthermore, intestinal infections with geohelminths, trichuris or ascaris can usually be identified on stool microscopy.

The most likely diagnosis here is infection with Schistosoma mansoni, which is very prevalent in Uganda (about 25% nationally). The parasitic worms are transmitted as cercariae on contact with fresh water, which is the habitat of their intermediary hosts (freshwater snails). The cercariae develop into schistosomulae, which migrate throughout the vascular system and ultimately land in the liver. There, they develop and migrate further to the venules of the intestinal tract, where a male and a female reside in copula (“doin’ the deed”). How do they find each other? Well, that’s easy: They find each other delightful!

As a consequence of this delight, eggs are produced and shed in the stool, contaminating fresh water yet again (with S. haematobium, this happens in the bladder). The eggs hatch into meracidiae, which penetrate into the snail and exit and cercariae again. Sometimes, fish and other aquatic creatures can serve as paratenic hosts, which means that they provide transportation only.

The first symptom of schistosomiasis is usually the so-called swimmers itch, which presents as a maculopapular rash at the point of entrance on the skin. Acute systemic symptoms may include fever, dry cough, muscle aches, hepatosplenomegaly, diarrhea and abdominal pain. Symptoms of chronic schistosomiasis depend on where the worms migrate and lay eggs. The symptoms range from acute bowel obstruction and intestinal ulcers to esophageal varices, ascites (as seen in our patient), cancer of the bladder (with S. haematobium), seizures or even motor impairment if the brain is affected. Some patients infected with schistosomiasis do not experience any symptoms at all.

The diagnosis is usually confirmed by detecting eggs in the stool or urine. Other methods include PCR testing and antibody detection. The two main treatment options for schistosomiasis are praziquantel and oxamniquine. Praziquantel is cheaper and therefore more commonly used, but is only effective against adult schistosomes and not against eggs and immature worms. The eggs may be excreted by people infected with schistosomiasis for weeks after having received treatment and the immature worms have the ability to survive and develop into adult schistosomes following praziquantel therapy. Because of this, it is advised to perform repeated testing of the stool and/or urine for schistosomiasis about four to six weeks following the treatment with praziquantel.

Avoiding contact with or ingestion of contaminated water in endemic regions is the key to prevention of this disease. In high-risk populations, mass treatment with praziquantel is sometimes used for prevention.

Thank you for this great case. All the best, 

Michelle and Alexander from the First Vienna Parasitology Passion Club

Kimona writes:

Dear TWiP Team,

The two soil-transmitted helminths, Ascaris lumbricoides and Strongyloides stercoralis, came up as my two final contenders for this 14 yr old boy’s illness. Both are quite prevalent in Sub-Saharan Africa and can cause a swollen belly and peripheral eosinophilia. The abdominal distention in A. lumbricoides can be from the bulk of worm burden and eventual intestinal obstruction which can lead to death (and perhaps the demise of his older brother). Strongyloides stercoralis and S. fuelleborni can both also cause abdominal distention and anorexia but seems also associated with diarrhea, which was not described. Daniel notably mentions ascites, which is a fluid accumulation usually due to serum hypoalbuminemia (i.e., low protein levels), which due to an osmotic effect draws fluid into extravascular spaces like the peritoneum. In advanced liver failure it is due to lack of albumin production by the liver, whereas in infections like A. lumbricoides, they mention malabsorption of fat, protein and lactose intolerance with anorexia – all of which would cause a severe protein malnutrition and could lead to ascites. And since the PD-7 chapter on Ascaris has a picture of a child with a swollen belly…….. I’ll go with this.

Ascaris eggs are described as being incredibly hardy and infection is via the fecal-oral route, typically in contaminated foods. The embryonated egg is swallowed, the parasite hatches in the alkaline environment of the small intestine, penetrates a capillary and is carried to the portal circulation of the liver. It then travels via the bloodstream to the heart and further into the pulmonary circulation where it ruptures into the alveolar space. It can then crawl up into the pharynx, be swallowed and end up in the intestinal lumen a second time, where it molts, matures, grows, and eventually mates.

I imagine this boy became infected at a very young age and is likely being continuously re-infected, since one adult female worm produces on average 200,000 eggs per day, and the sanitary conditions are likely poor. It is possible that he at some time experienced a pneumonitis, known as Loeffler’s syndrome, with bronchospasm resembling asthma. Mention is also made of the worms migrating in response to irritation, like fevers, and can lead to perforation or obstruction of the biliary tract, or peritonitis.

Diagnosis is by identification of eggs on stool exam, as well as serological tests to Ascaris antibodies and PCR/molecular tests. In suspicion of hepatobiliary ascariasis, ultrasound and ERCP may be helpful. I imagine that Dr. Daniel may have examined the boy’s stool, as the eggs are often prevalent. But maybe they could be seen by portable ultrasound when diagnosing the abdominal ascites.

Treatment of choice is with albendazole and mebendazole, which are used in de-worming programs for children. Intestinal obstruction may of course require surgical intervention.

As always, eager for the next TWiP to drop.

Kimona

Ps – At the end of a recent TWiV, I was thrilled to hear a listener email (Maureen from SUNY New Paltz) that was a dear grad-student friend in Fred Alt’s lab back in the 90s. This inspired me to reconnect. And as for my interest in TWiP, I can simply state that as the SARS-CoV-2 pandemic was unfolding, colleagues at work began turning to me with questions about virology and basic immunology, which led me first to TWiV and eventually most of the other TWiXs. A slightly reduced work-load, and inspiration from Daniel, led me to a volunteer experience with Floating Doctors in Panama this summer with my 17 yr old daughter. So, here is my plug – we both had a very uplifting and bonding experience and are soon returning for a few weeks in late February – a tradition we hope to continue as she flees to college next year. My monthly response to TWiP cases keeps me learning. And, someday I would love to visit you in the incubator! Maybe I’ll bring Maureen along…..

Elise writes:

Dear TWiP Collective, 

It’s January and I’m back after being seriously out of step with you all for months. I hope the new year is treating all of you well. It is sunny and windy and weirdly temperate (for January) here in Lower Manhattan (52 degrees F, 11.11 degrees C). 

I am writing today with an attempted diagnosis for this poor child who lived on Lake Victoria. My concern is that he has  a Schistosoma infection. This parasite is quite common in much of their world, and for this case,  in Lake Victoria, It is transmitted to humans  by snails, which live in water bodies (such as Lake Victoria)  and are intermediate hosts for the worm larvae. 

Schistosoma infections can take different forms depending on how the body of the host responds to the worm larvae and where they take up residence. Initial symptoms of an infection can take the form of flu type symptoms, but left untreated a wide range of gastric and renal symptoms can manifest as they have done in this child and, in all likelihood, his brother. 

A diagnosis can be most readily  made with a blood sample, and the parasite can be eliminated with  a course of praziquantel. I do, of course, have questions about how to treat this child’s other symptoms, particularly his abdominal ascites. Does this resolve on its own? Would he need to have fluid manually drained? Will he be able to recover somewhat after treatment? I did read that very young children experiencing these infections can experience learning delays which largely resolve after treatment, but since this boy has been ill for so long, will the effects be able to be reversed? 

As always thank you so much for your amazing work. I may have fallen off the map for a moment, but please know that I am here and taking so much interest and pleasure in everything you have to say.

Best best wishes

Elise (in lower Manhattan)

Andrew writes:

Kia ora from Pongaroa.

I have been remiss in sending in a case guess recently but I have a reasonable excuse. I have been helping a friend turn her PhD thesis into a book. Having to explain English prepositions to an Italian native speaker left me exhausted. The English language is far from logical. But the book is with the publisher and undergoing peer-review. I was too mentally exhausted to tackle any problems requiring thought. I even stopped doing Redactle.

Here is my guess for TwiP 212

The location and the ascites made me think of bilharzia caused by Schistosoma mansoni. I wanted a second opinion so I asked the AI chatGPT, here is its answer.

The most likely parasite responsible for the symptoms described in a 14-year-old boy with a history of slow progressive development of abdominal ascites over years, who appears wasted and malnourished, is Schistosoma mansoni. This parasite is a common cause of abdominal ascites and malnutrition in regions where the parasite is endemic, such as near Lake Victoria. The infection is acquired through contact with contaminated water, and it is common in areas where people swim, bathe, or wash in freshwater sources.

I checked this against my copy of PD7 and it looks good.

Nā,

Andrew

Martha writes:

Dear TWiPers, 

Again phone typing:  brief and no italics.

A 14 yo boy who has abdominal distension from ascites is described as appearing small for his age and malnourished. His older brother died with a similar condition. He is from Lake Victoria region 

Eukaryotic parasites that can cause ascites. Hookworm infestation can result in severe anemia and hypoalbuminemia which produces ascites from decreased colloid oncotic pressure. Strongyloides can also produce ascites by this mechanism of action.

But since the Hx includes Lake Victoria, then Schistosoma mansoni pops up to the top of the list. Eggs from worms in the mesenteric vessels can get into the portal branches in the liver where inflammation causes fibrosis and stricture. Children develop hepato-splenomegaly and portal HTN.

So my guess is Schistosoma mansoni causing hepato-splenic schistosomiasis, portal HTN and ascites

best wishes to all

Martha

Felix writes:

Dear Twip-Team,

I hope this guess reaches you in time! I’m a med student from southern Germany who has recently been to Africa, where I got interested in tropical diseases.

The weather near the alps is finally getting cold and maybe on the weekend we will have enough snow to start the backcountry skiing season!

Regarding the case, my first guess would be schistosoma mansoni. This water-borne parasite perfectly fits the geographic description. The common hepatosplenal manifestation will cause periportal fibrosis which leads to intrahepatic portal hypertension which then leads to ascites. It can later develop into cardiopulmonary schistosomiasis. The diagnosis can be made by microscopic stool examination, serology would probably not be useful for diagnosing in endemic areas. Praziquantel is listed as drug of choice for treatment.

I do not know much about the time course of the portal hypertension or potential esophageal varices after initiating treatment but I guess in some cases medication like propranolol or even interventions would be useful, if available.

Some more unlikely and less parasitic differentials would be ascites from malnutrition or neoplastic disease.

Greetings

Felix

Aaron writes:

Greetings all from an overcast St. Louis where the temperature is currently 36F (2C).

My guess for the case presented in episode 212 is Ascaris lumbricoides. I’ll be brief since I’m *just* a Web Developer at WashU School of Medicine, but I’d like to think that working on all of the websites for the school, some of the knowledge from the doctors I’ve worked with has found its way into my brain. Actually it was Vincent’s comment about the similar picture in PD 7th edition that led me to my diagnosis, that poor child. I hope the child from this case was treated with mebendazole like the case presented in the book and was able to recover.

My wife and I found the microbe.tv family of podcasts in January 2020 when one of her coworkers suggested we listen to the experts about this emerging virus. It turns out that our connection to Dickson goes back much further than that. “Monsters Inside Me” was (and still is) must see TV in our house. So when I found TWiP we said “wow, this is JUST like a podcast version of the show!”, and low and behold it truly is thanks to Dickson.

Thank you for all you do and keep up the good work!

Alice writes:

Hello TWIP doctors, 

Thank you microbe TV and TWIP for enriching my ID education with evidence based and clinical cases of parasite education. 

In regards to this week’s case, after spending some time in Kampala and Entebbe and seeing patients with complications from Lake Victoria, I suspect this patient has complications of chronic infection of Schistosoma mansoni. Manifestation of chronic disease is due to chronic egg deposition within tissues such as intestine and liver leading to granulomas. This then leads to hepatomegaly from portal fibrosis and subsequent splenomegaly, leading to this patient’s large abdomen. Treatment for chronic schistosomiasis is praziquantel. In young children, I have read that this might reverse some of the portal fibrosis. Therefore I hope this child is young enough to see benefits. 

I have received a book recently, therefore please do not include me in the draw. 

Thank you all. 

Alice  

— 

Alice Lehman MD, CTropMed® (she/her)

Adult and Pediatrics Infectious Diseases Fellow

Tom writes

Dear twip hosts,

First time emailer long time listener (more than 10 years!). I am an infectious disease fellow at the University of Minnesota  and work a bit in Uganda and have made stops at Montefiore (internal medicine residency) and the London School of hygiene and Tropical Medicine. I’m writing now from Kampala so this case seemed fitting for my first guess.  

For our young man living on lake Victoria he is showing unfortunate signs of portal hypertension and an older brother recently died of the same disease. The list of parasites causing these symptoms is relatively short. The diagnosis is Schistosomiasis. Eggs can be detected on a stool sample though the sensitivity is not great. Treatment is praziquantel. 

Until next time,

Tom McHale

Kampala, Uganda