Day 3: Party time aka sleeping sickness, leishmaniasis

Started off today with another awesome breakfast, strawberry pancakes, chicken sausages, exotic pastries… and 4 different kinds of fresh juices. I did like four journeys to the buffet and if the bus didn’t come I probably wouldn’t have stopped. I’m still being sorted out from jetlag and so work up at 4 am, but was productive! People seemed a little burnt out from yesterday’s talks, I can imagine that with limited training in infectious disease this is a lot to take in, however I feel the talks are all at my level, and feel I’m learning about things I’ve heard about and touched on, but now learning more detailed management, diagnostics and treatments.

I also found a little study group to review things at breaks, they are local (Indian) infectious disease fellows/doctors and so can really give context to things as they’ve seen lots of tropical diseases.

The material below is a bit much :)

First talk was about a case of a 64 year old male from Norway, who was in Uganda and developed high fevers and confusion, he had a negative malaria test, he was given doxycycline while there and shortly after had returned home. He was admitted for ongoing fevers, he was in renal failure, low platelets, and had elevated bilirubin. His blood smear done to examine his platelets revealed a worm consistent with Trypanosoma Brucei. Given the severity of disease, it was suspected this was T. B. Rhodisense, which was confirmed by PCR. As mentioned previously, zoonotic infections often cause more severe disease in humans, body responds more quickly as it appears more foreign, but they also can recover more quickly.

It was suspected this patient had CNS disease, something important with African sleeping sickness as treatment changes.

Congo has the highest amount of reported cases.

The vector for this is the TseTse fly (I remember it like Z Z.. fly for its sleeping sickness stuff). Apparently only 0.1% of flies carry it, it carries his reticular wings on over its abdomen, it only feeds on blood – T.B. Rhodisense is in more rural areas, close to cattle or animals. T.B. Gambiense is found more near rivers, its main vector is man.

The initial bite can cause a large chancre, which occurs after many days and can take weeks to disappear. After weeks, patient’s develop myalgias, fever, and cervical lymphadenopathy (winterbottoms sign), or submandibular, axillary and inguinal – more common with Rhodisiense. Diagnosing West African Sleeping sickness is easy as can use serology test (CATT) which is very sensitive. However for the East kind, you’d be searching the blood for the parasite.

Other things to recognize is that these bites are very painful, they bite in the day time (similar to black flies, and aedes mosquito), and are attracted to blue. DEET does not work. I’m going to Ethiopia in Feb. fortunately it does not appear to be transmitted there. 

The ongoing symptoms related to the ability of the parasite to change is surface glycoproteins, thus casing fluctuating parasitemia. As it’s a protozoan, would not expect eosinophilia to be a tip off like helminthic infections.

Treatment of these infections is not simple, WHO has a contact person to get a hold of melarsoprol for CNS involvement, apparently the drug itself has about a 5% mortality!

Next we had a talk about Chagas (T. Cruzi) disease, this felt mostly a review, when end organ is involved, not much is done (cardiomegaly, dilated colon/esophagus). It is transmitted by the reduvid bug. Mainly a disease south US but more importantly South America, Bolivia and then argentia having the highest prevalence. This bug has a huge animal reservoir. 30% develop chronic from of the disease, it was stressed the importance of screening blood donors and pregnant women. A case was presented of a patient post heart transplant, who had reactivation of T. Cruzi manifesting as skin rash, and hospitals often have a protocol to repeat regular PCR of T Cruzi post heart transplant. in infected individuals to look for reactivation.

Next we had a talk about intestinal protozoa which also is what we went over in the lab session.

Diagnosing and treating this stuff is probably appeared not very sexy. Other than Entamoeba liver abscess where here most will drain the abscess and send the fluid for PCR, the other one’s are often self-limiting, or have no clinical significance.  Interestingly in Chicago, I did see a patient with Endolinux nana (this was just colonization).

And here is a picture of me looking at sh*t through a microscope (stool sample).

The last talk was on leishmaniasis, this was an intense talk by Dr. Libman, who was also one of the authors on the recent guidelines.

The sandfly is the vector, it has V shaped wings, they have feathered edges, they fly low to the ground and not far. So one of the ways to try and prevent this is sleeping elevated, ideally the second floor of anything, windy places make it hard for these bugs to fly. They also can get through most mosquito nets, so ideally they should be net impregnated with DEET.

I think what’s so surprising about this disease is the cutaneous form can look like so many different things, it can be ulcerative like pyoderma, nodular (sporotrichoid spread), verrucous lesions, plaques or macules; and examples were shown for all of them.

Indian most often has L. Donovani causing visceral leishmaniasis as I saw a patient who was recovering yesterday.

A few pearls:

Leishmania residivans – looks like a central scar, with lesions around this, suspect this is an intense immune reponse, characteristic of L. tropica.

90% of VL cases are from Ganges river (North East India) + neighboring areas – Nepal and Bangladesh, Sudan, and Brazil.

Most African VL will have LAD, which is rare in Indian VL.

Sand flies can get through most mosquito nets, so they should be impregnated with DEET.

Patient’s who develop post Kala Azar dermal Leishmanisis may serve as a vector for transmitted disease.

The last lecture was on entomology, mostly a review of the lots of the vectors previously seen. I don’t think this would really help with being a good clinician, more like knowing some cool party tricks… however, I like party tricks

When we went to the hospital, we followed a pediatric neurologist, who took us around the wards.

1.    Firstly we saw a 14 year old male who was recovering from TB meningitis, the story of how he presented was fevers for 2 weeks and then a seizure, he was treated for 2 years and she noted that radiologic signs can be very slow to improve. He is left with some learning and behavior disorders.

2.     A 2 year old child was seen for encephalopathy, from North India, results were pending but we were told that the case was highly suspicious for Japanese encephalitis with basal ganglia lesions.

3.     We saw a 1.5 year old child with TB meningitis complicated by hydrocephalus. Sadly, apparently his grandfather had active TB. Interestingly, there was no culture results, and often patients with symptoms of chronic meningitis, LP findings with low glucose, high WBCs (with lymphocytes) protein, and MRI findings that are infra-tentorial are classic cases of TB meningitis.

  We went over multiple cases of neurocysticercosis, interestingly they were all parenchymal involved. Here with minimal lesions (1 or 2), patients are given antiepileptic therapy and CT heads are repeated in ~6 months, we saw some impressive before and after picture. Serology has low sensitivity and not heavily relied on, but MRI findings have many characteristic features (fluid within the lesion, size >20 mm, supra-tentorial, seeing a scolex, and patient not being immunosuppressed).