Day 4: more virus talk (dengue), cool cases, and leprosy oh my

Still having issues with jetlag, but I really like how the course is going. The day was started off by a fantastic lecture on dengue, how to interpret serology and antigen testing (NS1, IgM, IgG), as well as going over details of the aedes aegypti mosquito, how it actually feeds during the day, likes stagnant water (especially inside), and how it takes multiple blood meals during each feed  - thus explaining how several family members can present at the same time with dengue.  It is also referred to as the tiger mosquito. Generally, dengue hemorrhagic fever is when one gets dengue for a second time and with a different serotype (where there are 4). Although management is supportive, patients will die from complications, and recognising who has warning signs is key. Things such as abdominal pain, persistent vomiting, cold extremities, narrow pulse pressure, edema, blood in stool, or hematuria are somethings that should raise suspicion for a patient that may progress to severe dengue.

Note the striped legs (aka tiger mosquito), there is another aedes (A. Albopictus), which bites animals, is more rural, and takes a full meal from one human. This bastard also transmits zika, chickungunya, yellow fever, and even filariasis.

The illness consists of three phases

1.     Febrile

2.     Critical (plasma leak)

3.     Convalescence (resorption).

I think he take home message is patient can appear overloaded during the critical phase, but can be intravascular depleted and thus need fluids. Patient’s are at risk of volume overload/pulmonary edema during convalescence phase. Symptoms typical of dengue can be non-specific, but retro-orbital pain seems to be a prominent feature, they do get rash and the classic island of white in a sea of red usually is seen during the convalescent phase. Leukopenia, elevated liver enzymes (AST>ALT, thrombocytopenia and lymphocytosis is classic.

There is a vaccine for dengue, it is recommended in high endemic areas (>70%), the idea being that if you vaccinate people, potentially they can get severe dengue. It is recommended for those 9 or older.

We then had a talk about ebola which was excellent. The professor was present in Africa during the 2014 outbreak and was able to really go over his experience. It is believes it was transmitted by bats. Although people would wear extensive gear when treating this patients, it is actually thought to be only droplet spread, just highly infectious. In parts of Africa, the burial process involves significant contact with the deceased and this likely caused significant spreading among families.

We then had a talk on hemorrhagic fevers, a little much but in a nutshell, ribavirin does work for Lassa fever, a hemorrhagic fever in west Africa. It actually has been shown to have mortality benefit. It also can be given for prophylaxis as well. A weird feature of this virus is hearing loss, compared to rift valley fever (more in East Africa) which can cause vision loss (and has increase mortality with ribavirin).

And briefly touched on hanta virus, which can be associated with a pulmonary syndrome; ARDS, or renal disease (where ribavirin may work).

We had 3 very interesting cases presented to us (clinical vignettes) which is my favorite part of the courses.

1.     A 40 year old Thai female who had headache and fever x 1 week after returning back from Northern Thailand (had eosinophilic meningitis and was angiostrongylus, patient better after a lumbar puncture and was fine after a week)

2.     A 40 something year old male from west Africa (forget which country) who came to Norway from refugee camp, was diagnosed with relapsing fever (had relatively sudden onset of headache, myalgias). Of note, this is carried by body lice (which also transmits, trench fever- bartonella Quintana, as well as R. Prowazakii aka epidemic typhus.

3.     A 30 something year old female from Malawi with diarrhea, rash – diagnosed with pellagra, she had a classic rash around the neck (Casal’s Necklace)

The clinic today was really interesting; we went to a dermatology clinic where we got a break down of some common skin conditions seen in the tropics. We got a primer on leprosy, the 5 stages from tuberculoid to lepromatous, related to TH1 vs TH2 immune responses which dictate what kind of leprosy you will get. Tuberculoid being that your symptoms are more so from the inflammatory reaction, biopsy showing granulomatous inflammation, low amount of bacteria present, and classic hypopigmented, hypaesthesic patches.  Neuropathy is usually along the nerves where the lesions are, and this can be as foot drop, or ulnar nerve palsy (which we saw in clinic). Lepromatous is associated with more nodular lesions and often skin scrapings of multiple bacilli, neuropathy is more general. It is thought that leprosy is caused by the respiratory route, not easily transmissible. In general, it is poorly understood. Most patients fit somewhere in the middle of lepromatous and tuberculoid.

Differential of hypopigmented patches relate to sarcoid, TB, vitiligo, syphilis, post kala azar dermal leishmaniasis, tinea versciolor

When to consider leprosy?

- Hypopigmented or reddish patch(es) on the skin

- Diminished sensation or loss of sensation within skin patch(es)

- Paresthesias (tingling or numbness in the hands or feet)

- Painless wounds or burns on the hands or feet

- Lumps or swelling on the earlobes or face

- Tender, enlarged peripheral nerves

We reviewed type 1 (reversal reaction) and type 2 (erythema nodosum leprosum). Type 1 is an increased cellular immunity, and can occur prior to treatment, might be seen as a hypopigmented lesion turning more erythematous or worsening neuronitis. Type 2 reaction can cause more systematic symptoms (fever, malaise) and cutaneous nodules. One theory is that this is immune complex drive. Both reactions can be treated with steroids, for type 1, with severe nerve injury this is often given as 1 mg/kg and slowly tapered over weeks to months.

We then discussed the many skin manifestations of TB, of which lupus vulgaris (plaque like lesions, usually in one area, is most common).

Finally, we reviewed some presentations of Madura foot, mycetoma and actinomycetoma. Where we try and get a description of white kind of “grains” are coming out from the patient. Ideally discharge from the wound is use to make a presumptive diagnosis, one diagnosis seen in the tropics is chromoblastomycosis, where seeing copper penny bodies on histo can be helpful in making a diagnosis.

Ulnar nerve palsy in a female with leprosy.

This was a male in his 40s who actually had what seemed like carpal tunnel syndrome, he underwent decompression surgery and after biopsy of his nerve was suggestive of leprosy. He had clear thickening of his ulnar nerve, and this inconspicuous lesion on the dorsum of his left hand.

Not shown here but one women was missing fingers, she had progressed to quite a late stage of neuropathy, her findings were almost what I’d see in a severe diabetic neuropathy.

Treatment for mild forms is usually monthly rifampicin and daily dapsone (while checking G6PD prior to).

20 something year old farm with lesion on knee for several years, non-painful. This was highly suspicious for cutaneous TB (lupus vulgaris), biopsy was just done.

Chronic drainage lesion in a blacksmith, suspicious for mycetoma (waiting to see if this is fungal or bacterial).