AIDS, TB and Leprosy: a crash course

Ok, so for those of you who are physiologically, epidemiologically, or clinically inclined– please cut me some slack on this. For the rest of you, this is just a crash course in the basics (very, very basic basics) of HIV and AIDS, and also a little on leprosy just to provide some context about what I am doing. Some of you guys have emailed me questions concerning the diseases, concerning my potential for contracting the diseases, and what exactly I am doing from 9-4, so maybe I can clear some stuff up? Bear with me on this.

So AIDS (acquired immune deficiency syndrome) is caused by the virus HIV (human immunodeficiency virus) which belongs to a family of viruses called “Retroviruses.” Most living things transcribe DNA into RNA and then translate RNA into proteins. Retroviruses, however, are bizarre little antigens because they transcribe their RNA into DNA, which is backwards (hence the name, “retro” virus). Interestingly enough, at SRH we refer to our patients as having “retro-virus disease” or RVDs, since there is such a terrible social stigma associated with the term “AIDS.”

Anyhow, this backwards transcription is accomplished by a specific protein called reverse transcriptase. Reverse transcriptase has a big job. It has to transcribe RNA into DNA and then that DNA is inserted into the host cell’s DNA, which is then transcribed into RNA (again) by the host cell’s machinery. This is then used as the instructions to made HIV proteins. Reverse transcriptase is prone to error though, and makes lots of mistakes. And as I’m sure you can guess, mistakes in genetics often result in mutants! Some of these mutations just happen to benefit the virus in the presence of certain types of drugs (drug resistant strains).

So what we do to prevent the rise of drug resistant strains, is to treat patients with multi-drug therapy. This way, the virus is getting killed on lots of different fronts. Its really important that the patients follow the drug regimen to prevent the emergence of drug resistant strains (which, since none of the ART centers in Andhra Pradesh can supply any kind of second line ART, a first line resistant strain would be really really bad).

HIV specifically attacks the helper T cells of the immune system, which are an important component in the arms race of fighting off antigens (bad guys). Helper T cells do exactly what their name suggests: they help. They help macrophages eat up antigens, they help B cells get activated so that they can produce antibodies, they even help activate complement which is a system of proteins that kills infected cells. Helper T cells work in many ways throughout the entire immune system, so without them, a patient is immuno-compromised and their body struggles to fight off infection. Another name (a more technical name) for Helper T cells is “CD4 cells.”  Our patients have to get CD4 counts, which is an important test that helps the doctors (and hopeful medical students from America who follow the doctors around) to understand how the patient’s body is holding up against the virus. When a patient infected with HIV has a CD4 count less than 200 cells (per microliter of blood) they officially have AIDS. This point is an important marker for medication. The children, however, start medication when their CD4 drops below 500.

As the CD4 count drops, the immune system becomes weaker and weaker. As a result, patients get lots of opportunistic infections. Opportunistic infections are caused by other bacteria or antigens (not HIV) who are taking advantage of the weakened patient. The most common opportunistic infection in patients with HIV that we see at Sivananda (and the most common globally) is tuberculosis (this is often referred to as HIV/TB co-infection). Generally speaking, TB is not a highly infectious disease, and in a healthy individual it is pretty difficult to contract.  Additionally, patients receiving treatment are not infectious (therefore, it is possible that I could contract TB, but it is really, really unlikely that I would, so please don’t worry about that either). The bacterium that causes TB, Mycobacterium tuberculosis, is very very slow growing, and oftentimes (95% of the time in imuuno-competent individuals) the immune system kills it before it can get fully established.

Commonly, TB is found in the lungs. This if for a few reasons, one: the immune system generally tries to stay out of the lungs, because I mean, the less stuff in there the better. Two: TB is spread through droplets, so it is inhaled, and then sets up infection in the lungs, because that’s where it lands. However, since HIV patients have such weak immune systems, the TB has some pretty free range. It can a little haywire and sets up all over the place! This is called extra-pulmonary TB. I’ve seen X-rays and ultrasounds of patients with TB in their kidneys, in their brains, and even in their pancreas. From a social standpoint, its really sad and terrible, but from a clinical standpoint it is very interesting. Sure enough, India is the TB capital of the world. Andhra Pradesh has the highest percent of TB in the country, and Hyderabad is the capital of A.P. So I mean really, if you want to see some serious TB—this is the place to be. TB is curable, and is treated with multi-drug therapy to prevent drug resistant strains (same as with HIV). Drug resistant strains of TB do exist, and it has occasionally been the cause of some pretty scary international panic.

Dr. Yadavalli (my supervisor in Ohio) and his team of students (myself included) have been working in the HIV clinic creating a computer database of the patient records and collect the data from usable patient cases. I have zero contact with serum or blood, so do not, under any circumstances, worry yourself about me contracting HIV. Our goal is to write and publish a paper about the types of opportunistic infections that we are seeing, the CD4 counts (along with some other lab data such as lymphocyte count and hemoglobin) and the patient demographics. This data is important on a global perspective, because it helps keep the medical community abreast to what it is happening in the developing world, and the relationship between the struggles and resources available. Millions of doctors and scientists are working very hard to bring down the cost of HIV tests and treatment, and to increase the efficiency. Additionally, a publication is important source of PR for Sivananda.

Feeling overwhelmed? You’re doing great! Ok, so let’s switch gears to leprosy.

Leprosy is caused by bacteria, Mycobacterium leprae, (same family as TB actually), and like Mycobacterium tuberculosis, it grows very slowly. In fact, it is the slowest growing of all known bacteria. Because of this leprosy is 1. not very contagious and 2. very curable.

Leprosy is a disease that primarily affects the nerves. The skin lesions, infections, muscle atrophy etc are all complications which arise from the damaged nerves. The bacterium prefers cooler temperatures, so it usually localizes away from core body temperatures in the limbs and the face. Therefore we see most of the damage in the hands and the feet. The bacteria settle in the Schwann cells and causes the nerve to demyelinate. The nerve becomes very thick, and the doctors can physically feel it. The thickening nerve results in a lack of feeling to the given area.

In the case of the ulnar nerve (take a second to bend your elbow. Now feel between the two little bumps at the end of your funny bone. If you don’t feel a thick nerve bulging a little that is sore when you push on it, there’s a good chance you don’t have leprosy) the thickening results in “clawing” of the hands. The fingers bend completely at the top two knuckles, so the palm is open, but the fingers are rolled down. The hand freezes in this position. At SRH, the doctors perform reconstructive surgery to straighten the fingers out and angle them opposite of the thumb. They are still frozen in this position, but at least the patient can pick things up and use their hands a little bit, as opposed to the claw hand, with is pretty useless.

The WHO (and Sivananda) classify leprosy into two types: PB (pauci-bacillary) and MB (multi-bacillary). MB is more severe, and is characterized by more bacteria in the body, and more extensive anesthesia. Most of our patients are MB. Patients are treated with multi-drug therapy: two drugs for 6 months for patients with PB, and three drugs for 12 months for patients with MB. The WHO provides free medicine to any patient in the world with leprosy. Once on the treatment, the bacteria in the patient’s body gets killed off very effectively, and no new nerve damage occurs. The problem is, any previous damage is permanent. Additionally, new complications are always arising from old damage. We have many patients each day who get some really heinous ulcers. The patients injure themselves, but don’t know it (no feeling) and then the injury becomes infected. The ulcers, lesions, gangrene etc. that result from these injuries are where leprosy gets the stigma of uncleanliness.

Globally, leprosy is really on the decline. India and Brazil make up over 80% of all leprosy cases in the world, and with available treatment, people are cured left and right. It’s a great success story, but its really important to recognize that patients who are “cured” of the disease still live a long life of complications, disfigurement, and are socially stigmatized. SRH does a really good job of treating the whole patient, not just Mycobacterium leprae. Patients who are too disfigured to function outside live here. They have dignified work, food, clothing and a welcoming community. There are weaving factories on campus where linens and bandages are made of the hospital and the community. Rehabilitated patients can receive training to do LPN work, secretarial work, or even learn a trade. Additionally, my night watchman is a cured leprosy patient. It really is remarkable to live and work in such an interesting community.

So there’s a little bit on HIV/AIDS and leprosy (and some TB thrown in to boot!) If you’re interested in further reading try:

and of course: