I am not a demon-on-the-dancefloor. I shuffle about like a grandfather (without cardigan or slippers I might add) when dancing at wedding celebrations. My mother tried to encourage me to learn ballroom dancing, saying how wonderful it would feel to be gliding around the dancefloor with a pretty girl in my arms. But I must have bisinisterpody (a neologism meaning two left feet). I haven’t watched Strictly on TV in UK, because it didn’t interest me. However, last Saturday, I could see what all the fuss was about. It looked like a marvellous spectacle. And I am tempted to try it out with a willing partner who can dance in protective footwear. Paola Uribe, the lab specialist, on the other hand, attends dancing classes four days a week after work. She is even a qualified Aqua-Zumba instructor. Maybe there is hope for me yet.
They were both gliding around the dance floor, waltzing to perfection. The tango was modern and jazzy, not the classical Argentinian style. Their foxtrot was smooth and flowing, but the damage was done during the quickstep. Their rotations, hops and runs must have jiggled something loose.
Ten years ago at the 38th American Football Superbowl, Justin Timberlake and Janet Jackson were entertaining the crowd during the half time show. Justin ripped off part of Janet’s costume to reveal a breast. It was on display for less than a second, and the nipple was covered with a shield. Scandal! The Federal Communication Commission tried to fine her half a million dollars.
In the audience, just Marguerite Sheriff and I noticed the indiscretion. It was nothing compared to the hundreds of thousands nipples on display at the Umhlanga Reed Dance Festival a month ago. But the dancer might have had a point taken off.
These two contestants were competing at level one. They began shuffling around the dancefloor, with their eyes glued to their feet. Gradually they got into the swing of things and they loosened up. He kept his eyes on her, making sure he was following her lead. Then he made an error. I didn’t see what it was, perhaps he stood on her toe. She was furious with him and gave him a slap. Perhaps you would like to provide a running commentary?
If I had the luxury of a choice between being infected with TB or HIV, I think I’d choose HIV. Most of my patients don’t have that choice; if you have HIV, you have a 50% chance of developing TB. And if you are diagnosed with multi-drug resistant TB (MDR-TB) at the same time as you are diagnosed with HIV, there is a 50% chance you won’t survive the next month.
Tuberculosis is a horrible disease. My mother used to call it “consumption”. Two hundred years ago the “white death” accounted for about 20% of deaths in Europe. With improvements in public health, nutrition and housing, the incidence of TB fell dramatically, and new drugs for TB virtually finished it off. But over the past fifty years, there has been a resurgence of TB, especially drug resistant TB, in Eastern Europe, Asia and Africa. The epidemic of TB has been driven by HIV in Swaziland, as we have the highest prevalence of both in the world. I treat patients with TB every day in the clinic.
A cough officer screens every patient coming to the clinic for TB. Anyone with symptoms suggestive of TB is diverted to a separate building outside the clinic which we know as “TB Suspect”. Patients (and their accompanying relatives or friends) are given a mask at this point. Cough for two weeks or more, night sweats, loss of weight and close contact with a person who has or had TB recently – these are the main symptoms we look for. But fever, blood stained sputum, anorexia, chest pain, fatigue and general malaise are also common.
We are fortunate to have several geneXpert machines in our laboratory. Any tuberculosis DNA in a sample of sputum, aspirate or other material from a patient gets amplified in the machine. Not only do we get a result in two and a half hours, it also tells us if the TB is resistant to the most useful anti-TB drug we have, rifampicin. It is incredibly sensitive, detecting as few as 150 germs per millilitre of fluid/sputum. In contrast, looking for TB germs using a fancy microscope and a special fluorescent stain will only detect infections where there are more than 10,000 germs per millilitre of sputum.
A man who was born after me, but who looked twenty years older, was brought into the clinic in a wheelchair by his son. His legs had gradually become weak and he was now unable to walk. He didn’t live locally, so I asked him why he’d come to our clinic. He told me he had attended a local health centre, but they had told him to come to Matsapha MSF for treatment. Did they think it was too difficult for them to treat, or were they just passing the buck to a clinic where they knew he would get the best treatment?
His chest sounded grim and I saw that there was an angle in his spine (called a “gibus” after the Frenchman who invented the concertina-folding top hat) where one of his vertebrae had collapsed, probably because of infection with TB, damaging his spinal cord, resulting in paralysis. He had Pott’s Disease( after Percival Pott, the English surgeon, who was more famous for discovering the link between boy chimneysweeps and cancer of the scrotum).
His geneXpert test showed he had MDR-TB. He needs twenty months of treatment and I hope that he will regain some of the function in his legs. The cocktail of drugs he will receive is not pleasant. Pyrazinamide, an injection of Kanamycin (with a 30% risk of becoming deaf), a fluoroquinolone (we use levofloxacin usually), ethionamide, cycloserine and terizodone, for starters.
TB can attack any part of the body. Another thin, ill man saw me last week with a massive swelling in the scrotum. It looked as if it was about to burst. I stuck in a needle and the tuberculous pus was under so much pressure that it leaked out around the side of the needle. The pus wasn’t homogeneous, there were chunks of curd-like, white material suspended in it. He was coughing up sputum, too. Both sputum and pus grew MDR-TB.
Two weeks ago, I saw a middle-aged man who had lost 15kg over the past three months, had night sweats and fever for three weeks. He said he was desperate to get proper treatment. He had been admitted to hospital, treated for a chest infection and discharged because they could not detect any TB germs. He then went to the local TB centre, where he was prescribed even more antibiotics. He even gave a history of having a brother who died of TB last year.
His chest radiograph showed fluid at the base of his right lung and a massive boot-shaped heart. A cardiac ECHO (ultrasound) showed fluid around the heart in the pericardial sac. He knew that he was HIV positive, but he said his recent test did not indicate he should start treatment.
I understand that people are cautious about initiating anti-TB medication on flimsy evidence, but I felt there were strong grounds to start this man on treatment. He was so relieved. He knew what had happened to his brother. He is improving already.
All people diagnosed with TB are offered an HIV test. If this is reactive, we don’t start treatment for HIV until the patient has had two weeks of anti-TB treatment. This is to avoid immune reconstitution syndrome (IRIS) where the recovering immune system attacks the TB bacteria causing massive inflammation.
A young man recently diagnosed HIV reactive had some blood tests as a baseline before he started anti-retroviral therapy (ART). His immune system was very depleted, with a CD4 count of just 40 (normal is >500). His liver function tests were abnormal and he had abdominal pain. There were no signs of TB on his chest Xray but he had a dry cough and was given some amoxicillin. His liver function tests improved, hepatitis screening was negative, and we were about to start ART when he fell ill again, with his liver function tests becoming seriously deranged. He had developed a fever and was becoming anaemic. A scan of his abdomen showed an enlarged lymph node close to the liver.
He was admitted to hospital where it was found that his CD4 count had dropped to 11. He had received a blood transfusion and suddenly massive glands appeared in his neck. These were very suspicious of extrapulmonary TB. It was as though his immune system was finally packing up and any TB germs which had been kept under control were now flourishing. Co-infection with HIV and TB is a potent cause of anaemia.
It can be difficult to diagnose children with TB. Young ones may not be able to produce sputum, so we get the child to breathe nebulised saline, which loosens any secretions. If that doesn’t work, we try aspirating stomach contents to detect TB germs which come from the lungs but the child has swallowed. Sometimes all we have is a desperately ill child who is losing weight drastically, or who has some lymph nodes in his neck or groin, or who has a family history of TB. Rather than insisting on a microbiological diagnosis, we treat the child on clinical grounds and look for symptomatic improvement.
At “TB Suspect”, patients are clerked and get a tutorial on how to produce a good sample of sputum. This is sent for Xpert and culture. If there are chest signs, the nurse might order a chest Xray and treat with antibiotics. I have learned to be suspicious of any ill patient who gets better with antibiotics, as it is possible to have TB with an additional infection in their lungs.
Patients with HIV and low CD4 counts get Pneumocystis pneumonia (the name has changed, but everyone still calls it PCP). These patients have a very rapid pulse and respiratory rate, fever, chest pain and a dry cough. Even worse is Kaposi Sarcoma in the lungs. These illnesses teach me to keep an open mind, not to jump to conclusions, and to keep me on my toes.
Another man in his late fifties saw me complaining of shortness of breath on exertion. He had been treated several times for tuberculosis, but he told me that it had never been proven with a positive smear or culture. His chest Xray looked grossly abnormal. I took an occupational health history and he told me that he had worked in an asbestos mine for eleven years. It was highly likely that he had asbestosis or another industrial chest disease. I discovered that the Ministry of Labour sends an occupational physician to a clinic in Manzini on one day a fortnight. It took half an hour on the telephone, but I finally managed to make him an appointment. I am not sure we can help him, but instead of giving him yet another ineffective course of TB treatment, at least he might get some compensation.
I have learned never to take anything for granted. Small improvements may be welcome but can lull you into a false sense of security. It really is important to keep a close eye on patients, and this is difficult when our facility doesn’t have inpatient beds. Our project includes looking after the TB ward at Mankayane Hospital, where we admit seriously ill patients. Sadly, the death rate remains high, despite all the care and attention that MSF provides.
No, this is not how to mix a cocktail of cider and lager. I am discussing envenomation. Swaziland is home to over sixty species of snake, but only seven are likely to do you serious damage.
Judy Chovan asked me on Facebook how to deal with snakebite. The correct answer is to avoid being bitten in the first place. Stay clear of snakes, well clear. Mozambique spitting cobras can squirt their venom eight feet. Don’t hassle snakes, let them escape. They don’t want to pick a fight with you as you are too big to eat. Snakes have poor eyesight but can detect movement, so stay still. It isn’t a good idea to try to kill a snake. If you are close enough to whack it, you are within its strike range.
There are two reasons why you shouldn’t handle a dead snake. Some snakes play dead as a defence mechanism. Even when it is dead, the snake can still bite and inject venom as a post-mortem reflex. (In South Sudan in 1980, a boomslang fell out of a tree onto a chair while we were sitting around a campfire. I was so shocked that I hacked both the snake and the chair to death with a machete. The head was still gaping and closing for an hour after it had been severed, so I put it into the flames. Do you remember, Geoff Collins?)
It is common sense to wear decent shoes and long trousers when walking in the bush during spring and summer. Don’t put your hands into holes and be careful when messing about with a woodpile or compost heap. Use a torch to light your way if you are walking outside at night. Keep the grass in your garden cut short. Put up screens on doors and windows to prevent snakes from coming into the house seeking shade. Snakes eat rats, mice, frogs, small birds. Where you have chickens, you get rodents, so keep the coop away from the house and store feed in closed containers. Where there are weaver nests in a tree, there is bound to be a resident snake, looking to eat fledglings. And don’t forget to look in the toilet bowl before you sit down. My worst nightmare.
Right, let’s say you have been bitten. It might seem an impossible request but try to keep calm. The snake may not have been venomous, or if it was, it may not have injected a significant amount of venom. Most people haven’t a clue what type of snake bit them. Venomous snakes tend to be longer (four to six feet), rear up and make a hood (cobras) or inflate their neck, have bands/bars/stripes on their body (Mozambique spitting cobra and rinkhals), hiss and open their mouths wide. Don’t try to catch the snake for identification purposes, you will only get bitten again.
First Aid for Snakebite
Tell someone you have been bitten and get help. If there is some water available, pour it over the site of the bite to wash off any venom that hasn’t been injected. If you have been bitten on a hand or foot, remove your watch, rings, shoe before any swelling occurs. Draw a circle around the bite if you have a pen. Note the time – by writing it beside the bite if possible. If you do not know what kind of snake bit you, apply a pressure bandage and keep calm. Inform the hospital that you are coming. Don’t cut and try to suck out the venom. Don’t apply ice or lotions/potions. Keep calm and as still as possible.
Identifying the snake is often impossible, but a bit of local knowledge will help:
Puff adders are short, fat snakes that are active at night. They might appear sluggish as they don’t immediately slither away when disturbed, but that is part of their defence mechanism. They actually have the most rapid strike speed of any snake. They usually hiss fiercely and make an “S” shape winding up before striking.
Mozambique spitting cobras are active both day and night. They are inquisitive snakes that will enter homes. They rear up, spread a hood and spit or strike. If they strike, they may do so repeatedly. Some Swazis think that the second strike sucks out the venom from the first strike, but this is wishful thinking.
Rinkhals live in cooler climatic areas of Swaziland. Its defence mechanism is to play dead, often turning onto its back. It rears up when threatened, and spits or strikes.
Snouted cobras prefer hot climates. They are very aggressive and active in the daytime. The Swazis don’t distinguish between rinkhals and snouted cobras.
Black mambas are thin, grey-coloured or brown-coloured snakes, which can reach 8 feet in length. To defend themselves, they rear up alarmingly high and open their jaws to reveal a jet-black oral mucosa (hence their name). They hiss and can strike multiple times. It might seem strange, but their bite is not painful.
Venom works in three ways:
Neurotoxic venom attacks the nervous system and causes blurred vision, weakness, vomiting, thirst, difficulty swallowing and finally respiratory distress, followed by death within the hour if untreated. (Black mamba, snouted cobra and rinhkals)
Cytotoxic venom destroys tissues and initially causes painful swelling. This may proceed to necrosis, or tissue death, resulting in the loss of a digit or an ulcer requiring surgical intervention. (Mozambique spitting cobra, puff adder, rinhkals)
Haemotoxic venom stops the blood from clotting. It can take upto two days before the effects become evident. You bleed from every orifice. Vomiting, mental confusion and sweating are common. (Puff adder, boomslang, vine snake)
The treatment should counter the effect of the venom. For example, it is vitally important to slow down the transit of neurotoxic venom into the bloodstream and to the central nervous system. Pressure bandages or tourniquets are very effective at buying you more time if you have been bitten by a snouted cobra or black mamba. You need a wide elasticated bandage. Start beyond the bite and wrap the bandage tightly up the limb towards the heart. Adding a splint to the bandage is helpful. Don’t remove any clothing and keep still. For bites on the hand, use a sling.
The treatment for cytotoxic envenoming is just the opposite. If the venom is restricted to the bite site, it causes much more damage. You need to dilute the venom by spreading it around your body. If you have been bitten on the hand, lift it up above your head, move it around for five minutes. Do not apply a pressure bandage.
The more astute readers will realise that rinkhals have a venom which has both cytotoxic and neurotoxic effects. The latter is more life-threatening, so apply a pressure bandage.
Haemotoxic envenoming takes longer to appear, so the patient should be in hospital.
Two snakes in Swaziland spit venom when they are threatened (Mozambique spitting cobra and rinkhals). Their range is about twice the length of their body and they aim for the eyes. Venom sprayed onto flesh is harmless, just wash it off. If it gets into your eyes it stings worse than chillies. Rinse with copious amounts of water for twenty minutes. Don’t rub your eyes. You do not need antivenin but you should visit a doctor to check your eyes and to get some antibiotic eye ointment.
Antivenin is produced by injecting repeated tiny doses of venom into a horse without killing it. The horse’s immune system produces antibodies to the venom. It is polyvalent – meaning the horse is exposed to several different kinds of venom – so it can be used in situations where the snake is unknown. The local antivenin has been produced for decades in South Africa, where Mozambique spitting cobras are less common. Its venom was added to the mix more recently, but it is not as effective. I understand that a specific monovalent antibody is in preparation to treat this venom and should be available next year. (In Swaziland, 80% of serious envenomation is caused by the Mozambique spitting cobra.) There is also a monovalent antivenin for boomslang bites, but this rarely occurs.
Antivenin is given in hospital, intravenously, before any tourniquet or pressure bandage has been released. As the serum is horse protein, allergic reactions are common, so give prophylactic adrenaline intramuscularly (0.25ml of 1:1,000 for adults, 0.01ml/kg for children). Most doctors inject the antivenin via a peripheral line, 10ml per minute. You should get some improvement after 15-30 minutes. If you don’t, then you probably haven’t given enough.
For unknown snakebites, after five ampoules of polyvalent antivenin, release the tourniquet and look at the site. If the site is swelling, mark the edge with a line and time, then give an additional 20ml every hour until symptoms cease. You need 8 vials for a black mamba bite and 10 vials for Mozambique spitting cobras, with an additional 20ml every hour until symptoms cease.
Neurotoxic effects of envenomation will start to improve 30 minutes after adequate treatment with antivenin. However, once respiratory paralysis has begun, you need to begin artificial respiration by whatever means available. Antivenin just reduces the time this is required. Some victims have survived 12 days of respiratory support and have made a full recovery.
Antivenin has a shelf-life of three years, but it is so expensive that in Zambia, I have kept supplies in a refrigerator (NOT a freezer) well past this expiry date as long as the liquid has not become turbid. If using out of date stock, it is wise to assume some diminution of potency. Here in Swaziland, there is a co-operative scheme where families will buy a single vial of polyvalent antivenin which is kept in a central location, along with the stocks from many other families. In the event of someone being bitten, this antivenin is used, and the stock is replenished by the victim’s family, to keep a “float”. If you leave Swaziland, you could “sell on” your antivenin to a new arrival.
Good Shepherd Hospital is a private mission hospital in the most snake-infested part of Swaziland. They use up antivenin so quickly (they see 40 snake-bitten patients a month in peak season) that it has been possible to trade stocks which are a year from their expiry date for new antivenin. Thank you, Good Shepherd!
Haemotoxic envenomation is treated by transfusing blood and blood products to keep pace with loss.
MSF used to keep antivenin in Matsapha clinic, but as we have no inpatient beds, and Raleigh Fitkin Memorial Hospital is just 20km away, we no longer stock it. That relieves me of a big responsibility, but I’m occasionally called upon to treat the after-effects of cytotoxic envenomation (thank you for your advice, Professor Joe Dias).
For this posting, I am extremely indebted to Thea Litschka, who runs the Antivenom Swazi Foundation. She gives a great lecture, well illustrated with slides. She also runs an annual course on snakebite for medical staff in Swaziland. Check her out on YouTube, “Black Mamba, White Witch”, especially the part where she removes a black mamba from a hotel bedroom.