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.

My predecessor at the clinic, Dr Karen, examining a chest X-ray for possible TB.
My predecessor at the clinic, Dr Karen, examining a chest X-ray for possible TB.

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).

Our well-ventilated sputum production room
Our well-ventilated sputum production room

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.

Recording data about TB treatment has to be meticulous.
Recording data about TB treatment has to be meticulous.

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.

Child waiting in "TB Suspect"
Child waiting in “TB Suspect” with his father.

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.

By Dr Alfred Prunesquallor

Maverick doctor with 40 years experience, I reduced my NHS commitment in 2013. I am now enjoying being free lance, working where I am needed overseas. Now I am working in the UK helping with the current coronavirus pandemic.

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