South Africans with HIV-related pain are surprisingly active, but not due to their resilience.

Antonia Wadley

When one thinks about chronic conditions that are commonly painful, HIV doesn’t typically spring to mind. However, more than 50% of HIV-positive individuals experience painful conditions like headache, chest pain or neuropathy, and that pain is frequently experienced as moderate to severe in intensity.


What struck researchers from the Brain Function Research Group (BFRG) at Wits University as odd was that despite this high burden of pain in HIV, a couple of papers have emerged suggesting that, having asked patients, functional interference (having difficulty with things like walking or going to work) was not as great as they might have expected. One of these papers was from the BFRG and had been completed locally in Johannesburg, South Africa.


To investigate whether pain does actually affect function in HIV (as it does in many other clinical conditions), researchers Dr Antonia Wadley, Emeritus Professor Duncan Mitchell and Associate Professor Peter Kamerman from the BFRG, based in the School of Physiology, Faculty of Health Sciences at Wits, conducted a cross-sectional study.

The results from the study, titled: Resilience does not explain the dissociation between chronic pain and physical activity in South Africans living with HIV, are published today, 13th September, in the journal PeerJ.


To explain why pain may not affect function, the researchers first put it down to African patients being resilient – the ability to cope with adversity.


Explains Wadley: “Nobody’s assessed resilience in people living with HIV and chronic pain before. We hypothesised that people living with HIV would generally be pretty resilient and those who were more resilient, would be more active and report lower pain intensity.”


Measuring resilience in HIV-patients objectively for the first time

For the study, the researchers recruited HIV-positive patients from an HIV clinic in Johannesburg: half with chronic pain (defined as having had pain most days for at least three months) and half without. They then assessed resilience and, as well as asking patients about their activity, the researchers measured it objectively for the first time in a subset of patients using accelerometers, which are like sophisticated pedometers. They also asked the patients about their day to day worries.


“It turns out,” Wadley says, “that we were right on one thing, HIV-positive patients in our study were really resilient, but our hypothesis was wrong: being more resilient didn’t associate with being more active or having lower pain intensity. In fact, the activity results astounded us. Not only was patients’ activity not as affected as one might expect, it wasn’t affected at all.”


There was no difference in activity intensity, duration, or time spent at different intensities of activity between those with and without chronic pain. “This is something you just don’t see in other types of long term pain,” she adds.

The researchers then looked at how frequently patients worried about their health, money, food and family. “We thought that if patients were worried about money and having enough food that pain might be relegated to a lower priority.” They found that patients in chronic pain worried more frequently about each of these things compared to their pain-free counterparts and that health was lowest down the list.

“So it really does appear that if you are poor, pain may be relegated to a lower priority. Indeed, our analysis showed that worrying more about food associated with higher levels of activity,” says Wadley.


Going forward

The researchers also asked the patients in pain what else they worried about and who they had told about their pain.


“It turns out that HIV-related stigma is a real problem and that half the patients in pain had not told their closest friends and some not even their family about their pain, for fear that it might reveal their HIV status.”


Wadley says it thus seems that economic stresses and fear of HIV-related stigma may drive people to maintain high levels of activity, even when they are in severe pain.


“What’s not clear is whether this kind of level of activity in the face of pain is helpful or harmful and that’s something we will be looking into next,” she adds.

PainSA Congress 13th -15th May 2016, Umhlanga

Toni Wadley


Last month, I headed over to Umhlanga with some of the other Pain lab members for the annual PainSA Congress. PainSA  is the South African chapter of the International Association for the Study of Pain and the Congress is a meeting of health care professionals and scientists from across the country who work with pain.


PainSA Group photo

Me (far right) and the rest of the team, (from the left) Sean Chetty, Peter Kamerman, Prinisha and Dershnee Devan at the PainSA congress. (Photo by Toni Wadley)


In the pain lab, we’re always going on about how pain is under-recognised and under-treated in African HIV+ patients. Every PainSA congress, the sentiment that access to opioids in Africa for severe pain is woefully inadequate is repeated. Yet at this year’s congress we heard the opposite angle. US.  Professor Tracy Jackson, medical director of outpatient pain clinics at Vanderbilt, gave hard hitting talks about the ineffectiveness of current chronic pain therapies despite the US spending $630 billion a year on the problem. She spoke about the over-reliance on opioids in a country that uses 80% of the world’s stock and where opioid overdose is the leading cause of accidental death.


Tracy is a big advocate of non-pharmacological interventions including functional rehabilitation programmes. These programmes are residential and involve an entire multidisciplinary team of healthcare professionals aimed at getting patients back to being functional, even if that means their pain staying the same. Her new take on these programmes is to offer ‘Relief retreats’ where restoration programmes are held at retreat centres rather than in a typical clinic setting.


Tracy is really entertaining to listen to. Follow this link for a TEDx talk she gave in Nashville very recently on the topic of non-pharmaceutical treatment of chronic pain.


The theme of getting patients with chronic pain back to work was echoed throughout the congress. Dershnee, an MSc student in the pain lab, gave a workshop on the topic. Dershnee has a background in occupational therapy. Through her current work in medical insurance she knows only too well that absenteeism from work costs South Africa R12 billion a year.


Peter, the head of our pain lab, gave a plenary talk on “Neuropathic Pain: so many people, so few drugs”. Sean Chetty, a pain lab PhD student and anaesthesiologist, gave a plenary on pain management being a human right. In the largest research paper session a PainSA congress has had, I spoke about the effect of HIV stigma on pain, and Prinisha presented some of her PhD data about the pharmacological treatments that are actually being used in the clinic for HIV-associated sensory neuropathy. Prinisha won the joint first prize for best talk along with Tory Madden a new postdoc at UCT.  Well done Prinisha!


Prinisha giving her winning talk. Photo by Toni Wadley

Combating the ills of opioids (and saving rhinos)

Anna Haw


A field of brightly-coloured, flowering poppies is as spectacular to the brain as it is to the eye. Opioids, drugs derived from the opium poppy, act on receptors in the brain to bring about sensations such as euphoria and pain relief. Just as the wind through a field of poppies can capture your gaze and keep you mesmerized for hours, so too can opioids hook your brain; a phenomenon well understood by heroin addicts. Sadly, euphoria and pain relief are not the only opioid-induced effects. Another side-effect blocks the drive to breathe, resulting in the death of an estimated 69,000 people worldwide each year.



Opioids were first isolated from poppy seeds and are famous for their effect on the brain. Photo by Anna Haw.


Opioids block pathways in the brain that regulate breathing and dampen the feedback loops that tell the brain to take deeper breaths or more breaths when oxygen levels are low. Without enough oxygen in our blood, cells die and ultimately the heart will stop beating.


While opioid use in humans, with the subsequent consequences, is well recognized, opioid use in wildlife is perhaps not so widely understood. Have you ever wondered how wildlife veterinarians capture, treat and transport enormous wild animals such as rhinoceros and elephant? How do vets make these two-ton (or more) animals sleep by firing a measly dart into them? The secret lies in those fields of brightly-coloured poppies. Potent opioids, such as a drug commonly referred to as M99, are an essential component of a wildlife vet’s armory and the only class of drug capable of bringing about a deep sleep (or immobilisation) in large herbivores like the rhino and elephant. A major advantage of opioids is that their effect can be reversed with an antidote. When a vet has finished working with an animal, she injects the antidote and within seconds to minutes, the sleeping beast is awake and wandering back into the African bush.


However, the picture is not always so rosy. Sometimes the animals don’t get up, or sometimes they get up, only to suffer consequences of the event in days, weeks or months to come. It so happens that the white rhinoceros, currently needing the most hands-on interventions in the face of escalating poaching levels, is one of the species that is most severely affected by M99’s ill-effects. Just as opioids can kill humans, so too can they kill wildlife, with the white rhino being particularly susceptible to this fate.


White rhino are so severely affected by M99 that vets have been experimenting with different treatment options in an attempt to improve the oxygen levels in the immobilised rhino’s blood and reduce the risk of death. However, with many different vets trying variations on a similar theme, one standard approach, scientifically proven to improve oxygen levels, has been lacking. Therefore, with a team of researchers from the University of the Witwatersrand (Wits), University of Pretoria and SANParks, I systematically tested different available treatment options, firstly in boma-housed rhino and then in free-ranging rhino within the Kruger National Park. In the bomas, we were surprised to find that giving a high volume of oxygen through the rhino’s nostril made the physiological imbalances caused by M99 even worse and did not improve breathing. Another treatment option, currently used by many veterinarians, is a drug called butorphanol. Butorphanol partially reverses the effects of M99, and it is believed that the negative side-effects are reversed more than the positive effects, such as immobilisation. However, the advantages of butorphanol are not clear-cut and, invariably, some arousal occurs together with improved breathing. In a two-ton, confused wild rhino, unwanted arousal can be problematic. We also found that butorphanol did not fully correct the oxygen levels in the rhino. So we combined the administration of oxygen through the nostril with an injection of butorphanol. To our delight, this treatment option completely corrected the dangerously low oxygen levels, thus significantly improving the safety of rhino immobilisation.


rhino pic

Immobilised white rhino receiving oxygen through its nostrils. Photo by Andrea Fuller.


As the fight against poaching intensifies, more rhino need to be immobilised for procedures such as translocation and the fitting of tracking devices. Moreover, vets are increasingly faced with severely injured rhino that have survived a poaching incident. These compromised animals require repeated immobilisations for intensive veterinary care and often cannot survive any additional physiological stress. Thankfully, as a result of our research, rhino capture need no longer be such a risky procedure and wildlife vets across South Africa have already adopted the approach of administering oxygen and butorphanol to immobilised rhino.



Haw AJ, Meyer LCR, Fuller A. 2016. Nalbuphine and butorphanol reverse opioid-induced respiratory depression but increase arousal in etorphine-immobilized goats (Capra hircus). Veterinary Anaesthesia and Analgesia.

Haw AJ, Hofmeyr M, Fuller A, Buss P, Miller M, Fleming G, Meyer LCR. 2015. Butorphanol with oxygen insufflation improves cardiorespiratory function in field-immobilised white rhinoceros (Ceratotherium simum). Journal of the South African Veterinary Association, 86: Art #1276.

Haw AJ, Hofmeyr M, Fuller A, Buss P, Miller M, Fleming G, Meyer LCR. 2014. Butorphanol with oxygen insufflation corrects etorphine-induced hypoxaemia in chemically immobilized white rhinoceros (Ceratotherium simum). BMC Veterinary Research, 10:253.

How to do an ELISA (or A day in the Fever Lab)

Arista Botha


An example of a 96-well ELISA plate. Photo by Arista Botha


When you are writing up your PhD protocol, your experiments all seem simple. Then, when it gets to actually carrying out the experiment, things are often a lot more complicated than what they appeared like on paper. For example, my methods description was strewn with all of the blood chemistry tests one could possibly think of. Once my protocol and my ethics were approved, I had to start making it happen. How hard could it be?


As it turns out, finding an ELISA kit for any animal other than humans, rats or mice is tricky, so I ended up sending about twenty emails back and forth to various companies. Finally I found a company that could send me the right ELISA kit. The second surprise came when I saw what ELISA kits cost! I never knew that such a small thing could be so expensive. Luckily, my supervisor had a grant that was just about the right amount to cover my ELISA kits. So I had a product, a supplier, a quote and a grant. Satisfied, I placed my order. I was so excited when, a few days later, my kits were delivered. Like a little kid opening a Christmas present, I unpacked my kits, marked them clearly with my name, and stored them neatly into the fridge.


I stood back and thought: Now what!


Panic started to set in. During my Master’s degree I had spent most of my time in the field, tracking my study animals and doing behavioural observations. The result being that I have not spent any time in a laboratory since my undergraduate degree! How did I get myself into this?


Luckily Tanya and Lois from the Fever Lab were doing ELISA’s for their research, and they agreed that I could tag along and they would teach me how to do an ELISA. So I joined the Fever Lab for a day.


First off, I have to say that the Physiology Department have the most amazing equipment in Monica’s assay lab! To start off with, Tanya used an ultrasonic homogenizer (also called a sonicator) to prepare rat brain tissue before performing an ELISA for detecting rat IL-1β protein. A sonicator is similar in purpose to a homogeniser (or the blender in your kitchen) except that a sonicator uses ultrasonic sound waves to disintegrate the tissue. ULTRA-SONIC SOUND WAVES! That sounds like something from a science fiction movie…



An ultrasonic liquid processor (sonicator) is used in our lab to sonicate the samples. Photo by Arista Botha


And then, they have this “super-pipette”, which we call the “Pipette-man”! The first part of doing an ELISA is pipetting your sample and other solutions provided by your ELISA kit into the sample wells. This little piece of equipment makes a big difference in speeding up the whole process.



This pipette allows you to pipette simultaneously into eight wells, saving a lot of time during the ELISA process. Photo by Arista Botha


After incubating your samples the wells have to be washed out properly. You can either manually empty each well and then wash it out with wash buffer using an ordinary pipette (repeat times five!), or (the better option) you can use an automatic well washer, such as the one shown below:




The automatic well washer saves you hours of repeatedly pipetting wash buffer into each well. Photo by Arista Botha.


After washing your samples, you add a substrate solution (consisting of colour reagents), which makes your samples turn blue, if for example, IL-1β is present in your sample. After leaving it to incubate for a set time period you add the stop solution, which changes the colour from blue to yellow.



Adding the stop solution changes the sample colour from blue to yellow. Arista Botha


The final step in the ELISA process is, of course, getting the results! The concept is that the darker yellow your samples, the higher the concentration of the substance you want to measure in your sample (in this case, IL-1β). You put your 96-well plate into a microplate reader, which is set at a certain wavelength, and which will give you optical density (OD) readings. Further calculation of these OD readings ultimately will give you your sample concentration.



The ELISA microplate reader measures the optical density of each well, which you then use to calculate the concentration of your sample. Photo by Arista Botha


After spending the day with the Fever Lab, I feel a lot more confident (and excited) about doing my own ELISAs. I am so glad that we have these equipment and skilled people in our research group and that we can learn from one another. This is why the BFRG is a team and why we do research TOGETHER!

Our genetics can be painful

Liesl Hendry

“It must be in your genes”. This is a phrase that gets thrown around quite often, usually to explain some sort of behaviour or (often unwanted) physical trait. Our genes and the variation within them can, to a large extent, tell us a lot about ourselves, why we are the way we are and explain what makes us different from other humans and other organisms. Interestingly, we are about 99.5% genetically similar (when looking at the DNA sequence) to our fellow humans and about 98% similar to our furry chimpanzee friends. We do, however, differ in some parts of our genome and it is this unique “pattern” or variation that, along with some environmental and other factors, influences the way we look, the way we behave and the way we respond to certain things. For example, something as simple as whether or not one tastes the unpleasant bitter taste of Brussels sprouts is determined by the presence or absence of a certain genetic variant!


I have been interested in the field of genetics for a while now and am fascinated by the role that genetics plays in our lives. A more serious part of genetics and a main focus of research in the field is that of genetics related to disease. Our genetic makeup is believed to influence our susceptibility to developing certain diseases and the seriousness of a particular illness or associated symptom. My first exposure to this line of research was during my MSc degree where I was involved in a joint project between the Human Genetics department at Wits/NHLS and the pain lab of the BFRG. My research investigated the association of previously associated neuropathy and pain genes with susceptibility to developing HIV-associated sensory neuropathy (HIV-SN) and pain and variation in pain intensity. This was looked at in a black Southern African population. The population of choice was specifically significant as African populations have been largely understudied in the field of disease genetics compared to non-African populations. Based on the knowledge of genetic susceptibility to disease, it comes as no surprise that the risk of experiencing pain and neuropathy as well as the intensity of the pain experienced in HIV patients are considered to have a genetic component, but the big (and still not completely answered) question is exactly what genes and variants within the genes are involved? Having a supervisor from both the genetics and physiology departments offered the necessary expertise to understand the relationship between the genes and phenotypes under investigation and to try to come a bit closer to answering this question.


The project was an extension of work being done at the time by Toni Wadley for her PhD, with a deeper look into some of the regions of the genome that she had looked at, and was part of a larger study, headed by Prof Peter Kamerman, looking at various aspects of HIV-SN. The project used DNA samples from adult HIV positive patients, attending the Virology Clinic at the Charlotte Maxeke Johannesburg Academic Hospital, who had been on antiretroviral therapy for at least six months. This DNA was genotyped for a range of carefully selected single nucleotide polymorphisms (mutations/variants within genes) across the genes under investigation with the aim of being able to determine, as best we could, the role that the genes play in neuropathy and/or pain.


Apart from the specific statistical associations which resulted from analysing the genotype data against the phenotype data (HIV-SN status, pain status and pain intensity, etc; there is too much to mention here!), the research led to several observations/conclusions. The first thing to point out is that pain is very common in individuals with HIV-SN. Over 90% of individuals with the neuropathy experienced some sort of pain, mostly moderate to severe in nature. This made studying pain risk in these individuals rather difficult as the number of cases (those with pain) far out-weighed the number of controls (those without pain), therefore making the reliability of the pain risk results questionable. Secondly, it is clear that both HIV-SN and pain are complex traits. Unlike disorders such as Huntington’s disease or cystic fibrosis, which are monogenic, the results pointed towards several genes being associated with HIV-SN and pain risk and pain intensity. This brings about a particular challenge: how do we know what the exact causative genes/variants are? To answer this question, genetic association studies need to be coupled with functional studies to determine the actual functional role that the variants play, for example in altering the expression of the gene product, which could ultimately lead to differences in disease susceptibility and intensity. Lastly, there were inconsistencies between what was previously discovered in non-African populations and what we discovered in our African population, leading to us concluding that associations (in this study and in fact in most genetic association studies) are population-specific. This could be explained by the differences in diversity and structure of the genome among populations of different ethnicity, leading to different variants within different genes being associated with a particular trait.


A question you may have on your minds (possibly as non-geneticists) is “why is it so important to discover which genes are associated with a particular trait?”. Apart from the hunger for knowledge, one of the biggest factors to consider is that of treatment. Looking specifically at HIV-SN, treatment generally involves slowing the progression of the neuropathy or managing symptoms, rather than actually curing the neuropathy. What I haven’t yet mentioned is that the neuropathy and associated symptoms are often caused by the antiretrovirals that the individuals receive. Identifying individuals who are at a greater risk genetically for developing HIV-SN and pain associated with the neuropathy can result in these individuals being monitored more carefully and having the chance of being administered different antiretrovirals in the future.


The questions that I’m sure many geneticists ask themselves…Will the research ever end? Have we found all the answers yet? The answer, quite simply, is “no”. The genetic differences between populations and the complex and multifactorial nature of many traits/diseases make the research in this field anything but simple. With the advancing technologies and the increased ability to handle and analyse large sets of data, researchers seem to be getting a little closer, but, in many cases, the findings recorded so far are just the beginning with so much still to be uncovered…



1) Hendry L, Lombard Z, Wadley A, Kamerman P. KCNS1, but not GCH1, is associated  with pain intensity in a black southern African population with HIV-associated sensory neuropathy: a genetic association study. J Acquir Immune Defic Syndr. 2013 May 1;63(1):27-30. doi: 10.1097/QAI.0b013e318285cf36. PubMed PMID: 23314412.


2) Wadley AL, Hendry LM, Kamerman PR, Chew CS, Price P, Cherry CL, Lombard Z. Role of TNF block genetic variants in HIV-associated sensory neuropathy in black  Southern Africans. Eur J Hum Genet. 2015 Mar;23(3):363-8. doi: 10.1038/ejhg.2014.104. Epub 2014 Jun 4. PubMed PMID: 24896147; PubMed Central PMCID: PMC4326702.



3) Hendry LM, Wadley AL, Cherry CL, Price P, Lombard Z, Kamerman PR. TNF Block Gene Variants Associate With Pain Intensity in Black Southern Africans With HIV-associated Sensory Neuropathy. Clin J Pain. 2016 Jan;32(1):45-50. doi: 10.1097/AJP.0000000000000224. PubMed PMID: 25756557.


Born to be a Kalahari kid

Wendy Panaino


Pangolin face

A pangolin looks up from its ant meal. Photo by Wendy Panaino

It’s hard to think that almost a year ago, I had barely even heard of pangolins, and now I get to spend most nights with these incredible creatures in the most beautiful place. My MSc research involves investigating the body temperature and activity patterns of free-living ground pangolins (Smutsia temminckii) at Tswalu Kalahari Reserve in the Northern Cape Province. It has taken me a while to sit down and put into words the incredible journey I have been on this year. As I sit and wait for a pangolin to emerge from its burrow, I have plenty of time to gaze at the stars and reflect on my 2015 adventure. How could I possibly put this incredible year into one blog post? So many spectacular stories can be told here, but for now I’ll stick to telling you about my daily field work life at Tswalu.


After a successful week of surgery to implant pangolins with temperature data loggers, my adventure into a mind-blowing world was to begin. I’d be away from home longer than ever before, and fending for myself for the first time. I could never have dreamed that I would end up here, living in such a spectacular reserve. I dived right into things, venturing over the sandy dunes of the Kalahari, tracking the pangolins each day with a VHF receiver and antenna. There are few things more thrilling than hearing that first beep coming from your receiver, indicating that the animal you seek is nearby. Whether it takes you five minutes or an hour, you can’t help but feel the excitement boiling inside you when you know you’re getting close. There it is… a beautifully structured burrow that houses the precious scaly creature you’ve been seeking. I place a camera trap, mark the burrow on my GPS and get a slight sense of victory as I walk away.


Kalahari Kid tracking (2)

Tracking pangolins in the Kalahari. Photo by Lizelle du Preez

Camera trap

A camera trap in front of a pangolin burrow. Photo by Wendy Panaino


Daylight passes and the glorious night sky awakens. The way the moon rises over the mountains is more spectacular here than anywhere I’ve ever seen. This is my FAVOURITE part. I arrive at the burrow that I had marked earlier in daylight hours. I use the VHF receiver to ensure that the pangolin has not left its burrow yet. Providing that it is still in its burrow, I carefully position myself somewhere close by and down-wind. Here I sit and wait for the sound of the pangolin emerging from its burrow. Such a unique sound it is for a mammal, with the scales brushing against each other, a sound that could easily be mistaken for grasses rustling with the evening breeze. However, after spending many nights with these little animals, I have finally developed an ear for the unique sound. The moment I hear the animal in motion, my heart starts to race and the butterflies in my stomach emerge. I am about to lay my eyes on one of South Africa’s most elusive animals; the animal that I have chosen to devote an entire year to study. What a privilege!


Pangolin tracker (2)

A pangolin with a tracking device attached. Photo by Wendy Panaino


After the pangolin emerges, I follow the scaly critter from a distance as it forages for ants and termites through parts of the night. Recently I have managed to catch a pangolin in the act of laying a scat. How many people have seen a pangolin in the wild, let alone seen its scat? That’s a component that is lacking in most “tracks and signs” wildlife field guides. To take things even further, I have had the most incredible experience of being able to watch a female pangolin emerge from her burrow with her offspring. This may be the highlight of all my experiences here at the ever-so mesmerizing Tswalu, and I’ve only just begun! I cannot wait to see what lies in store for me in 2016.


Pangolin baby (2)

A pangolin female with her offspring clinging to her back. Photo by Wendy Panaino.


When I am not tracking or following pangolins, I am sitting counting ants that have been collected from pitfall traps. Although this takes many hours out of each day, it somehow gives me a sense of peace and I have learned to embrace it, since I am so fortunate to be doing it in this beautiful reserve. I never thought I’d end up working with insects, but I’ve recently taken it upon myself to learn as much as possible about the various insects and other little creatures that I find in these traps. The endless urge to keep learning and my continuous curiosity is what drives my passion for science and research, and so I encourage myself to embrace every opportunity that comes my way, no matter how small. Looking at each day with utter optimism is what makes my journey so special to me, and is what drives my excitement for this project and this place. And what would such an adventure be without the people I get to share it with? Living with such a diverse group of researchers has been a whole new world of fun, and each person (albeit unknowingly) drives my passion and excitement even further. I have met some of the most incredible people in this spectacular place. Tswalu is possibly the best place I’ve ever had the opportunity to visit. It is so unique and different to any other place I know and I have now started thinking that maybe, just maybe, I was born to be a Kalahari kid.


group photo

A few of the researchers and students at Tswalu that inspire me every day. Photo by Wendy Panaino.


Kruger behind the scenes

Malek J Murad


When the student protests finally ended, we went to the Kruger National Park, the biggest national park in South Africa (the park is as big as Belgium), to collect data for a research project on buffalo. I was looking forward for our trip really badly and I was so excited when we finally got there.



First time in Kruger! Photo by Malek Murad


How did it feel to be in Kruger for the first time? Incredible! We were sitting outside, having dinner, while a gecko was catching a moth and some mosquitoes by the light of the lapa. A perfect symbiosis. I hate mosquitoes.


In Kruger, it is never quiet. You fall asleep to the sound of the crickets chirping. You wake up in the middle of the night and the crickets are still chirping. Then you lie awake for two hours, because you are so excited. There is always an animal calling somewhere. Was that a hyena maybe? In Kruger, it is never quiet. And your heart isn’t either.


If you have never been to Kruger you should add a visit to your to-do-list. On our way to our camp, we watched an elephant herd taking a bath from 100 m away. Readers who have seen an elephant bull from up close will know what I mean; he’s not just big, he’s huge! And at that moment in time I did not yet know how close I would get to an elephant bull during my visit…


IMG_0873 (3)

Elephants enjoying the water on a hot day. Photo by Arista Botha


After a short night in Kruger Vetcamp, we left early the next day to start with our research work. So this is how wildlife research works: You get up at 4 o’ clock to start work at 5. What is the benefit of that? You have to work in the cooler morning hours and finish before noon to prevent heat stress for the animals during immobilisation. What is the benefit for yourself? You can go for a game drive in the afternoon!


So why did we go to Kruger National Park? What did we do there? Arista Botha, PhD student at BFRG, is currently doing research on African buffalo. The buffalo have to be sedated so that we can collect samples and weigh them. No sooner said than done. The well-rehearsed team of the Kruger State Veterinarians sedated, weighed and measured all the buffalo and collected all the samples well before noon. The Kruger veterinarians allowed me to help out where I could.



The buffalo were immobilised to collect samples and to weigh them. Photo by Malek Murad


The director of the BFRG, Professor Andrea Fuller, asked the senior manager of Kruger Veterinary Wildlife Services, Dr Peter Buss, if I could help out with any other projects during my stay in Kruger. Luckily, there was an elephant bull that had to be routine-sampled the next day. So we went into the bush with a 4×4 vehicle and a helicopter to look for the bull.



The helicopter manoeuvres into position to dart the elephant bull. Photo by Malek Murad


I was very close when the one ton elephant bull was darted from the helicopter. It was incredible to see how accurate the helicopter pilot controlled his machine. He was able to position the helicopter perfectly for the veterinarian to dart the bull from up there. Shot – Strike! You could easily see that the dart had hit its mark by the pink feather on the end of the dart. We then had to follow the elephant, who was running away from us into the bush. The effect of the anaesthetic is not immediate; it usually takes a few minutes before the animal goes down. We drove through the bush for 1,5 kilometres until we found him. As soon as we were there, we started routine sampling, measurements and a general health check-up on the elephant.



Elephant bull undergoing routine sampling and health check. Photo by Malek Murad


My first trip to one of the South African National Parks (SANParks) was fantastic. Not only could I enjoy the wonderful scenery, but I was able to observe, from up close, the SANParks Veterinarians doing their job with their impressively elaborate and professional routine. It is the dream of every veterinary student to be a part of that.


“I think you get born with the spirit of a vet. I don’t know anybody who decided to become a vet at the age of 18. I mean there are many other possibilities to earn more money without getting that dirty.” – Lou (24), qualified in veterinary medicine this June.

At the end of our last day in Kruger we watched the sunset at Lake Panic. We watched the hippos playing in the water and just enjoyed ourselves and Kruger.


Sunset over Lake Panic. Photo by Arista Botha


I am so glad that I had made the decision to come over to Africa. I was very lucky – I met the right people who gave me the help and support I needed. People who gave me the opportunity to develop and to use the skills I have. Not only here in Africa, but also at home in Germany. They taught me to be confident. I especially have to thank my parents who always support me and back me in everything I do. I can always rely on them. There were many hurdles to overcome before I could get here. My wish for everybody who has a dream in life, is that he will take his chance and that he will find people who will back him when he needs them.