THE ELITE world of taxonomic microbiologists – the people who get to decide what we call our microscopic friends – is divided into the “lumpers” and the “splitters.” The lumpers try to minimise the number of families and genuses that bacteria, viruses and other pathogens can scientifically be classified into, while the splitters rejoice in discovering subtle and minor differences between micro-organisms, and love to distinguish them as new species or occasionally to create a new genus. Even as a practising infectious diseases specialist I have trouble keeping up with the names of bugs: every month or so our laboratory sends me a report which names a pathogen that I have never heard of. At the time of writing this, the most recent was Nesterenkonia halobia. I had to ask a colleague what it was.
“Used to be a micrococcus,” she said. “At least I could spell that.”
There is a degree of hypocrisy in this complaint, for I myself belong to a research group that changed the name of a bug. In my defence, however, we showed that our germ belonged to an established genus, one whose properties – and spelling – were well known to the mainstream microbiological world. We brought our little charge in from the obscurity and loneliness of an unpronounceable genus – it was the sole species of the genus Calymmatobacter – and added it to a warm and loving family, the Klebsiellae.
But my pedantic taxonomic colleagues seem to delight in taking a relatively well-known bug and, through a process reminiscent of Winston Smith’s work in George Orwell’s novel Nineteen Eighty-Four, depriving it of identity with the stroke of a pen. A paper is published and you wake the next day to find that what you knew before you went to bed isn’t so today. Yesterday’s Branhamella is today’s Moraxella – or was it the other way round?
The taxonomy of some bugs, however, is so established that reclassifying and renaming them would be unthinkable, and perhaps the best example of this is Staphylococcus aureus. Although doctors will abbreviate the name to Staph aureus, most likely you will know it under another name – golden staph. An aureus was a Roman gold coin and staphylococcus is from the Greek “staphyle” (a bunch of grapes) and “coccus” (granule). The Greco-Roman name beautifully describes the appearance of the bacteria in the laboratory – they really do look like a bunch of grapes under the microscope, and the colonies that grow on an agar plate are yellow.
I took very little notice of Staph aureus as a student and junior doctor. It was, to my mind, a pedestrian sort of bug. There was little romance associated with it – everybody had it on their skin, up their nose or in their groin. It caused tedious things like skin infections and abscesses and it had no international allure. Its main claim to fame was that some strains had developed a special characteristic that made them stand out in a crowd – resistance. The most famous strain is known mainly by its acronym, MRSA (Methicillin-resistant Staphylococcus aureus).
Antibiotic resistance is a fashionable subject in the early twenty-first century. Some authorities believe that we may be in the last decades of the Antibiotic Age, that soon the bacteria will win and we will be back to the 1930s, before the advent of sulphur drugs and penicillin. It is hard to pick up a medical journal without reading about the appearance of a germ that has mutated so that it is resistant to most antibiotics. There is no better way to frighten patients than to inform them that they have an infection caused by a resistant organism. “Oh my god, that’s a superbug isn’t it?” they usually say, and you can see family members trying to hide the fact that they have taken a small step back from the bedside. Often the patient’s perception is that MRSA has flesh-eating capabilities and they will be banished to an isolation ward in the basement of the hospital, somewhere between the incinerator and the morgue.
In reality, MRSA is no more, and possibly less, dangerous than the common-or-garden variety Staph aureus. The so-called superbugs may be resistant to antibiotics but they are no more virulent than their antibiotic-sensitive cousins. Indeed, there is an evolutionary cost of developing resistance: the bacteria may actually become less pathogenic. The problem is that MRSA must be treated using antibiotics that are less effective than the usual choices, have serious side-effects and toxicities, or are extremely expensive. For example, the drug linezolid, which is sometimes used to treat MRSA, costs around $120 a tablet, and a patient needs two tablets a day for a minimum of a week for the simplest infection, and much longer in the case of complicated infections.
MRSA is usually transmitted from patient to patient in hospital, mainly on the hands of the doctors and nurses who care for them. In our hospital, which has quite low rates of resistant organisms, we isolate all patients who are known to have MRSA to minimise its spread. This can have a negative psychological effect on some people, as they often feel stigmatised (conversely, others enjoy the quiet and relative privacy of the single room that their “unclean” status confers). Some hospitals have so much MRSA that they are unable to offer enough single rooms, and so the patients are not segregated. Without antibiotic treatment most people with MRSA will naturally become clear of the bacteria over time, but this can take many months or even years.
While I am never happy when I learn that a patient has had MRSA isolated from some part of his or her body, I only really get worried when it has grown in a specimen that was taken from a site in the body that should be sterile – say, an artificial joint or, worse, the bloodstream. But if growing MRSA from the blood of a hospitalised patient is bad, I am even more disturbed when I learn of a patient who has not been in hospital and who has grown a Staph aureus in their blood that is sensitive to the routine antibiotics. Most doctors who are not specialists in infectious diseases don’t get too fussed about this, but it is one of the most serious diagnoses that I can make.
MEDICAL systems around the world respond to certain problems in a stereotypical way. The reason that someone with chest pain triggers an immediate response in an emergency department is that a heart attack can kill you quickly and early intervention reduces the risk of subsequent complications or death. In the 1970s if you survived a heart attack long enough to get to hospital the chance of leaving alive was about 80 per cent, and in the 1980s around 85 per cent. Today the chance of your making it home is about 93 per cent. One of the reasons for the continuing decline in the mortality rate from heart attacks among people admitted to hospital has been the rapidity of the medical response. The quality of a cardiology or emergency department can be gauged by the time it takes to get from the door of the hospital to the catheter laboratory where the patient’s blocked artery can be opened up. A hospital’s reputation can hinge on how quickly it achieves this, and it would be impossible for a doctor not to see a heart attack as an emergency requiring an immediate response.
Unfortunately, the response of most hospital systems to patients presenting with infections, even the most obvious and serious types, is much more relaxed. A patient who has grown Staph aureus in his or her blood is said to have bacteraemia or, more colloquially, blood poisoning. The bug can get into the bloodstream through small breaches in the skin caused by simple cuts and scratches, via things inserted for medical reasons – an intravenous cannula, for example – and from needles used to inject illicit drugs. A patient with Staph aureus bacteraemia initially feels unwell, may develop a headache and muscle and back pains, and experiences chills and rigours (shivering fits). If the disease progresses the infected person suffers a drop in blood pressure, becomes delirious and eventually slips into a coma.
The severity of the disease varies enormously from patient to patient, depending on age, general state of health and, it would seem, providence. Although it is no surprise that elderly patients with heart disease and diabetes will do very poorly if they get a Staph aureus infection, I have seen fit young people with the same infection become sick in the morning, be in intensive care that night and be dead by the end of the week.
It is reasonable to assume that the earlier that patients with Staph aureus in their blood receive antibiotics the better their chance of survival. At Canberra Hospital we have been collecting data on patients with infections in their blood for over ten years, and the information provides a unique insight into what happens to patients with these infections in Australia. The study has shown that patients who develop Staph aureus bacteraemia have about a 25 per cent chance of being dead within six months (the percentage is higher in many countries) regardless of how healthy or old they are when they get the infection. In other words, if you go into hospital with Staph aureus in your blood you are between three and four times more likely to be dead within the year than if you had arrived with a heart attack. This is a fact little known to doctors – or their patients – and few hospitals have the same protocols in place for the rapid identification and treatment of bloodstream infections as they do for heart attacks. Few, if any, hospitals could tell you how long it takes a patient with bacteraemia to receive antibiotics.
Recently, two of my students calculated the time it took for patients in our hospital with suspected meningitis, another condition where every second counts, to receive antibiotics. The median time of just over three hours was consistent with results from overseas hospitals, but it highlights the different approach that medical staff take when it comes to infections compared to affairs of the heart.
Why do intelligent and motivated people act so differently when the results of delay can be so devastating? Perhaps it is the immediacy of a heart attack’s consequences that prompts medical staff into action: the patient’s heart can stop without a second’s warning, the muscle of the heart can be damaged so badly that it can’t pump enough blood around the body, and the effect – a breathless, gasping patient – is right in front of the doctor’s eyes.
Every week we diagnose at least one new staph bloodstream infection in our hospital. I know that the earlier we diagnose the infection, the better the patient’s chances of a full recovery, but I also know that a proportion of patients will not receive the right antibiotic, given at the right dose, for the right duration. As a result, this invisible little bunch of grapes will have seeded itself in occult parts of the human body that it has invaded and will reappear in a few days or weeks. This time it will demand treatment by dint of its severe manifestations – a heart valve may be infected, or an abscess may have formed in the spine or a muscle or the brain. Those of us who treat these complications appreciate what the absence of an urgent initial response can lead to, but we have failed in the main to convey this sense of urgency to our colleagues who have the opportunity to initiate treatment.
Most serious bloodstream infections start in the community – well before the patient has been anywhere near a hospital – and there is not a lot that we can do to prevent them occurring in the first place. Sometimes, however, the infection is the fault of the medical system, and the consequences can be a grizzly showcase for its failings.
HE WAS admitted to the hospital after a fight outside a nightclub. He had been punched in the face by a drunk who was aiming at someone else. The blow had fractured the man’s cheekbone, and his face had been badly cut when he fell on broken glass in the gutter. After the ambulance arrived a paramedic inserted an intravenous cannula in his left arm, just at the elbow. When he got to the hospital a surgeon assessed that he needed a procedure to push his jaw back into place, but there was no theatre time available that night, or the next day, and it was forty-eight hours before he had his operation. He recovered well after the surgery but on the third day after admission he developed a high temperature. He was seen by a series of residents over three shifts. They examined his face, chest and wounds, took blood tests and requested a chest X-ray, but didn’t order any antibiotics. His temperature fluctuated, and while he felt reasonable for most of the day, when it went up he looked and felt dreadful.
On the fourth day he developed rigours and a set of blood cultures was taken. The next day, a Saturday, he was much sicker, and his girlfriend said she thought he was not making any sense. The laboratory rang the ward to say the blood cultures were positive for Staphylococcus aureus. The medical registrar was called, but it was an hour before he could see the patient. When he arrived he was appalled by what he saw: from the end of the bed it was apparent to him that the patient had developed septic shock. He made an emergency call, and soon the room was full of doctors, nurses and orderlies.
“He needs to move to the intensive care immediately,” the registrar said. Toxins from the multiplying bacteria had entered the patient’s circulation and initiated a cascade of events. His heart rate had risen but his blood pressure had fallen, so the heart was unable to pump enough blood to provide adequate oxygen to all the tissues. The body’s automatic response was to regulate the flow of blood, supplying the most important organs – the brain and heart – at the expense of the kidneys, liver and gut. Organs can only continue to function with a reduced blood flow for a short time before they start to fail – the kidneys first, then the lungs and finally the brain. The patient was confused and delirious, then his consciousness faded – a sequence of events very difficult to reverse.
On the ward he was given intravenous fluid to try to increase his blood pressure. Additional oxygen was also administered, but it was clear his blood oxygen level was still falling. A tube was inserted into his trachea, but his lungs were waterlogged and stiff from fluid that had escaped from capillaries leaking because of the bacteria in his blood. His blood pressure remained dangerously low and he needed to be transferred to the intensive care unit urgently so that he could receive the adrenaline-like drugs that could bring it up to a safer level. The bedside was cluttered with people busy with lines and tubes and monitors. His mother stood outside the room, silent, ashen, trying to hold on to her composure as she felt it running away from her. The intensive care registrar was there now. “Everyone needs to hurry up a bit and get this move under way please,” she said as she walked around the bed while the medical registrar filled her in on the details. She was listening and examining the patient at the same time. Suddenly, she interrupted her colleague in mid-sentence.
“What is this?” she asked, pointing to the intravenous cannula in the patient’s left arm, at the elbow. “How long has this been in?” She looked more closely. The cannula site was red, and as she touched the surrounding skin a drop of yellow pus welled up at the edge of the plastic tube. The medical registrar didn’t know when the cannula had been inserted: there was nothing written on the dressing around the cannula and no documentation in the medical notes. The only reference to when it was put in came from the ambulance officer’s notes from five days before.
The intensive care registrar pulled out the cannula and handed it to the nurse, telling him to send the tip of the cannula to the laboratory for culture. This was a formality: the Staph aureus almost certainly entered the man’s bloodstream soon after the assault, through the breach in the skin caused by inserting the cannula. As the days passed the number of bugs multiplied exponentially, so that by the time the intensive care registrar spotted the cannula the bacteria were well established in the man’s circulation. The patient was wheeled out of the ward, his bed now a moving intensive care unit, packed with monitors, infusion machines, oxygen bottles and suspended fluids. The medical registrar stayed in the ward. The intensive care staff were in control now.
A medical student, who had been watching the events play out from a corner of the room, asked the medical registrar how this could have happened.
“That cannula should have been removed as soon as he arrived in the emergency department and a new one put in,” the registrar said. “The new one should have come out within forty-eight hours, seventy-two hours max.”
“The hospital should have a policy about this,” said the student.
“It does – I’ve just told you the policy,” the registrar replied, shrugging his shoulders.
“But why don’t people follow the policy if there is one?” asked the student.
“You tell me,” said the registrar, walking out of the room. “Just don’t mention any of this in front of his mother, will you.”
The patient died later that night – his lungs were so damaged that it was impossible to get enough oxygen into them. His heart stopped and could not be restarted. He was twenty-four years old.
WE COULD use that tragedy to pick apart any number of systemic failings, but my main point is to illustrate the potency of a common bacterium. Resistance to antibiotics is an important subject for discussion, but it can be a little distracting. Staphylococcal infections kill hundreds of Australians each year and put thousands in hospital, yet the vast majority of the responsible strains are sensitive to cheap and safe antibiotics. There is no vaccine available for Staph aureus and there is nothing on the horizon.
The generations who grew up in the pre-antibiotic age knew very well the capacity of bland bacteria to cause terrible sickness. But today respect for the power of bacteria sometimes seems to be limited to those who see the late manifestations of infections. In hospital practice, working at the bottom of a “diagnostic sieve” that funnels the sickest our way, my fellow “infectionistas” and I have frequent opportunities to see the uncommon life-threatening consequences of bacterial invasion. Perhaps we are too nice, maybe we lack the swagger and metaphorical cojones of the cardiologists, because we are unable to get many of our colleagues to recognise that an infection in the blood is a slow-motion heart attack – less dramatic when played at normal speed, but just as deadly in fast-forward. •
This is an edited extract from Gone Viral: The Germs that Share Our Lives, by Frank Bowden, published recently by NewSouth. Some details of the case discussed have been changed by the author to protect the privacy of the people involved.