Since mid-1991 New Zealand has been in the grip of a significant epidemic of meningococcal meningitis.
Though not dramatic enough to make the headlines every day, the epidemic has warranted steady media coverage. In early September, for instance, Middlemore Hospital in Auckland claimed that it was admitting a case each day, and in the previous month two fatalities had resulted.
Usually, New Zealand has an annual meningococcal disease incidence of 1-1.5 cases per 100,000—perhaps 50 cases a year. Now it is more than 11 per 100,000—up to 80 cases in some months.
According to Michael Baker of the Communicable Disease Centre of the Institute of Environmental Science and Research in Wellington, meningococcal disease has become the most closely scrutinised infectious disease in the country.
“About one person in 20 who contracts the disease locally dies from it, which makes it a pretty lethal disease for us,” he says. “Worldwide, perhaps 10-15 per cent die, so we are doing better than many, but it’s still a major concern.”
The main manifestation of meningococcal disease is meningitis, but the relationship between the two is not completely straightforward.
Meningitis gets its name from the meninges, membranes that surround the brain and spinal cord. In meningitis, the meningeal lining becomes inflamed. Any one of more than half a dozen bacterial species can cause this inflammation, but there are three main culprits. In children under five—the main group afflicted by meningitis—Hemophihis influenzae has been behind most illnesses, but the introduction of a successful vaccine in 1994 has reduced the incidence of cases attributable to this organism by 80 per cent, and Streptococcus pneumoniae is now the main cause. In teenagers, among whom a smaller peak of infections occur, and the rest of us (who have a generally low incidence) Neisseria meningitidis is the chief cause. When the disease is caused by this bacterium, it is termed meningococcal meningitis.
The bacteria don’t actually have to get into the brain to cause problems. Even in the blood they can prove lethal. Meningococci (dead or alive) stimulate the host to produce defence proteins which often precipitate a fatal drop in blood pressure by increasing the permeability of blood vessel walls, especially in the extremities. The term “meningococcal disease” covers both meningococcal meningitis and blood-based septicemia.
The bacterial culprits which cause meningitis are not exotic rarities, descending on our humble bodies like aliens from other planets. Far from it: they are everyday inhabitants of our throats—part of our domestic microbiological gardens, where they for the most part reside without causing problems.
At any given time,between two and ten per cent of healthy people carry meningococci (the least common of the three bacteria), and probably all of us have been carriers at some time. The epithelium that lines the throat normally keeps the bacteria out of our bodies proper, but occasionally, for unknown reasons, they manage to breach it and invade the blood. From there, a few may succeed in crossing the tightly interlinked cells in the brain’s blood vessels that constitute the blood-brain barrier. Once over that hurdle, the bugs are able to multiply rapidly in the cerebrospinal fluid, and inflame the meninges, causing meningitis.
The presence of 100,000 bacteria per ml in cerebrospinal fluid triggers the release of host defence chemicals, which themselves disrupt the blood-brain barrier, allowing immune system cells to enter and fight the bacteria, but exacerbating inflammation as well. It is the rapid rise in fluid pressure exerted on the brain which proves fatal.
Typical symptoms of meningitis include fever, irritability and drowsiness—all pretty similar to a bout of viral influenza—but these can be accompanied by seizures, headache, dislike of bright lights, neck stiffness, vomiting and coma (all signs that the bacteria have invaded the meningeal membranes), and often death. A rash which resembles tiny red-purple spots or bruises caused by bleeding under the skin is a distinctive and ominous feature.
Treatment usually takes the form of large doses of injected penicillin, only a small amount of which will leak across the blood-brain barrier. Anti-inflammatory agents are often given along with the antibiotic to curtail the host’s release of defence system proteins that, in the case of meningitis, seems only to make matters worse.
Speed of treatment is the difference between life and death. Unfortunately, the unspecific nature of many of the symptoms helps not at all. Without treatment the disease is usually fatal, often within not much more than 24 hours from the onset of symptoms.
“About 75 per cent of the cases of meningococcal disease occur in spring and winter, not just here but in many countries,” says Michael Baker. “Whether this is due to everyone huddling together indoors, and therefore sharing infectious microbes, or whether some other seasonal throat infection is enabling the meningococcus to get into the blood stream, we just don’t know.”
There are also a few other quirks to meningococcal disease. Pacific Islanders and Maori are more susceptible than pakeha, and people in Southland and Taranaki have a particularly high incidence. “Measles and influenza epidemics tend to sweep the whole country, and a high percentage of the population becomes infected quickly. This disease isn’t like that. Only one person in 10,000 comes down. It’s not invasive, and there is no great clustering of cases,” Baker says.
There are several varieties of N. meningitides, termed A, B, and C. Diana Martin, also of the Communicable
Disease Centre, says that the majority of cases in New Zealand (as in most developed countries) are group B, against which there is no vaccine, but about 25 per cent are group C, for which a vaccine has recently become available. Plans are afoot to vaccinate in Taranaki, where C is common.
Says Martin: “Group A causes massive outbreaks of meningitis in sub-Saharan Africa and elsewhere in the developing world, in which thousands of cases can occur in a few weeks. There was actually a modest epidemic of group A in Auckland during the 1980s, which was controlled by vaccination. Most unusual for a developed country.”
With meningococcal disease the unusual seems disconcertingly possible.