Australia's century of meningococcal disease: development and the changing ecology of an accidental pathogen

Abstract

Trends in meningococcal disease (MD) over the 20th century in Australia, as in other industrialised countries, have been characterised by epidemics during the two World Wars, a transient rise in incidence in the 1950s followed by endemic disease, and in the 1980s the emergence of a sustained hypersporadic phase. Epidemics occur at times of social upheaval and among marginalised populations, and resolve when living conditions improve. Periodic serogroup A epidemics have been replaced since the 1950s by endemic disease caused mainly by serogroups B and C meningococci. The current hypersporadic plateau in Australia, as in other industrialised countries, is associated with the intercontinental spread of hypervirulent clones of meningococci. The conjugate serogroup C vaccine has reduced the incidence of MD and carriage rates of serogroup C meningococci. However, the vaccine is expensive and its long‐term impact on the emergence of non‐vaccine strains and on nasopharyngeal microecology is unknown. A rising incidence of MD should not be viewed as the action of a virulent microbe exploiting a vulnerable population, but as the emergence of an “accidental pathogen” from an evolving host–microbial ecology. While it is essential to monitor the impact of vaccines on this ecology, we must find ways that can optimise our coexistence with microbes.

Impact of meningococcal C conjugate vaccine use in Australia

“…In the past 100 years there have many dramatic fluctuations in the incidence of meningococcal disease in Australia, as https://doi.org/10.5694/j.1326-5377.2007.tb00837.x describes in this issue of the Journal 1 . Rising socioeconomic status with reduced household crowding has probably been the major factor in curbing the overall incidence of the disease in recent decades, 1 but the introduction in early 2003 of a routine vaccination against serogroup C for all infants (and a catch‐up campaign for those aged under 20 years) has also had an undeniably impressive impact.…”

“…Without a vaccine, it is questionable whether behaviour modification would mitigate risk. Patel claims that “the societal determinants of the current hypersporadic disease pattern are unknown” 1 . This is at odds with Australian and overseas data clearly showing that crowded environments, including university colleges and nightclubs, and risk‐taking behaviour (eg, smoking and multiple deep‐kissing contacts) are important risk factors 12 and may be modifiable.…”

“…This is at odds with Australian and overseas data clearly showing that crowded environments, including university colleges and nightclubs, and risk‐taking behaviour (eg, smoking and multiple deep‐kissing contacts) are important risk factors 12 and may be modifiable. Despite the recent unravelling of sequence data for the entire genomes of representative strains of meningococcal serogroups A, B and C, the hypermutable meningococcus will likely continue as an “accidental tourist” causing havoc in a small proportion of vulnerable hosts 1 and go on challenging public health control measures throughout the 21st century.…”

Trends in meningococcal disease: challenges for vaccine control when disease is rare

“…However, they are not the only drivers of change. Data from long established surveillance systems show patterns of peaks and troughs in the rates of disease over periods of decades 7 . This variation probably reflects interactions between the (disease‐associated) fitness of the prevalent clones and population immunity, which is acquired via nasopharyngeal colonisation and reduces the circulation of bacterial clones over time 8 .…”

“…Data from long established surveillance systems show patterns of peaks and troughs in the rates of disease over periods of decades. 7 This variation probably reflects interactions between the (disease-associated) fitness of the prevalent clones and population immunity, which is acquired via nasopharyngeal colonisation and reduces the circulation of bacterial clones over time. 8 Without vaccination or reductions in risk factors for transmission and disease, the arrival of a new strain, for which population immunity is limited, is likely to lead to increased disease; a recent rise in disease in the United Kingdom caused by a highly invasive capsular group W clone of N. meningitidis illustrates this point.…”