Each year millions of Muslims make their way to Mecca, the birthplace of Islam’s prophet Muhammad and site of its holiest city, about 50 miles from the Red Sea on the western border of Saudi Arabia. This Hajj, the ritual pilgrimage to Mecca, is a conditional obligation to be performed at least once in the lifetime of every follower of Islam.¹ Early in its history, pilgrims arrived solely by sea or via caravan along numerous distinct overland routes from ‘distant’ lands like Syria, Iraq, and Egypt. In modern times, the sojourner is more apt to arrive by airplane from any number of places around the world.

Participants in the holy pilgrimage have at times been exposed to more than just prayer and reflection; infectious diseases have been constant companions of the worshippers throughout history. Epidemic diseases tend to thrive under environmental conditions that promote their spread from person to person, such as those engendered by large crowds that place people in close proximity to each other. Although this dynamic is amplified by indoor crowding—an explanation for the rapid spread of respiratory infections in schools, military barracks, and college dormitories—the overarching principle has to do with the density of people and the relative distances from one person’s nose to that of another. The way most respiratory pathogens are spread from person to person is by tiny liquid droplets that get expelled from infected people through coughing, sneezing, or even breathing and then get inhaled by others in close—usually less than six feet—proximity.

Situations that bring together crowds of people with varying levels of health, especially those people who might harbor infectious agents or who might be vulnerable to them because of other medical conditions, have the potential to promote the spread of epidemic disease. Because the Hajj amasses immense groups of people from varying backgrounds together in close quarters and at least in earlier times under suboptimal sanitary conditions, it is not entirely surprising that serious health issues have accompanied this event.

In the nineteenth century, during the height of epidemic cholera throughout the world, it was this disease that was imported into Mecca, killing tens of thousands of pilgrims in its episodic occurrence between 1865 and 1912.¹ Cholera at the Hajj was eventually brought under control through the appropriate use of quarantine—the temporary isolation of non-ill individuals to ensure that they were not harboring a communicable disease—and the natural waxing and waning cycles of the infection worldwide. Seventy-five years later another epidemic disease—meningococcal meningitis—would become a major health threat to the masses on their spiritual journey, causing travel restrictions, policy changes, and sparking new outbreaks as pilgrims returned to their home soil carrying their infectious guest in their nasal passages.²

Most infections are initially recognized as distinct entities by the circumstances surrounding individual—“sporadic”—and epidemic cases and the clinical manifestations of their disease. The distribution, patterns, and determinants of infections are known as the epidemiology of disease; clinical manifestations refer to the symptoms—what the patient complains of—and signs—what the health care provider finds on examination—that the disease provokes.

Some illnesses, like the common cold, are recognized as syndromes. Colds can be caused by a variety of different respiratory viruses that share certain epidemiologic features and clinical manifestations. Epidemiologically, colds tend to occur in cooler months, affect younger individuals more frequently than older ones, and usually cause relatively mild illness. Clinically, colds are widely recognized by their symptoms: runny and/or stuffy nose, general malaise or feeling rundown, sore throat, cough, and in some cases fever. Most cases improve and resolve over a few days. It is difficult, based upon epidemiologic and clinical features alone to discern one cause of a cold from another. However, other infectious diseases, such as measles, influenza, or malaria, can be defined as specific entities by their distinctive clinical appearance in the context of certain epidemiologic patterns. Cerebrospinal meningitis falls into this category.

Sporadic—episodic—cases of bacterial meningitis can be caused by a variety of microorganisms, but more than nighty percent of cases in children and adults are caused by one of three bacteria: Streptococcus pneumoniae, the “pneumococcus”; Neisseria meningitidis, the “meningococcus”; and Hemophilus influenzae, H. flu.³ Of these, the pneumococcus, so named because of its historical primacy in causing bacterial pneumonia—an acute infection of the lungs—accounts for the vast majority of adult cases of meningitis and more than a third of childhood cases. Hemophilus influenzae, originally but erroneously thought to be the cause of influenza at the turn of the twentieth century (an illness subsequently found to be caused by a virus in the 1930s), had played a dominant role in childhood bacterial meningitis until the introduction of effective vaccines three decades ago. It now accounts for only a small fraction of cases in developed countries.

Meningococcal meningitis accounts for approximately fifteen to forty percent of bacterial meningitis cases among children and young adults in the United States and is associated with a very high mortality rate—ten percent. Although the incidence of disease appears to have decreased somewhat in the United States over the past decade, for unclear reasons but perhaps in part related to vaccination,3 meningococcal meningitis remains a significant cause of lethal, sporadic disease among children and young adults and occasional outbreaks in the same age groups. When epidemics do occur, they are usually confined to semi-enclosed, densely populated environments, such as college dormitories, prisons, military barracks, and child-care centers.

In the developing world, the dynamics of invasive, meningococcal disease are markedly different. There, meningococcal meningitis remains a global health problem of immense proportions. Outbreaks have occurred worldwide, from Brazil to China to New Zealand to Africa to the Hajj pilgrimage in Saudi Arabia. Children, adolescents, and young adults are primarily affected and are the unfortunate recipients of the death and nervous system destruction left in the wake of meningococcal epidemics.

The northern portion of sub-Saharan Africa is a region of tropical savannah that is characterized by two main seasons: a rainy season from June to September, and the dry season, which lasts from December to June and is punctuated by the “harmattan,” a hot, dry wind that blows south from the Sahara desert, carrying sand and other particulate matter with it. Nearly 50 years ago, Leon Lapeyssonnie, a renowned French epidemiologist with substantial field experience in Africa, produced the definitive epidemiologic descriptions of the epicenter of worldwide epidemic meningitis.⁴

Lapeyssonnie’s first assignment to Francophone Africa in 1942 involved a military investigation into the incidence and prevalence of trypanosomiasis—sleeping sickness, a disease causing widespread illness and death in French West African colonies in Bobo-Dioulasso, Upper Volta—now Burkina Faso. While there, he and his colleagues also witnessed firsthand the human toll of epidemic meningitis, which by that time was already a well-known cause of recurrent, explosive outbreaks in Africa.

Two decades later, after serving in a variety of leadership positions and achieving senior academic rank within the French public health system, Lapeyssonnie returned to Africa as a World Health Organization consultant to countries experiencing meningitis epidemics. Because of his stature in the field, he had access to the many official and unofficial reports that had been published over the preceding 30 years; he used these and his own astute observations to accurately define the epidemiology of meningitis in Africa. He comprehensively described this in the 1963 classic monograph that for the first time, referred to the affected area as the “African meningitis belt”.⁴

Lapeyssonnie described the wave-like dynamics of epidemic meningitis in Upper Volta, Niger, Chad, Nigeria, and Sudan and underscored some of the characteristics that have continued to make the disease such a formidable public health problem, such as the impossibility of accurately predicting where or when epidemics will strike. He provided detailed descriptions of the focality, seasonality, and the kinetics of epidemics there. Additionally, he delineated the basic epidemiology and bacteriology of meningococcal epidemics in Africa: the overwhelming predominance of one type of germ—group A Neisseria meningitidis as the causative agent; the distribution of epidemics over two to three consecutive years; the age distribution of cases with a predominance in young children and teenagers; and the human costs engendered by the long-term, neurologic sequelae in those ‘lucky’ enough to survive an episode of meningitis—deafness, mental retardation, seizures, and amputation, due to compromise of the blood supply to limbs.⁴