Epidemics

EPIDEMICS

The characterization of epidemics and their recognition in a community involve several quantitative measures and some specific epidemiologic definitions. Infectivity, in epi-demiologic terms, equates to attack rate and is measured as the frequency with which an infection is transmitted when there is contact between the agent and a susceptible individ-ual. The disease index of an infection can be expressed as the number of persons who de-velop the disease divided by the total number infected. The virulence of an agent can be estimated as the number of fatal or severe cases per the total number of cases. Incidence, the number of new cases of a disease within a specified period, is described as a rate in which the number of cases is the numerator and the number of people in the population under surveillance is the denominator. This is usually normalized to reflect a percentage of the population that is affected. Prevalence, which can also be described as a rate, is primarily used to indicate the total number of cases existing in a population at risk at a point in time.

The prerequisites for propagation of an epidemic from person to person are a suffi-cient degree of infectivity to allow the organism to spread, sufficient virulence for an in-creased incidence of disease to become apparent, and sufficient level of susceptibility in the host population to permit transmission and amplification of the infecting organism. Thus, the extent of an epidemic and its degree of severity are determined by complex in-teractions between parasite and host. Host factors such as age, genetic predisposition, and immune status can dramatically influence the manifestations of an infectious disease. To-gether with differences in infecting dose, these factors are largely responsible for the wide spectrum of disease manifestations that may be seen during an epidemic.

The effect of age can be quite dramatic. For example, in an epidemic of measles in an isolated population in 1846, the attack rate for all ages averaged 75%; however, mortality was 90 times higher in children less than 1 year of age (28%) than in those 1 to 40 years of age (0.3%). Conversely, in one outbreak of poliomyelitis, the attack rate of paralytic polio was 4% in children 0 to 4 years of age and 20 to 40% in those 5 to 50 years of age. Sex may be a factor in disease manifestations; for example, the likelihood of becoming a chronic carrier of hepatitis B is twice as high for males as for females.

Prior exposure of a population to an organism may alter immune status and the fre-quency of acquisition, severity of clinical disease, and duration of an epidemic. For exam-ple, measles is highly infectious and attacks most susceptible members of an exposed population. However, infection gives solid lifelong immunity. Thus, in unimmunized pop-ulations in which the disease is maintained in endemic form, epidemics occur at about 3-year intervals when a sufficient number of nonimmune hosts has been born to permit rapid transmission between them. When a sufficient immune population is reestablished, epidemic spread is blocked and the disease again becomes endemic. When immunity is short-lived or incomplete, epidemics can continue for decades if the mode of transmission is unchecked, which accounts for the present epidemic of gonorrhea.

Prolonged and extensive exposure to a pathogen during previous generations selects for a higher degree of innate genetic immunity in a population. For example, extensive exposure of Western urbanized populations to tuberculosis during the 18th and 19th cen-turies conferred a degree of resistance greater than that among the progeny of rural or geographically isolated populations. The disease spread rapidly and in severe form, for example, when it was first encountered by Native Americans. An even more dramatic ex-ample concerns the resistance to the most serious form of malaria that is conferred on peoples of West African descent by the sickle-celled trait . These in-stances are clear cases of natural selection, a process that accounts for many differences in racial immunity.

Occasionally, an epidemic arises from an organism against which immunity is essen-tially absent in a population and that is either of enhanced virulence or appears to be of enhanced virulence because of the lack of immunity. When such an organism is highly in-fectious, the disease it causes may become pandemic and worldwide. A prime example of this situation is the appearance of a new major antigenic variant of influenza A virus against which there is little if any cross-immunity from recent epidemics with other strains. The 1918 – 1919 pandemic of influenza was responsible for more deaths than World War I (about 20 million). Subsequent but less serious pandemics have occurred at intervals because of the development of strains of influenza virus with major antigenic shifts . Another example, acquired immunodeficiency syndrome (AIDS), illustrates the same principles but also reflects changes in human ecologic and social be-havior.

A major feature of serious epidemic diseases is their frequent association with poverty, malnutrition, disaster, and war. The association is multifactorial and includes overcrowding, contaminated food and water, an increase in arthropods that parasitize hu-mans, and the reduced immunity that can accompany severe malnutrition or certain types of chronic stress. Overcrowding and understaffing in day-care centers or institutes for the mentally impaired can similarly be associated with epidemics of infections.

In recent years, increasing attention has been given to hospital (nosocomial) epi-demics of infection. Hospitals are not immune to the epidemic diseases that occur in the community; and outbreaks result from the association of infected patients or persons with those who are unusually susceptible because of chronic disease, immunosuppressive ther-apy, or the use of bladder, intratracheal, or intravascular catheters and tubes. Control depends on the techniques of medical personnel, hospital hygiene, and effective surveil-lance.