Preliminary Programme

This paper analyses the epidemiologic factors involved in contemporary endemic trachoma in Spain, which affected various regions in the country up until the 1960s, paying particular attention to the factors related to the prevalence of childhood trachoma. As trachoma is regarded as a consequence of hardship and poverty, a study of this illness may help to explain the multi-causal model used to account for the incidence of infectious diseases, such as measles, which are considered childhood diseases and share the common characteristic of being preventable. In order to carry out the research, primary sources such as reports and publications produced in the context of health campaigns against trachoma will be used, in addition to information regarding the initiatives implemented by school health inspection services in the mid 20th century. (Show less)

One of the most contagious of all human viruses, the measles virus is estimated to have killed more than 200 million persons in the last 150 years. Although virtually eradicated in the developed world by the introduction of a vaccine fifty years ago, worldwide there are still 40 million cases and over half a million deaths per year from measles. Many that survive are left with life-long disabilities: blindness, deafness or brain damage. This explains the persisting interest about the dynamics of measles epidemics and the risk factors involved in measles mortality. These include gender, frailty, malnutrition, overcrowding, hygiene, climatic conditions.
With some adaptations, the analytical framework used for less developed countries can be adopted in historical studies of measles epidemics. This paper follows such an approach, focusing on two measles outbreaks which hit Venice in 1854 and 1861, causing over 600 deaths. The study uses a large mid-nineteenth century longitudinal sample of the Venetian population drawn from the local population register. The life histories of the population under study are reconstructed and framed in the changing context of their families, households, and neighborhood. Other source materials provide further pieces of information concerning the causes of death, daily outdoor temperatures, staple food prices, housing conditions. The unique richness and quality of such a data set will make possible to test some of the major hypotheses concerning measles mortality in a historical setting. (Show less)

The Reproductive Number of an epidemic is the number of secondary cases produced by each primary case in a totally susceptible population. Its magnitude, together with the Serial Interval between primary and secondary cases, is an important factor in the transmissibility of the disease and the possibility for intervention. For the epidemic to die out, the Reproductive Number must fall to less than unity. Large values indicate epidemics that may not be susceptible to interventions designed to reduce transmissibility below the critical threshold. Demographers are already familiar with these concepts from population dynamics as the Reproductive Number is equivalent to the Net Reproduction Rate and the Serial Interval is equivalent to generation length.

It is surprising, given its importance for epidemic preparedness, that there are relatively few estimates of the Reproductive Number for 1918. Analyses of this pandemic in the United States and North-West Europe produce estimates of around 1.2 to 3.75. These values are surprisingly low when compared with estimates as high as 20 for other influenza epidemics, and when compared with other infectious diseases. It suggests that the 1918 disaster was caused by very high case fatality rates, rather than by extreme transmissibility, and that control might have been feasible with aggressive intervention.

The Madrid data comprise individual death records which allow us to contrast different methodologies for estimating Reproductive Numbers and to examine a number of hypotheses with regard to covariates such as age, sex, marital status and geographical propinquity. Aggregate studies show that the Relative Mortality Risk for infants was close to unity in 1918, but rose sharply with age so that children over 4 were at high risk. We will also contrast the 1889-90 pandemic with the successive waves of 1918-20. It is known that the age-specific response in these two pandemics was different and that the former occurred in an era when influenza had almost disappeared as a cause of morbidity and mortality, so that the proportion of the population with a naïve immune response to influenza was probably much higher than in 1918.

The city of Madrid represents an important example as there is evidence that the rise in relative mortality during 1918 was greater in Spain and Italy than in North-West Europe, North America and Australasia. So far, the explanations have been speculative rather than quantitative. This paper offers a clear example of the way in which historic data can contribute to the understanding of contemporary problems. (Show less)