M.V. Martínez de Aragón

Increase of pertussis incidence in 2010 to 2012 after 12 years of low circulation in Spain.

In Spain, whole cell pertussis vaccination started in 1975, with three doses before the age of 6-7 months. Doses at 15-18 months and 4-6 years were introduced in 1996 and 2001, respectively. Spain switched to an acellular vaccine in 2005. From 1998 to 2009, pertussis incidence rates remained ≤1.5 cases/100,000 inhabitants but increased from 2010 to 7.5 cases/100,000 in 2012. Data from 1998 to 2012 were analysed to assess disease trends and susceptible populations. We defined four epidemic periods: 1998-2001 (reference), 2002-05, 2006-09 and 2010-12. In 2002-05, the incidence rate increased in individuals aged 15-49 years (IRR: 1.41 (95% CI: 1.11-1.78)) and ≥50 years (IRR: 2.78 (95% CI: 1.78-4.33)) and in 2006-09 increased also in infants aged <3 months (IRR: 1.83 (95% CI: 1.60-2.09)). In 2010-12, the incidence rate increased notably in all age groups, with IRRs ranging between 2.5 (95% CI: 2.3-2.8) in 5-9 year-olds and 36.0 (95% CI: 19.4-66.8) in 20-29 year-olds. These results, consistent with the countrys vaccination history, suggest a progressive accumulation of susceptible individuals due to waning immunity after years of low incidence. Further vaccination strategies should be assessed and implemented to prevent pertussis in pre-vaccinated infants, in whom the disease is more severe.

CIRCULATION OF MUMPS VIRUS GENOTYPES IN SPAIN FROM 1996 TO 2007.

ABSTRACT Although the WHO recommends the use of genotyping as a tool for epidemiological surveillance for mumps, limited data on mumps virus (MV) genotype circulation that may be used to trace the patterns of virus spread are available. We describe the first complete series of data from Spain. The small hydrophobic region was sequenced from 237 MV-positive samples from several regions of Spain collected between 1996 and 2007. Six different genotypes were identified: A, C, D (D1), G (G1, G2), H (H1, H2), and J. Genotype H1 was predominant during the epidemic that occurred from 1999 to 2003 but was replaced by genotype G1 as the dominant genotype in the epidemic that occurred from 2005 to 2007. The same genotype G1 strain caused concomitant outbreaks in different parts of the world (the United States, Canada, and the United Kingdom). The remaining genotypes (genotypes A, C, D, and J) appeared in sporadic cases or small limited outbreaks. This pattern of circulation seems to reflect continuous viral circulation at the national level, despite the high rates of vaccine coverage.

Childhood and adolescent cancer in Spain: Mortality time trends 1956–1990

Using log-linear Poisson modelling, trends in childhood cancer mortality among the population under 20 years of age in Spain are described over the 35-year period from 1956 to 1990. Overall cancer mortality and seven specific sites were considered: all leukaemias, Hodgkins disease, non-Hodgkins lymphomas, malignant brain tumours, kidney cancer, malignant bone neoplasms, and a broad category of ill-defined tumours. An age-period-cohort model was used to analyse the influence of age, period of death and birth cohort. Recent trends were estimated by restricting analysis to the last three 5-year periods. In general, mortality began to decline at the beginning of the 1970s, with reductions of 36% in males and 45% in females being registered between 1966-1970 and 1986-1990. The use of age-period-cohort models revealed an initially rising period effect attributable to diagnostic advances. The decline in mortality in post-1965 generations and the final downturn in the period effect are both most certainly a consequence of the remarkable progress achieved in the treatment of such tumours. During the final 15 years, there was a relative decline in mortality of approximately 20% every 5 years. However, in the case of malignant renal tumours in males and malignant bone tumours and non-Hodgkins lymphomas in both sexes the situation remained stable.

Mumps Virus Genotyping: Basis and Known Circulating Genotypes~!2009-11-20~!2009-11-26~!2010-02-16~!

Although mumps virus (MV) is considered antigenically monotypic, twelve different genotypes of MV based on genetic variation in the SH gene (A to L) are currently recognised by the WHO. Both dominance of a single genotype and co-circulation of different genotypes in the same geographical area, as well as temporal replacement of genotypes have been described in different countries. The different histories of genotype importation, variations in vaccine coverage and the use of different vaccine strains in each country results in a complex picture that could be the cause of the different geographical patterns of mumps virus genotype circulation observed in different countries. Lack of full cross-protection between different genotypes has been reported and has been suggested as a cause of vaccine failure, especially for vaccine strains belonging to genotype A, which is genetically distant to the remaining genotypes that include most of the currently circulating wild strains. Finally, a differential ability to invade the neural system has been suggested for some particular strains belonging to genotype D.

Actualización en varicela

Primary infection by varicella-zoster virus causes chickenpox and herpes zoster. At 14 years of age, 91% of the population have already suffered the illness and after 30 years, more than 95% have done so. In 1999, the hospitalization rate was 2.4 per 1,000 chickenpox cases in those under 14 and 15.5 per 1,000 cases in those over 14. A total of 73% of deaths recorded during the period 1991-2000 were in the older than 14 year old group. Efficacy of varicella vaccine after a 7-8 years period is 87%; a milder case of chickenpox (breakthrough) can appear in vaccinated people 42 days after vaccination. The introduction of the vaccine may be proposed to stop or decrease virus circulation among the population or to decrease complications and mortality from chickenpox. According to the objective proposed, different strategies that imply risks and benefits should be conducted.

Mortalidad en España en 1998. Evolución en la década 1989-1998. II. Mortalidad general, principales causas de muerte por sexo y edad

Ambos sexos —En los niños hasta los 5 años tienen peso sobre todo las causas de mortalidad infantil, especialmente las originadas en el período perinatal. En la última década la Mortalidad por anomalías congénitas cardiovasculares, por hipoxia, asfixia y distrés respiratorio y por inmadurez fetal disminuyó notablemente manteniéndose relativamente estables la mortalidad por complicaciones obstétrica y por infección perinatal. La evolución de la mortalidad general por edades en la última década reflejó el impacto de la epidemia de sida en los jóvenes y el inicio de su recuperación (figs. 1 y 2). En relación con el año anterior, sólo los jóvenes de 15 a 24 años aumentaron la mortalidad entre un 5% y un 3%. Todavía en 1998 la mortalidad de los hombres de 25 a 34 años era un 14% superior a la de 1980-82. La sobremortalidad masculina descendió en los jóvenes pero aumentó en las edades medias y avanzadas, reflejando la mayor disminución de la mortalidad en los hombres jóvenes en comparación con las mujeres y un comportamiento inverso entre los mayores. La razón de masculinidad para todas las edades se mantuvo en un 1,80 (fig. 3). Las principales causas por grupo de edad y sexo se presentan en la tabla 1 y figuras 4 y 5 donde puede verse la situación en 1998, la evolución en la década y el cambio desde 1980-82. Se han considerado principales causas Mortalidad en España en 1998. Evolución en la década 1989-1998. II. Mortalidad general, principales causas de muerte por sexo y edad