jueves, 11 de marzo de 2010

Meningococcal Outbreak, Greater Aachen Region, Germany | CDC EID



EID Journal Home > Volume 16, Number 3–March 2010

Volume 16, Number 3–March 2010
Research
Vaccine Preventability of Meningococcal Clone, Greater Aachen Region, Germany
Johannes Elias, Leo M. Schouls, Ingrid van de Pol, Wendy C. Keijzers, Diana R. Martin, Anne Glennie, Philipp Oster, Matthias Frosch, Ulrich Vogel,1 and Arie van der Ende1
Author affiliations: University of Wuerzburg, Wuerzburg, Germany (J. Elias, M. Frosch, U. Vogel); National Institute for Public Health and Environment (RIVN), Bilthoven, the Netherlands (L.M. Schouls, I. van de Pol); Academic Medical Center, Amsterdam, the Netherlands (W.C. Keijzers, A. van der Ende); Institute of Environmental Science and Research, Porirua, New Zealand (D.R. Martin, A. Glennie); and Novartis Vaccines, Siena, Italy (P. Oster)


Suggested citation for this article

Abstract
Emergence of serogroup B meningococci of clonal complex sequence type (ST) 41/44 can cause high levels of disease, as exemplified by a recent epidemic in New Zealand. Multiplication of annual incidence rates (3.1 cases/100,000 population) of meningococcal disease in a defined German region, the city of Aachen and 3 neighboring countries (Greater Aachen) prompted us to investigate and determine the source and nature of this outbreak. Using molecular typing and geographic mapping, we analyzed 1,143 strains belonging to ST41/44 complex, isolated from persons with invasive meningococcal disease over 6 years (2001–2006) from 2 German federal states (total population 26 million) and the Netherlands. A spatially slowly moving clone with multiple-locus variable-number tandem repeat analysis type 19, ST42, and antigenic profile B:P1.7–2,4:F1–5 was responsible for the outbreak. Bactericidal activity in serum samples from the New Zealand MeNZB vaccination campaign confirmed vaccine preventability. Because this globally distributed epidemic strain spreads slowly, vaccination efforts could possibly eliminate meningococcal disease in this area.
Our work describes the epidemiology of invasive meningococcal disease (IMD) caused by meningococci of clonal complex (cc) 41/44 in the Netherlands and the 2 bordering German states Lower Saxony and North-Rhine-Westphalia during 2001–2006. Neisseria meningitis is a gram-negative bacterium that occasionally causes invasive disease in humans, primarily meningitis or sepsis (1). Notwithstanding low incidence rates in most industrialized countries, IMD remains a serious public health problem because of its predilection for affecting young persons and its ≈10% death rate despite antimicrobial drug treatment. In contrast to the meningitis belt in Africa, where epidemic waves cause incidence rates up to 300 cases/100,000 population (2), epidemics or case clusters are rare in industrialized countries (3). Meningococci are antigenically diverse bacteria that can be divided into 12 serogroups by variation of their polysaccharide capsules. Despite increased findings of serogroup C meningococci in several countries, serogroup B has clearly controlled the epidemiology of IMD in western Europe for the past 20 years. Dominance of serogroup B has further been compounded by numerous vaccination campaigns with polysaccharide C conjugate vaccine leading to a decline in serogroup C disease (4). Unfortunately, the serogroup B polysaccharide is an unsuitable vaccine antigen because of poor immunogenicity. Despite substantial progress in the development of vaccines based on membrane-associated antigens (5,6), a universal vaccine against meningococci has yet to be licensed.

Typing of N. meningitidis is critical for tracking transmissions and recognition of disease clusters. In recent years, focus has shifted to portable molecular typing methods with high discriminatory power. The preferred method for sequence-based typing of meningococci is multilocus sequence typing (MLST) (7), which enables identification of strains belonging to hypervirulent clonal complexes responsible for most cases of the invasive disease (8). MLST is complemented by antigen sequence typing of the variable regions of the outer membrane proteins PorA and FetA (9). Moreover, multiple-locus variable-number tandem repeat analysis (MLVA), which shows slightly higher discriminatory ability than MLST (10), represents a recent addition to the arsenal of portable typing methods for N. meningitidis.

Differences in the antigenic makeup of meningococcal clonal complexes (cc) (11) likely influence reported disparities in spatiotemporal spread. Whereas strains belonging to the multilocus sequence type (ST) 5 complex (cc5/subgroup III) (12) and ST-11 complex (cc11/ET-37 complex) (13) depend on migration to survive, strains of the ST41/44 complex (cc41/44/lineage 3) have been described as causing stationary and persistent hyperendemic disease, as exemplified by the New Zealand serogroup B epidemic, which lasted more than a decade (14).

cc41/44 is a large hypervirulent complex that revolves around 2 STs instead of 1 central ST, namely ST41 and ST-44 (15). It was first described in the Netherlands in the 1980s (16), where it caused a substantial increase in disease incidence (17,18). Subsequently, this lineage was reported in Belgium in the early 1990s (19), then New Zealand since 1991 (14). In New Zealand an epidemic with incidences up to 17.4 cases/100,000 population in 2001 prompted an immunization campaign with custom made outer-membrane-vesicle vaccine MeNZB (Novartis Vaccines and Diagnostics, Siena, Italy) (20).

abrir aquí para acceder al documento CDC EID completo (muy extenso):
Meningococcal Outbreak, Greater Aachen Region, Germany | CDC EID

Suggested Citation for this Article
Elias J, Schouls LM, van de Pol I, Keijzers WC, Martin DR, Glennie A, et al. Vaccine preventability of meningococcal clone, Greater Aachen Region, Germany. Emerg Infect Dis [serial on the Internet]. 2010 Mar [date cited].

http://www.cdc.gov/EID/content/16/3/464.htm

DOI: 10.3201/eid1603.091102

No hay comentarios:

Publicar un comentario