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Chairmen:
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Fernando Baquero
César Nombela |
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Place: Euroforum Infantes,
El Escorial (Madrid)
Date: November 19 & 20, 2004 |
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| Viernes
/ Friday 19th |
| 08:15 |
Recogida
de Acreditaciones / Registration |
| 08:45 |
Opening and welcome addresses:
Why this symposium. |
| 09:00 |
Keynote Address
Moderador/Chairperson: Fernando Baquero |
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Bruce R Levin
Professor of Biology
Emory University, Department of Biology. Atlanta, USA. |
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Population biology, evolution and infectious
disease: an opinionated perspective /Biología poblacional,
evolución y enfermedad infecciosa: una perspectiva obstinada.
For more than two decades, investigators trained in precious,
academic population and evolutionary biology have been studying
infectious diseases and their treatment and prevention. What
have they accomplished? In this talk I will review what I consider
to be the major achievements of this enterprise and consider
the kinds of questions and issues that I believe people in this
area should be addressing. My talk will be unabashedly opinionated
and our own work in this area will, doubtless, be over represented.
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| SESION 1
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The Interplay of Human and
Microbial Evolutionary Biology / La interacción entre
las evoluciones humana y microbiana.
Moderador / Chairperson: Antonio Rodríguez
Noriega. |
| 09:40 |
Jörg Hacker
Professor, Head of the Institute for Molecular Biology of Infectious
Diseases University of Würzburg. Germany. |
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Making friends: from pathogenicity to commensalisms
/ Haciendo amigos: de la patogenicidad al comensalismo
The genome of pathogenic as well as non-pathogenic microbes
consists of a core region and of a so-called flexible gene pool.
Genomic islands represent parts of the flexible gene pool and
they can encode “additional factors”, which may
be necessary for adaptation of non-pathogenic microbes to certain
habitats, but also for disease-related processes of pathogens.
The aim of the presentation is to describe genomic islands of
pathogenic and non-pathogenic enterobacteria and to show how
the respective gene products interact with host factors in order
to increase the fitness as well as the pathogenicity of particular
bacterial isolates. |
| 10:10 |
Carmen Álvarez Domínguez
Investigador Facultativo, Servicio de Inmunología
Hospital Universitario Marqués de Valdecilla, Santander.
Spain. |
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From commensalism to intracellularity / Del comensalismo
a la intracelularidad
Pathogens have adapted to intracellular spaces mainly to remain
hidden from the host defense mechanisms and find specialized
niches that fulfilled their nutrient requirements. Actually
the regulation of this specialized trafficking known as phagocytosis
is beginning to be unrevealed. The identification of both, host
regulators and microbial factors involved in the phagocytic
trafficking will discover the strategies of pathogens to survive
intracellularly and evade the immune system. |
| 10:40 |
Café/Coffee |
| 11:10 |
César Nombela
Catedrático de Microbiología y Director de la
Cátedra Extraordinaria MSD de Genómica y Proteómica
Facultad de Farmacia. Universidad Complutense de Madrid. Spain. |
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Breaking the equilibrium: multifactorial basis
for opportunistic pathogenicity of Candida albicans / Rompiendo
el equilibrio: bases multifactoriales para la patogenicidad
oportunista de Candida albicans
Candida albicans is a successful commensal in the human body
that can invade multiple sites, thus producing a wide range
of infections, from superficial to deep-seated. More than 50
gene products have been identified as required for virulence
in model systems used for experimental infection. Our approach
to analyse the transition to a pathogenic state is, on one hand,
to study the activation of fundamental signalling pathways (cell
integrity, high osmolarity glycerol) under the challenging conditions
that the fungus must face in the host. The response is based
on a regulated cross-talk between signalling pathways controlled
by MAP kinases Mkc1 and Hog1. On the other hand, by proteome
technology we observed specific changes in protein expression
during the Candida-macrophages interaction. We have identified
36 fungal proteins whose expression is altered by interaction
with the macrophage, several of them being induced by the oxidative
products related to the phagocyte anticandidal activity. |
| 11:40 |
Marc Lipsitch
Associate Professor, Epidemiology and Immunology and Infectious
Diseases
Harvard School of Public Health. Boston, MA, USA. |
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What maintains diversity and virulence
in pathogens? / ¿Qué mantiene la diversidad
y virulencia en los patógenos?
Conventional wisdom has answered the twin questions
of: why are surface structures of pathogens variable (because
host immunity directed against one variant creates selective
pressures favoring the others), and why do pathogens harm
their hosts (as a by-product of selection for reproduction
within and transmission between hosts). While there are multiple
examples consistent with each of these stories, especially
in viruses, there are also many important microbes for which
these explanations are difficult to support. Understanding
the diversifying and virulence-maintaining forces in natural
populations is important for basic population biology and
for applications such as vaccine design. This talk will briefly
examine some of the examples, supportive and otherwise, for
these generalizations and consider some alternative and possibly
general mechanisms for maintenance of diversity and virulence.
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| 12:10 |
Discussion General
Topic 1 |
| 12:45 |
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| 13:45 |
Almuerzo |
| SESION 2 |
Changing Ecology and Evolution of
Infectious Diseases / Cambiando la ecología y evolución
de las enfermedades infecciosas
Moderador / Chairperson: José María Eirós
BouzaCentro Nacional de Microbiología, Instituto
de Salud Carlos III. Spain.
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| 15:15 |
Dieter Ebert
Professor, Zoological Institute
University of Basel. Basel, Switzerland.
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Host-parasite coevolution / Coevolución
huésped-parásito
What evidence do we have for antagonistic coevolution by negative
frequency dependent selection? In the first part of my talk
I introduce a couple of experiments aimed to test for aspects
of antagonistic coevolution between hosts and parasites. In
the second part I discuss the consequences of coevolution for
the genetic structure of populations and for their evolution. |
| 15:45 |
Juan Ortín
Profesor de Investigación
Centro Nacional de Biotecnología, CSIC. Madrid, Spain.
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From animal to human viruses: the case of
respiratory pathogens / De los virus animales a los humanos:
el caso de los patógenos respiratorios
The Influenza A viruses are members of the Orthomyxoviridae
family that contain as genome a set of 8 ssRNA molecules of
negative polarity. These RNAs form RNP structures that transcribe
and replicate independently in the nucleus of the infected cell.
Influenza A viruses are genetically and antigenically variable.
Many subtypes can be distinguished, depending on the structure
of the surface antigens HA and NA. All viral subtypes replicate
in wild avian species, without signs of pathology, while a subset
of these subtypes infect mammals, including man, and produce
disease. Normally new Influenza viruses can enter the human
host by reassortment of RNPs in individuals infected by a normal
human virus and an avian virus, but recently some avian viruses
have crossed the species barrier and produced disease in man.
The possibility that these viruses may develop into a new pandemic
strain has raised special concern. The possibility of crossing
the species barrier is limited for avian Influenza viruses by
the lack of adaptation to replicate in the mammalian host. Thus,
the steps of adsorption to cells, membrane fusion, transcription
and replication of virus RNA and modulation of the cell antivirus
response involve virus-host interactions that are optimized
for each virus-host pair. The interspecies shift needs to overcome
the barriers imposed by inexistent or inefficient interactions.
Unfortunately, the large heterogeneity of the influenza virus
populations, their continuous evolution and the possibility
for the avian viruses to incorporate human-adapted RNPs by reassortment
will allow the appearance of new viruses in the human population
and eventually a new pandemic. The consequences of such pandemic
for human health will depend upon the pathogenicity of the virus
strain, the time elapsed until identification of the new virus
and the public health measures adopted worldwide. |
| 16:15 |
David Heymann
Representative of the Director-General for Polio Eradication
World Health Organization. Geneva, Switzerland. |
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Factors in the evolution of infectious diseases
/ Factores en la evolución de las enfermedades infecciosas
The microbes that cause infectious diseases are complex, dynamic,
and constantly evolving. They reproduce rapidly, mutate frequently,
and adapt with relative ease to new environments and hosts,
and they develop resistance to the drugs used to treat them.
Social, economic and environmental factors linked to a host
of human activities often accelerate and amplify the natural
phenomena that modify infectious disease patterns in humans,
increasing the ease at which the microbes that cause them adapt
to new environments and hosts, and the speed with which they
develop resistance to the antimicrobial agents that treat them. |
| 16:45 |
Michel Tibayrenc
Director, Unit of Research Genetics and Evolution of Infectious Diseases
UMR CNRS/IRD 9926. Montpellier, France. |
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Human genetic diversity and the evolution
of infections
Environmental factors are crucial for the transmission
and severity of infectious diseases. However, for the same
socioeconomical and medical environment, we are unequal before
transmissible diseases. Resistance genes have been evidenced,
for example in the case of malaria, lepra and schistosomiasis,
and family studies have detected important individual differences.
However, resistances to transmissible diseases are complex
phenotypes. It is my belief that: (i) the genetic background
of these complex phenotypes is also complex, that is to say:
multigenic; (ii) the target of natural selection for these
complex phenotypes is much more the population, even the ethnic
group, rather than the individual (Tibayrenc, 2004). When
ethnic groups are concerned, it has been proposed that the
morphological and colorimetrical diversity of our species
is the result of sexual selection (Harpending, 2002). However
natural selection by climatic parameters plays an obvious
role in it. Since the transmission of infectious diseases
is strongly influenced by climatic factors, I suggest that
ethnic diversity is a relevant parameter for the study man
genetic susceptibility to transmissible diseases.In this seminar,
I will expose what is known presently on the overall genetic
diversity of our species and on the genetic differences (in
particular HLA polymorphism) that could explain why some population
are overall more resistant to given infectious diseases than
other populations. I will speak also on the potential interest
of the “Human Diversity Genome Project” (HDGP)
for the study of transmissible diseases (Tibayrenc, 2003).
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| 17:15 |
Discussion general Topic
2 |
| 17:45 |
Café
/ Coffee |
| 18:15 |
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| Sábado
/ Saturday 20 |
| SESSION
3 |
Intervention Strategies and the Evolution
of Infectious Diseases / Estrategias de intervención
y la evolución de las enfermedades infecciosas
Moderador / Chairperson: Jerónimo Pachón
Servicio de Enfermedades Infecciosas Hospital Universitario
Virgen del Rocio. Sevilla, Spain. |
| 09:00 |
Javier Garau
Head, Department Of Medicine
Hospital Mutua Terrasa, Barcelona, Spain. |
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Antibiotics and the evolution of infectious
diseases / Antibióticos y evolución de las
enfermedades infecciosas
In the past 60 years, the ecology and treatment of ID have changed
greatly. As a result of excessive demand and use of antibiotics
in humans, and the deployment of antibiotics in animal husbandry,
the number of organisms demonstrating resistance has increased
dramatically, and there is now a well established pool of antibiotic
resistance genes in nature. Antibiotic resistance has become
a major deterrent to effective treatment and control of many
infectious diseases. Changes in the susceptible human such as
reduction of immunocompetence, in social behavior and in the
environment have also taken place. Bacteria will continue to
evolve under these pressures. The impact of such basic changes
will be reviewed. |
| 09:30 |
Fernando Baquero
Jefe de Servicio de Microbiología
Hospital Ramón y Cajal & Centro de Astrobiología,
CSIC / INTA. Madrid, Spain. |
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Antibiotics and emergent behaviour of bacterial
pathogens / Antibióticos y comportamiento emergente
de los patógenos bacterianos
Antimicrobial agents used in chemotherapy constitute a major
component of the environment of bacteria associated with humans.
Bacterial adaptation to antibiotic challenges is either based
on mutational events or on extensive combinatorial trade-off
of locally available genetic sequences. As a result of the later
process, a number of these sequences are amplified by selection
and become increasingly available for future adaptive combinations.
Both mutational events and local engineering inputs facilitate
in some cases, and prevent in others, the building-up of new
bacterial behaviors in particular bacterial clones. Successful
clones may spread efficiently, disseminating in novel microbial
environments the genetic tools that have contributed to their
wealth. |
| 10:00 |
Café
/ Coffee |
10:30
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Gail Cassell
Vice President, Scientific Affairs, Eli Lilly and Company
Lilly Corporate Center. Indianapolis, USA. |
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Immunomodification and the Evolution of Infectious Diseases: The Challenge of Mycobacterium tuberculosis / Modificación inmunitaria y evolución de las enfermedades infecciosas: el reto del Mycobacterium tuberculosis
Immunodification of infectious agents no doubt contributes to the agent's ability to persist within a host as well as cause disease. Tuberculosis is one of the oldest known and well studied infectious diseases form with regards to host/parasite interactions. Yet one third of the world's population is latently infected with this organism. Every 15 seconds at least one person dies of this disease. This presentation will review what is known about immunomodulation and its involvement from both the perspective of the host and the parasite. Lastly, the threat from multi-drug resistant tuberculosis will be discussed as an emerging global crisis. |
| 11:00 |
Sunetra Gupta
Reader in Epidemiology of Infectious DiseaseDepartment of
Zoology, University of Oxford. UK.
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Inmmunoselection and the evolution of pathogenicity
/ Inmunoselección y evolución de la patogenicidad
I will discuss the effects of immune selection on the evolution
of antigenic diversity both at the within-host and between-host
level with particular reference to Plasmodium falciparum malaria.
I will show how partially cross-protective immune responses
can structure a pathogen population in to antigenically distinct
‘strains’, and also enable the orchestration of
antigenic variation as a within-host immune evasion strategy. |
| 11:30 |
Discussion General
Topic 3 |
| 12:00 |
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| 13:00 |
Closure Address
Moderador / Chairperson: César Nombela |
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Julian Davies
Professor, Department of Microbiology and Immunology
University of British Columbia. Vancouver, Canada. |
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Human–microbe interactions: the future
/ Interacciones humano-microbio: el futuro
In the past 25 years, cellular microbiology has provided amazing
insights on human-microbe interactions, both parasitic and commensal.
The evolution of microbial diseases is a real-time phenomenon;
in 1980, E. coli 0157 was not known as a human pathogen. Future
work must be concerned with the rapidity that new pathogens
can appear and whether or not this can be predicted. What are
the origins of pathogenicity genes and how are they acquired?
More importantly, what makes a pathogenicity gene? |
| 13:40 |
Farewell
Fernando Baquero
César Nombela
José Antonio Gutiérrez Fuentes
Juan Carlos Gómez Pérez
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| Seminarios: dirigidos a
la discusión y orientación de los aspectos prácticos
relacionados con la prevención, el diagnóstico
y el tratamiento |
| (*)SEMINARIOS |
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SEMINARIO 1 |
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Ponente: Fernando Cháves
Adjunto, Servicio de Microbiología
Hospital Universitario Doce de Octubre, Madrid |
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Tuberculosis, una enfermedad en evolución.
Novedades diagnósticas / Tuberculosis, an evolving
disease. Diagnosis innovations
La tuberculosis es un problema de salud pública de importancia
global. Las características singulares de Mycobacterium
tuberculosis, la resistencia a los fármacos, y los nuevos
fenómenos epidemiológicos que se están
sucediendo, suponen importantes retos para el control de la
enfermedad. Las nuevas técnicas de epidemiología
molecular están aportando importante información
en la transmisión de la tuberculosis, patogenicidad,
manejo clínico de los pacientes, y en la evaluación
de los programas para el control de la enfermedad. |
| SEMINARIO
2 |
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Ponente: Rafael Cantón
Adjunto, Servicio de Microbiología, Hospital Ramón
y Cajal y Profesor Asociado del Departamento de Microbiología,
Facultad de Farmacia, Universidad Complutense, Madrid
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La explosión de las beta-lactamasas
de espectro extendido: valoración y control / Outburst
of extended spectrum beta-lactamases. Assessment and control
Las beta-lactamasas de espectro extendido (BLEE), detectadas
inicialmente al principio de la década de los 80, se
han convertido en paradigma de la dispersión de los mecanismos
de resistencia, no sólo en el ambiente hospitalario sino
también en la comunidad. Las BLEE están codificadas
en unidades genéticas de transferencia horizontal y con
frecuencia se asocian a otros genes de resistencia. Los procesos
de co-selección y la movilidad de los genes BLEE pueden
haber tenido un papel relevante en su diseminación. El
control de la explosión de las BLEE constituye un reto
actual para la microbiología y las enfermedades infecciosas.
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| SEMINARIO
3 |
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Ponente: Jordi Vila
Profesor de Microbiología, Facultad de Medicina, Universidad
de Barcelona, y Consultor del Departamento de Microbiología
Clínica del Hospital Clinic Barcelona. |
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Human migrations and infectious diseases /
Migraciones humanas y enfermedades infecciosas
Las enfermedades infecciosas son la primera causa de muerte
en el mundo. El riesgo de padecer una de estas enfermedades
se ve influenciado por diferentes factores, entre los cuales
se hallan la globalización del comercio mundial, los
movimientos migratorios, y el creciente tráfico aéreo.
En este seminario, se discutirán estos factores, así
como la diseminación de microorganismos específicos,
y como esta puede ser prevenida y controlada.
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| Viernes
19 |
Sábado
20 |
| 12:45
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18:15
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12:00 |
| SEM- 1 |
SEMI-2 |
SEM- 1 |
SEM- 3 |
SEM- 2 |
SEM- 3 |
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PROMOCION
Y PATROCINIO: Fundación Lilly |
| COMITÉ CIENTÍFICO (ORGANIZADOR) |
LUGAR DE CELEBRACIÓN DEL
SIMPOSIO |
César Nombela
Fernando Baquero
Juan Carlos Gómez
José A Gutiérrez Fuentes |
Euroforum Infantes.
El Escorial,
Madrid, Spain |
| CONFERENCIANTES
– SPEAKERS |
JÁlvarez Domínguez, C (Sp)
Baquero, F (Sp)
Levin, B (US)
Cantón R (Sp)
Cassell, G (US)
Chaves, F (Sp)
Davies, J (Can)
Ebert, D (Sw)
Eiros JM (Sp)
Garau, J (Sp)
|
Gupta, S (UK)
Hacker, J (Al)
Heymann, D (Sw)
Lipsitch, M (US)
Nombela, C (Sp)
Ortín, J (Sp)
Pachón J (Sp)
Rodríguez Noriega, A (Sp)
Tibayrenc, M (Fr)
Vila J (Sp) |
| INFORMACIÓN
GENERAL |
La acreditación supondrá la asistencia a todas
las sesiones plenarias y, como mínimo, a dos seminarios.
Las
conferencias tendrán una duración de 30
minutos y se verán seguidas por un coloquio de 10
minutos, estando abiertas al público en general.
Los
seminarios se impartirán dos veces cada uno.
Al acreditarse,
los asistentes harán una opción previa sobre los
seminarios a los que desean asistir, limitándose el número
de participantes en cada uno de ellos un máximo de 70
(se respetará rigurosamente el orden de inscripción). |
| SECRETARIA |
Fundación Lilly: Calle Velázquez 94, 6º
Izq. 28006 Madrid
Tel: 91 781 50 70-71 / 629 86 14 16
Fax: 917815079
E-mail: fundacionlilly@lilly.com
/ www.fundacionlilly.com
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