Description of measles D4-Hamburg outbreak in Hamburg, Germany, December 2008 to June 2009, which disproportionally affected a local Roma community.

From December 2008 to June 2009 a measles outbreak occurred in the Federal State of Hamburg, Germany. The outbreak affected 216 persons and was caused by a new measles strain termed D4-Hamburg which led to consecutive outbreaks between 2009 and 2011 in at least 12 European countries. Here, we describe epidemiological characteristics of the outbreak and evaluate the control measures taken in Hamburg. In one of the seven boroughs of Hamburg a local Roma community comprised more than 50% of the notified cases.We compared in a stratified analysis the age distribution of these cases with cases of fellow citizens who did not belong to the Roma community. The age group of infants (0-11 months) comprised 33% among the non-Roma measles cases, while in the Roma community only 4% belonged to this stratum. In the stratum of 5-17 year-olds only 8% were affected among the non-Roma cases, whereas in the Roma community 50% belonged to this age group. We discuss the influencing factors that might have led to this difference in age distribution between the two groups.

[Pancytopenia, fever, and splenomegaly in a 2-year-old boy]. / Panzytopenie, Fieber und Splenomegalie bei 2-jährigem Jungen.

HISTORY: Suspected of having a systemic malignancy a 22-month-old boy was admitted to hospital with fever, pancytopenia and hepatosplenomegaly. The boy was of ethnically German origin and no travel abroad was reported. DIAGNOSIS: Intensive search for a focus of infection, laboratory tests and bone marrow microscopy failed to be diagnostic. Serological findings and detection of Leishmania DNA in bone marrow by polymerase chain reaction (PCR) led to the diagnosis of visceral leishmaniasis. On explicit questioning the child's parents reported a stay in Greece 18 months before onset of symptoms. TREATMENT AND COURSE: On the fourth day of i.v. therapy with liposomal amphotericin B, 3mg/kg/d for 10 days, the fever subsided. Platelets and leukocytes regained normal levels. The child was discharged after 10 days of treatment and received two more doses on days 14 and 21. CONCLUSION: Negative results on microscopic bone marrow inspection do not rule out visceral leishmaniasis. Detection of anti-Leishmania antibodies may support the suspected diagnosis and provide the indication for PCR technique.

No life without death--apoptosis as prerequisite for T cell activation.

The orchestrated death of infected cells is key to our understanding of CD8 T cell activation against pathogens. Most intracellular bacteria including Mycobacterium tuberculosis, the etiologic agent of tuberculosis, remain enclosed in phagosomes of infected macrophages. CD8 T cells play a critical role in defense of infection and recognize antigens originating from the cytosol presented by MHC-I molecules. Since mycobacteria do not gain access to the cytosolic MHC-I presentation pathway, the fundamental question as to how CD8 T cells encounter mycobacterial antigens remains to be solved. In this review, we focus on solutions for this enigma and describe the detour pathway of T cell activation. Mycobacteria induce cell death of infected macrophages which thereby leave a last message by releasing apoptotic vesicles. Subsequently, these antigen-containing entities are engulfed by dendritic cells which process the mycobacterial cargo for efficient antigen presentation and CD8 T cell activation. Since the dying infected cell is the origin of a protective T cell response destined to preserve life and individuality, the detour pathway represents an altruistic principle at a cellular level which corresponds to the macroscopic world where death is the precondition to perpetuate the living.

Factor H and disease: a complement regulator affects vital body functions.

Factor H is a multidomain and multifunctional protein. As a complement regulator factor H determines the fate of newly formed C3b and controls formation and stability of C3 convertases both in the fluid phase and on cell surfaces. In addition, this plasma protein displays functions outside complement control as it has been suggested to act as an adhesion protein, to be a ligand for the cellular integrin receptor CR3 (CD11b/CD18) and to display chemotactic activity. Genetic and pathophysiological analyses describe a role for factor H in vital body functions. Depletion or the absence of factor H due to genetic reasons leads to unrestricted C3 consumption. A reduced amount of factor H in plasma or mutations within the factor H gene may lead to glomerulonephritis (type II MPGN) or hemolytic uremic syndrome (HUS). Certain pathogenic organisms have been shown to evade complement attack by binding factor H from the host. Such specific factor H binding components have been demonstrated on the surface of microbes, e.g., Streptococcus pyogenes and Neisseria gonorrhoeae. Here, we summarize the current knowledge how abnormalities in function of the central complement regulator factor H are associated with human diseases.