Bernhard Nocht Institute for Tropical Medicine

Hamburg, Germany

Bernhard Nocht Institute for Tropical Medicine

Hamburg, Germany

Bernhard Nocht Institute for Tropical Medicine; is a medical institution based in Hamburg, Germany which is dedicated to research, treatment, training and therapy of tropical and infectious diseases.The body responsible for the BNI is the Federal Ministry of Health and the Government Agency for Social Affairs, Family Affairs, Health and Environment of Hamburg.The BNI is allied with the Kwame Nkrumah University in Ghana, where there is a laboratory complex named the Kumasi Centre for Collaborative Research in Tropical Medicine. Today, there is a staff of approximately 400 people working in Hamburg and Kumasi combined. Presently, it is considered the most important research facility regarding tropical medicine in Europe. Wikipedia.

SEARCH FILTERS
Time filter
Source Type

Osterloh A.,Bernhard Nocht Institute for Tropical Medicine
Medical Microbiology and Immunology | Year: 2017

Rickettsiae are small intracellular bacteria that can cause life-threatening febrile diseases. Rickettsioses occur worldwide with increasing incidence. Therefore, a vaccine is highly desired. A prerequisite for the development of a vaccine is the knowledge of the immune response against these bacteria, in particular protective immunity. In recent years murine models of rickettsial infections have been established, and the study of immune response against rickettsiae in mice provided many new insights into protective and pathological immune reactions. This review summarizes the current knowledge about immune mechanisms in protection and pathology in rickettsial infections. © 2017 The Author(s)


News Article | September 14, 2016
Site: www.nature.com

Ebola survivors are teaching scientists some surprising lessons. Long-term studies have revealed that the virus lasts longer in survivors’ bodies than previously suspected. The findings, presented on 12 September at an Ebola-virus conference in Antwerp, Belgium, underscore the need for extended tracking of people who have beaten Ebola and other rare infections. Researchers have long known that the virus can persist in people who have recovered from the infection. But the size of the West African outbreak, coupled with improved monitoring technologies, is changing how scientists view life after Ebola — and how to prevent future outbreaks. “Now that you have tens of thousands of survivors and systemic approaches to follow them, you can detect things that happen more rarely and attribute them to Ebola,” says physician and epidemiologist Daniel Bausch of the World Health Organization in Geneva, Switzerland. Researchers will soon publish the first confirmed report of a person without obvious Ebola symptoms infecting another person. A seemingly healthy mother in Guinea passed the virus to her nine-month-old daughter in breast milk, and the child died from Ebola-virus infection in August 2015, according to a European Union-funded team led by Sophie Duraffour from the Bernhard Nocht Institute for Tropical Medicine in Hamburg, Germany. A study due to be presented at the Antwerp meeting also suggests that some people who became infected during the recent outbreak escaped detection. Miles Carroll, an epi­demiologist at Public Health England in Porton Down, and his colleagues tracked 80 people who had contact with Ebola patients in Guinea but did not themselves become noticeably ill. Yet 15–20% of these contacts developed immune responses capable of neutralizing Ebola viruses, suggesting that they had contracted mild infections that went undetected. This ‘sub-symptomatic’ or ‘asymptomatic’ Ebola was known to exist, but the latest studies involve more people who have been studied more intensively than in the past. Researchers caution, however, that it is still rare for Ebola lingering in a person’s body to spark new outbreaks. The phenomenon would probably have escaped notice if the recent epidemic had been smaller. Thousands of men who are infected have survived, but until recently scientists did not know that the Ebola virus could be transmitted in semen beyond three months, says Mary Choi, an epidemiologist at the US Centers for Disease Control and Prevention. The agency and the Liberian government are running the largest-ever investigation of Ebola viruses in the semen of survivors. So far, the team’s study of 466 men has detected virus fragments in semen up to 18 months after a man has recovered from his infection1. In February, two months after the outbreak was declared over in Guinea, Duraffour and her colleagues traced a cluster of new Ebola cases to a man who transmitted the virus to a sexual partner 17 months after recovering from his infection2. Yet another study, which examined 26 male Ebola survivors, found that the vast majorityeliminated the virus from their semen within 4 months of recovery3. The precise timing varied widely from person to person, however. Choi says that the virus probably lasts for longer than 18 months in semen. Her team will continue to monitor the virus’s persistence, while counselling survivors to use condoms or abstain from sex until their semen tests negative twice. “The primary takeaway is that semen testing should be incorporated earlier on as part of services that survivors receive,” Choi says. Researchers must show sensitivity in communicating such findings, says virologist Stephan Günther of the Bernhard Nocht Institute, and take care not to make life more difficult than it already is for Ebola survivors, who face discrimination and lingering health problems. “We have to be careful to stress that these are very, very rare events.”


Muller I.B.,Bernhard Nocht Institute for Tropical Medicine | Hyde J.E.,University of Manchester
Molecular and Biochemical Parasitology | Year: 2013

Malaria still poses one of the most serious threats to human health worldwide and the prevailing lack of effective, clinically licensed, vaccines means that prophylaxis and treatment depend heavily on a small number of compounds whose efficacies are progressively compromised at varying rates by the inevitable emergence of drug-resistant parasite populations. Of these antimalarials, those inhibiting steps in folate metabolism, along with chloroquine, are the oldest synthetic compounds, with origins dating back three-quarters of a century. Despite widespread parasite resistance, the antifolates still play an important role in malaria control, and our understanding of the underlying mechanisms of folate metabolism and genesis of drug resistance has increased considerably over the last twenty years. Folate de novo synthesis in the parasite, interconversion of active folate derivatives and their utilisation as multifunctional cofactors involve numerous enzymes, although only two of these have ever served as targets of clinical antimalarial inhibitors. The current application of antifolates, resistance to this class of drugs, new insights into folate metabolism in the parasite, its potential for providing novel targets of inhibition and some of the questions that are still outstanding are reviewed here. © 2013 Elsevier B.V. All rights reserved.


Muller I.B.,Bernhard Nocht Institute for Tropical Medicine
Future Microbiology | Year: 2010

Malaria represents one of the most serious threats to human health worldwide, and preventing and curing this parasitic disease still depends predominantly on the administration of a small number of drugs whose efficacy is continually threatened and eroded by the emergence of drug-resistant parasite populations. This has an enormous impact on the mortality and morbidity resulting from malaria infection, especially in sub-Saharan Africa, where the lethal human parasite species Plasmodium falciparum accounts for approximately 90% of deaths recorded globally. Successful treatment of uncomplicated malaria is now highly dependent on artemisinin-based combination therapies. However, the first cases of artemisinin-resistant field isolates have been reported recently and potential replacement antimalarials are only in the developmental stages. Here, we summarize recent progress in tackling the problem of parasite resistance and discuss the underlying molecular mechanisms that confer resistance to current antimalarial agents as far as they are known, understanding of which should assist in the rational development of new drugs and the more effective deployment of older ones. © 2010 Future Medicine Ltd.


Mosquitoes and other arthropods may transmit medically important pathogens, in particular viruses such as West Nile virus. The presence of suitable hosts and competent vectors for those zoonotic viruses is essential for an enzootic transmission, which is a prerequisite for epidemics. To establish reliable risk projections, it is an urgent need for an exact identification of mosquito species, which is especially challenging in the case of sibling species, such as Culex. pipiens pipiens biotypes pipiens and molestus. To facilitate detection of different Culex pipiens forms and their hybrids we established a multiplex real-time PCR. Culex pipiens samples were obtained by egg raft collection and rearing until imago stage or adult sampling using CO2 baited traps and gravid traps. In total, we tested more than 16,500 samples collected all over Germany in the years 2011 and 2012. The predominant species in Germany are Culex pipiens pipiens biotype pipiens and Culex. torrentium, but we also detected Culex pipiens pipiens biotype molestus and hybrids of the two pipiens biotypes at sites where both species occur sympatrically. This report of a potentially important bridge vector for West Nile virus might have major impact in the risk projections for West Nile virus in Germany.


Marti M.,Harvard University | Spielmann T.,Bernhard Nocht Institute for Tropical Medicine
Current Opinion in Microbiology | Year: 2013

The continuous multiplication of Plasmodium parasites in red blood cells leads to a rapid increase in parasite numbers and is responsible for the disease symptoms of malaria. Survival and virulence of the parasite are linked to parasite-induced changes of the host red blood cells. These alterations require export of a large number of parasite proteins that are trafficked across multiple membranes to reach the host cell. Two classes of exported proteins are known, those with a conserved Plasmodium export element (PEXEL/HT) or those without this motif (PNEPs). Recent work has revealed new aspects of the determinants required for export of these 2 protein classes, shedding new light on the mode of trafficking during the different transport steps en route to the host cell. © 2013 Elsevier Ltd.


Meyer C.G.,Bernhard Nocht Institute for Tropical Medicine | Thye T.,Bernhard Nocht Institute for Tropical Medicine
Seminars in Immunology | Year: 2014

Early observations, candidate gene studies and, more recently, genome-wide association studies have shown that susceptibility to tuberculosis has a host genetic component. Because the value of candidate gene studies has been doubted due to major limitations such as lack of sufficient power and small study groups, lack of reproducibility in independent groups and, often, ambiguous or even contrasting results in attempts of replication, much hope and expectancy has been put on the progress the genome-wide association approach has created. However, much less than initially expected became clear by the results obtained in genome-wide studies, emphasizing the need of increasing sample sizes, e.g. through meta-analyses, and of increasing the density of genetic variants studied across the human genome. A further reason why a rather low number of associated genetic variants were identified to date in infectious diseases in general and tuberculosis in particular might be the fact that selection acts strongly in diseases that affect the reproductive success. As in most genome-wide association studies performed so far, significant signals, often most likely surrogate marker only, have been found in non-coding regions of genomes, the identification of truly causative genetic variation and of the functionality of associated factors needs urgent attention. In the following we briefly discuss genetic studies in tuberculosis and describe new technologies that are currently employed in the search for responsible genetic elements involved in tuberculosis susceptibility. © 2014 Elsevier Ltd.


Jonsson F.,Bernhard Nocht Institute for Tropical Medicine
PloS one | Year: 2012

Dynamic changes in the actin cytoskeleton are essential for immune cell function and a number of immune deficiencies have been linked to mutations, which disturb the actin cytoskeleton. In macrophages and dendritic cells, actin remodelling is critical for motility, phagocytosis and antigen presentation, however the actin binding proteins, which control antigen presentation have been poorly characterized. Here we dissect the specific roles of the family of ADF/cofilin F-actin depolymerizing factors in macrophages and in local immune responses. Macrophage migration, cell polarization and antigen presentation to T-cells require n-cofilin mediated F-actin remodelling. Using a conditional mouse model, we show that n-cofilin also controls MHC class II-dependent antigen presentation. Other cellular processes such as phagocytosis and antigen processing were found to be independent of n-cofilin. Our data identify n-cofilin as a novel regulator of antigen presentation, while ADF on the other hand is dispensable for macrophage motility and antigen presentation.


Thye T.,Bernhard Nocht Institute for Tropical Medicine
Nature genetics | Year: 2010

We combined two tuberculosis genome-wide association studies from Ghana and The Gambia with subsequent replication in a combined 11,425 individuals. rs4331426, located in a gene-poor region on chromosome 18q11.2, was associated with disease (combined P = 6.8 x 10(-9), odds ratio = 1.19, 95% CI = 1.13-1.27). Our study demonstrates that genome-wide association studies can identify new susceptibility loci for infectious diseases, even in African populations, in which levels of linkage disequilibrium are particularly low.


Spielmann T.,Bernhard Nocht Institute for Tropical Medicine | Gilberger T.-W.,Bernhard Nocht Institute for Tropical Medicine
Trends in Parasitology | Year: 2010

Intracellular malaria parasites export numerous proteins into their host cell, a process essential for parasite survival and virulence. Many of these proteins are defined by a short amino acid sequence motif termed PEXEL or VTS that mediates their export, suggesting a collective trafficking route. The existence of several PEXEL-negative exported proteins (PNEPs) indicates that alternative export pathways might also exist. We review recent data on the sequences mediating export of PNEPs and compare this process to PEXEL export taking into account novel findings on the function of this motif. Based on this we propose that, despite the lack of a PEXEL in PNEPs, both groups of proteins might converge in a single export pathway on their way into the host cell. © 2009 Elsevier Ltd. All rights reserved.

Loading Bernhard Nocht Institute for Tropical Medicine collaborators
Loading Bernhard Nocht Institute for Tropical Medicine collaborators