Welcome to the Microbiology Information

Onchocerciasis is an infection caused by Onchocerca volvulus, a parasite nematode worm transmitted to humans by a species of black fly of the Simulium genus whose larvae develop in fast-flowing rivers.

Infected subjects suffer not only from severe skin lesions but also eye damage that can lead to irreversible of−loss of sight, hence the name ‘river blindness’. A huge majority (99%) of the 37 million people
infected by the parasite live in SubSaharan. Ivermectin, a medicine capable of killing the parasite
embryos (the microfilariae) circulating in the organism of patients and temporarily interrupting the nematode’s reproduction, is the only treatment used for onchocerciasis control.

Since 1995, the African Programme for Onchocerciasis Control (APOC) has been covering 19 of the
continent’s 28 countries hit by the disease. Access to this treatment is possible for 70 million people and has
significantly diminished the onchocerciasis-induced morbidity. However, the doubling of cases of infection in
certain communities of Ghana between 2000 and 2005, in spite of annual treatments, created fear of the emergence of ivermectin-resistant strains. Such apprehension appears particularly justified in that a high degree of therapeutic cover is achieved during mass distribution campaigns and hence only a tiny part of the parasite population targeted remains unexposed to drug treatment pressure.

Since 1994, a team of IRD researchers, working jointly with Cameroon researchers and others from McGill University of Montreal, has been monitoring a cohort of Cameroon patients benefiting from repeated treatments with ivermectin. Regular parasite sampling from these subjects was performed over a 13-year period in order to determine the changes in the genetic structure of Onchocerca volvulus
populations. Each occasion involved measurement of the genotype frequency of heterozygotes and homozygotes for the gene coding β-tubulin, a protein involved in the organization of the parasite’s cells. The team focused on this particular gene because it acts as a marker of resistance to ivermectin in other nematode species parasitic on cattle. As a control, they monitored the changes in genotype frequency
of two other genes, known for their high evolutionary stability over time. The proportion of homozygotes and heterozygotes for these two genes remained stable throughout the investigation, but the situation was
completely different for the β-tubulin gene.

Between 1994 and 1998, the percentage of parasites showing a genotype homozygous for this gene fell from 79 to 31% in subjects receiving quarterly treatment with ivermectin. At the same time, the proportion of heterozygous genotypes changed in the opposite sense, rising from 21 to 69%. These results could be the sign of adaptation of nematode worm populations to repeated treatments using this drug. The research team inferred that the parasites showing a genotype homozygous for β-tubulin are more susceptible to
it. As courses of treatment progressed, they would therefore gradually disappear, to the benefit of the more resistant heterozygous strains. Ivermectin’s effect on microfilariae, other than its direct one, is to prevent them from leaving the uterus of adult worms, for several months after treatment: this is its embryostatic effect. Post-treatment, there were more microfilariae in the uterus of homozygous female parasites than in those of heterozygous females.

This could mean that, in the latter, the microfilariae succeed in leaving the uterus, as they usually do in the absence of treatment, and therefore that the embryostatic effect of ivermectin would be diminished. Contrary to the effect anticipated, the repeated exposure to treatments could in this way select those worms more able to keep up the production of new generations. Nevertheless, the drug’s direct action on the moment, there is no reason to call into question the current control strategy against the disease based on annual treatments with ivermectin.

Affirmation of the results requires further investigations1, starting from new cohorts subjects infected by Onchocerca volvulus who have not yet been treated with ivermectin. This type of approach should bring more information on the risks of the parasite’s resistance to this drug. If such risks were confirmed, then the whole onchocerciasis control strategy would probably have to be revised. Nevertheless, for many years to come, ivermectin could well remain the sole drug applicable for mass treatment in measures to control river blindness.

Healthy consumers can handle the low levels of bacteria occasionally found in cosmetics. But for severely ill patients these bacteria may trigger life-threatening infections, as patients in the intensive care unit at one Barcelona hospital discovered after using contaminated body moisturiser. The Burkholderia cepacia bacteria outbreak is detailed in the open access journal, Critical Care.

Five patients suffered from infection including bacteremia, lower respiratory tract infection and urinary tract infection associated with the bacterial outbreak in August 2006. Skin care products sold in the European Union are not required to be sterile, but there are limits to the amount and type of bacteria that are permitted. The Hospital Universitari del Mar, Universitat Autònoma de Barcelona’s routine infection control surveillance pinpointed the unwelcome bacteria in five patients’ biological samples.

Researchers tested a number of environmental samples, and discovered that moisturizing body milk used in the patients’ care was a B. cepacia reservoir. Pulsed-field gel electrophoresis experiments confirmed that all of the strains of B. cepacia bacteria found in patient and environmental samples were from the same bacterial clone. Tests on sealed containers of the moisturizer confirmed that the bacteria had not invaded the product after it had been opened, but that it was contaminated during manufacturing, transportation or
storage.

“This outbreak of nosocomial infection caused by B. cepacia in five severely ill patients supports a strong
recommendation against the use cosmetic products for which there is no guarantee of sterilization during the manufacturing process,” says study author Francisco Álvarez-Lerma. B. cepacia is a group or “complex” of bacteria that can be found in soil and water. They have a high resistance to numerous antimicrobials and antiseptics and are characterised by the capacity to survive in a large variety of hospital microenvironments These bugs pose little medical risk to healthy people. However, those with weakened immune systems or chronic lung diseases, particularly cystic fibrosis, may be more susceptible to B. cepacia infection. B
cepacia is a known cause of hospital infections.

Moisturizing body milk as a reservoir of Burkholderia cepacia: outbreak of nosocomial infection in a multidisciplinary intensive care unit. Francisco Alvarez-Lerma, Elena Marull, Roser Terradas, Concepcion Segura, Irene Planells, Pere Coll, Hernando Knobel and Antonia Vazquez. Critical Care (in
press).

Finding should aid those developing anti-virus vaccines. Vaccines have led to many of the world’s greatest public health triumphs, but many deadly viruses, such as HIV, still elude the best efforts of scientists to develop effective vaccines against them.

An improved understanding of how the immune system operates during a viral infection is critical to designing successful anti-virus vaccines. Scientists from the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH), have added an important dimension to this knowledge.

Focusing on mouse lymph nodes—bean-shaped organs that contain a variety of immune cells and are distributed throughout the body—the researchers discovered that immune cells confront viruses just inside of the lymph node and not deep within these organs as previously thought. The study, led by Jonathan Yewdell, M.D., Ph.D., chief of the NIAID Cellular Biology Section and his NIAID colleague, Heather Hickman, Ph.D., is described in a report online in Nature Immunology.

The results are significant, the authors say, as they observed in detail the interaction of viruses and immune cells inside a living organism, in this case, mice. Combining expertise from disciplines such as imaging, immunology, virology and other specialties, the scientists first extracted and then purified specific T cells—killer T cells—from mice. Killer T cells, which attack and kill infected or cancerous cells, are major
weapons in the immune system arsenal. The scientists labelled the T cells with a fluorescent marker, injected them back into the mice, and then infected the animals with vaccinia virus, the virus used to make smallpox vaccine, engineered to express a brilliantly coloured protein.

Using a multiphoton microscope, a highly specialized microscope that enables scientists to peer into a living
organism, the scientists could now look into the lymph nodes of the infected mice and see that the viruses had infected cells just inside the lymph node surface, triggering a swarm of T cells. These virus-specific T cells form an elaborate and dynamic communications network that activates them to divide and travel to the site of viral infection, where they kill virus-infected cells.

“A key challenge in viral vaccine research is developing strategies for immunizing against lethal viruses such as HIV that have eluded the standard vaccine approaches,” notes Dr. Yewdell. “We have contributed a page to the handbook of understanding how to rationally design vaccines to elicit a T-cell response.” According to the NIAID team, pinpointing where in the lymph node immune cells fight the virus should help efforts to design effective anti-virus vaccines.