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09.19.2013

more on the antibiotic resistance crisis

bacteriaThe New York Times editoriaizes on the CDC study that found 23,000 people a year die each year due to infections from drug resistant bacteria:

The new report, for the first time, puts 17 drug-resistant bacteria and a dangerous fungus into three categories based on how big a threat they pose. Three were deemed “urgent threats,” including a bacterium, known as CRE, that is resistant to most drugs and kills a high percentage of people who become infected with it. Though it is rare, causing 600 deaths a year, it has been identified in health facilities in 44 states. Further spread of the germ or transfer of its resistance genes to other germs could lead to a “nightmare scenario,” the agency said. Twelve drug-resistant strains, including such common germs as salmonella, tuberculosis and MRSA, were classified as “serious threats.”

Scientific American also covers a paper published in JAMA Internal Medicine that links pig manure fertilizer to MRSA (methicillin-resistant staphylococcus aureus infections in humans. From Scientific American:

The team analyzed cases of two different types of MRSA — community-associated MRSA (CA-MRSA), which affected 1,539 patients, and health-care-associated MRSA (HA-MRSA), which affected 1,335 patients. (The two categories refer to where patients acquire the infection as well as the bacteria’s genetic lineages, but the distinction has grown fuzzier as more patients bring MRSA in and out of the hospital.) Then the researchers examined whether infected people lived near pig farms or agricultural land where pig manure was spread. They found that people who had the highest exposure to manure — calculated on the basis of how close they lived to farms, how large the farms were and how much manure was used — were 38% more likely to get CA-MRSA and 30% more likely to get HA-MRSA.

Expect to hear about this more and more.

12.19.2012

resistant bacteria from labs enter rivers in china

bacteria

In China, resistant bacteria from molecular biology experiments are turning up in rivers and streams. Molecular biologists use different resistant strains in order to clone bacteria and produce different proteins. In the US, academic and industrial labs have implemented steps to prevent these resistant genes from being introduced into our environment. China, it appears, still has a ways to go before they get a handle on this. From C&EN:

But because this technique is still commonly used in molecular biology labs, some researchers have been concerned that these experiments could release resistance genes into the environment. To search for antibiotic-resistance genes introduced by synthetic plasmids, Jun-Wen Li at the Institute of Health and Environmental Medicine, in Tianjin, China, and his colleagues took water samples from six Chinese rivers downstream of densely populated cities. They extracted plasmids from the samples and transferred the DNA into Escherichia coli. Then they screened the bacteria for a gene commonly used in academic and industrial labs that confers resistance to the antibiotic ampicillin. To determine if a gene in a sample came from a manmade source, they used polymerase chain reaction to look for sequences unique to several synthetic plasmids.

The researchers found synthetic resistance genes in all six rivers. Of all of the ampicillin-resistance plasmids they found in the rivers, about 27% had the synthetic vector-sourced gene.

More here.

12.13.2012

platelets confer resistance to parasites

Platelets prevent parasitic infestation. Image from Sciencemag.org

From Science magazine this week, a report on how platelets express genes to help kill parasites. An excerpt from the perspective:

The six Plasmodium parasite species that cause disease in humans (P. falciparum, P. vivax, P. malariae, P. ovale wallickerie, P. ovale curtisii, and P. knowlesi) appear to have independently colonized hominids and influenced the genetic composition of different human populations (3). For example, the genes responsible for sickle cell anemia, thalassemia, and glucose-6-phosphate dehydrogenase deficiency have a higher frequency in populations where malaria is, or was once, endemic. These genes provide protection against severe malaria syndromes and likely evolved in response to the disease by providing a survival advantage (4). Another of these genes encodes the Duffy-antigen receptor for chemokines (DARC/Fy glycoprotein/CD234) found on red blood cells. This protein also acts as a receptor for P. vivax (5), and human red blood cells lacking this receptor are resistant to invasion by this species and by P. knowlesi (6, 7). The impact of this genetic selection can be seen in the geographical distribution of P. vivax. This parasite is spread throughout tropical regions of the world, but is rare in large areas of central and western Africa where many individuals lack Duffy-antigen receptor expression on red blood cells. Thus, this “Duffy-negative” phenotype appears to have evolved as an innate resistance mechanism to P. vivax infection.

McMorran et al. extend previous work that demonstrated an important role for platelets in resistance to malaria (8) by identifying platelet factor 4 (PF4) as a key molecule in platelet-mediated killing of P. falciparum. PF4 is released from α granules in activated platelets to promote blood coagulation (9). It binds the Duffy-antigen receptor, along with several other chemokines (10). McMorran et al. found that a functional Duffy-antigen receptor is required for the antiparasitic activity of PF4.

Also check out the scientific research paper here [subscription required].

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