Portion of U.s. beekeepers
affected by colony collapse
Portion, on average, of
total hives lost by those
Honeybee death suspects spotted
Colony collapse disorder linked to virus-fungus conspiracy
by eva emerson
A one-two punch by a gut parasite and
viruses may help explain the mysterious
decline in U. S. honeybees in recent years.
Bees infected with both the fungal parasite Nosema ceranae and with any one
of a family of viruses were more likely to
come from declining hives than healthy
hives, researchers reported May 25.
The finding represents a new twist in
a complex problem termed colony col-
lapse disorder, which has caused severe
losses for U.S. beekeepers since 2006.
Over a quarter of beekeepers have been
affected, according to the Apiary Inspec-
tors of America, an industry group. These
beekeepers, including honey producers
as well as many who lease out their bees to
pollinate food crops, have reported losing
bet ween 30 and 90 percent of their hives.
bees may fall prey to a fungal parasite
and viruses in cases of colony collapse.
by bacteria talk
Blocking microbial signaling
might help close skin wounds
by eva emerson
Chatter between bacterial cells may stall
healing of skin wounds, and sabotaging
that chitchat could offer another way to
battle infection, new research suggests.
Making Pseudomonas aeruginosa bacteria deaf to each other’s talk would offer a
kind of antibiotic therapy that doesn’t kill
bacterial cells but rather strikes at their
ability to attack human cells en masse,
Jasper Jacobsen of the Statens Serum
Institute in Copenhagen said May 24.
When P. aeruginosa infects human
tissue, the bacteria coordinate their
offensive using a method called quorum
sensing. As the number of bacteria present grows, signaling molecules involved
in quorum sensing build up. These signal-
ing molecules bind to proteins encoded by
two master quorum sensing genes: lasR
and rhlR. This switches on the production
of a battery of compounds secreted by the
bacteria to promote infection. The two
genes are also involved in the creation of
a biofilm — a layered bacterial growth that
is harder for the immune system to combat than free-floating microbes.
Jacobsen and colleagues compared
secretions released by a normal strain
of P. aeruginosa with those from a strain
in which the two quorum sensing genes
had been turned off. “We wanted to see
whether this ‘language’ could impair
wound healing in cells,” he said.
The researchers arranged human skin
cells in lab dishes with a gap in the middle
to model a skin gash. Secretions from normal bacteria reduced the ability of skin
cells to fill the gap (a key process in wound
healing called migration) substantially
more than secretions from the strain with
disabled quorum sensing genes.
Most affected were cells called kerati-
nocytes, which form the outermost layer
of people’s skin. In these, normal strain
secretions led to substantially less cell
migration—about 55 percent wound
closure compared with 75 percent for
the altered strain. The normal strain
also decreased migration of fibroblast
cells, which are abundant in the skin
layer below, but to a lesser extent. Neither
strain substantially affected cell growth
or the migration of skin endothelial cells.