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RESEARCH BRIEFS
Diagnosis of Lice May Be LousyFlecks of white in the hair and the skin-crawling sensation of tiny bodies on the scalp can mean only one thing: lice. Or so many people think—but they are wrong, according to Richard Pollack, instructor in immunology and infectious diseases at HSPH. In a paper in the August Pediatric Infectious Disease Journal, he and colleagues report that physicians and others may misdiagnose head lice more often than not, indiscriminately labeling other insects, egg casings from previous louse infestations, and even dandruff with the scarlet L. As a result, many children who go to schools with "no nits" policies miss classes unnecessarily. More worrisome, the study found that those misdiagnosed with lice used prescription delousing medications four times more often than those with bona fide cases. Pollack says the insecticide-containing products, though generally safe, can be hazardous if used incorrectly. Too frequently, doctors and pharmacists may not explain how to apply them. Pollack, with research fellow Anthony Kiszewski, and professor of tropical public health Andrew Spielman, both of HSPH, solicited samples of lice or nits by posting a form on a website. For the study, they analyzed 614 submissions, some from as far away as Japan. Less than two thirds turned out to be louse-related, and of those, only about half included a louse or a viable egg. (Dead or hatched eggs cannot be considered evidence of an active case because the "glue" that keeps eggs stuck to hair can last years after an infestation.) What's more, just one in five respondents who reported a doctor had diagnosed the condition actually had lice, compared with three out of four diagnosed by parents, teachers, and nurses. So why are doctors lousy at recognizing lice? Despite the stigma attached to it, the louse is a lightweight as parasites go and receives little attention in medical school, says Pollack. Also, many doctors seem to diagnose lice over the phone. Anyone unsure about how to identify lice may get help at the HSPHheadlice website, which includes photographs of the parasites. Pollack is on a campaign to quell fears about the relatively innocuous insects. They are more difficult to acquire than most people believe, which calls into question school "no nits" policies. "Hysteria seems far more contagious than are the head lice themselves," he says.
Distinguishing between a viable and a dead egg may seem like nitpicking, but it could make or break a correct diagnosis of head lice. The egg on the right is about one day from hatching; the egg on the left has been dead for more than two weeks. Courtesy of Richard Pollack Sequence of Cholera Genome May Yield More Potent VaccinesOn the heels of the announcement of a working draft of the human genome comes news of the genetic sequencing of one of man's longtime antagonists, cholera. Researchers including John Mekalanos, the Adele Lehman professor of microbiology and molecular genetics and head of the department at HMS, published the findings in the Aug. 3 Nature. Unlike most bacteria, which contain a single circular chromosome, Vibrio cholerae boasts two. The larger is the site of most of the genes responsible for the bacteria's basic cellular functions and pathogenicity. The smaller chromosome, however, is suspiciously similar to a plasmid, which can insinuate itself into other cells and replicate. The genetic resemblance has led the authors to speculate that "the small chromosome may originally have been a megaplasmid that was captured by an ancestral Vibrio species." The small chromosome, found in most Vibrio species, likely enables the bacteria to survive—and thrive—as free living aquatic organisms. Other human pathogens, such as E. coli and H. pylori, which lack a second chromosome, do not live in the water, says Mekalanos. "There's a smoking gun there," he says. The megaplasmid theory also explains the small chromosome's abundance of DNA originating in other organisms. V. cholerae is mystifyingly diverse—the weedy pathogen flourishes in marine and fresh water, in virulent and innocuous forms, sometimes invading zooplankton and other sea life. Researchers hope the sequence information, along with a DNA chip being constructed, will shed light on the causes of this diversity and settle questions about whether environmental conditions trigger epidemics. The sequence data also has revealed new potential virulence factors and motility genes. They could be used to fine-tune cholera vaccines, such as those already created by Mekalanos that employ genetically immobilized bacteria. Researchers used the whole genome random sequencing method pioneered by co-author Craig Venter of Celera Genomics to complete the four-year project. Collaborators also came from The Institute for Genomic Research and the University of Maryland. Test Reveals Vulnerability to Hearing LossWhen it comes to hearing loss, George Orwell was right: some animals are more equal than others. Under the same noise conditions, individuals—both human and animal—show a vast range of vulnerability to acoustic injury. Now, researchers at the Massachusetts Eye and Ear Infirmary have developed a simple test to predict who is at risk for noise-induced hearing loss. The test takes advantage of the ear's feedback system. After cells in the inner ear convert mechanical vibration into electrical energy, the brain sends an electrical message back to the ear via the olivocochlear (OC) efferent pathway. Part of this feedback system is thought to protect against hearing loss by signaling the outer hair cells, which amplify the sound signal, to turn down their "gain." In addition, the system modulates sounds actually produced by these cells, so-called otoacoustic emissions, which are distortions of the original input signal. It is this distorted echo that researchers measured in guinea pigs. Holding up a thumb-sized device—which can produce sound and measure otoacoustic emissions—to the ears of the animals, Charles Liberman, HMS professor of otology and laryngology, and research fellow Stephane Maison measured the decibel levels of the distortion products. From this, they could determine the strength of the sound-evoked OC feedback system that affects the outer hair cells. They later exposed the animals to protracted, moderate sound levels and tested the resulting hearing loss. Guinea pigs with strong reflexes had little hearing loss, and those with weak reflexes suffered greater damage. Liberman is developing a study to test the reflex system in construction workers and is looking for the genes responsible for a mouse strain recently discovered with "ears of steel." The current research appears in the June 15 Journal of Neuroscience. Crystal Structure Shows Finer Points of a SneezeIt's the immunoglobulin that makes you sneeze and wheeze, and it's not quite how Jean-Pierre Kinet, HMS professor of pathology at Beth Israel Deaconess Medical Center, imagined it would look in action. But after a long pursuit, Kinet and a team from Northwestern University headed by Theodore Jardetsky have a clear view of how the immunoglobulin IgE touches off the body's allergic response when its Fc portion binds to its high-affinity receptor. Their solution of the crystal structure of the IgE–Fc bond to its receptor alpha subunit was published in the July 20 Nature. It's an important connection. It sets off a cascade of intracellular signals that are central to allergic response, anaphylaxis, and the immune response to parasites. With asthma and other diseases linked to environmental antigens on the rise, the precise structure of the IgE–Fc bond to its receptor is a matter of considerable interest. Fourteen years after he first cloned the Fc receptor for IgE, Kinet got a good look at the binding. "The structure of the cocrystal was a surprise," says Kinet. "The stoichiometry of binding was known to be 1 IgE:1 receptor. The domain on IgE that binds to the receptor was known to be the Cepsilon3 domain (part of the Fc fragment). Antibodies are symmetrical and thus have two Cepsilon3 domains. Since in principle, both Cepsilon3 domains have a capacity to bind the receptor, it follows that one antibody has the potential to bind two receptors. The fact that it does not had generated a number of hypotheses, the most prevalent being that once one domain binds, there is a conformational change preventing the other from binding another receptor." "In fact, both domains bind asymmetrically to two different sites on one receptor alpha chain. Hence the 1:1 stoichiometry," Kinet says. "That was unexpected." |
