Stay up-to-date on the latest infectious disease news by checking out our top 5 articles of the week.
The closing plenary session of ID Week 2017 looked ahead to the fight against infectious diseases. James Crowe, Jr, MD, Vanderbilt University Medical Center, Nashville, Tennessee, struck an optimistic note. “I believe we are in the midst of a sea change in moving from antibiotics to antibodies to combat infectious diseases,” he said.
Traditional vaccine development is a laborious failure-and-success process that can take decades. The old timetable just won’t work any longer. “Antibody technology is mature enough and affordable enough to now be considered as a first approach,” said Dr. Crowe. The path from the discovery of an antigenic target to antibody availability is measured in months, not decades. Formulations with half-lives of up to 90 days are being developed. The manufacture of antibodies and their safe administration is well established. All these facts argue for antibody-based strategies as the go-to tool in infectious diseases.
To read more about the closing plenary, just click here.
A treatment algorithm for staphylococcal bloodstream infections (BSIs) featuring markedly shorter antibiotic therapy than the conventional standard of care produces similar rates of success and serious adverse events. For complicated infections, the algorithm approach is better than standard care. The good news from the randomized, multinational, open-label, adjudicator-blinded trial was presented at the ID Week 2017 meeting in San Diego, California.
“The optimal duration of treatment for staphylococcal bacteremia is unknown. Long-course or short-course treatment may place the patient at risk. If treatment is too prolonged, there is a greater risk of the development of antibacterial resistance and antibiotic-associated adverse events. On the other hand, if the treatment duration is too short, there can be a greater chance of relapse due to inadequately treated infection,” said Thomas L. Holland, MD, Duke University Medical Center, Durham, North Carolina, on behalf of the Bacteremia Study Group.
With this in mind, the researchers sought to provide clarity concerning treatment time. “Our study rationale was that a strategy to identify patients with staphylococcal BSI who can safely be treated with shorter courses of therapy would improve care,” explained Dr. Holland.
Read more about staphylococcal bloodstream infections here.
Clinical trials are a linchpin of clinical science. They are designed to evaluate the prowess of an antibacterial, antifungal, and antiviral compounds. The busy clinical trial terrain results in a barrage of data. Sifting through all this information to discover studies that describe drugs that are practice-changing can be challenging for a busy clinician.
A session at the year’s ID Week in San Diego, California came to the rescue. The speakers were tasked with summarizing recent important clinical trials involving viruses, bacteria, and fungi. Francisco Marty, MD, Division of Infectious Diseases, Brigham and Women's Hospital, Boston, Massachusetts, reviewed recent antiviral trials, excepting those involving HIV. His focus was the herpes zoster subunit vaccine, intravenous (IV) influenza drugs, and letermovir for prevention of post-transplant cytomegalovirus (CMV) infection.
Read more about anti-infective trials presented at ID Week here.
A survey of Americans hospitalized for treatment of candidemia has revealed the presence of Clostridium difficile (C. difficile) co-infection in almost 10% of the cases.
Infections caused by C. difficile and Candida species are important healthcare-associated infections. A multistate survey carried out in 2014 by the US Centers for Disease Control and Prevention (CDC) reported C. difficile and Candida in 61 of 504 (12.1%) and 32 of 504 (6.3%) infections, with C. difficile responsible for 70% of all recorded gastrointestinal infections and Candida responsible for 22% of all bloodstream infections. Both infections carry a high mortality rate.
Read more about Candida-C. difficile co-infection here.
Although international health organizations often focus on the nearly 37 million people worldwide who live with HIV, another sexually transmitted disease—herpes simplex 2 (HSV-2), the main cause of genital herpes, is a far more common condition. According to the World Health Organization, as of 2012, there were 417 million people globally between the ages of 15 and 49 with HSV-2, many of them, like most with HIV, reside in sub-Saharan Africa. And while HSV-2 on its own is not fatal, having the condition makes an individual more likely to contract HIV, just as having HIV raises a person’s risk of HSV-2.
This symbiosis and what it means for a vulnerable population was behind a British team’s effort to document the risk of HIV acquisition in people infected with HSV-2. Scientists at the University of Bristol and Imperial College London delved into multiple studies conducted up to 2017, mostly in Africa, that examined the connection between these 2 chronic infections. They found that individuals with HSV-2 had a decidedly higher risk of acquiring HIV than those without HSV-2. This risk was nearly tripled among the general population and doubled for people in high-risk categories, such as women engaged in sex work, men who frequent sex workers, and men who have sex with men. And when the data was analyzed to separate out individuals who had acquired HSV-2 after the study began versus those who had been infected with it earlier, the team found that the risk of contracting HIV was 5 times greater in the general population.
“The greater cofactor effect for incident HSV-2 infection than for prevalent HSV-2 infection might be because newly acquired HSV-2 infection is associated with an increased frequency and severity of genital ulceration, viral shedding, and inflammation in the genital tract, symptoms and manifestations that decrease with time after infection,” the authors wrote in the discussion section of their report. An HSV-2 infection that is active and symptomatic generates CD4-positive T cells. HIV targets these cells, and genital ulceration and viral shedding can enable HIV to break through the mucosal barrier in the genital area. Once infected with HIV, an individual with HSV-2 is likely to experience increased viral shedding that makes his or her infection more transmissible to others.
Read more about HSV-2 and HIV here.