User:Dsaraceni/sandbox

Article Critique

• Most articles referenced were critique articles
• Good explanation of basic bacterial features
• Good explanation of identification methods in a lab
• Missing History section-- want to add this and expand how policies/ guidelines became implemented
• Expand Virulence paragraph to explain how infections occur in the body and in the baby
  • ascending bacteria colonize cervix and infect amniotic sac/fluid
  • can also be added in 'GBS infections in newborns' section
• More detail needed under prevention and screening sections
• Detailed explanation of difference between EOD and LOD

History

Evidence of infection and death in mothers and infants can be dated back to Hippocratic writings and Hindu texts in 1500_BC. Although there are records of puerperal infections, it was not a major source of mortality until the 17th century. Before this time, women primarily gave birth at home, but 17th century Europe marks the development of "lying-in" hospitals. These hospitals provided advancements in medicine and obstetrics, but caused the spread of infection at accelerated rates. Major issues were attributed to contaminated tools, over crowded facilities, and excessive vaginal examinations. Infection incidence continued to increase and in the mid-1800's, puerperal sepsis (or childbed fever) was identified as the major contender in the morbidity and mortality of pregnant and postpartum women. Up to this point, little was known about the pathogenesis of the disease, but Ignác Semmelweiss, a Hungarian obstetrician, began to unravel the mystery through observation. A colleague of Semmelweiss was performing an autopsy on a woman that had died of puerperal sepsis when he himself caught the disease and died. Through this observation, Semmelweiss was able to conclude that this infection had a direct mode of transmission and implemented the practice of hand washing with chlorine before touching patients to reduce incidence of the infectious agent.

In 1935, Group B Streptococcus (Streptococcus agalactiae) was identified as one of the causative bacterial agents in puerperal sepsis. Scientiest Rebecca Lancefield developed a grouping system for hemolytic properties of streptococci allowing the isolation of the infectious pathogen. Initially, group A streptococci (Streptococcus pyogenes) was deemed the leading pathogen in puerperal sepsis, and group B streptococci (Streptococci agalactiae) was considered a commensal bacteria isolated from normal deliveries. It was not until 1938, when Fry reported several fatal cases of sepsis associated with group B streptococci, that it was linked to women and newborns as an infectious agent. The next notable advance in the discovery of group B streptococci as an pathogen came in the 1960's and 70's. At this time, group B streptococci infections were considered the leading cause of death in neonates under 3 months old and was recognized as passed from mother to baby. Of the infants infected, between 50 and 55% resulted in death. Clinical trials for treatments and prevention measures began in the early 1980's ultimately reducing the mortality rate in infants to 10-15%. This is when it was discovered that treating mothers intrapartum with ampicillin or penicillin was the most effective treatment option if a woman was positively colonizing GBS in their vaginal canal, but since there was a major lack in an effective and uniform testing method, this problem was not presented as a major concern in the medical and public health communities. Many clinicians felt that until there was a clear method of collection and identification of the bacteria in women, prevention methods could wait, and so they did. In 1992, the American Academy of Pediatrics implemented recommendations for prophylactic treatment initiating the prevention measures of GBS in pregnant women, but it was not until a consensus was made with the Center for Disease Control and Prevention (CDC) in 1996 that the recommendations would be taken seriously across the United States. These guidelines ensured that women in their last 5 weeks of pregnancy were screened for colonization as well as women that were considered to have risk factors such as high fever or ruptured membranes. After implementation of the guidelines, mortality rate from group B sepsis in infants decreased to 5%. In 2002, the CDC modified the guidelines to only administer intrapartum treatment to women that tested positive for GBS colonization because of the fear of antibiotic resistance. GBS has already shown resistance to erythromycin, the antibiotic originally administered to women that were allergic to penicillin. Today, in the guidelines, penicillin is the treatment of choice for positive GBS cultures because all strains of the bacteria are still most sensitive to this antibiotic. Ampicillin was used and is still considered a second line of treatment, but because there is such a wide range of antimicrobial effect, it is not opt for in fear of selecting a resistant bacterias.