User:Dsaraceni/sandbox
Article Critique
[edit]- 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
[edit]Evidence of infection and death in mothers and infants can be dated back to Hippocratic writings and Hindu texts in 1500BC.[1] Although there are records of puerperal infections, it was not a major source of mortality until the 17th century.[1] Before this time, women primarily gave birth at home, but 17th century Europe marks the development of "lying-in" hospitals.[1] These hospitals provided advancements in medicine and obstetrics, but caused the spread of infection at accelerated rates.[1] Major issues were attributed to contaminated tools, over crowded facilities, and excessive vaginal examinations.[1] 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.[2] 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.[2] 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.[2]
In 1935, Group B Streptococcus (Streptococcus agalactiae) was identified as one of the causative bacterial agents in puerperal sepsis.[2] Scientiest Rebecca Lancefield developed a grouping system for hemolytic properties of streptococci allowing the isolation of the infectious pathogen.[3][2] 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.[3] 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.[3] 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.[2] Of the infants infected, between 50 and 55% resulted in death.[4][3] Clinical trials for treatments and prevention measures began in the early 1980's ultimately reducing the mortality rate in infants to 10-15%.[4][3] 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.[4][3] 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.[3] 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.[4][3][2] 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.[2][4] After implementation of the guidelines, mortality rate from group B sepsis in infants decreased to 5%. [4] 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.[2] GBS has already shown resistance to erythromycin, the antibiotic originally administered to women that were allergic to penicillin.[2] 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.[2] 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.[4]
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- ^ a b c d e De Costa, Caroline (2002). "The contagiousness of childbed fever: a short history of puerperal sepsis and its treatment" (PDF). Medical Journal of Australia. 177 (11): 668–671. doi:10.5694/j.1326-5377.2002.tb05004.x. PMID 12463995. S2CID 12164328.
- ^ a b c d e f g h i j k Koenig, Joyce M.; Keenan, William J. (2009). "Group B Streptococcus and Early-Onset Sepsis in the Era of Maternal Prophylaxis". Pediatric Clinics of North America. 56 (3): 689–708. doi:10.1016/j.pcl.2009.04.003. PMC 2702484. PMID 19501699.
- ^ a b c d e f g h Schuchat, Anne (2001). "Group B Streptococcal Disease: From Trials and Tribulations to Triumph and Trepidation" (PDF). Clinical Infectious Diseases. 33 (6): 751–6. doi:10.1086/322697. PMID 11512078.
- ^ a b c d e f g Dermer, Peggy; Lee, Connie; Eggert, Julie; Few, Brian (2004). "A history of neonatal group B streptococcus with its related morbidity and mortality rates in the United States". Journal of Pediatric Nursing. 19 (5): 357–363. doi:10.1016/j.pedn.2004.05.012. PMID 15614260.