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Logsdon, Beth A., and Daniel T. Casto. "Prevention of Group B Streptococcus Infection in Neonates." Annals of Pharmacotherapy 31, no. 7-8 (July 1997): 897–906. http://dx.doi.org/10.1177/106002809703100718.
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OBJECTIVE: To review the epidemiology of group B Streptococcus (GBS) infection, risk factors for infection, and clinical manifestations of disease in the neonate, as well as the role of chemoprophylaxis and immunoprophylaxis in prevention of GBS disease and current recommendations for prevention. DATA SOURCES AND STUDY SELECTION: MEDLINE searches (1976–1997) of the English-language literature. DATA SYNTHESIS: Despite clinical advances in health care in the past two decades, GBS remains a leading cause of serious neonatal infection. Most early-onset GBS infections can be prevented through the use of intrapartum antimicrobial chemoprophylaxis. Preventing GBS infection in neonates is more cost-effective than treating GBS infections, and implementing prevention programs can reduce morbidity and mortality resulting from GBS disease. Many proposals have been made regarding prevention strategies; however, they have not been implemented widely and consistently in the US. To coordinate both pediatric and obstetric supported strategies, the Centers for Disease Control and Prevention (CDC) recently published recommendations for prevention of neonatal GBS disease through two possible strategies. In the first strategy, intrapartum antibiotic chemoprophylaxis should be offered to all women identified by prenatal culture as colonized and those who develop premature membrane rupture or onset of labor at less than 37 weeks gestation. The second strategy involves administration of intrapartum antibiotics to all women who develop one or more risk factors at the time of membrane rupture or onset of labor. CONCLUSIONS: GBS is difficult to eradicate, causing many women to be colonized with the organism during pregnancy and labor, thereby infecting their infant. Prevention strategies have been published for more than 10 years without successful implementation. Although optimal prevention management has not been defined, following one of two strategies recommended by the CDC can prevent the majority of GBS infections in neonates.
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Zappernick, Taissa, Brigid Wilson, Richard Banks, Daniel Baechle, Sunah Song, Janet Briggs, Robin L. Jump, and Federico Perez. "220. Characteristics and Outcomes of Veterans with Invasive Group B Streptococcal Infection Vary with the Type of Syndrome." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S128—S129. http://dx.doi.org/10.1093/ofid/ofz360.295.
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Abstract Background Surveillance from the US Center for Disease Control and Prevention (CDC) has detected an increase in the prevalence of invasive Group B streptococcus (GBS) infections between 2008 and 2016 among non-pregnant adults. Here, we use data from the US Veterans Health Administration (VHA) to assess the underlying clinical characteristics and outcomes associated with specific types of invasive GBS infection among veterans. Methods We used the VA Corporate Data Warehouse to identify patients with invasive GBS infection diagnosed between 2008–2017 using CDC’s surveillance definitions. Data on the microbiological source of infection (e.g., GBS in cultures from blood, bone or sterile fluids) and associated International Classification of Disease (ICD) codes were used to classify the type of invasive infection. We determined associated co-morbid conditions and 30-day all-cause mortality for incident cases. Results Between 2008 and 2017, there were 4780 incident cases of invasive GBS infection in veterans with a mean age of 66.6 years (±11.7) and30-day all-cause mortality of 8%. The most common syndrome was osteomyelitis (23%, N = 1078) with 30-day mortality of 1%. Other common infections, such as bacteremia (20%; N = 972), skin and soft-tissue infections (18%, 853), and pneumonia (14%, N = 664), had higher mortality (13%, 4% and 17%, respectively; Figure). In patients with GBS peritonitis, present in 3% (N = 138) incidence cases, 46% had chronic liver disease with a 30-day mortality of 28%. Diabetes mellitus (DM) occurred in 66% of patients with any invasive GBS infection and in 86% of patients with GBS osteomyelitis. Chronic heart, kidney, or lung disease affected >25% of patients (table). Conclusion Invasive GBS infection is a burden for veterans with DM and other high-risk conditions, with some types of infections associated with substantial mortality. Osteomyelitis, the most common type of infection, was associated with lower mortality compared with other invasive GBS infections. DM and chronic lung, kidney and heart disease are common among veterans with invasive GBS infection. Disclosures All authors: No reported disclosures.
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Briggs, Janet, Brigid Wilson, Taissa Zappernick, Richard Banks, Daniel Baechle2; Sunah Song, Robin L. Jump, and Federico Perez. "206. Variations in the frequency and impact of polymicrobial cultures in adults with invasive Group B Streptococcal (GBS) infection at the US Veterans Health Administration." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S122. http://dx.doi.org/10.1093/ofid/ofz360.281.
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Abstract Background GBS, a colonizer of human skin, genitourinary and gastrointestinal tracts, is responsible for increasing rates of invasive infection among non-pregnant adults in the United States. GBS is often isolated with other bacteria; however, the clinical significance of polymicrobial cultures in patients with invasive GBS infection is unknown. Our aim was to characterize polymicrobial cultures in patients with invasive GBS infection and explore their impact on mortality at 30 days. Methods Within the VHA Corporate Data Warehouse, we identified veterans active in VHA between 2008–2017 with invasive GBS infection according to CDC’s surveillance definitions. Reports of cultures from blood, bone and sterile fluid with GBS were assessed for the presence of other bacteria.We used International Classification of Disease (ICD) codes to define the type of invasive GBS infection. We compared 30-day all-cause mortality between patients with cultures that identified only GBS (monomicrobial cases) and patients with cultures that identified GBS and other bacteria (polymicrobial cases). Results Of 4780 incident cases of invasive GBS infection identified between 2008–2017, 1204 (25%) were polymicrobial. The proportion of polymicrobial cases varied by type of invasive GBS infection, ranging from 58% in osteomyelitis to 10–15%in meningitis, endocarditis, skin and soft-tissue infections, and septic arthritis (table). Staphylococcus aureuswas found in 516 (43%) of polymicrobial cases;there were variations in the bacteria isolated by type of infection (figure). Overall, there was no difference in 30-day mortality between polymicrobial and monomicrobial cases of invasive GBS infection (both 8%). However, when compared with monomicrobial cases, 30-day mortality was doubled in polymicrobial cases of pneumonia and bacteremia (15% vs. 31% and 11% vs. 22%, respectively). Conclusion The frequency, composition and mortality of polymicrobial cases vary according to the type of invasive GBS infection. Polymicrobial infection could be an important determinant of outcome in certain invasive GBS infections. The effect of polymicrobial infection involving GBS, relative to age, severity of illness and underlying comorbidities, needs further exploration. Disclosures All authors: No reported disclosures.
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Halpin, A. Laufer, W. Gu, M. E. Wise, J. J. Sejvar, R. M. Hoekstra, and B. E. Mahon. "Post-Campylobacter Guillain Barré Syndrome in the USA: secondary analysis of surveillance data collected during the 2009–2010 novel Influenza A (H1N1) vaccination campaign." Epidemiology and Infection 146, no. 13 (July 10, 2018): 1740–45. http://dx.doi.org/10.1017/s0950268818001802.
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AbstractGuillain Barré syndrome (GBS), which is triggered by autoantibodies produced in response to antigenic stimuli such as certain infections and vaccinations, is the most common cause of acute flaccid paralysis worldwide. Campylobacter, the most common bacterial enteric infection in the USA, is reported to be the most commonly diagnosed antecedent of GBS, yet little information is available about the risk of post-Campylobacter GBS. Data collected through active, population-based surveillance in the Emerging Infections Program during the 2009–2010 novel Influenza A (H1N1) vaccination campaign allowed us to compare confirmed and probable GBS cases to non-cases to determine whether antecedent Campylobacter infection (or a diarrhoeal illness consistent with campylobacteriosis) was more common among cases and to assess the risk of GBS following Campylobacter infection. We estimate that 8–12% of GBS cases in the USA are attributable to Campylobacter infection (or a diarrhoeal illness consistent with campylobacteriosis), with 434–650 cases of post-diarrhoeal GBS annually and about 49 cases of GBS per 100 000 Campylobacter infections. These results provide updated estimates for post-Campylobacter GBS incidence in the USA and highlight an important benefit of effective measures to prevent Campylobacter infections.
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Gendrin, Claire, Jay Vornhagen, Lisa Ngo, Christopher Whidbey, Erica Boldenow, Veronica Santana-Ufret, Morgan Clauson, et al. "Mast cell degranulation by a hemolytic lipid toxin decreases GBS colonization and infection." Science Advances 1, no. 6 (July 2015): e1400225. http://dx.doi.org/10.1126/sciadv.1400225.
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Ascending infection of microbes from the lower genital tract into the amniotic cavity increases the risk of preterm birth, stillbirth, and newborn infections. Host defenses that are critical for preventing ascending microbial infection are not completely understood. Group BStreptococcus(GBS) are Gram-positive bacteria that frequently colonize the lower genital tract of healthy women but cause severe infections during pregnancy, leading to preterm birth, stillbirth, or early-onset newborn infections. We recently described that the GBS pigment is hemolytic, and increased pigment expression promotes GBS penetration of human placenta. Here, we show that the GBS hemolytic pigment/lipid toxin and hyperpigmented GBS strains induce mast cell degranulation, leading to the release of preformed and proinflammatory mediators. Mast cell–deficient mice exhibit enhanced bacterial burden, decreased neutrophil mobilization, and decreased immune responses during systemic GBS infection. In a vaginal colonization model, hyperpigmented GBS strains showed increased persistence in mast cell–deficient mice compared to mast cell–proficient mice. Consistent with these observations, fewer rectovaginal GBS isolates from women in their third trimester of pregnancy were hyperpigmented/hyperhemolytic. Our work represents the first example of a bacterial hemolytic lipid that induces mast cell degranulation and emphasizes the role of mast cells in limiting genital colonization by hyperpigmented GBS.
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Wu, Dongning, Kenneth Bromberg, and Roberto Jodorkovsky. "Invasive Group B Streptococcal Disease in Two Pediatric Patients with Systemic Lupus Erythematosus." Case Reports in Pediatrics 2013 (2013): 1–3. http://dx.doi.org/10.1155/2013/896014.
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Systemic lupus erythematosus (SLE) is an autoimmune disease associated with high morbidity and mortality, often caused by infection. We report two patients with SLE who were treated with steroids and immunosuppressive medication and then developed invasive Group BStreptococcus(GBS) infections. While GBS infection is rare in the nonneonatal pediatric age group, GBS should be considered when treating SLE patients presenting with signs of infection.
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Mawla, Nurun Nahar, Shahin Sultana, and Nayareen Akhter. "Guillain-Barré Syndrome and Campylobacter jejuni Infection: A Review." Delta Medical College Journal 2, no. 1 (January 29, 2014): 28–35. http://dx.doi.org/10.3329/dmcj.v2i1.17794.
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Guillain-Barré syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illness precedes 50%-75% of the GBS cases. Although many infectious agents have been associated with GBS, the strongest documented association is with Campylobacter infection. The first line of evidence supporting Campylobacter infection as a trigger of GBS is anecdotal reports. The second line of evidence is serological surveys, which have demonstrated that sera from GBS patients contain anti Campylobacter jejuni antibodies, consistent with recent infection. Finally, culture studies have proven that a high proportion of GBS patients have C. jejuni in their stools at the time of onset of neurological symptoms. One of every 1058 Campylobacter infections results in GBS. Sialic acid containing lipooligosaccharides (LOS) biosynthesis gene locus are associated with GBS and the expression of ganglioside mimicking structures. GM1a was the most prevalent ganglioside mimic in GBS associated strains. Molecular mimicry between C. jejuni LOS and gangliosides in human peripheral nerves, and cross-reactive serum antibody precipitate the majority of GBS cases in Bangladesh, like worldwide. DOI: http://dx.doi.org/10.3329/dmcj.v2i1.17794 Delta Med Col J. Jan 2014; 2(1): 28-35
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&NA;. "Preventing neonatal GBS infection." Inpharma Weekly &NA;, no. 1143 (June 1998): 3. http://dx.doi.org/10.2165/00128413-199811430-00004.
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Singh, Mary. "Group B streptococcus-an update." Morecambe Bay Medical Journal 4, no. 12 (September 1, 2005): 356–57. http://dx.doi.org/10.48037/mbmj.v4i12.916.
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Group B streptococcus (GBS) infection has long been recognised as an important cause of neonatal morbidity. It is now known to be the most common serious neonatal infection in the developed world. In the United Kingdom (UK), it is estimated that 1 in 1000 babies develops a GBS infection. A recent London study, however, estimated the incidence of culture-proven plus suspected cases of GBS infection to be significantly higher (approximately 3.6 per 1000 babies born). Despite this, there is no standard of practice in the UK for stopping GBS infections in newborn babies. Mary Singh, specialist registrar at the Royal Lancaster Infirmary, explains.
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Dourado Junior, Mario Emilio Teixeira, Bruno Fernandes de Sousa, Nathaly M. Coelho da Costa, and Selma Maria Bezerra Jeronimo. "Cytomegalovirus infection in Guillain-Barré syndrome: a retrospective study in Brazil." Arquivos de Neuro-Psiquiatria 79, no. 7 (July 2021): 607–11. http://dx.doi.org/10.1590/0004-282x-anp-2020-0464.
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ABSTRACT Background: Guillain-Barré syndrome (GBS) is currently the most common cause of acute flaccid paralysis worldwide. Risk factors for GBS include previous viral or bacterial infections or vaccination. Recently, an outbreak of Zika virus led to an outbreak of GBS in Latin America, mostly in Brazil, concomitant to continuous circulation of dengue virus serotypes. However, there is no study about cytomegalovirus (CMV) infection as a risk for GBS in Brazil. Objectives: In this study, we report a series of cases of GBS with the aim of determining the prevalence of CMV and the characteristics associated with the infection. Methods: A cohort of 111 GBS cases diagnosed between 2011 and 2017 in Natal, northeastern Brazil, was studied. Presence of CMV IgM antibodies was determined by means of electrochemiluminescence. The analysis was performed considering CMV infection status and the clinical outcome. Results: We found seroprevalence of 15.3% (n = 17) for CMV. CMV patients were younger (26 vs. 40; p = 0.016), with no apparent gastrointestinal (p = 0.762) or upper respiratory infections (p = 0.779) or sensory loss (p = 0.03). They presented more often with a classic GBS sensorimotor variant (p = 0.02) and with a demyelinating pattern in electrophysiological studies (p < 0.001). Conclusion: In Brazil, the clinical-epidemiological profile of GBS associated with CMV infection is similar to that described in other countries. Better understanding of the relationship between infectious processes and GBS is a key component of the research agenda and assistance strategy for global health initiatives relating to peripheral neuropathic conditions.
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Hon, Kam L., Tai C. Chow, Tsun S. Cheung, Wai T. Lam, Lok T. Hung, King W. So, I. P. Margaret, and Su Y. Qian. "Severe Group A and Group B Streptococcus Diseases at a Pediatric ICU: Are they Still Sensitive to the Penicillins?" Current Clinical Pharmacology 15, no. 2 (October 14, 2020): 125–31. http://dx.doi.org/10.2174/1574884714666190926124714.
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Background: Group A β-hemolytic streptococcus (GAS) and Group B streptococcus (GBS) are two common pathogens that are associated with many diseases in children. Severe infections as a result of these two streptococci are albeit uncommon but associated with high mortality and morbidity, and often necessitate intensive care support. This paper aims to review mortality and morbidity severe infection associated with GAS and GBS isolations at a Pediatric Intensive Care Unit (PICU). Methods: All children admitted to PICU of a teaching hospital between October 2002 and May 2018 with laboratory-proven GAS and GBS isolations were included. Results: There were 19 patients (0.7% PICU admissions) with streptococcal isolations (GAS, n=11 and GBS, n=8). Comparing to GAS, GBS affected infants were younger (median age 0.13 versus 5.47 years, 95% CI, 1.7-8.5, p=0.0003), and cerebrospinal fluids more likely positive (p = 0.0181). All GAS and GBS were sensitive to penicillin (CLSI: MICs 0.06 – 2.0 μg/mL), with majority of GAS sensitive to clindamycin and erythromycin, and half of the GBS resistant to clindamycin and erythromycin. Co-infections were prevalent, but viruses were only isolated with GAS (p=0.024). Isolation of GAS and GBS was associated with nearly 40% mortality and high rates of mechanical ventilation and inotropic supports. All non-survivors had high mortality (PIM2) and sepsis scores. Conclusions: Severe GAS and GBS are rare but associated with high mortality and rates of mechanical ventilation and inotropic supports in PICU. The streptococci are invariably sensitive to penicillin. The high PIM2 and Sepsis scores suggest that prompt recognition of sepsis and timely judicious institution of antibiotics and intensive care support may be life-saving for these devastating infections.
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Dev, Nishant, Rahul Kumar, and Dilip Kumar. "Guillain–Barre syndrome: a rare complication of leptospirosis and scrub typhus co-infection." Tropical Doctor 49, no. 3 (March 21, 2019): 248–49. http://dx.doi.org/10.1177/0049475519836038.
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Guillain–Barré syndrome (GBS) is a potentially life-threatening immune-mediated acute inflammatory polyneuropathy associated with several antecedent infections. We report a 20-year-old man with GBS associated with concurrent leptospirosis and scrub typhus infection. GBS was confirmed with clinical examination and nerve conduction studies. There have been case reports of GBS in association with Leptospira and Orienta tsusugamushi separately. However, this may be the first case report of GBS associated with concurrent diseases.
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Mada, Pradeep Kumar, Gabriel Castano, and Andrew Stevenson Joel Chandranesan. "Invasive Group B Streptococcal Infection with Toxic Shock-Like Syndrome in a Postsplenectomy Patient." Case Reports in Infectious Diseases 2020 (February 13, 2020): 1–3. http://dx.doi.org/10.1155/2020/4048610.
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The incidence of invasive group B streptococcal disease (GBS) in nonpregnant population is increasing. As per the Centers for Disease Control and Prevention (CDC), there are 10 cases in every 100,000 nonpregnant adults each year, and 1 in 20 nonpregnant adults with serious GBS infections die. GBS infection is almost always associated with underlying risk factors such as diabetes mellitus or malignancy. We present a 47-year-old female with a remote history of splenectomy presented with toxic shock-like syndrome secondary to invasive GBS infection.
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SAKOVETS, T. G., E. I. BOGDANOV, G. R. KHUZINA, and R. Z. MUKHAMETZYANOV. "Особенности синдрома Гийена - Барре, ассоциированного с инфекцией COVID-19." Practical medicine 19, no. 4 (2021): 45–49. http://dx.doi.org/10.32000/2072-1757-2021-4-45-49.
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In December 2019, an epidemic of coronavirus infection SARS-CoV-2 (Severe acute respiratory syndrome-related coronavirus 2) emerged in Wuhan (China). In February 2020, the World Health Organization assigned the official name to the infection caused by the new coronavirus SARS-CoV-2 — Coronavirus disease 2019 or COVID-19, which was accompanied by various neurological complications, including Guillain — Barre syndrome. The purpose — to study the features of Guillain — Barre syndrome (GBS) with a new COVID-19 infection. Results. Recently, various neurological complications of COVID-19 have been described: severe viral hemorrhagic encephalitis, toxic encephalopathy, acute demyelinating lesions, acute cerebral disorders blood circulation, etc. It is proposed to consider Guillain — Barre syndrome (GBS) a neurological complication of CO VID-19, since the main route of coronavirus infection is respiratory, and most patients with GBS describe a respiratory infection before the development of neurological symptoms. Typically, GBS develops 11-13 days after the onset of COVID-19. Recent studies have shown that GBS is one of the most common lesions of the peripheral nervous system in COVID-19. The clinical picture, as a rule, is represented by increasing flaccid tetraparesis, less often there is respiratory failure. In a pandemic, it is advisable to test patients with GBS for COVID-19 if there are no respiratory disorders, since laboratory signs of SARS-CoV-2 infection were detected in a number of patients with acute neuropathy. Given the higher demand for respiratory support in GBS patients infected with CoV-2, it is assumed that COVID-19 may trigger the progression of neurological symptoms. Diagnosing GBS in SARS-CoV-2 patients is particularly challenging because symptoms such as shortness of breath and fatigue can be misinterpreted as a consequence of SARS-CoV-2 lung damage, delaying the timely diagnosis of GBS. Conclusion. Successful GBS management depends on clinical vigilance and its early diagnosis in patients with COVID-19.
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Lund, Sean J., Kathryn A. Patras, Jacqueline M. Kimmey, Asami Yamamura, Gilberto Hernandez, Omar Lakhdari, Alyssa M. McCoy, Victor Nizet, and Lawrence S. Prince. "Polysaccharide capsule allows Group B Streptococcus to avoid killing in a newborn pneumonia model." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 117.30. http://dx.doi.org/10.4049/jimmunol.200.supp.117.30.
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Abstract Group B Streptococcus (Streptococcus agalactiae, GBS) causes severe infections in neonates. While not a common adult pathogen, GBS is the leading cause of congenital pneumonia. To determine the molecular mechanisms of neonatal susceptibility, we developed a murine GBS pneumonia model. Neonatal, juvenile, and adult C57BL/6 mice were inoculated intranasally with 2800 CFU/g of GBS (COH1). After 7 d, survival was 100 % in adults and juveniles, with 10 % of neonates dying within 3 d after infection. Histopathological assessments showed severe lung injury scores 24 h after infection, with adult and juvenile mice demonstrating resolution of injury at 3 d post infection and normal histology after 7 d. In contrast, neonatal lungs had persistent lung injury up to 7 d post infection. By FACS, GBS induced rapid neutrophil recruitment into adult lungs and increased CD11b expression on adult lung macrophages. In neonatal lungs, GBS neither increased neutrophil numbers nor altered macrophage marker expression. Confocal imaging showed GBS in adult lungs almost entirely localized to alveolar macrophage phagolysosomes. However in neonatal lungs, GBS was only rarely phagocytosed by macrophages. These data were consistent with GBS killing data, which showed complete GBS killing within 24 h in adult and juvenile mice, but persistent GBS viability within the lung for up to 3 d in neonates. Defective GBS killing in neonates appeared to require the GBS capsule. Neonatal mice were much more efficient in killing the ΔcpsD capsule mutant compared to wild type GBS. Adult mice showed equal killing of ΔcpsD or wild type GBS. Our data suggest that the GBS capsule prevents killing by the newborn lung innate immune system, leading to neonatal disease susceptibility.
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H. Wahid, Hanan, Puteri F. D. Mustapha Rounal, Ayesha Bahez, Mohammed I. A. Mustafa Mahmud, Norhidayah Kamarudin, Arvind R. Selvakumaran, Ahmad M. Ahmad Mustafa, and Hamizah Ismail. "A REVIEW OF GROUP B STREPTOCOCCUS (GBS) VAGINAL COLONIZATION AND ASCENDING INTRAUTERINE INFECTION: INTERACTION BETWEEN HOST IMMUNE RESPONSES AND GBS VIRULENCE FACTORS." Acta Scientifica Malaysia 6, no. 1 (2022): 17–22. http://dx.doi.org/10.26480/asm.01.2022.17.22.
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Vaginal colonization with Group B streptococcus (GBS) or Streptococcus agalactiae can potentially cause ascending intrauterine infection among pregnant women, and hence it is known as one of the risk factors for preterm delivery. Ascending intrauterine infection may also cause the transmission of GBS to the fetus in utero and the newborn during delivery, leading to the development of early onset of neonatal infection. GBS are β-hemolytic, gram-positive bacteria that are opportunistic commensal of the gastrointestinal and urogenital tract of approximately 18% of pregnant women globally. Intrapartum antibiotic prophylaxis (IAP) only reduces the rate of early onset neonatal infection, but not the late onset neonatal infection. Thus, the development of GBS vaccine is thought to be important to decrease the rate of preterm delivery and neonatal infections particularly in low-and-middle income countries where IAP program is not feasible. Vaccination can also be cost-effective for the healthcare system when executed together with IAP program. The aim of the current review is to summarize the mechanisms on how the GBS virulence factors interact with host immune components in the gestational tissues, leading to cervicovaginal colonization and ascending intrauterine infection. The elucidation of these mechanisms is essential for expediting the development of vaccines and novel therapeutic measures targeting these GBS virulence factors that will hamper the vaginal colonization, ascending intrauterine infection and conceptus tissue invasion by GBS. These strategies are crucial to potentially reduce the rate of preterm delivery and subsequent serious complications in the newborn.
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Kline, Kimberly A., Drew J. Schwartz, Warren G. Lewis, Scott J. Hultgren, and Amanda L. Lewis. "Immune Activation and Suppression by Group B Streptococcus in a Murine Model of Urinary Tract Infection." Infection and Immunity 79, no. 9 (June 20, 2011): 3588–95. http://dx.doi.org/10.1128/iai.00122-11.
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ABSTRACTGroup B streptococcus (GBS) is a common commensal of the gastrointestinal and vaginal mucosa and a leading cause of serious infections in newborns, the elderly, and immunocompromised populations. GBS also causes infections of the urinary tract. However, little is known about host responses to GBS urinary tract infection (UTI) or GBS virulence factors that participate in UTI. Here we describe a novel murine model of GBS UTI that may explain some features of GBS urinary tract association in the human host. We observed high titers and heightened histological signs of inflammation and leukocyte recruitment in the GBS-infected kidney. However, extensive inflammation and leukocyte recruitment were not observed in the bladder, suggesting that GBS may suppress bladder inflammation during cystitis. Acute GBS infection induced the localized expression of proinflammatory cytokines interleukin-1α (IL-1α), macrophage inflammatory protein-1α (MIP-1α), MIP-1β, and IL-9, as well as IL-10, more commonly considered an anti-inflammatory cytokine. Using isogenic GBS strains with different capsule structures, we show that capsular sialic acid residues contribute to GBS urinary tract pathogenesis, while high levels of sialic acid O-acetylation attenuate GBS pathogenesis in the setting of UTI, particularly in direct competition experiments.In vitrostudies demonstrated that GBS sialic acids participate in the suppression of murine polymorphonuclear leukocyte (PMN) bactericidal activities, in addition to reducing levels of IL-1α, tumor necrosis factor alpha, IL-1β, MIP-1α, and KC produced by PMNs. These studies define several basic molecular and cellular events characterizing GBS UTI in an animal model, showing that GBS participates simultaneously in the activation and suppression of host immune responses in the urinary tract.
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Whidbey, Christopher, Maria Isabel Harrell, Kellie Burnside, Lisa Ngo, Alexis K. Becraft, Lakshminarayan M. Iyer, L. Aravind, Jane Hitti, Kristina M. Adams Waldorf, and Lakshmi Rajagopal. "A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta." Journal of Experimental Medicine 210, no. 6 (May 27, 2013): 1265–81. http://dx.doi.org/10.1084/jem.20122753.
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Microbial infection of the amniotic fluid is a significant cause of fetal injury, preterm birth, and newborn infections. Group B Streptococcus (GBS) is an important human bacterial pathogen associated with preterm birth, fetal injury, and neonatal mortality. Although GBS has been isolated from amniotic fluid of women in preterm labor, mechanisms of in utero infection remain unknown. Previous studies indicated that GBS are unable to invade human amniotic epithelial cells (hAECs), which represent the last barrier to the amniotic cavity and fetus. We show that GBS invades hAECs and strains lacking the hemolysin repressor CovR/S accelerate amniotic barrier failure and penetrate chorioamniotic membranes in a hemolysin-dependent manner. Clinical GBS isolates obtained from women in preterm labor are hyperhemolytic and some are associated with covR/S mutations. We demonstrate for the first time that hemolytic and cytolytic activity of GBS is due to the ornithine rhamnolipid pigment and not due to a pore-forming protein toxin. Our studies emphasize the importance of the hemolytic GBS pigment in ascending infection and fetal injury.
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Daner, William E., Brett D. Meeks, William C. Foster, and Norman D. Boardman. "Group B Streptococcal Septic Arthritis of the Shoulder and Potential Association with Pelvic Examination and PAP Smear." Case Reports in Orthopedics 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/5294517.
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Group B streptococcal (GBS) infection of a native joint in a nonpregnant adult is uncommon. While many women are colonized with this flora, it rarely becomes pathogenic in its adult host. GBS associated joint infections have been reported, most of which have been related to hematogenous seeding from unknown sources. To our knowledge, there are no published case reports of a GBS joint infection in association with a pelvic exam and Papanicolaou (PAP) smear. In this case report, we present a case of GBS sepsis of a native shoulder, possibly resulting from a routine pelvic exam and PAP smear.
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Rowen, D. "Streptococci and the Genital Tract." International Journal of STD & AIDS 4, no. 2 (March 1993): 63–66. http://dx.doi.org/10.1177/095646249300400201.
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Streptococci of Lancefield Group B (GBS) are known to cause maternal sepsis and neonatal infection, whereas streptococci Lancefield Group A (GAS) cause vulvo-vaginitis in both children and adults. Prevalence of SGB colonization of the lower genital tract of normal women is between 4–18%, with higher rates found in hospital personnel and delivery rooms. Such high carriage rates may be a significant factor in nosocomial transmission of GBS to neonates. Symptomatic infection is uncommon and usually secondary to other pathological states. Amnionitis is a complication of vaginal carriage of GBS and there is now evidence that chorioamnionitis is associated with pre-term labour and its attendant problems. GBS infection of the male genitalia has also been described. Intrapartum chemoprophylaxis has been shown to prevent early onset GBS disease of the neonate. Prevalence of GAS in the genital tract is lower than that for GBS, but is more likely to be symptomatic. The response to penicillin is usually prompt. Optimal drug regimens need to be determined, particularly for use in pregnancy.
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SMITH, E. M., M. A. KHAN, A. REINGOLD, and J. P. WATT. "Group B streptococcus infections of soft tissue and bone in California adults, 1995–2012." Epidemiology and Infection 143, no. 15 (April 1, 2015): 3343–50. http://dx.doi.org/10.1017/s0950268815000606.
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SUMMARYGroup B streptococcus (GBS) is an increasing cause of disease in adults. We present long-term trends in incidence of overall infections and identify characteristics of patients with GBS cellulitis, bone and joint infections. Active, population-based surveillance was conducted from 1995–2012 in three California counties and the data were analysed retrospectively. All cases had isolation of GBS from a normally sterile site. Cases of cellulitis were classified based on clinical diagnosis. GBS bone or joint infection was defined as isolation of GBS from a bone or joint or a diagnosis of osteomyelitis or septic arthritis. Medical charts were reviewed for demographic and clinical information. There were 3917 cases of GBS; the incidence of disease increased from 5·8 to 8·3 cases/100 000 persons (P < 0·001) from 1995 to 2012. In adults aged ⩾40 years, the overall incidence of GBS increased from 8·5 to 14·2 cases/100 000 (P < 0·001) persons during the study period. The incidence of cellulitis increased from 1·6 to 3·8 cases/100 000 (P < 0·001), bone infection increased from 0·7 to 2·6 cases/100 000 (P < 0·001), and the incidence of joint infection remained approximately constant at an average rate of 1·0 case/100 000. The highest incidence rates were observed in men, persons aged ⩾80 years, non-Hispanic blacks and Hispanics. Diabetes was the most common underlying condition (51·2% cellulitis cases, 76·3% bone infections, 29·8% joint infections).
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Harlow, Olivia S., Kara G. Greenfield, and Kathryn Knoop. "Group B Streptococcus does not translocate the gut epithelium of neonatal mice." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 59.18. http://dx.doi.org/10.4049/jimmunol.208.supp.59.18.
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Abstract Neonatal sepsis remains a leading cause of death in preterm and low-birthweight infants and can be separated into two groups: early-onset sepsis (EOS) and late-onset sepsis (LOS). Previous studies have shown that LOS can result from translocation of enteric bacteria across the intestinal epithelium, resulting in bloodstream infection. Through metagenomic sequencing we have observed, unsurprisingly, potential sepsis-causing organisms such as Escherichia coli, Staphylococcus aureus, Enterobacter cloacae, and Group B Streptococcus (GBS) in the stool of neonatal intensive care unit patients. Our previous work has shown E. coli can disseminate from the intestines via goblet cells in a model of LOS, but how other bacterial pathogens disseminate remains unclear. GBS is often associated with EOS following in utero infections and vertical transmission from the mother during pregnancy and delivery. However, the ability of gut-residing GBS to cause sepsis in a murine model of LOS is still unknown. Here we infected five-day-old mice by oral gavage with different strains of GBS, but we did not observe GBS translocating the intestinal epithelium in the pups, unlike E. coli. We next induced EOS in newborn mice by vaginally inoculating pregnant mice to assess GBS dissemination and compare the EOS model to our LOS model. After in utero infection, most pups were intestinally colonized with GBS and, interestingly, only pups with GBS colonies in the lungs had systemic GBS infections. This data suggests neonates are at risk of GBS infection in utero, but not following delivery, even if GBS colonizes the neonatal intestine. This work could elucidate the pathogenesis of EOS as compared to LOS, leading to a deeper understanding of modes of GBS transmission. Supported by NIH: DK122187
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Mosites, Emily, Tammy Zulz, Dana Bruden, Leisha Nolen, Anna Frick, Louisa Castrodale, Joseph McLaughlin, Chris Van Beneden, Thomas Hennessy, and Michael Bruce. "1625. Risk of Invasive Group A Streptococcus, Group B Streptococcus, and Streptococcus pneumoniae Infection Among Adults Experiencing Homelessness—Anchorage, Alaska, 2002–2015." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S593. http://dx.doi.org/10.1093/ofid/ofz360.1489.
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Abstract Background People experiencing homelessness (PEH) have an increased risk of infectious disease. However, for many infections, this increased risk has not been clearly quantified. For example, the risk of invasive streptococcal infection has not been established among PEH in the United States. Methods We compared the incidence of detected cases of invasive group A Streptococcus (GAS) infection, group B Streptococcus (GBS) infection, and Streptococcus pneumoniae (pneumococcal) infection among adult PEH to that in the general adult population in Anchorage, Alaska from 2005 through 2015 using data from the CDC Arctic Investigations Program surveillance system, the US census, and the Anchorage Point in Time count (PIT [a yearly census of PEH]). Results During 2005–2015, the PIT counted a mean number of 970 adults (minimum 795, maximum 1486) in Anchorage who were homeless, which accounted for 0.4% of the total population. Compared with the general population, PEH were 53 times as likely to have invasive GAS infection (95% CI 47–61), 7 times as likely to have invasive GBS infection (95% CI 6, 8), and 36 times as likely to have invasive pneumococcal infection (95% CI 33, 40). Of all invasive GAS cases in Anchorage over the time period, 19% occurred within the homeless population, while 3% of invasive GBS cases and 14% of invasive pneumococcal cases were within the homeless population. Additionally, the predominant subtypes of GAS and pneumococcus differed among PEH compared with the general population. Conclusion A disproportionate burden of invasive streptococcal disease in Anchorage was detected among PEH, indicating a need for further focus on this high-risk group. Disclosures All authors: No reported disclosures.
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Sharma, Mridula B., Rama Chaudhry, Irum Tabassum, Nishat Hussain Ahmed, Jitendra Kumar Sahu, Benu Dhawan, and Veena Kalra. "The presence of Mycoplasma pneumoniae infection and GM1 ganglioside antibodies in Guillain-Barré syndrome." Journal of Infection in Developing Countries 5, no. 06 (March 4, 2011): 459–64. http://dx.doi.org/10.3855/jidc.1508.
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Introduction: Guillain-Barré syndrome (GBS) is an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infection. GBS patients are known to have antecedent bacterial infections associated with auto-antibodies to various gangliosides. This investigation aimed to evaluate GBS patients for serological evidence of Mycoplasma pneumoniae infection and anti GM1 ganglioside antibodies. Methodology: This cross-sectional study included 57 pediatric GBS patients, 42 neurological controls (i.e., non-GBS Acute Flaccid Paralysis cases) and 35 non-neurological controls. Enzyme linked immune sorbent assay (ELISA) was performed on the sera of the subjects to detect IgM and IgG antibodies against Mycoplasma (M.) pneumoniae and GM1 gangliosides. Results: The results showed that 15.79% and 21.05% GBS patients were positive for IgG and IgM antibodies against M. pneumoniae as compared to 2.38% (P < 0.05) and 14.2% in non-GBS-AFP and 5.7% and 14.2% in non-neurological controls respectively. Additionally, 43.85% and 38.54% GBS patients were positive for IgG and IgM antibodies against GM1 gangliosides as compared to 38.09% and 28.57% in non-GBS-AFP and 14.2% and 2.84% in non-neurological controls respectively (P < 0.05). Conclusions: Significant difference in levels of IgG antibodies against M. pneumoniae was observed between GBS patients and neurological controls, suggesting M. pneumoniae to be an important antecedent to GBS. Significant difference in levels of anti GM1 ganglioside antibodies (IgG & IgM) was seen between GBS patients and non-neurological controls, highlighting its possible role in the pathogenesis of GBS.
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Spencer, Brady, Norhan Alhajjar, and Kelly Doran. "T cell response during Group B Streptococcus vaginal colonization and ascending infection." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 82.15. http://dx.doi.org/10.4049/jimmunol.204.supp.82.15.
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Abstract Pre-term birth, miscarriage, and other adverse pregnancy outcomes remain the primary cause of neonatal death and are associated with bacterial ascending infections within the female reproductive tract. Group B Streptococcus (GBS), a vaginal tract colonizer, is a leading contributor to adverse pregnancy outcomes and neonatal invasive disease. We have developed a mouse model of GBS vaginal colonization and ascending infection and have observed increased IL-17 production in mice that cleared GBS colonization compared to those still colonized. Thus, we hypothesize that IL-17 and IL-17-producing cells may be important for host defense; yet, the immune dynamics during GBS vaginal persistence and ascending infection/adverse pregnancy outcomes remain unknown. T cells are a major source of IL-17 in the mucosa. To assess the role of adaptive immunity during GBS colonization, we colonized RAG1+/+ and RAG1−/− mice with GBS and observed increased persistence of GBS in the vaginal tract of the RAG1−/− mice. To determine the cellular source of IL-17 within the reproductive tract of GBS-colonized mice, we isolated immune cells from vaginal, cervical, and uterine tissues at the time of GBS clearance and performed flow cytometry. TCRɣδ+ cells comprised the highest percentage of RORɣT+ immune cells in the vagina, cervix, and uterus. We further observed an increased percentage of TCRɣδ+ cells in the uterus of GBS-colonized mice compared to naïve mice at day 9 post-inoculation, at which point half the mice had cleared. We hypothesize that IL-17-producing TCRɣδ+ cells contribute to GBS clearance in the murine reproductive tract. Future studies will assess GBS vaginal persistence and ascending infection in IL-17- and TCRɣδ-deficient mouse lines.
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Steele, Russell W. "Control of Neonatal Group B Streptococcal Infection." Journal of the Royal Society of Medicine 86, no. 12 (December 1993): 712–15. http://dx.doi.org/10.1177/014107689308601213.
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Group B β-haemolytic streptococcus (GBS) is the leading cause of life-threatening perinatal infection in developed countries. As immunization of women is not yet available, selective intrapartum chemoprophylaxis appears to be the best current strategy for preventing disease. All pregnant women should be screened for GBS at 26 to 28 weeks gestation. During labour, all colonized women with risk factors for invasive GBS neonatal infection should be treated with intravenous penicillin or ampicillin. Risk factors include preterm labour, premature rupture of membranes, intrapartum fever, multiple births, prolonged rupture of membranes, maternal diabetes, previous sibling with invasive GBS disease, and maternal GBS bacteriuria. The latter two categories warrant chemoprophylaxis regardless of maternal colonization status.
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Yeo, Kee Thai, Monica Lahra, Barbara Bajuk, Lisa Hilder, Mohamed E. Abdel-Latif, Ian M. Wright, and Ju-Lee Oei. "Long-term outcomes after group B streptococcus infection: a cohort study." Archives of Disease in Childhood 104, no. 2 (July 17, 2018): 172–78. http://dx.doi.org/10.1136/archdischild-2017-314642.
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ObjectiveTo describe the risk of death and hospitalisation until adolescence of children after group B streptococcus (GBS) infection during infancy.DesignPopulation-based cohort study.SettingNew South Wales, Australia.PatientsAll registered live births from 2000 to 2011.InterventionsComparison of long-term outcomes in children with the International Statistical Classification of Diseases and Related Health Problems-10th Revision discharge codes corresponding to GBS infections and those without.Main outcome measuresDeath and hospitalisation.ResultsA total of 1206 (0.1%) children (936 (77.6%)≥37 weeks’ gestation) were diagnosed with GBS infection. Over the study period, infection rates decreased from 2.1 (95% CI 1.8 to 2.4) to 0.7 (95% CI 0.5 to 0.9) per 1000 live births. Infants with GBS infection were born at lower gestation (mean 37.6 vs 39.0 weeks), were more likely very low birth weight (<1500 g, OR 9.1(95% CI 7.4 to 11.3)), born premature (OR 3.9(95% CI 3.4 to 4.5)) and have 5 min Apgar scores ≤5 (OR 6.7(95% CI 5.1 to 8.8)). Children with GBS had three times the adjusted odds of death (adjusted OR (AOR) 3.0(95% CI 2.1 to 4.3)) or rehospitalisations (AOR 3.1(95% CI 2.7 to 3.5)). Thirty-six (3.0%) with GBS died, with >50% of deaths occurring <28 days. Children with GBS were hospitalised more frequently (median 2 vs 1), for longer duration (mean 3.7 vs 2.2 days) and were at higher risk for problems with genitourinary (OR 3.1(95% CI 2.8 to 3.5)) and nervous (OR 2.0 (95% CI1.7 to 2.3)) systems.ConclusionsDespite decreasing GBS rates, the risk of poor health outcomes for GBS-infected children remains elevated, especially during the first 5 years. Survivors continue to be at increased risk of death and chronic conditions requiring hospitalisations, such as cerebral palsy and epilepsy.
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McDonnell, Erin P., Nicole J. Altomare, Yesha H. Parekh, Ram C. Gowda, Payal D. Parikh, Mark H. Lazar, and Martin J. Blaser. "COVID-19 as a Trigger of Recurrent Guillain–Barré Syndrome." Pathogens 9, no. 11 (November 19, 2020): 965. http://dx.doi.org/10.3390/pathogens9110965.
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Coronavirus 2019 (COVID-19) has been reported to trigger Guillain–Barré syndrome (GBS). While uncommon, recurrent GBS (rGBS) episodes, triggered by antecedent viral infections, have been reported in a small proportion of GBS patients, here we describe a patient with a recurrent case of GBS, occurring secondary to COVID-19 infection. Before this patient’s episode, he had two prior GBS flares, each precipitated by a viral infection followed by complete recovery besides intermittent paresthesias. We also consider the nosology of this illness in the spectrum of rGBS and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), with their differing natural histories, prognosis, and therapeutic approaches. For patients who have a history of inflammatory demyelinating polyradiculopathies who develop COVID-19, we recommend close observation for neurologic symptoms over the next days and weeks.
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Savino, Wilson, Carolina V. Messias, Daniella A. Mendes-da-Cruz, Pamela Passos, Ana Carolina A. F. Ferreira, and Osvaldo J. Nascimento. "Zika Virus Infection in the Elderly: Possible Relationship with Guillain-Barré Syndrome." Gerontology 63, no. 3 (December 22, 2016): 210–15. http://dx.doi.org/10.1159/000453579.
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The Zika virus (ZIKV) outbreak in French Polynesia, in 2013, and in Brazil, in 2015, was correlated with neurological complications, which comprised, among others, congenital microcephaly and Guillain-Barré syndrome (GBS), which includes a group of acute autoimmune neuropathies generally reported after respiratory or gastrointestinal infectious diseases. Despite being relatively rare, the incidence rate of GBS rises with age, which makes GBS more frequent in the elderly, in whom it is also a more severe disease with slower recovery than in younger patients. Different forms of GBS have been described having diagnostic confirmation of a previous infection with the ZIKV virus. Although we do not have enough evidence that elderly people are a particularly susceptible population to developing GBS following ZIKV infection, this is plausible. We should consider this possibility, particularly taking into account that aging subjects are more susceptible to infections. In this context, a deeper understanding of how the immune system in the elderly functions in relation to ZIKV infection is necessary, as well as an understanding of what kind of alterations of the nervous system such an infection triggers in the elderly, beyond GBS. This will be relevant for better therapeutic interventions and for designing vaccine candidates that can be applied in an aging population, particularly those prone to develop ZIKV-induced autoimmunity.
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Wang, Zhixia, Wenyuan Pu, Qi Liu, Meifeng Zhu, Qinlei Chen, Yingchun Xu, and Chunxiang Zhou. "Association of Gut Microbiota Composition in Pregnant Women Colonized with Group B Streptococcus with Maternal Blood Routine and Neonatal Blood-Gas Analysis." Pathogens 11, no. 11 (November 4, 2022): 1297. http://dx.doi.org/10.3390/pathogens11111297.
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Group B Streptococcus (GBS) colonizes the vaginal and rectal mucosa in a substantial proportion of healthy women, and GBS is a risk factor for GBS-associated adverse birth outcomes, such as bacterial infection, in neonates. Whether changes in the gut microbiota of GBS-infected pregnant women are associated with maternal complete blood cell count (CBC) and neonatal blood-gas analysis is unknown. To explore the relationship between the intestinal microecological composition of pregnant women and maternal blood routine and neonatal blood-gas analysis, we collected intestinal microecology samples of 26 pregnant women in clinic. They were divided into a positive group(GBS positive,GBS +) and a negative group (GBS negative, GBS-), with 12 in the positive group and 14 in the negative group. 16S rRNA gene sequencing was used to examine the gut microbiota profile from a fecal sample of pregnant women. CBC was carried out in enrolled pregnant women and umbilical arterial blood-gas analysis (UABGA)was conducted for analysis of intestinal microbiota composition, maternal blood routine and neonatal blood gas. Our results showed significant differences in the total number of organisms and microbial diversity of intestinal microbiota between healthy pregnant women and GBS-positive pregnant women. Particularly, abundances of Lentisphaerae, Chlorobi, Parcubacteria, Chloroflexi, Gemmatimonadetes, Acidobacteria, Fusobacteria and Fibrobacteres were only detected in participants with GBS colonization. Blood-gas analysis revealed that neonates born to mothers with GBS colonization had significantly higher fractions of carboxyhemoglobin (FCOHb) and lower methemoglobin (FMetHb), and abundances of OTU80, OTU122, OTU518 and OTU375 were associated with blood-gas indicators, such as carboxyhemoglobin, methemoglobin, PCO2, PH and ABE. Interestingly, there were significant correlations between OTU levels and inflammatory indexes in pregnant women with GBS infection. Together, this study revealed for the first time that altered gut microbiota compositions are related to the inflammatory state in GBS-positive pregnant women and neonatal blood-gas indicators. GBS colonization may lead to significant changes in the gut microbiome, which might be involved in the pathogenesis of the maternal inflammatory state and neonatal blood gas abnormalities.
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Hon, Kam Lun, King Hang Chan, Pak Long Ko, King Woon So, and Alexander K. C. Leung. "Late Onset Streptococcus agalactiae Meningitis following Early Onset Septicemia: A Preventable Disease?" Case Reports in Pediatrics 2017 (2017): 1–4. http://dx.doi.org/10.1155/2017/8418105.
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We report a neonate who presented with early onset Streptococcus agalactiae or group B streptococcus (GBS) septicemia within 24 hours of birth. After discharge at day 14, she went on to develop late onset GBS meningitis at 36 days of age. The infant was treated with intravenous antibiotics on both occasions and eventually discharged home with no apparent sequelae. We address issues associated with GBS infection in infancy including the demographics, risk factors, and the risk of late onset GBS meningitis following an early onset GBS infection. The major source of GBS in early onset GBS disease is maternal birth canal GBS colonization. On the other hand, nosocomial cross-infection is an important source of GBS in late onset disease. Penicillin remains the current treatment of choice for GBS infection. Given the rapid onset and progression within hours of birth and lack of an effective solution for preventing late onset GBS, administration of an effective GBS vaccine in pregnancy could provide a sensible and cost-effective solution in all settings.
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Tissi, Luciana, Francesco Bistoni, and Manuela Puliti. "IL-4 Deficiency Decreases Mortality but Increases Severity of Arthritis in Experimental Group BStreptococcusInfection." Mediators of Inflammation 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/394021.
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IL-4 is an anti-inflammatory cytokine that inhibits the onset and severity in different experimental arthritis models. Group B streptococci (GBS) have been recognized as an ever-growing cause of serious invasive infections in nonpregnant adults. Septic arthritis is a clinical manifestation of GBS infection. To investigate the role of IL-4 in experimental GBS infection, IL-4 deficient or competent mice were inoculated with1×107GBS/mouse. Mortality, appearance of arthritis, GBS growth in the organs, and local and systemic cytokine and chemokine production were examined. IL-4–/– mice showed lower mortality rates but increased severity of arthritis and exhibited a lower microbial load in blood, kidneys, and joints than wt mice. Increased local levels of IL-1β, IL-6, TNF-α, MIP-1α, and MIP-2 accompanied the more severe arthritis in IL-4–/– mice. Our results suggest a detrimental role of IL-4 in GBS sepsis, whereas it plays a beneficial effect on GBS-induced arthritis.
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EKELUND, K., and H. B. KONRADSEN. "Invasive group B streptococcal disease in infants: a 19-year nationwide study. Serotype distribution, incidence and recurrent infection." Epidemiology and Infection 132, no. 6 (November 16, 2004): 1083–90. http://dx.doi.org/10.1017/s0950268804002808.
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During the period 1984–2002, 472 cases of invasive group B streptococcal (GBS) disease in infants aged 0–90 days in Denmark were registered. The overall incidence was 0·4/1000 live births. Most infants (73%) had early-onset GBS infection with 53% registered within the first day. Serotype III predominated (59%) with other serotypes as follows: Ia (16%), Ib (8%), NT (7%), II (6%), other serotypes (5%). Recurrence of GBS infection was registered in six infants, and the interval with no antibiotic therapy varied from 2 to 39 days. The serotypes of the isolates obtained from first and second episodes were identical (serotype III in five, and serotype Ia in one infant). Paired isolates were indistinguishable by PFGE and antibiotic susceptibility testing. Invasive GBS infections in infants are still a problem in Denmark, and recurrent infections are registered in 1% of these infants.
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Nyati, Kishan Kumar, and Roopanshi Nyati. "Role ofCampylobacter jejuniInfection in the Pathogenesis of Guillain-Barré Syndrome: An Update." BioMed Research International 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/852195.
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Our current knowledge onCampylobacter jejuniinfections in humans has progressively increased over the past few decades. Infection withC. jejuniis the most common cause of bacterial gastroenteritis, sometimes surpassing other infections due toSalmonella,Shigella, andEscherichia coli.Most infections are acquired due to consumption of raw or undercooked poultry, unpasteurized milk, and contaminated water. After developing the diagnostic methods to detectC. jejuni, the possibility to identify the association of its infection with new diseases has been increased. After the successful isolation ofC. jejuni, reports have been published citing the occurrence of GBS followingC. jejuniinfection. Thus,C. jejuniis now considered as a major triggering agent of GBS. Molecular mimicry between sialylated lipooligosaccharide structures on the cell envelope of these bacteria and ganglioside epitopes on the human nerves that generates cross-reactive immune response results in autoimmune-driven nerve damage. ThoughC. jejuniis associated with several pathologic forms of GBS, axonal subtypes followingC. jejuniinfection may be more severe. Ample amount of existing data covers a large spectrum of GBS; however, the studies onC. jejuni-associated GBS are still inconclusive. Therefore, this review provides an update on theC. jejuniinfections engaged in the pathogenesis of GBS.
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Robischon, Kathleen, and Marvin S. Amstey. "Evidence for In Utero Hematogenous Transmission of Group B β-hemolytic Streptococcus." Infectious Diseases in Obstetrics and Gynecology 2, no. 4 (1994): 184–85. http://dx.doi.org/10.1155/s1064744994000621.
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Background: The presumed ascending route of group B β-hemolytic streptococcus (GBS) infection from the colonized maternal genital tract is well accepted. This case report proposes a hematogenous, selective infection of one unruptured amniotic sac over the other ruptured amniotic sac in a twin gestation in a patient with known GBS vaginal colonization.Case: This is a case report of GBS sepsis in twin B with intact membranes. Twin A, with 28 h of ruptured membranes, failed to show any signs of infection. The pathology of the placenta confirmed chorioamnionitis in twin B and the absence of infection in twin A.Conclusion: The presence of culture-positive GBS sepsis in the twin with the unruptured amniotic sac, as well as the absence of GBS infection in the twin with the ruptured sac, suggests an alternative means of infection for GBS infection, such as hematogenous transplacental transmission.
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SMITH, JAMES L. "Campylobacter jejuni Infection during Pregnancy: Long-Term Consequences of Associated Bacteremia, Guillain-Barré Syndrome, and Reactive Arthritis†." Journal of Food Protection 65, no. 4 (April 1, 2002): 696–708. http://dx.doi.org/10.4315/0362-028x-65.4.696.
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Campylobacter jejuni infections are the main cause of foodborne gastroenteritis in the United States and other developed countries. Generally, C. jejuni infections are self-limiting and treatment is not necessary; however, infections caused by this organism can lead to potentially dangerous long-term consequences for some individuals. Bacteremia, Guillain-Barré syndrome (GBS; an acute flaccid paralytic disease), and reactive arthritis (ReA) are the most serious of the long-term consequences of C. jejuni infections. During pregnancy, foodborne infections may be hazardous to both the woman and the fetus. C. jejuni–induced bacteremia during pregnancy may lead to intrauterine infection of the fetus, abortion, stillbirth, or early neonatal death. Infection of a newborn by the mother during the birth process or shortly after birth may lead to neonatal enteritis, bacteremia, and/or meningitis. C. jejuni enteritis is the inducing antecedent infection in approximately 30% of cases of GBS. Thus, pregnant women infected with C. jejuni may contract GBS. GBS during pregnancy does not affect fetal or infant development and does not increase spontaneous abortion or fetal death; however, it may induce spontaneous delivery during the third trimester in severe cases. Reactive arthritis occurs in approximately 2% of C. jejuni enteritis cases and leads to the impaired movement of various joints. Pregnant women with C. jejuni–induced reactive arthritis can be expected to deliver a normal infant. A pregnant patient with GBS or ReA may be unable to care for a newborn infant because of the physical impairment induced by these diseases. Since C. jejuni infections put both fetuses and pregnant women at risk, pregnant women must take special care in food handling and preparation to prevent such infections.
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Alshengeti, Amer. "Group B Streptococcus among Pregnant Women and Neonates in Saudi Arabia: A Systemic Review." Pathogens 11, no. 9 (September 10, 2022): 1029. http://dx.doi.org/10.3390/pathogens11091029.
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Sepsis caused by Group B Streptococcus (GBS) continues to cause mortality and morbidity in newborns, especially in developing countries. Bacterial sepsis in newborns varies nationally and even within countries. Developing countries have reported 34 deaths per 1000 live births compared to 5 in developed countries. This systemic review aimed to assess the prevalence of GBS colonization among pregnant women and the incidence of neonatal GBS sepsis in Saudi Arabia. A literature search of PubMed, MEDLINE Ovid, and Google Scholar was conducted. A total of 21 studies were found: 15 described maternal GBS colonization and 6 studies described neonatal GBS infections. The GBS colonization prevalence among pregnant women ranged from 2.1% to 32.8%. Inconsistencies in the reporting method for neonatal GBS infection rates were observed. Only two studies have the incidence of neonatal GBS as the primary outcome. No national multicenter studies exist on the GBS rates among neonates. Nationwide studies are warranted to assess the burden of GBS infections in neonates. These studies would guide appropriate GBS screening strategies during pregnancy for application in a national public health program.
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Martin, Denis, Stéphane Rioux, Edith Gagnon, Martine Boyer, Josée Hamel, Nathalie Charland, and Bernard R. Brodeur. "Protection from Group B Streptococcal Infection in Neonatal Mice by Maternal Immunization with Recombinant Sip Protein." Infection and Immunity 70, no. 9 (September 2002): 4897–901. http://dx.doi.org/10.1128/iai.70.9.4897-4901.2002.
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ABSTRACT The protective potential of antibodies directed against group B streptococcus (GBS) Sip surface protein was determined by using the mouse neonatal infection model. Rabbit Sip-specific antibodies administered passively to pregnant mice protected their pups against a GBS lethal challenge. In addition, active immunization with purified recombinant Sip protein of female CD-1 mice induced the production of specific antibodies that also confer protection to the newborn pups against GBS strains of serotypes Ia/c, Ib, II, III, and V. These data confirm that Sip-specific antibodies can cross the placenta and conferred protective immunity against GBS infections.
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Hummel, K., J. Dunn, K. Muldrew, S. Gogia, E. Kravitz, E. Johnson, A. Berra, I. Stafford, I. Martin, and E. Munson. "Mycoplasma Genitalium And Streptococcus Agalactiae Colonization In Pregnant Women: An Emerging Relationship." American Journal of Clinical Pathology 154, Supplement_1 (October 2020): S159. http://dx.doi.org/10.1093/ajcp/aqaa161.347.
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Abstract Introduction/Objective Mycoplasma genitalium has been identified as an emerging sexually transmitted infection (STI) causing cervicitis, pelvic inflammatory disease and other gynecologic pathology. The prevalence of M. genitalium in pregnant women has not been determined, nor has frequency of co-infection with Streptococcus agalactiae (GBS). Neonatal sepsis caused by GBS is associated with black race and young maternal age with approximately 10%-30% of pregnant women colonized. The aim of this retrospective study was to investigate the possible association between M. genitalium infection and colonization with GBS in a large cohort of pregnant women from a tertiary care center in Houston, Texas. Methods Remnant endocervical samples collected from pregnant women attending clinics at the Baylor College of Medicine between September 2019 and December 2019 were screened for M. genitalium by transcription mediated amplification (Hologic, Inc. Marlborough, MA). Demographic, STI co-infection [Human papillomavirus (types 16,18), Trichomonas vaginalis, Chlamydia trachomatis, Neisseria gonorrhoeae, Treponema pallidum, and Herpes simplex virus], and GBS status data were recorded. Fisher’s exact test was performed for statistical analysis. Results 719 total samples were collected and tested for M. genitalium. Of these, 41 (5.7%) were positive. The mean age of infected women was younger than noninfected women (24.9 vs. 28.1 years respectively p = 0.0004). More black women (34.2%) were infected with M. genitalium compared to white (14.6%) or other (51.2%) (p = 0.0003). Rates of GBS colonization was significantly higher among women infected with M. genitalium compared to women who tested negative (58.3% vs. 16.1% respectively p = 0.002) and increased compared to national reported rates of GBS colonization. M. genitalium also showed a significant association with T. vaginalis (p=0.03), but no other STI co- infections studied. Conclusion Our data demonstrates that infection with M. genitalium may be associated with persistent GBS colonization. Further prospective studies are needed to further elucidate this relationship.
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Winram, Scott B., Mechthild Jonas, Emil Chi, and Craig E. Rubens. "Characterization of Group B Streptococcal Invasion of Human Chorion and Amnion Epithelial Cells In Vitro." Infection and Immunity 66, no. 10 (October 1, 1998): 4932–41. http://dx.doi.org/10.1128/iai.66.10.4932-4941.1998.
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ABSTRACT Group B streptococci (GBS) have been cultured from the chorioamnionic membrane of pregnant women, usually in association with chorioamnionitis and premature labor (K. A. Boggess, D. H. Watts, S. L. Hillier, M. A. Krohn, T. J. Benedetti, and D. A. Eschenbach, Obstet. Gynecol. 87:779–784, 1996). Colonization and infection of placental membranes can be a prelude to neonatal GBS infections even in the presence of intact membranes (R. L. Naeye and E. C. Peters, Pediatrics61:171–177, 1978), suggesting that GBS cause chorioamnionitis or establish amniotic fluid infections by partial or complete penetration of the placental membranes. We have isolated and grown cultures of primary chorion and amnion cells from human cesarean-section placentas. This has provided a biologically relevant model for investigating GBS adherence to and invasion of the two epithelial barriers of the placental membrane. GBS adhered to chorion cell monolayers to a high degree. Pretreatment of GBS with trypsin reduced adherence up to 10-fold, which suggested that the bacterial ligand(s) was a protein. GBS invaded chorion cells at a high rate in vitro, and invasion was dependent on cellular actin polymerization. GBS could be seen within intracellular vacuoles of chorion cells by transmission electron microscopy. We also demonstrated that GBS were capable of transcytosing through intact chorion cell monolayers without disruption of intracellular junctions. GBS also adhered to amnion cells; in contrast, however, these bacteria failed to invade amnion cells under a variety of assay conditions. GBS interactions with the chorion epithelial cell layer shown here correlate well with epidemiological and pathological studies of GBS chorioamnionitis. Our data also suggest that the amnion cell layer may provide an effective barrier against infection of the amniotic fluid.
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Paoletti, Lawrence C., and Lawrence C. Madoff. "Vaccines to prevent neonatal GBS infection." Seminars in Neonatology 7, no. 4 (August 2002): 315–23. http://dx.doi.org/10.1053/siny.2002.0114.
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&NA;. "Surfactant beneficial in neonatal GBS infection." Inpharma Weekly &NA;, no. 1265 (November 2000): 16. http://dx.doi.org/10.2165/00128413-200012650-00037.
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Jiang, Shengmei, and Michael R. Wessels. "BsaB, a Novel Adherence Factor of Group B Streptococcus." Infection and Immunity 82, no. 3 (December 16, 2013): 1007–16. http://dx.doi.org/10.1128/iai.01014-13.
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ABSTRACTStreptococcus agalactiae(group BStreptococcus[GBS]) is a leading cause of neonatal sepsis and meningitis, peripartum infections in women, and invasive infections in chronically ill or elderly individuals. GBS can be isolated from the gastrointestinal or genital tracts of up to 30% of healthy adults, and infection is thought to arise from invasion from a colonized mucosal site. Accordingly, bacterial surface components that mediate attachment of GBS to host cells or the extracellular matrix represent key factors in the colonization and infection of the human host. We identified a conserved GBS gene of unknown function that was predicted to encode a cell wall-anchored surface protein. Deletion of the gene and a cotranscribed upstream open reading frame (ORF) in GBS strain 515 reduced bacterial adherence to VK2 vaginal epithelial cellsin vitroand reduced GBS binding to fibronectin-coated microtiter wells. Expression of the gene product inLactococcus lactisconferred the ability to adhere to VK2 cells, to fibronectin and laminin, and to fibronectin-coated ME-180 cervical epithelial cells. Expression of the recombinant protein inL. lactisalso markedly increased biofilm formation. The adherence function of the protein, namedbacterialsurfaceadhesin of GBS (BsaB), depended both on a central BID1 domain found in bacterial intimin-like proteins and on the C-terminal portion of the BsaB protein. Expression of BsaB in GBS, like that of several other adhesins, was regulated by the CsrRS two-component system. We conclude that BsaB represents a newly identified adhesin that participates in GBS attachment to epithelial cells and the extracellular matrix.
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Korir, Michelle L., Shannon D. Manning, and H. Dele Davies. "Intrinsic Maturational Neonatal Immune Deficiencies and Susceptibility to Group B Streptococcus Infection." Clinical Microbiology Reviews 30, no. 4 (August 16, 2017): 973–89. http://dx.doi.org/10.1128/cmr.00019-17.
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SUMMARY Although a normal member of the gastrointestinal and vaginal microbiota, group B Streptococcus (GBS) can also occasionally be the cause of highly invasive neonatal disease and is an emerging pathogen in both elderly and immunocompromised adults. Neonatal GBS infections are typically transmitted from mother to baby either in utero or during passage through the birth canal and can lead to pneumonia, sepsis, and meningitis within the first few months of life. Compared to the adult immune system, the neonatal immune system has a number of deficiencies, making neonates more susceptible to infection. Recognition of GBS by the host immune system triggers an inflammatory response to clear the pathogen. However, GBS has developed several mechanisms to evade the host immune response. A comprehensive understanding of this interplay between GBS and the host immune system will aid in the development of new preventative measures and therapeutics.
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Yamana, Masaki, Motoi Kuwahara, Yuta Fukumoto, Keisuke Yoshikawa, Kazuo Takada, and Susumu Kusunoki. "Guillain-Barré syndrome and related diseases after influenza virus infection." Neurology - Neuroimmunology Neuroinflammation 6, no. 4 (May 21, 2019): e575. http://dx.doi.org/10.1212/nxi.0000000000000575.
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ObjectiveWe examined the clinical and serologic features of Guillain-Barré syndrome (GBS)-related diseases (GBSRDs), including GBS, Fisher syndrome (FS), and Bickerstaff brainstem encephalitis (BBE), after influenza virus infection (GBSRD-I) to reveal potential underlying autoimmune mechanisms.MethodsWe retrospectively investigated the presence of antiglycolipid antibodies against 11 glycolipids and the clinical features of 63 patients with GBSRD-I. Autoantibody profiles and clinical features were compared with those of 82 patients with GBSRDs after Campylobacter jejuni infection (GBSRD-C).ResultsThe anti-GQ1b seropositivity rate was significantly higher, whereas the GM1 and GD1a seropositivity rates were significantly lower in GBSRD-I compared with GBSRD-C. Anti-GQ1b and anti-GT1a were the most frequently detected antiglycolipid antibodies in GBSRD-I (both 15/63, 24%). Consequently, FS was more frequent in GBSRD-I than GBSRD-C (22% vs 9%, p < 0.05). In addition, as for GBS, cranial nerve deficits, sensory disturbances, and ataxia were more frequent in the cases after influenza infection (GBS-I) than in those after C. jejuni infection (GBS-C) (46% vs 15%, 75% vs 46%, and 29% vs 4%, respectively; all p < 0.01). Nerve conduction studies revealed acute inflammatory demyelinating polyneuropathy (AIDP) in 60% of patients with GBS-I but only 25% of patients with GBS-C (p < 0.01).ConclusionsAnti-GQ1b antibodies are the most frequently detected antibodies in GBSRD-I. Compared with GBS-C, GBS-I is characterized by AIDP predominance and frequent presence of cranial nerve involvement and ataxia.
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Brigtsen, Anne Karin, Anne Flem Jacobsen, Lumnije Dedi, Kjetil Klaveness Melby, Cathrine Nygaard Espeland, Drude Fugelseth, and Andrew Whitelaw. "Group B Streptococcus colonization at delivery is associated with maternal peripartum infection." PLOS ONE 17, no. 4 (April 1, 2022): e0264309. http://dx.doi.org/10.1371/journal.pone.0264309.
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Background Group B Streptococcus (GBS) is a major cause of serious neonatal infection but its role in maternal morbidity has received little investigation. The aim of this study was to determine whether GBS colonization at delivery is associated with increased risk of maternal peripartum infection. Methods In this prospective cohort study, 1746 unselected women had a vaginal-rectal culture taken at the onset of labor. Diagnosis of maternal peripartum infection was based on a combination of two or more signs or symptoms including fever, breast pain, severe wound or pelvic pain, purulent discharge and abnormal laboratory tests including C-reactive protein and white blood cell count occurring from labor until 2 weeks postpartum. The main outcome measure was the proportion of women with maternal peripartum infection according to GBS colonization status. Results A total of 25.9% (452/1746) women were colonized with GBS. The rate of peripartum infection was almost twice as high in colonized women (49/452 [10.8%]) vs. non-colonized women (81/1294 [6.3%]); OR 1.82 [1.26–2.64], p = 0.002). This association was confirmed in a multivariable model (OR 1.99 [1.35–2.95], p = 0.001). Women diagnosed with peripartum infection had a significantly longer hospital stay compared to women without peripartum infection (4 days (median) vs. 3 days, p < 0.001). Length of hospital stay did not differ between colonized and non-colonized women. Serotype IV GBS was more frequent in colonized women with peripartum infection than in women without peripartum infection (29.3% vs. 12.5%, p = 0.003). Conclusions GBS colonization at delivery is associated with increased risk of peripartum infection. Whether this increase is due directly to invasion by GBS or whether GBS colonization is associated with a more general vulnerability to infection remains to be determined.
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Wilson, Brigid, Taissa Zappernick, Richard Banks, Daniel Baechle2; Janet Briggs, Sunah Song, Federico Perez, and Robin L. Jump. "466. Elevated Risk of Invasive Group B Streptococcal Infection Among Veterans with Poorly Controlled Diabetes Mellitus or at Extremes for Body Mass Index." Open Forum Infectious Diseases 6, Supplement_2 (October 2019): S228—S229. http://dx.doi.org/10.1093/ofid/ofz360.539.
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Abstract Background Diabetes mellitus (DM) and obesity have been identified as risk factors for invasive Group B Streptococcal (GBS) infection in non-pregnant adults. We used data from the US Veterans Health Administration (VHA) to confirm these findings and determine if poor diabetic control (elevated hemoglobin A1C (HbA1c)) or extreme weight (body mass index (BMI)) impacted risk. Methods We examined the VHA Corporate Data Warehouse to identify veterans active in VHA between 2008 and 2017 with invasive GBS infection according to the US Centers for Disease Control and Prevention surveillance definitions. We used International Classification of Disease (ICD) codes to determine a diagnosis of DM and stratified veterans by the highest HbA1c and first BMI in a given year. Absent HbA1c among those with DM were recorded as such. For years without BMI, the most recent BMI was carried forward. Results Between 2008 and 2017, the rate of invasive GBS infection for veterans with HbA1C ≥9.5% ranged from 55 to 104 /100,000 person-years (Figure 1). Rates in the next-highest risk group (HbA1c 7.5%–9.4%) were 24 to 36/100,000 person-years. Veterans with a BMI ≥40 (extremely obese; n = 798) or ≤18.5 (underweight; n = 99) had similarly elevated rates of invasive GBS infection (26 to 37/100,000 and 15 to 33/100,000 person-years, respectively) while those with BMI of 18.5–40 ranged from 6 to 13/100,000 person-years (Figure 2). Among those with HbA1c ≥9.5%, the most common type of infection was osteomyelitis (500/1,182; 42%; Table 1). Pneumonia was most common among patients with a BMI, Table 2. Conclusion Our study confirms that DM and obesity are notable risk factors for invasive GBS infection among veterans. The risk is substantially increased in patients with poorly controlled DM and morbid obesity. The high rate of invasive GBS infections among the small proportion of underweight veterans may reflect long-standing type 1 DM or other chronic diseases. Effective interventions to reduce the burden of invasive GBS infection among veterans should target individuals with poorly controlled DM, morbid obesity and those markedly underweight. Disclosures All authors: No reported disclosures.
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Bonadio, William A., William Jeruc, Yvonne Anderson, and Douglas Smith. "Systemic Infection Due to Group B Beta-Hemolytic Streptococcus in Children." Clinical Pediatrics 31, no. 4 (April 1992): 230–33. http://dx.doi.org/10.1177/000992289203100408.
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We reviewed 75 outpatient cases of systemic infection due to group B beta-hemolytic streptococcus (GBS) evaluated during a 13-year period. Patient ages ranged from five days to eight months; 75% were younger than two months. Early-onset (<seven days of age) GBS disease occurred in 10% of the patients, and late-onset GBS disease in 90%. The racial distribution was 60% black, 35% white, and 5% Hispanic. Symptoms included fever, irritability, lethargy, and altered-feeding pattern which lasted less than 24 hours in 88% of patients. On presentation, 33% were afebrile (eight had GBS meningitis); 32% did not appear ill (six had GBS meningitis). Of the total, 40% had GBS meningitis, of these, a greater proportion had either early-onset GBS disease or neutropenia. Infection other than meningitis was identified in 24% of all patients: pneumonia (six cases), cellulitis/adenitis (six cases), osteomyelitis/septic arthritis (five cases), and otitis media (one case). All patients survived. Systemic GBS infection in an outpatient population can involve infants up to eight months old, is more common in blacks than in whites, can be present without fever or compromised appearance, and usually has low mortality.
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Dryżałowski, Paweł, Elżbieta Sołowiej, Damian Okruciński, and Sergiusz Jóźwiak. "Guillain-Barre syndrome as a paraneoplastic syndrome in a 17-year- old boy." Child Neurology 29, no. 58 (2020): 86–88. http://dx.doi.org/10.20966/chn.2020.58.463.
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Guillain-Barre syndrome (GBS) is an acute inflammatory polyneuropathy, characterised by progressive, symmetrical muscle weakness and sensory disorder due to autoimmunologic myelin nerve sheats and/or peripheral nerves axonal damage. The course of the disease in children is usually milder than in adults. The most common variant of GBS is acute inflammatory demyelinating polyneuropathy (AIDP). GBS is a rare disorder with morbidity rate of 0,5-1,5/100 000/ year, more often seen in males. The course of disease in children is usually milder than in adults. Early diagnosis and proper treatment enables complete recovery in 80% of cases, while approximately 10% of patients suffer from symptoms recurrence, mainly after infection. Almost 2/3 of GBS cases are preceded by upper respiratory or gastrointestinal infection. The emergence of antibodies in various mechanisms, which cross react with nerve sheats or axon antigens (through a phenomenon known as molecular mimicry), leads to development of the syndrome. Known triggers inducing GBS include viral and bacterial infections, injuries, surgery, bone marrow transplantation and rarely childhood vaccinations. In still rarer cases, GBS may develop in the course of paraneoplastic syndrome (PNS), and be the first symptom of an underlying neoplastic process.
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Szymański, Sławomir, Katarzyna Szczerba, and Violetta Konstanty-Kurkiewicz. "The effect of perinatal antibiotic prophylaxis on an early onset of symptomatic infections in newborns." Pielegniarstwo XXI wieku / Nursing in the 21st Century 16, no. 3 (September 26, 2017): 17–24. http://dx.doi.org/10.1515/pielxxiw-2017-0024.
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Abstract Aim. The aim of the study was to evaluate the effectiveness of preventive perinatal antibiotic therapy on the occurrence of an earlysymptomatic infections in newborns. Material and Methods. The studied material consisted of data obtained from medical records of 1,328 born alive infants and their mothers. Advanced parameters were described with appropriate numbers, arithmetic means, standard deviation, median as well as minimum and maximum values. The level of statistical significance was p<0.05. Results. When it comes to 6.62% of newborns, they demonstrated the presence of early signs of infection. The Group B Streptococcus (GBS) infection was found in 14 cases, but only in 5 of them pure GBS strains were isolated. E. coli bacteria was reported in 33 neonates, while the other bacteria naming: Enterococcus faecalis, Enterobacteriaceae, taphylococcus epidermidis, Staphylococcus aureus were isolated from 42 newborns. Among 24 newborns showing clinical signs of infection and positive indicators of inflammation in laboratory tests, simultaneously negative results of bacteriological cultures were reported. Conclusions. In connection with the introduction of an obligation to perform tests for GBS, amount of used antibiotics is increasing. However, the effectiveness of intrapartum antibiotic therapy and its prevalence appear to be unsatisfactory. The color of amniotic fluid may have an impact on the occurrence of intrauterine infection, including early symptoms of the GBS infection.