Streptococcus agalactiae: Difference between revisions
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==Ecology== | ==Ecology== | ||
S. agalactiae inhabits a human host, colonizing the lower gastrointestinal tract and the genitourinary tract. Colonization is frequent in pregnant women, where the bacteria is colonized in 15% to 45% of women and more specifically, 10%-30% of pregnant women (textbook and woods). In pregnant women, colonization can be transferred in utero to the fetus, or transferred from the birth canal during delivery. <ref name=online /> | S. agalactiae inhabits a human host, colonizing the lower gastrointestinal tract and the genitourinary tract. Colonization is frequent in pregnant women, where the bacteria is colonized in 15% to 45% of women and more specifically, 10%-30% of pregnant women (textbook and woods). In pregnant women, colonization can be transferred in utero to the fetus, or transferred from the birth canal during delivery. <ref name=online /> | ||
==Pathology== | ==Pathology== | ||
S. agalactiae colonization can result in infection and serious diseases in pregnant women, infants, men and non-pregnant women. S. agalactiae virulence and pathology varies amongst the various sereotypes of the bacteria, with types Ia, II, III, and V found to be the most virulent ( | S. agalactiae colonization can result in infection and serious diseases in pregnant women, infants, men and non-pregnant women. S. agalactiae virulence and pathology varies amongst the various sereotypes of the bacteria, with types Ia, II, III, and V found to be the most virulent <ref name=glasergenomeGlaser, Philippe, et. al. “Genome sequence of Streptococcus agalactiae, a pathogen causing invasive neonatal disease.” Molecular Microbiology (2002), 1499-1513</ref>. The bacteria is well known for the serious infections and complications it causes in pregnant women and neonates. While carriage rates for pregnant women are very high (10%-30%), infection rates are much lower. In fact, the majority of pregnant women colonized with the bacteria are asymptomatic, with only 2%-4% of patients diagnosed with the most common infection associated with pregnant women and the bacteria, a urinary tract infection <ref name=CDC>Schrag, Stephanie, et al. “Prevention of Perinatal Group B Streptococcal Disease: Revised Guidelines from CDC” Center for Disease Control and Prevention, August 16 2002</ref>. These infections occur during and after pregnancy and generally clear up quite quickly. In very few cases, more serious complications such as endocarditos, meningitis, and osteomyelitis can occur.<ref name=txtbk /> | ||
S. agalactiae colonization complicates childbirth, as the rate of passing along colonization to the newborn is extremely high. In fact, over half – approximately 60% - of colonized mothers pass along the bacteria to their newborns. (textbook). Various risk factors such as heavy colonization, premature delivery, prolonged membrane rupture, and fever during labor increase the probability of passing along colonization. Colonization in the baby can occur while the baby is still developing in utero, at birth, or in the first few months after the baby is born. While many infants acquire S. agalactiae colonization from their mothers, a very small percentage of those infants that are colonized – only 1%-2% develop diseases as a result of colonization <ref name=online />. In utero and birth colonization can result in early onset disease, which is present within the first week of birth. Early onset disease as a result of S. agalactiae colonization usually presents itself as bactermia, pneumonia or meningitis.<ref name=online /> In fact, S. agalactiae is considered the main cause of these diseases in infants | |||
S. agalactiae colonization complicates childbirth, as the rate of passing along colonization to the newborn is extremely high. In fact, over half – approximately 60% - of colonized mothers pass along the bacteria to their newborns. (textbook). Various risk factors such as heavy colonization, premature delivery, prolonged membrane rupture, and fever during labor increase the probability of passing along colonization. Colonization in the baby can occur while the baby is still developing in utero, at birth, or in the first few months after the baby is born. While many infants acquire S. agalactiae colonization from their mothers, a very small percentage of those infants that are colonized – only 1%-2% develop diseases as a result of colonization <ref name=online />. In utero and birth colonization can result in early onset disease, which is present within the first week of birth. Early onset disease as a result of S. agalactiae colonization usually presents itself as bactermia, pneumonia or meningitis.<ref name=online /> In fact, S. agalactiae is considered the main cause of these diseases in infants <ref name=glasergenome /> . In addition, fetal aspiration of colonized amniotic fluid can lead to serious complications such as stillbirth, neonatal pneumonia or sepsis. <ref name=CDC /> Medical advancements have lead to more efficient diagnosis and care of newborns colonized with S. agalactiae and have reduced the mortality rate to less than 5%. However, while the mortality rate is low, many infected newborns do not completely recover from meningitis and develop neurologic sequelae, an immulogical condition that often includes mental retardation, blindness and deafness. S. agalactiae colonization can also occur in older infants, resulting in late-onset diseases that occur from one week after birth to 3 months of age. Such infections usually present as sepsis, pneumonia, meningitis, osteomyelitis or septic arthritis <ref name=online />.<ref name=CDC /> While the mortality rate is low for infants with late onset disease, developmental complications from meningitis are common.<ref name=txtbk /> | |||
S. agalactiae colonization occurs in individuals throughout the population, including nonpregnant women and in men. In such individuals, colonization in conjunction with compromised immunity can result in diseases such as bacteremia, pneumonia, bone and joint infections, and skin and soft-tissue infections. Mortality is higher for these patients and falls between 15% and 32%. <ref name=txtbk /> | S. agalactiae colonization occurs in individuals throughout the population, including nonpregnant women and in men. In such individuals, colonization in conjunction with compromised immunity can result in diseases such as bacteremia, pneumonia, bone and joint infections, and skin and soft-tissue infections. Mortality is higher for these patients and falls between 15% and 32%. <ref name=txtbk /> | ||
Much research has gone into how to treat S. agalactiae colonization in pregnant patients, as a means to prevent the dangerous infections that may result from colonization. The Center for Disease Control and Prevention (CDC) has issued guidelines (most recently updated in 2002) for detecting and treating S. agalactiae colonization in pregnant patients, and these guidelines have been largely responsible for the lowered infant mortality rate. The CDC promotes two methods of detecting colonization. The risk-based method analyzes a particular patient’s risk of colonizing the bacteria by identifying risk factors correlated with S. agalactiae infections. The presence of these factors, which include premature delivery (before 37 weeks), having a temperature (greater than 100.4 degrees Fahrenheit) during labor and delivery, or premature rupture of the amniotic fluid (premature rupture of membranes), indicate a high probability of S. agalactiae colonization <ref name=CDC />. The screening-based method cultures swabs taken from pregnant women (between 35 and 37 weeks pregnant) to test for vaginal and rectal S. agalactiae colonization. Both methods indicate that a colonized patient should receive antibiotics during labor in order to reduce the risk of passing along colonization to the infant. While penicillin is generally regarded as the first choice for intrapartum antibiotic prophylaxis, ampicillin can be used for patients with penicillin allergies.<ref name=CDC /> | |||
As S. agalactiae can cause many different infections and complications, various different medical treatments are often used to treat patients sickened by this bacteria. Current research is focusing on the development of a vaccine to create immunity against the bacteria and many in the medical community are rallying to work on ways to better diagnose and treat non pregnant patients with colonization. <ref name=epi>Phares Christina R, Lynfield Ruth, Monica M. Farley, et al. “Epidemiology of Invasive Group B Streptococcal Disease in the United States, 1999-2005.” JAMA. 2008; 299(17):2056-2065</ref> | |||
== | ==Epidemiology== | ||
S. agalactiae affects three main groups within the population: pregnant women, infants, and non pregnant women and men. Following the 2002 release of the CDC’s guidelines on how to deal with the diseases, a major epidemiological study (Phares, et. al) was published studying the trends of S. agalactiae disease within the population. The study, conducted from 1999-2005 and studying the population in 10 U.S. states, found that there 14,573 cases of S. agalactiae disease. 9.25%, or 1,348 of these cases resulted in death. The incidence of early onset disease (which the study defined as from birth until 6 days old) decreased during the study, as from 1999-2001 the rate was 0.47 per 1000 live births and from 2003-2005 the rate decreased by 0.12 to 0.34 per 1000 live births. The study also measured the incidence of late onset disease <ref name=epi /> | |||
==Current Research== | ==Current Research== | ||
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| Streptococcus agalactiae | ||||||||||||||
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| Streptococcus agalactiae |
Description and significance
Streptococcus agalactiae, also known as Group B streptococci are gram positive cocci that range from 0.6 to 1.2 um. These cocci arrange themselves in chains, forming shorter chains in clinical specimens and longer chains in a culture specimen. They are distinguished from other streptococci by the presence of the group B antigen.[1]
S. agalactiae colonizes in a woman’s vaginal and gastrointestinal tracts in a commensal relationship that is present in 25-40% of healthy women. When the organism is introduced to a weakened or susceptible host (including individuals with compromised immunity and newborns), S. agalactiae causes bacterial sepsis, pneumonia and meningitis in newborns and can also cause postpartum infection, neonatal sepsis and other infections in infected hosts.[2] [3]
Cell structure and metabolism
S. agalactiae are facultative anerobes that are both B-hemoltyic and non hemolytic[1] (hemolysis is the breakdown of red blood cells before the natural course of the red blood cell’s life).[4]
Different strains of Streptococcus agalactiae have been identified by serologic markers that have classified different groups based on the prescence of either a B antigen or group specific cell wall polysaccharide antigen, a type-specific capsular polysaccharides or the presence of the surface (C) protein. The type-specific capsular polysaccharides have been lableled Ia, Ia/c, Ib/c, II, IIc, III, IV, V, VI, VII, VIII and are used as epidemiologic markers.[1]
The cell structure of S. agalactiae helps to contribute to the organism’s virulence in several different ways. S. agalactiae contains a thick peptidoglycan cell wall layer which prevents dessication and allows for the organism to live on dry surfaces. The capsular polysaccharides Ia, III and V further contribute to the organism’s virulence by preventing the immune response of complement mediated phagocytosis. In addition, the organism’s virulence is heightened by the presence of hydrolytic enzymes that aide in the spread of bacteria and allow for host tissue destruction.[1]
Genome structure
As there are several isolates of S. agalactiae, the genome sequence of different isolates have been determined and comparatively analyzed with other S. agalactiae strains. The study found that the circular S. agalactiae genome consists of 2,160,267 base pairs, including a G + C content of 35.7%, 80 tRNAs, 7 rRNAs and 3 sRNAs. The project predicted that the genome encodes for 2,175 proteins, 61% of which (1,333) were identified, while the remaining proteins coded by the genome are “of unknown function.”[2]
In addition, the genome sequencing experiment identified various genes that act as possible virulence factors. Several genes such as Sip (SAG0032), CAMP factor (SAG2043), R5 protein (SAG1331), Streptococcal enolase (SAG0628), hyaluronidase (SAG1197) and hemolysin/cytolysin (cylE, SAG0669), have been identified as coding for surface proteins or secretory proteins that contribute to the organisms virulence or aide in the organism’s immunity against host defenses.[2]
The genome project highlighted the unique membrane structure of S. agalactiae as it identified the S. agalactiae genomic sequences that code for the B antigen present on the surface of all S. agalactiae strains and the capsular polysaccharide specific to each strain of S. agalactiae. The project also recognized nine differing capsular polysaccharides types, each one containing salic acid structures. These units are part of a repeating structure that prevent the activation of the host’s alternative complement pathway and thereby contribute to the organism’s virulence.[2]
The sequencing project also undertook comparative genomics, comparing the genome of S. agalactiae to that of its common streptococci, S. pneumoniae and S. pyogenes. The analysis discovered 1,060 homologous genes in the three genomes and identified 683 genes specific to S. agalactiae only. These findings are in line with the relationships between the different strains, which must have similar gene factors as they all cause invasive diseases, but cannot have identical genomes as they each colonize and invade different areas and cause different diseases. For example, while S. agalactiae codes for the synthesis of arginine, asparate and citruline, it is missing the genes that S. pneumoniae and S. pyogenes use to synthesize fucose, lactose, mannitol, raffinose, lysine, and threonine. The differining genes are most probably a reflection of the differening hosts between the organisms.[2]
While there are various different serotypes of S. agalactiae, the genomic variations between and within serotypes are not well recognized. It has been hypothesized, however, that these variations are mainly unique to S. agalactiae, as while 260 (38%) of S. agalactiae’s unique 683 genes vary amongst different S. agalactiae serotypes, only 47 (4%) of the genes found in all three streptococci strains vary amongst different S. agalactiae serotypes.[2]
Ecology
S. agalactiae inhabits a human host, colonizing the lower gastrointestinal tract and the genitourinary tract. Colonization is frequent in pregnant women, where the bacteria is colonized in 15% to 45% of women and more specifically, 10%-30% of pregnant women (textbook and woods). In pregnant women, colonization can be transferred in utero to the fetus, or transferred from the birth canal during delivery. [3]
Pathology
S. agalactiae colonization can result in infection and serious diseases in pregnant women, infants, men and non-pregnant women. S. agalactiae virulence and pathology varies amongst the various sereotypes of the bacteria, with types Ia, II, III, and V found to be the most virulent Cite error: Invalid <ref> tag; invalid names, e.g. too many. These infections occur during and after pregnancy and generally clear up quite quickly. In very few cases, more serious complications such as endocarditos, meningitis, and osteomyelitis can occur.[1]
S. agalactiae colonization complicates childbirth, as the rate of passing along colonization to the newborn is extremely high. In fact, over half – approximately 60% - of colonized mothers pass along the bacteria to their newborns. (textbook). Various risk factors such as heavy colonization, premature delivery, prolonged membrane rupture, and fever during labor increase the probability of passing along colonization. Colonization in the baby can occur while the baby is still developing in utero, at birth, or in the first few months after the baby is born. While many infants acquire S. agalactiae colonization from their mothers, a very small percentage of those infants that are colonized – only 1%-2% develop diseases as a result of colonization [3]. In utero and birth colonization can result in early onset disease, which is present within the first week of birth. Early onset disease as a result of S. agalactiae colonization usually presents itself as bactermia, pneumonia or meningitis.[3] In fact, S. agalactiae is considered the main cause of these diseases in infants [5] . In addition, fetal aspiration of colonized amniotic fluid can lead to serious complications such as stillbirth, neonatal pneumonia or sepsis. [6] Medical advancements have lead to more efficient diagnosis and care of newborns colonized with S. agalactiae and have reduced the mortality rate to less than 5%. However, while the mortality rate is low, many infected newborns do not completely recover from meningitis and develop neurologic sequelae, an immulogical condition that often includes mental retardation, blindness and deafness. S. agalactiae colonization can also occur in older infants, resulting in late-onset diseases that occur from one week after birth to 3 months of age. Such infections usually present as sepsis, pneumonia, meningitis, osteomyelitis or septic arthritis [3].[6] While the mortality rate is low for infants with late onset disease, developmental complications from meningitis are common.[1]
S. agalactiae colonization occurs in individuals throughout the population, including nonpregnant women and in men. In such individuals, colonization in conjunction with compromised immunity can result in diseases such as bacteremia, pneumonia, bone and joint infections, and skin and soft-tissue infections. Mortality is higher for these patients and falls between 15% and 32%. [1]
Much research has gone into how to treat S. agalactiae colonization in pregnant patients, as a means to prevent the dangerous infections that may result from colonization. The Center for Disease Control and Prevention (CDC) has issued guidelines (most recently updated in 2002) for detecting and treating S. agalactiae colonization in pregnant patients, and these guidelines have been largely responsible for the lowered infant mortality rate. The CDC promotes two methods of detecting colonization. The risk-based method analyzes a particular patient’s risk of colonizing the bacteria by identifying risk factors correlated with S. agalactiae infections. The presence of these factors, which include premature delivery (before 37 weeks), having a temperature (greater than 100.4 degrees Fahrenheit) during labor and delivery, or premature rupture of the amniotic fluid (premature rupture of membranes), indicate a high probability of S. agalactiae colonization [6]. The screening-based method cultures swabs taken from pregnant women (between 35 and 37 weeks pregnant) to test for vaginal and rectal S. agalactiae colonization. Both methods indicate that a colonized patient should receive antibiotics during labor in order to reduce the risk of passing along colonization to the infant. While penicillin is generally regarded as the first choice for intrapartum antibiotic prophylaxis, ampicillin can be used for patients with penicillin allergies.[6]
As S. agalactiae can cause many different infections and complications, various different medical treatments are often used to treat patients sickened by this bacteria. Current research is focusing on the development of a vaccine to create immunity against the bacteria and many in the medical community are rallying to work on ways to better diagnose and treat non pregnant patients with colonization. [7]
Epidemiology
S. agalactiae affects three main groups within the population: pregnant women, infants, and non pregnant women and men. Following the 2002 release of the CDC’s guidelines on how to deal with the diseases, a major epidemiological study (Phares, et. al) was published studying the trends of S. agalactiae disease within the population. The study, conducted from 1999-2005 and studying the population in 10 U.S. states, found that there 14,573 cases of S. agalactiae disease. 9.25%, or 1,348 of these cases resulted in death. The incidence of early onset disease (which the study defined as from birth until 6 days old) decreased during the study, as from 1999-2001 the rate was 0.47 per 1000 live births and from 2003-2005 the rate decreased by 0.12 to 0.34 per 1000 live births. The study also measured the incidence of late onset disease [7]
Current Research
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 R. Murray, S. Rosenthal and A. Pfaller. “Streptococcus.” Medical Microbiology, Fifth Edition, Chapter 23, p. 247-250, (2005)Elsevier Mosby
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Tettelin, Herve et. Al. “Complete genome sequence and comparitive genomic analysis of an emerging human pathogen, serotype V Streptococcus agalactiae.” PNAS. September 2002. Vol. 99, no. 19, 12391-12396.
- ↑ 3.0 3.1 3.2 3.3 3.4 Woods, Christian J. “Streptococcus Group B Infections.” Emedicine http://emedicine.medscape.com/article/229091-overview
- ↑ Medline Plus. 20 April 2002 http://www.nlm.nih.gov/medlineplus/ency/article/002372.htm
- ↑ Cite error: Invalid
<ref>tag; no text was provided for refs namedglasergenome - ↑ 6.0 6.1 6.2 6.3 Cite error: Invalid
<ref>tag; no text was provided for refs namedCDC - ↑ 7.0 7.1 Phares Christina R, Lynfield Ruth, Monica M. Farley, et al. “Epidemiology of Invasive Group B Streptococcal Disease in the United States, 1999-2005.” JAMA. 2008; 299(17):2056-2065