Epidemiology of streptococcus parasanguinis is the study of the distribution and determinants of the infection or colonization by the bacterium in human and animal populations. Epidemiology can help understand the risk factors, transmission modes, prevalence, incidence, morbidity, mortality, and control measures of streptococcus parasanguinis.
Some epidemiological aspects of streptococcus parasanguinis are:
Host range: Streptococcus parasanguinis is a common human commensal bacterium that colonizes multiple body sites, especially the oral cavity. It is a prevalent bacterium in the oral cavity of both adults and infants, and it plays a vital role in dental plaque formation and oral health. Streptococcus parasanguinis is also an opportunistic pathogen that can cause subacute endocarditis, a severe infection of the heart valves, in susceptible individuals. Streptococcus parasanguinis has also been reported as a new animal pathogen that can cause subclinical mastitis, a chronic mammary gland inflammation, in sheep.
Transmission modes: Streptococcus parasanguinis can be transmitted from person to person or from animal to person through direct or indirect contact with saliva, blood, or other body fluids. The main transmission route is through oral contacts, such as kissing, sharing utensils, or dental procedures. Streptococcus parasanguinis can also be transmitted through sexual contact, such as oral sex or vaginal intercourse. Streptococcus parasanguinis can also be transmitted from animals to humans through contact with infected milk or meat.
Prevalence and incidence: The frequency and prevalence of streptococcus parasanguinis infection or colonization vary depending on the host population, the body site, and the detection method. For example, one study found that streptococcus parasanguinis was detected in 86% of saliva samples and 67% of fecal samples from healthy adults using quantitative real-time PCR (qPCR) targeting the groEL gene. Another study found that streptococcus parasanguinis was detected in 17% of blood cultures from patients with infective endocarditis using conventional culture methods.
Morbidity and mortality: The prevalence and fatality rates of streptococcus parasanguinis infection or colonization depend on the host’s immune status, the site and severity of infection, and the availability of treatment. For example, streptococcus parasanguinis infection in the oral cavity can cause dental caries, gingivitis, periodontitis, or abscesses, which can affect the host’s quality of life and oral function. Streptococcus parasanguinis infection in the bloodstream can cause subacute endocarditis, leading to severe complications such as heart failure, embolism, abscess formation, or valve damage. The mortality rate of subacute endocarditis caused by streptococcus parasanguinis ranges from 10% to 30%, depending on the treatment regimen and the presence of comorbidities.
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: parasanguinis
Due to its division mode, Streptococcus parasanguinis is a spherical or ovoid-shaped bacterium typically occurring in pairs or chains (resembling a string of beads). It lacks the formation of spores and is non-motile, meaning it does not possess flagella for movement.
The cell wall of Streptococcus parasanguinis is composed of peptidoglycan, which provides structural support and protection. It also contains teichoic acids involved in cell division and binding to host tissues. The cell membrane lies beneath the cell wall and regulates the transport of molecules in and out of the bacterium.
Like other streptococci, S. parasanguinis has no capsule (a gel-like layer outside the cell wall). Still, it possesses various surface proteins, including adhesins, which enable it to adhere to surfaces such as tooth enamel and epithelial cells. These surface proteins play a significant role in their ability to colonize various host tissues.
Furthermore, S. parasanguinis possesses fimbriae or pili, hair-like appendages on the cell surface that assist in adhesion to host cells and the formation of biofilms. Communities of bacteria known as biofilms attach to surfaces and are encased in a protective matrix, which can contribute to developing dental plaque and other infections.
Antigenic types of streptococcus parasanguinis are different strains or variants of the bacterium with distinct antigenic properties, meaning they can elicit different immune responses in the host. Antigens are molecules that an immune system can detect the immune system, such as proteins, polysaccharides, or lipids.
One way to classify antigenic types of streptococcus parasanguinis is based on the groEL gene, which encodes a heat shock protein that is involved in protein folding and stress response. The groEL gene is highly conserved among bacteria, but it can also have some variations that can be used to differentiate between strains. Two species-specific PCR primers targeting the groEL gene, Spa146f-Spa525r, and Spa93f-Spa525r, were designed to quantify human oral and fecal streptococcus parasanguinis. These primers can also identify the antigenic types of streptococcus parasanguinis based on the sequence analysis of the amplified groEL gene.
Another way to classify antigenic types of streptococcus parasanguinis is based on the fap1 gene cluster, which encodes a fimbrial adhesin protein that mediates the attachment of the bacterium to oral surfaces and other bacteria. The fap1 gene cluster consists of 14 genes that are involved in the biosynthesis, glycosylation, and export of the Fap1 protein. The fap1 gene cluster is highly variable among strains of streptococcus parasanguinis, and it can be used to distinguish between antigenic types based depending on the presence or absence of genes or gene variants.
S. parasanguinis infection’s pathogenesis is not well understood, but some studies have suggested some possible mechanisms.
S. parasanguinis can adhere to the host tissues, such as the tooth enamel, the salivary pellicle, or the heart valves, by expressing various adhesins that bind to extracellular matrix (ECM) proteins, such as fibronectin, collagen, or laminin. For example, S. parasanguinis produces a fibronectin-binding protein (Spaf_1409) that mediates the attachment of the bacteria to fibronectin-coated surfaces and enhances biofilm formation. S. parasanguinis also produces a collagen-binding protein (CbpA) that binds to collagen type I and IV and promotes bacterial aggregation. These adhesins may facilitate the colonization and invasion of S. parasanguinis in the oral cavity and the endocardium.
S. parasanguinis can cause inflammation and tissue damage by producing various virulence factors, such as hydrogen peroxide, proteases, or hemolysins. For example, S. parasanguinis produces hydrogen peroxide that can kill competing bacteria, damage host cells, or modulate host immune responses. S. parasanguinis also produces a serine protease (SpaP) that degrades fibrinogen and interferes with blood clotting. S. parasanguinis also produces a hemolysin (SlyA) that lyses red blood cells and releases iron for bacterial growth. These virulence factors may contribute to the pathogenesis of S. parasanguinis in dental caries or endocarditis.
The host defenses of S. parasanguinis are not fully elucidated, but some studies have suggested some possible mechanisms.
S. parasanguinis can evade the host immune system by mimicking the host tissues or producing factors inhibiting the complement system or phagocytosis. For example, S. parasanguinis produces a polysaccharide capsule chemically like the host’s connective tissue and is non-antigenic. The capsule also protects the bacteria from opsonization and phagocytosis by neutrophils. S. parasanguinis also produces a surface protein called Fap1 that binds to factor H, a negative regulator of the complement system, and prevents the activation of the alternative pathway. Fap1 also inhibits the oxidative burst of neutrophils through a decrease in the generation of reactive oxygen species.
S. parasanguinis can adhere to the host surfaces and form biofilms by expressing various adhesins, such as pili, fimbriae, and surface proteins. These adhesins mediate the attachment of S. parasanguinis to salivary pellicles, extracellular matrix proteins, or other bacteria. S. parasanguinis is more likely to survive and persist when biofilms are present in the oral cavity and protect the bacteria from antimicrobial agents and host immune responses.
S. parasanguinis can also adapt to various environmental stresses, such as pH changes, oxidative stress, nutrient limitation, or antibiotic exposure, by regulating its gene expression or modifying its cell envelope. For example, S. parasanguinis can increase its resistance to acid stress by upregulating genes involved in glycolysis, amino acid metabolism, and proton efflux. S. parasanguinis can also increase its resistance to oxidative stress by upregulating genes involved in DNA repair, antioxidant enzymes, and iron homeostasis. S. parasanguinis can modify its cell envelope by altering its lipid composition, peptidoglycan cross-linking, or surface charge to increase its resistance to antibiotics or antimicrobial peptides.
Streptococcus parasanguinis (SP) is a type of bacteria that can cause post-streptococcal glomerulonephritis (PSGN), a kidney disease. PSGN usually occurs ten days following scarlet fever or strep throat and roughly three weeks following a GAS skin infection. Fatigue, swollen hands, feet, cheeks, less urine production or less desire to urinate, and dark, reddish-brown urine are all signs of PSGN. Depending on the location afflicted, red and painful swollen tissue, scabby sores, painful (strep) throat, and a rash may also be signs of SP infection.
SP is one of the significant early inhabitants of the human oral cavity’s dental surfaces. Pili and fimbriae, cell surface features, enable the bacteria to adhere to oral surfaces. These adhesion molecules are crucial for developing biofilms, promoting aggregation with late tooth colonizers to form dental plaque. The presence of SP in the oral cavity is associated with healthy microflora.
Diagnosis methods include culture, PCR, serology, or molecular typing. Culture is the traditional method that involves growing the bacterium on selective media, such as blood agar or mitis salivarius agar, and performing biochemical tests, such as catalase, bile solubility, and optochin sensitivity.
PCR is a molecular method that amplifies and detects specific DNA sequences of the bacterium, such as the groEL gene or the fap1 gene cluster. Serology is an immunological method that involves measuring the host’s antibody response to the bacterium, such as anti-streptolysin O (ASO) or anti-DNase B (ADB). Molecular typing is a genetic method that involves comparing the DNA sequences or patterns of different strains of the bacterium, such as multilocus sequence typing (MLST) or pulsed-field gel electrophoresis (PFGE).
Prevention methods for streptococcus parasanguinis and other infections:
Maintain good oral hygiene (brushing, flossing, regular dental visits).
Wash hands frequently with soap and water.
Avoid sharing personal items (toothbrushes, cups, utensils, towels, razors).
Practice safe sex (use condoms, limit partners).
Get vaccinated against preventable diseases (influenza, pneumonia, meningitis, tetanus, diphtheria, pertussis, HPV).
Use antimicrobial prophylaxis before surgery or dental procedures.
Streptococcus parasanguinis – an overview | ScienceDirect Topics
Structural insight into the role of Streptococcus parasanguinis Fap1 within oral biofilm formation – PMC (nih.gov)
Epidemiology of streptococcus parasanguinis is the study of the distribution and determinants of the infection or colonization by the bacterium in human and animal populations. Epidemiology can help understand the risk factors, transmission modes, prevalence, incidence, morbidity, mortality, and control measures of streptococcus parasanguinis.
Some epidemiological aspects of streptococcus parasanguinis are:
Host range: Streptococcus parasanguinis is a common human commensal bacterium that colonizes multiple body sites, especially the oral cavity. It is a prevalent bacterium in the oral cavity of both adults and infants, and it plays a vital role in dental plaque formation and oral health. Streptococcus parasanguinis is also an opportunistic pathogen that can cause subacute endocarditis, a severe infection of the heart valves, in susceptible individuals. Streptococcus parasanguinis has also been reported as a new animal pathogen that can cause subclinical mastitis, a chronic mammary gland inflammation, in sheep.
Transmission modes: Streptococcus parasanguinis can be transmitted from person to person or from animal to person through direct or indirect contact with saliva, blood, or other body fluids. The main transmission route is through oral contacts, such as kissing, sharing utensils, or dental procedures. Streptococcus parasanguinis can also be transmitted through sexual contact, such as oral sex or vaginal intercourse. Streptococcus parasanguinis can also be transmitted from animals to humans through contact with infected milk or meat.
Prevalence and incidence: The frequency and prevalence of streptococcus parasanguinis infection or colonization vary depending on the host population, the body site, and the detection method. For example, one study found that streptococcus parasanguinis was detected in 86% of saliva samples and 67% of fecal samples from healthy adults using quantitative real-time PCR (qPCR) targeting the groEL gene. Another study found that streptococcus parasanguinis was detected in 17% of blood cultures from patients with infective endocarditis using conventional culture methods.
Morbidity and mortality: The prevalence and fatality rates of streptococcus parasanguinis infection or colonization depend on the host’s immune status, the site and severity of infection, and the availability of treatment. For example, streptococcus parasanguinis infection in the oral cavity can cause dental caries, gingivitis, periodontitis, or abscesses, which can affect the host’s quality of life and oral function. Streptococcus parasanguinis infection in the bloodstream can cause subacute endocarditis, leading to severe complications such as heart failure, embolism, abscess formation, or valve damage. The mortality rate of subacute endocarditis caused by streptococcus parasanguinis ranges from 10% to 30%, depending on the treatment regimen and the presence of comorbidities.
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: parasanguinis
Due to its division mode, Streptococcus parasanguinis is a spherical or ovoid-shaped bacterium typically occurring in pairs or chains (resembling a string of beads). It lacks the formation of spores and is non-motile, meaning it does not possess flagella for movement.
The cell wall of Streptococcus parasanguinis is composed of peptidoglycan, which provides structural support and protection. It also contains teichoic acids involved in cell division and binding to host tissues. The cell membrane lies beneath the cell wall and regulates the transport of molecules in and out of the bacterium.
Like other streptococci, S. parasanguinis has no capsule (a gel-like layer outside the cell wall). Still, it possesses various surface proteins, including adhesins, which enable it to adhere to surfaces such as tooth enamel and epithelial cells. These surface proteins play a significant role in their ability to colonize various host tissues.
Furthermore, S. parasanguinis possesses fimbriae or pili, hair-like appendages on the cell surface that assist in adhesion to host cells and the formation of biofilms. Communities of bacteria known as biofilms attach to surfaces and are encased in a protective matrix, which can contribute to developing dental plaque and other infections.
Antigenic types of streptococcus parasanguinis are different strains or variants of the bacterium with distinct antigenic properties, meaning they can elicit different immune responses in the host. Antigens are molecules that an immune system can detect the immune system, such as proteins, polysaccharides, or lipids.
One way to classify antigenic types of streptococcus parasanguinis is based on the groEL gene, which encodes a heat shock protein that is involved in protein folding and stress response. The groEL gene is highly conserved among bacteria, but it can also have some variations that can be used to differentiate between strains. Two species-specific PCR primers targeting the groEL gene, Spa146f-Spa525r, and Spa93f-Spa525r, were designed to quantify human oral and fecal streptococcus parasanguinis. These primers can also identify the antigenic types of streptococcus parasanguinis based on the sequence analysis of the amplified groEL gene.
Another way to classify antigenic types of streptococcus parasanguinis is based on the fap1 gene cluster, which encodes a fimbrial adhesin protein that mediates the attachment of the bacterium to oral surfaces and other bacteria. The fap1 gene cluster consists of 14 genes that are involved in the biosynthesis, glycosylation, and export of the Fap1 protein. The fap1 gene cluster is highly variable among strains of streptococcus parasanguinis, and it can be used to distinguish between antigenic types based depending on the presence or absence of genes or gene variants.
S. parasanguinis infection’s pathogenesis is not well understood, but some studies have suggested some possible mechanisms.
S. parasanguinis can adhere to the host tissues, such as the tooth enamel, the salivary pellicle, or the heart valves, by expressing various adhesins that bind to extracellular matrix (ECM) proteins, such as fibronectin, collagen, or laminin. For example, S. parasanguinis produces a fibronectin-binding protein (Spaf_1409) that mediates the attachment of the bacteria to fibronectin-coated surfaces and enhances biofilm formation. S. parasanguinis also produces a collagen-binding protein (CbpA) that binds to collagen type I and IV and promotes bacterial aggregation. These adhesins may facilitate the colonization and invasion of S. parasanguinis in the oral cavity and the endocardium.
S. parasanguinis can cause inflammation and tissue damage by producing various virulence factors, such as hydrogen peroxide, proteases, or hemolysins. For example, S. parasanguinis produces hydrogen peroxide that can kill competing bacteria, damage host cells, or modulate host immune responses. S. parasanguinis also produces a serine protease (SpaP) that degrades fibrinogen and interferes with blood clotting. S. parasanguinis also produces a hemolysin (SlyA) that lyses red blood cells and releases iron for bacterial growth. These virulence factors may contribute to the pathogenesis of S. parasanguinis in dental caries or endocarditis.
The host defenses of S. parasanguinis are not fully elucidated, but some studies have suggested some possible mechanisms.
S. parasanguinis can evade the host immune system by mimicking the host tissues or producing factors inhibiting the complement system or phagocytosis. For example, S. parasanguinis produces a polysaccharide capsule chemically like the host’s connective tissue and is non-antigenic. The capsule also protects the bacteria from opsonization and phagocytosis by neutrophils. S. parasanguinis also produces a surface protein called Fap1 that binds to factor H, a negative regulator of the complement system, and prevents the activation of the alternative pathway. Fap1 also inhibits the oxidative burst of neutrophils through a decrease in the generation of reactive oxygen species.
S. parasanguinis can adhere to the host surfaces and form biofilms by expressing various adhesins, such as pili, fimbriae, and surface proteins. These adhesins mediate the attachment of S. parasanguinis to salivary pellicles, extracellular matrix proteins, or other bacteria. S. parasanguinis is more likely to survive and persist when biofilms are present in the oral cavity and protect the bacteria from antimicrobial agents and host immune responses.
S. parasanguinis can also adapt to various environmental stresses, such as pH changes, oxidative stress, nutrient limitation, or antibiotic exposure, by regulating its gene expression or modifying its cell envelope. For example, S. parasanguinis can increase its resistance to acid stress by upregulating genes involved in glycolysis, amino acid metabolism, and proton efflux. S. parasanguinis can also increase its resistance to oxidative stress by upregulating genes involved in DNA repair, antioxidant enzymes, and iron homeostasis. S. parasanguinis can modify its cell envelope by altering its lipid composition, peptidoglycan cross-linking, or surface charge to increase its resistance to antibiotics or antimicrobial peptides.
Streptococcus parasanguinis (SP) is a type of bacteria that can cause post-streptococcal glomerulonephritis (PSGN), a kidney disease. PSGN usually occurs ten days following scarlet fever or strep throat and roughly three weeks following a GAS skin infection. Fatigue, swollen hands, feet, cheeks, less urine production or less desire to urinate, and dark, reddish-brown urine are all signs of PSGN. Depending on the location afflicted, red and painful swollen tissue, scabby sores, painful (strep) throat, and a rash may also be signs of SP infection.
SP is one of the significant early inhabitants of the human oral cavity’s dental surfaces. Pili and fimbriae, cell surface features, enable the bacteria to adhere to oral surfaces. These adhesion molecules are crucial for developing biofilms, promoting aggregation with late tooth colonizers to form dental plaque. The presence of SP in the oral cavity is associated with healthy microflora.
Diagnosis methods include culture, PCR, serology, or molecular typing. Culture is the traditional method that involves growing the bacterium on selective media, such as blood agar or mitis salivarius agar, and performing biochemical tests, such as catalase, bile solubility, and optochin sensitivity.
PCR is a molecular method that amplifies and detects specific DNA sequences of the bacterium, such as the groEL gene or the fap1 gene cluster. Serology is an immunological method that involves measuring the host’s antibody response to the bacterium, such as anti-streptolysin O (ASO) or anti-DNase B (ADB). Molecular typing is a genetic method that involves comparing the DNA sequences or patterns of different strains of the bacterium, such as multilocus sequence typing (MLST) or pulsed-field gel electrophoresis (PFGE).
Prevention methods for streptococcus parasanguinis and other infections:
Maintain good oral hygiene (brushing, flossing, regular dental visits).
Wash hands frequently with soap and water.
Avoid sharing personal items (toothbrushes, cups, utensils, towels, razors).
Practice safe sex (use condoms, limit partners).
Get vaccinated against preventable diseases (influenza, pneumonia, meningitis, tetanus, diphtheria, pertussis, HPV).
Use antimicrobial prophylaxis before surgery or dental procedures.
Streptococcus parasanguinis – an overview | ScienceDirect Topics
Structural insight into the role of Streptococcus parasanguinis Fap1 within oral biofilm formation – PMC (nih.gov)
Epidemiology of streptococcus parasanguinis is the study of the distribution and determinants of the infection or colonization by the bacterium in human and animal populations. Epidemiology can help understand the risk factors, transmission modes, prevalence, incidence, morbidity, mortality, and control measures of streptococcus parasanguinis.
Some epidemiological aspects of streptococcus parasanguinis are:
Host range: Streptococcus parasanguinis is a common human commensal bacterium that colonizes multiple body sites, especially the oral cavity. It is a prevalent bacterium in the oral cavity of both adults and infants, and it plays a vital role in dental plaque formation and oral health. Streptococcus parasanguinis is also an opportunistic pathogen that can cause subacute endocarditis, a severe infection of the heart valves, in susceptible individuals. Streptococcus parasanguinis has also been reported as a new animal pathogen that can cause subclinical mastitis, a chronic mammary gland inflammation, in sheep.
Transmission modes: Streptococcus parasanguinis can be transmitted from person to person or from animal to person through direct or indirect contact with saliva, blood, or other body fluids. The main transmission route is through oral contacts, such as kissing, sharing utensils, or dental procedures. Streptococcus parasanguinis can also be transmitted through sexual contact, such as oral sex or vaginal intercourse. Streptococcus parasanguinis can also be transmitted from animals to humans through contact with infected milk or meat.
Prevalence and incidence: The frequency and prevalence of streptococcus parasanguinis infection or colonization vary depending on the host population, the body site, and the detection method. For example, one study found that streptococcus parasanguinis was detected in 86% of saliva samples and 67% of fecal samples from healthy adults using quantitative real-time PCR (qPCR) targeting the groEL gene. Another study found that streptococcus parasanguinis was detected in 17% of blood cultures from patients with infective endocarditis using conventional culture methods.
Morbidity and mortality: The prevalence and fatality rates of streptococcus parasanguinis infection or colonization depend on the host’s immune status, the site and severity of infection, and the availability of treatment. For example, streptococcus parasanguinis infection in the oral cavity can cause dental caries, gingivitis, periodontitis, or abscesses, which can affect the host’s quality of life and oral function. Streptococcus parasanguinis infection in the bloodstream can cause subacute endocarditis, leading to severe complications such as heart failure, embolism, abscess formation, or valve damage. The mortality rate of subacute endocarditis caused by streptococcus parasanguinis ranges from 10% to 30%, depending on the treatment regimen and the presence of comorbidities.
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Streptococcaceae
Genus: Streptococcus
Species: parasanguinis
Due to its division mode, Streptococcus parasanguinis is a spherical or ovoid-shaped bacterium typically occurring in pairs or chains (resembling a string of beads). It lacks the formation of spores and is non-motile, meaning it does not possess flagella for movement.
The cell wall of Streptococcus parasanguinis is composed of peptidoglycan, which provides structural support and protection. It also contains teichoic acids involved in cell division and binding to host tissues. The cell membrane lies beneath the cell wall and regulates the transport of molecules in and out of the bacterium.
Like other streptococci, S. parasanguinis has no capsule (a gel-like layer outside the cell wall). Still, it possesses various surface proteins, including adhesins, which enable it to adhere to surfaces such as tooth enamel and epithelial cells. These surface proteins play a significant role in their ability to colonize various host tissues.
Furthermore, S. parasanguinis possesses fimbriae or pili, hair-like appendages on the cell surface that assist in adhesion to host cells and the formation of biofilms. Communities of bacteria known as biofilms attach to surfaces and are encased in a protective matrix, which can contribute to developing dental plaque and other infections.
Antigenic types of streptococcus parasanguinis are different strains or variants of the bacterium with distinct antigenic properties, meaning they can elicit different immune responses in the host. Antigens are molecules that an immune system can detect the immune system, such as proteins, polysaccharides, or lipids.
One way to classify antigenic types of streptococcus parasanguinis is based on the groEL gene, which encodes a heat shock protein that is involved in protein folding and stress response. The groEL gene is highly conserved among bacteria, but it can also have some variations that can be used to differentiate between strains. Two species-specific PCR primers targeting the groEL gene, Spa146f-Spa525r, and Spa93f-Spa525r, were designed to quantify human oral and fecal streptococcus parasanguinis. These primers can also identify the antigenic types of streptococcus parasanguinis based on the sequence analysis of the amplified groEL gene.
Another way to classify antigenic types of streptococcus parasanguinis is based on the fap1 gene cluster, which encodes a fimbrial adhesin protein that mediates the attachment of the bacterium to oral surfaces and other bacteria. The fap1 gene cluster consists of 14 genes that are involved in the biosynthesis, glycosylation, and export of the Fap1 protein. The fap1 gene cluster is highly variable among strains of streptococcus parasanguinis, and it can be used to distinguish between antigenic types based depending on the presence or absence of genes or gene variants.
S. parasanguinis infection’s pathogenesis is not well understood, but some studies have suggested some possible mechanisms.
S. parasanguinis can adhere to the host tissues, such as the tooth enamel, the salivary pellicle, or the heart valves, by expressing various adhesins that bind to extracellular matrix (ECM) proteins, such as fibronectin, collagen, or laminin. For example, S. parasanguinis produces a fibronectin-binding protein (Spaf_1409) that mediates the attachment of the bacteria to fibronectin-coated surfaces and enhances biofilm formation. S. parasanguinis also produces a collagen-binding protein (CbpA) that binds to collagen type I and IV and promotes bacterial aggregation. These adhesins may facilitate the colonization and invasion of S. parasanguinis in the oral cavity and the endocardium.
S. parasanguinis can cause inflammation and tissue damage by producing various virulence factors, such as hydrogen peroxide, proteases, or hemolysins. For example, S. parasanguinis produces hydrogen peroxide that can kill competing bacteria, damage host cells, or modulate host immune responses. S. parasanguinis also produces a serine protease (SpaP) that degrades fibrinogen and interferes with blood clotting. S. parasanguinis also produces a hemolysin (SlyA) that lyses red blood cells and releases iron for bacterial growth. These virulence factors may contribute to the pathogenesis of S. parasanguinis in dental caries or endocarditis.
The host defenses of S. parasanguinis are not fully elucidated, but some studies have suggested some possible mechanisms.
S. parasanguinis can evade the host immune system by mimicking the host tissues or producing factors inhibiting the complement system or phagocytosis. For example, S. parasanguinis produces a polysaccharide capsule chemically like the host’s connective tissue and is non-antigenic. The capsule also protects the bacteria from opsonization and phagocytosis by neutrophils. S. parasanguinis also produces a surface protein called Fap1 that binds to factor H, a negative regulator of the complement system, and prevents the activation of the alternative pathway. Fap1 also inhibits the oxidative burst of neutrophils through a decrease in the generation of reactive oxygen species.
S. parasanguinis can adhere to the host surfaces and form biofilms by expressing various adhesins, such as pili, fimbriae, and surface proteins. These adhesins mediate the attachment of S. parasanguinis to salivary pellicles, extracellular matrix proteins, or other bacteria. S. parasanguinis is more likely to survive and persist when biofilms are present in the oral cavity and protect the bacteria from antimicrobial agents and host immune responses.
S. parasanguinis can also adapt to various environmental stresses, such as pH changes, oxidative stress, nutrient limitation, or antibiotic exposure, by regulating its gene expression or modifying its cell envelope. For example, S. parasanguinis can increase its resistance to acid stress by upregulating genes involved in glycolysis, amino acid metabolism, and proton efflux. S. parasanguinis can also increase its resistance to oxidative stress by upregulating genes involved in DNA repair, antioxidant enzymes, and iron homeostasis. S. parasanguinis can modify its cell envelope by altering its lipid composition, peptidoglycan cross-linking, or surface charge to increase its resistance to antibiotics or antimicrobial peptides.
Streptococcus parasanguinis (SP) is a type of bacteria that can cause post-streptococcal glomerulonephritis (PSGN), a kidney disease. PSGN usually occurs ten days following scarlet fever or strep throat and roughly three weeks following a GAS skin infection. Fatigue, swollen hands, feet, cheeks, less urine production or less desire to urinate, and dark, reddish-brown urine are all signs of PSGN. Depending on the location afflicted, red and painful swollen tissue, scabby sores, painful (strep) throat, and a rash may also be signs of SP infection.
SP is one of the significant early inhabitants of the human oral cavity’s dental surfaces. Pili and fimbriae, cell surface features, enable the bacteria to adhere to oral surfaces. These adhesion molecules are crucial for developing biofilms, promoting aggregation with late tooth colonizers to form dental plaque. The presence of SP in the oral cavity is associated with healthy microflora.
Diagnosis methods include culture, PCR, serology, or molecular typing. Culture is the traditional method that involves growing the bacterium on selective media, such as blood agar or mitis salivarius agar, and performing biochemical tests, such as catalase, bile solubility, and optochin sensitivity.
PCR is a molecular method that amplifies and detects specific DNA sequences of the bacterium, such as the groEL gene or the fap1 gene cluster. Serology is an immunological method that involves measuring the host’s antibody response to the bacterium, such as anti-streptolysin O (ASO) or anti-DNase B (ADB). Molecular typing is a genetic method that involves comparing the DNA sequences or patterns of different strains of the bacterium, such as multilocus sequence typing (MLST) or pulsed-field gel electrophoresis (PFGE).
Prevention methods for streptococcus parasanguinis and other infections:
Maintain good oral hygiene (brushing, flossing, regular dental visits).
Wash hands frequently with soap and water.
Avoid sharing personal items (toothbrushes, cups, utensils, towels, razors).
Practice safe sex (use condoms, limit partners).
Get vaccinated against preventable diseases (influenza, pneumonia, meningitis, tetanus, diphtheria, pertussis, HPV).
Use antimicrobial prophylaxis before surgery or dental procedures.
Streptococcus parasanguinis – an overview | ScienceDirect Topics
Structural insight into the role of Streptococcus parasanguinis Fap1 within oral biofilm formation – PMC (nih.gov)
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