Neisseria sicca, a member of the Neisseria genus, typically resides within the human respiratory tract as a commensal organism, signifying its non-harmful and non-beneficial relationship with the host. However, certain strains of Neisseria sicca have been implicated in causing septicemia, particularly in individuals with compromised immune systems.
While the literature contains a limited number of case reports, they underscore the potential for this bacterium to induce infections in specific circumstances.Neisseria sicca meningitis occurred in a 68-year-old woman with chronic lymphocytic leukemia after chemotherapy. Successful ceftriaxone treatment ensured complete recovery.
In another case, a previously healthy 34-year-old man experienced bacterial conjunctivitis caused by Neisseria sicca. Symptoms like ocular pain, discharge, and erythema underlined its capacity to incite ocular infections. Furthermore, Neisseria sicca was implicated in peritonitis within a 54-year-old cirrhotic man following a paracentesis procedure, underscoring its potential to trigger peritoneal infections.
Neisseria sicca‘s role in endocarditis became evident as a 23-year-old woman with congenital heart disease developed the condition, leading to multiple embolic brain infarcts. Additionally, instances of Bartholin’s gland abscess caused by Neisseria sicca have been observed. A 24-year-old woman’s case highlighted its association with this condition after unprotected intercourse, managed effectively with clindamycin treatment and incision drainage.
Kingdom: Bacteria
Phylum: Pseudomonadota
Class: Betaproteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus:Neisseria
Species:Neisseria sicca
Neisseria sicca is an oxidase-positive, gram-negative bacterium characterized by a thin peptidoglycan.
Neisseria sicca has a spherical or cocci shape-diplococci. They measure about 0.6 to 1.0 µm in diameter.
Typically, they are observed in pairs, with the adjacent sides of the cells flattened. This arrangement gives them a distinctive kidney-shaped or bean-shaped appearance.
Neisseria sicca has pili, hairlike filamentous appendages extending several micrometers from the cell surface.
The antigenic types of Neisseria sicca still need to be explored due to its status as a rare and opportunistic pathogen. Despite this, certain virulence factors have been identified, particularly its Outer Membrane Proteins (OMPs). These proteins play diverse roles, including serving as porins, adhesins, or receptors. The classification of OMPs comprises three categories: protein II (opa), protein III (rmp) & protein I (porin).
Protein I function as a porin, creating channels for the passage of small molecules through the outer membrane. Protein II, an opa protein, aids in adhering to host cells and penetrating mucosal barriers. Protein III, designated as a rmp protein, offers protection against complement-mediated killing, enhancing the bacterium’s ability to evade the immune system.
Several Neisseria sicca strains have been identified, shedding light on their origins and availability for research. These strains include N. sicca ATCC 29256, isolated from human saliva, and N. sicca CCUG 17620, originating from human blood and accessible from the Culture collection university of Gothenburg. Additionally, N. sicca DSM 13165, isolated from human blood. Lastly, N. sicca NCTC 12122, also sourced from human blood, represents another strain available for investigation.
The precise mechanisms through which Neisseria sicca triggers infections remain largely elusive, yet several factors contribute to its pathogenic potential. Notably, the bacterium might employ pili, elongated filamentous appendages protruding from its surface to secure attachment to host cells and tissues. Beyond attachment, pili also facilitate DNA uptake and exchange, potentially enhancing genetic diversity and adaptive capabilities within the bacterial population.
Neisseria sicca is believed to employ a range of enzymes, such as IgA1 protease, to undermine the host’s immune defenses and infiltrate mucosal barriers. This protease efficiently cleaves the hinge region of IgA1, a dominant immunoglobulin in mucosal secretions, thereby preventing its binding to the bacterium. Neisseria sicca can thwart initial defense mechanisms and establish infection by degrading host immune components.
It can modify its outer membrane proteins and lipooligosaccharides (LOS), molecular components that contribute to its outer structure. By altering these surface elements, the bacterium may evade recognition by antibodies and the complement system, a vital immune cascade. While the LOS is an endotoxin that elicits inflammation and tissue damage, it can also enhance Neisseria sicca‘s resistance to serum-mediated killing. The unique presence of an O-repeat structure in the LOS further suggests a potential role in bolstering bacterial resilience.
Neisseria sicca‘s capacity to spread from its initial site of infection to distant organs and tissues is facilitated by dissemination through the bloodstream or lymphatic system. Moreover, the bacterium can form biofilms, intricate bacterial communities encased within an extracellular matrix. These biofilms provide a sheltering environment that shields the bacteria from antibiotics and host immune responses.
The mucosal epithelium in the respiratory tract & oral cavity constitutes the first line of defense. It produces mucus, which obstructs attachment and invasion by Neisseria sicca. IgA antibodies and lactoferrin are also secreted, hampering bacterial colonization and virulence.
The LL-37 peptide, a derivative of human cathelicidin, emerges as a potent defender. It binds to Neisseria sicca, curbing its growth and restraining biofilm formation—a vital strategy bacteria use to resist host defenses.
Neutrophils and macrophages, essential phagocytic cells, play a pivotal role. They engulf and eliminate Neisseria sicca by producing reactive oxygen species, nitric oxide, and lysosomal enzymes, effectively neutralizing the threat.
An intricate web of the complement system adds to the defense. It opsonizes Neisseria sicca, enhancing its recognition by phagocytic cells, and can trigger lysis by activating the classical, alternative, or lectin pathways.
T cells & B cells are central to adaptive immunity. They identify Neisseria sicca antigens, producing cytokines and antibodies that bolster clearance and confer protection against reinfection. This dynamic response enhances clearance and affords protection against potential reinfection.
Neisseria sicca, typically regarded as a harmless saprophyte, has shown its potential to cause clinical issues, especially in individuals with compromised immune systems. Although infrequent, Neisseria sicca-related infections have been documented, highlighting its clinical significance.
Neisseria sicca has been found in sputum samples of patients with pneumonia, contributing to lung infection. The bacterium has also been linked to Bartholin’s gland abscess, causing pain and swelling in the vulva area, and osteomyelitis, characterized by bone infection and related symptoms.
Neisseria sicca is associated with endocarditis and meningitis. Symptoms comprise headache, fever, fatigue, vomiting, chest pain, and heart murmur. If not managed, endocarditis can lead to severe complications. Neisseria sicca has been identified through cerebrospinal fluid & blood cultures in patients.
Inflammation of the abdominal cavity lining, peritonitis, can result from Neisseria sicca infection. Indications involve abdominal pain, tenderness, swelling, fever, chills, and loss of appetite. This condition might arise due to organ rupture or wounds, allowing bacteria entry. Neisseria sicca has been detected in peritoneal fluid from peritonitis cases.
Culture method: Culture remains a fundamental and reliable method for Neisseria sicca detection. Patient samples like blood or cerebrospinal fluid are placed on specialized growth media; Thayer-Martin agar is commonly used for isolating Neisseria sicca. Incubation for 24 to 48 hours enables characteristic colonies to develop. These colonies exhibit distinct traits, typically appearing small, round, smooth, and grayish white. The oxidase-positive reaction, characterized by a blue or purple hue upon exposure to an oxidizing agent, further confirms the presence of Neisseria sicca.
Biochemical Tests: Biochemical assays assess Neisseria sicca‘s utilization and production of specific substances like sugars, amino acids, and enzymes. This aids differentiation from other Neisseria species or related bacteria. Neisseria sicca‘s ability to ferment glucose and maltose and its unique acid production patterns distinguish it. Likewise, its capacity to hydrolyze arginine and urea, not esculin or gelatin, is a discriminating trait in identifying the bacterium.
Distinguishing Neisseriamucosa, Neisseria sicca, and Neisseriasubflava biovar perflava through biochemical methods presents challenges. However, specific tests target the identification of Neisseria sicca. These tests encompass carbonic anhydrase, catalase, iodine test for polysaccharide synthesis from sucrose, nitrite reduction with gas production, oxidase (utilizing the Superoxol Test involving 30% hydrogen peroxide), and the enzyme-substrate test for prolyl aminopeptidase positivity. Together, this suite of tests forms a comprehensive toolkit for profiling, enabling the precise recognition of Neisseria sicca. Such identification is pivotal in comprehending its unique attributes and potential implications.
Molecular techniques: For Neisseria sicca identification, DNA-DNA hybridization (DDH) and phylogenetic analyses of the 16S ribosomal gene serve as additional molecular tools. However, relying solely on single loci like the 16S rRNA genes can be constrained by limited resolution and horizontal genetic transfer (HGT). To surmount this, implementing multi-locus sequence analysis (MLSA) has brought substantial differentiation enhancements.
MLSA methods, notably Multi Locus Sequence Typing (MLST) utilizing seven loci, ribosomal MLST (rMLST) encompassing 53 ribosomal genes, and the core genome MLST (cgMLST) engaging 246 loci across the Neisseria genus, have emerged as pivotal advancements. These methodologies markedly bolster classification accuracy, propelling the discrimination of Neisseria species to new heights. By incorporating a spectrum of genetic markers, MLSA techniques offer a more comprehensive and intricate understanding, effectively propelling the realm of Neisseria species distinction.
Encourage good hygiene habits, including frequent handwashing with water & soap, especially after sneezing, coughing, or touching surfaces. Proper hygiene helps limit the spread of bacteria from contaminated surfaces to the respiratory tract.
Immunization against other pathogens that can weaken the immune system, such as influenza and Streptococcus pneumoniae, can reduce the susceptibility to opportunistic infections, including those caused by Neisseria sicca.
Neisseria sicca, a member of the Neisseria genus, typically resides within the human respiratory tract as a commensal organism, signifying its non-harmful and non-beneficial relationship with the host. However, certain strains of Neisseria sicca have been implicated in causing septicemia, particularly in individuals with compromised immune systems.
While the literature contains a limited number of case reports, they underscore the potential for this bacterium to induce infections in specific circumstances.Neisseria sicca meningitis occurred in a 68-year-old woman with chronic lymphocytic leukemia after chemotherapy. Successful ceftriaxone treatment ensured complete recovery.
In another case, a previously healthy 34-year-old man experienced bacterial conjunctivitis caused by Neisseria sicca. Symptoms like ocular pain, discharge, and erythema underlined its capacity to incite ocular infections. Furthermore, Neisseria sicca was implicated in peritonitis within a 54-year-old cirrhotic man following a paracentesis procedure, underscoring its potential to trigger peritoneal infections.
Neisseria sicca‘s role in endocarditis became evident as a 23-year-old woman with congenital heart disease developed the condition, leading to multiple embolic brain infarcts. Additionally, instances of Bartholin’s gland abscess caused by Neisseria sicca have been observed. A 24-year-old woman’s case highlighted its association with this condition after unprotected intercourse, managed effectively with clindamycin treatment and incision drainage.
Kingdom: Bacteria
Phylum: Pseudomonadota
Class: Betaproteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus:Neisseria
Species:Neisseria sicca
Neisseria sicca is an oxidase-positive, gram-negative bacterium characterized by a thin peptidoglycan.
Neisseria sicca has a spherical or cocci shape-diplococci. They measure about 0.6 to 1.0 µm in diameter.
Typically, they are observed in pairs, with the adjacent sides of the cells flattened. This arrangement gives them a distinctive kidney-shaped or bean-shaped appearance.
Neisseria sicca has pili, hairlike filamentous appendages extending several micrometers from the cell surface.
The antigenic types of Neisseria sicca still need to be explored due to its status as a rare and opportunistic pathogen. Despite this, certain virulence factors have been identified, particularly its Outer Membrane Proteins (OMPs). These proteins play diverse roles, including serving as porins, adhesins, or receptors. The classification of OMPs comprises three categories: protein II (opa), protein III (rmp) & protein I (porin).
Protein I function as a porin, creating channels for the passage of small molecules through the outer membrane. Protein II, an opa protein, aids in adhering to host cells and penetrating mucosal barriers. Protein III, designated as a rmp protein, offers protection against complement-mediated killing, enhancing the bacterium’s ability to evade the immune system.
Several Neisseria sicca strains have been identified, shedding light on their origins and availability for research. These strains include N. sicca ATCC 29256, isolated from human saliva, and N. sicca CCUG 17620, originating from human blood and accessible from the Culture collection university of Gothenburg. Additionally, N. sicca DSM 13165, isolated from human blood. Lastly, N. sicca NCTC 12122, also sourced from human blood, represents another strain available for investigation.
The precise mechanisms through which Neisseria sicca triggers infections remain largely elusive, yet several factors contribute to its pathogenic potential. Notably, the bacterium might employ pili, elongated filamentous appendages protruding from its surface to secure attachment to host cells and tissues. Beyond attachment, pili also facilitate DNA uptake and exchange, potentially enhancing genetic diversity and adaptive capabilities within the bacterial population.
Neisseria sicca is believed to employ a range of enzymes, such as IgA1 protease, to undermine the host’s immune defenses and infiltrate mucosal barriers. This protease efficiently cleaves the hinge region of IgA1, a dominant immunoglobulin in mucosal secretions, thereby preventing its binding to the bacterium. Neisseria sicca can thwart initial defense mechanisms and establish infection by degrading host immune components.
It can modify its outer membrane proteins and lipooligosaccharides (LOS), molecular components that contribute to its outer structure. By altering these surface elements, the bacterium may evade recognition by antibodies and the complement system, a vital immune cascade. While the LOS is an endotoxin that elicits inflammation and tissue damage, it can also enhance Neisseria sicca‘s resistance to serum-mediated killing. The unique presence of an O-repeat structure in the LOS further suggests a potential role in bolstering bacterial resilience.
Neisseria sicca‘s capacity to spread from its initial site of infection to distant organs and tissues is facilitated by dissemination through the bloodstream or lymphatic system. Moreover, the bacterium can form biofilms, intricate bacterial communities encased within an extracellular matrix. These biofilms provide a sheltering environment that shields the bacteria from antibiotics and host immune responses.
The mucosal epithelium in the respiratory tract & oral cavity constitutes the first line of defense. It produces mucus, which obstructs attachment and invasion by Neisseria sicca. IgA antibodies and lactoferrin are also secreted, hampering bacterial colonization and virulence.
The LL-37 peptide, a derivative of human cathelicidin, emerges as a potent defender. It binds to Neisseria sicca, curbing its growth and restraining biofilm formation—a vital strategy bacteria use to resist host defenses.
Neutrophils and macrophages, essential phagocytic cells, play a pivotal role. They engulf and eliminate Neisseria sicca by producing reactive oxygen species, nitric oxide, and lysosomal enzymes, effectively neutralizing the threat.
An intricate web of the complement system adds to the defense. It opsonizes Neisseria sicca, enhancing its recognition by phagocytic cells, and can trigger lysis by activating the classical, alternative, or lectin pathways.
T cells & B cells are central to adaptive immunity. They identify Neisseria sicca antigens, producing cytokines and antibodies that bolster clearance and confer protection against reinfection. This dynamic response enhances clearance and affords protection against potential reinfection.
Neisseria sicca, typically regarded as a harmless saprophyte, has shown its potential to cause clinical issues, especially in individuals with compromised immune systems. Although infrequent, Neisseria sicca-related infections have been documented, highlighting its clinical significance.
Neisseria sicca has been found in sputum samples of patients with pneumonia, contributing to lung infection. The bacterium has also been linked to Bartholin’s gland abscess, causing pain and swelling in the vulva area, and osteomyelitis, characterized by bone infection and related symptoms.
Neisseria sicca is associated with endocarditis and meningitis. Symptoms comprise headache, fever, fatigue, vomiting, chest pain, and heart murmur. If not managed, endocarditis can lead to severe complications. Neisseria sicca has been identified through cerebrospinal fluid & blood cultures in patients.
Inflammation of the abdominal cavity lining, peritonitis, can result from Neisseria sicca infection. Indications involve abdominal pain, tenderness, swelling, fever, chills, and loss of appetite. This condition might arise due to organ rupture or wounds, allowing bacteria entry. Neisseria sicca has been detected in peritoneal fluid from peritonitis cases.
Culture method: Culture remains a fundamental and reliable method for Neisseria sicca detection. Patient samples like blood or cerebrospinal fluid are placed on specialized growth media; Thayer-Martin agar is commonly used for isolating Neisseria sicca. Incubation for 24 to 48 hours enables characteristic colonies to develop. These colonies exhibit distinct traits, typically appearing small, round, smooth, and grayish white. The oxidase-positive reaction, characterized by a blue or purple hue upon exposure to an oxidizing agent, further confirms the presence of Neisseria sicca.
Biochemical Tests: Biochemical assays assess Neisseria sicca‘s utilization and production of specific substances like sugars, amino acids, and enzymes. This aids differentiation from other Neisseria species or related bacteria. Neisseria sicca‘s ability to ferment glucose and maltose and its unique acid production patterns distinguish it. Likewise, its capacity to hydrolyze arginine and urea, not esculin or gelatin, is a discriminating trait in identifying the bacterium.
Distinguishing Neisseriamucosa, Neisseria sicca, and Neisseriasubflava biovar perflava through biochemical methods presents challenges. However, specific tests target the identification of Neisseria sicca. These tests encompass carbonic anhydrase, catalase, iodine test for polysaccharide synthesis from sucrose, nitrite reduction with gas production, oxidase (utilizing the Superoxol Test involving 30% hydrogen peroxide), and the enzyme-substrate test for prolyl aminopeptidase positivity. Together, this suite of tests forms a comprehensive toolkit for profiling, enabling the precise recognition of Neisseria sicca. Such identification is pivotal in comprehending its unique attributes and potential implications.
Molecular techniques: For Neisseria sicca identification, DNA-DNA hybridization (DDH) and phylogenetic analyses of the 16S ribosomal gene serve as additional molecular tools. However, relying solely on single loci like the 16S rRNA genes can be constrained by limited resolution and horizontal genetic transfer (HGT). To surmount this, implementing multi-locus sequence analysis (MLSA) has brought substantial differentiation enhancements.
MLSA methods, notably Multi Locus Sequence Typing (MLST) utilizing seven loci, ribosomal MLST (rMLST) encompassing 53 ribosomal genes, and the core genome MLST (cgMLST) engaging 246 loci across the Neisseria genus, have emerged as pivotal advancements. These methodologies markedly bolster classification accuracy, propelling the discrimination of Neisseria species to new heights. By incorporating a spectrum of genetic markers, MLSA techniques offer a more comprehensive and intricate understanding, effectively propelling the realm of Neisseria species distinction.
Encourage good hygiene habits, including frequent handwashing with water & soap, especially after sneezing, coughing, or touching surfaces. Proper hygiene helps limit the spread of bacteria from contaminated surfaces to the respiratory tract.
Immunization against other pathogens that can weaken the immune system, such as influenza and Streptococcus pneumoniae, can reduce the susceptibility to opportunistic infections, including those caused by Neisseria sicca.
Neisseria sicca, a member of the Neisseria genus, typically resides within the human respiratory tract as a commensal organism, signifying its non-harmful and non-beneficial relationship with the host. However, certain strains of Neisseria sicca have been implicated in causing septicemia, particularly in individuals with compromised immune systems.
While the literature contains a limited number of case reports, they underscore the potential for this bacterium to induce infections in specific circumstances.Neisseria sicca meningitis occurred in a 68-year-old woman with chronic lymphocytic leukemia after chemotherapy. Successful ceftriaxone treatment ensured complete recovery.
In another case, a previously healthy 34-year-old man experienced bacterial conjunctivitis caused by Neisseria sicca. Symptoms like ocular pain, discharge, and erythema underlined its capacity to incite ocular infections. Furthermore, Neisseria sicca was implicated in peritonitis within a 54-year-old cirrhotic man following a paracentesis procedure, underscoring its potential to trigger peritoneal infections.
Neisseria sicca‘s role in endocarditis became evident as a 23-year-old woman with congenital heart disease developed the condition, leading to multiple embolic brain infarcts. Additionally, instances of Bartholin’s gland abscess caused by Neisseria sicca have been observed. A 24-year-old woman’s case highlighted its association with this condition after unprotected intercourse, managed effectively with clindamycin treatment and incision drainage.
Kingdom: Bacteria
Phylum: Pseudomonadota
Class: Betaproteobacteria
Order: Neisseriales
Family: Neisseriaceae
Genus:Neisseria
Species:Neisseria sicca
Neisseria sicca is an oxidase-positive, gram-negative bacterium characterized by a thin peptidoglycan.
Neisseria sicca has a spherical or cocci shape-diplococci. They measure about 0.6 to 1.0 µm in diameter.
Typically, they are observed in pairs, with the adjacent sides of the cells flattened. This arrangement gives them a distinctive kidney-shaped or bean-shaped appearance.
Neisseria sicca has pili, hairlike filamentous appendages extending several micrometers from the cell surface.
The antigenic types of Neisseria sicca still need to be explored due to its status as a rare and opportunistic pathogen. Despite this, certain virulence factors have been identified, particularly its Outer Membrane Proteins (OMPs). These proteins play diverse roles, including serving as porins, adhesins, or receptors. The classification of OMPs comprises three categories: protein II (opa), protein III (rmp) & protein I (porin).
Protein I function as a porin, creating channels for the passage of small molecules through the outer membrane. Protein II, an opa protein, aids in adhering to host cells and penetrating mucosal barriers. Protein III, designated as a rmp protein, offers protection against complement-mediated killing, enhancing the bacterium’s ability to evade the immune system.
Several Neisseria sicca strains have been identified, shedding light on their origins and availability for research. These strains include N. sicca ATCC 29256, isolated from human saliva, and N. sicca CCUG 17620, originating from human blood and accessible from the Culture collection university of Gothenburg. Additionally, N. sicca DSM 13165, isolated from human blood. Lastly, N. sicca NCTC 12122, also sourced from human blood, represents another strain available for investigation.
The precise mechanisms through which Neisseria sicca triggers infections remain largely elusive, yet several factors contribute to its pathogenic potential. Notably, the bacterium might employ pili, elongated filamentous appendages protruding from its surface to secure attachment to host cells and tissues. Beyond attachment, pili also facilitate DNA uptake and exchange, potentially enhancing genetic diversity and adaptive capabilities within the bacterial population.
Neisseria sicca is believed to employ a range of enzymes, such as IgA1 protease, to undermine the host’s immune defenses and infiltrate mucosal barriers. This protease efficiently cleaves the hinge region of IgA1, a dominant immunoglobulin in mucosal secretions, thereby preventing its binding to the bacterium. Neisseria sicca can thwart initial defense mechanisms and establish infection by degrading host immune components.
It can modify its outer membrane proteins and lipooligosaccharides (LOS), molecular components that contribute to its outer structure. By altering these surface elements, the bacterium may evade recognition by antibodies and the complement system, a vital immune cascade. While the LOS is an endotoxin that elicits inflammation and tissue damage, it can also enhance Neisseria sicca‘s resistance to serum-mediated killing. The unique presence of an O-repeat structure in the LOS further suggests a potential role in bolstering bacterial resilience.
Neisseria sicca‘s capacity to spread from its initial site of infection to distant organs and tissues is facilitated by dissemination through the bloodstream or lymphatic system. Moreover, the bacterium can form biofilms, intricate bacterial communities encased within an extracellular matrix. These biofilms provide a sheltering environment that shields the bacteria from antibiotics and host immune responses.
The mucosal epithelium in the respiratory tract & oral cavity constitutes the first line of defense. It produces mucus, which obstructs attachment and invasion by Neisseria sicca. IgA antibodies and lactoferrin are also secreted, hampering bacterial colonization and virulence.
The LL-37 peptide, a derivative of human cathelicidin, emerges as a potent defender. It binds to Neisseria sicca, curbing its growth and restraining biofilm formation—a vital strategy bacteria use to resist host defenses.
Neutrophils and macrophages, essential phagocytic cells, play a pivotal role. They engulf and eliminate Neisseria sicca by producing reactive oxygen species, nitric oxide, and lysosomal enzymes, effectively neutralizing the threat.
An intricate web of the complement system adds to the defense. It opsonizes Neisseria sicca, enhancing its recognition by phagocytic cells, and can trigger lysis by activating the classical, alternative, or lectin pathways.
T cells & B cells are central to adaptive immunity. They identify Neisseria sicca antigens, producing cytokines and antibodies that bolster clearance and confer protection against reinfection. This dynamic response enhances clearance and affords protection against potential reinfection.
Neisseria sicca, typically regarded as a harmless saprophyte, has shown its potential to cause clinical issues, especially in individuals with compromised immune systems. Although infrequent, Neisseria sicca-related infections have been documented, highlighting its clinical significance.
Neisseria sicca has been found in sputum samples of patients with pneumonia, contributing to lung infection. The bacterium has also been linked to Bartholin’s gland abscess, causing pain and swelling in the vulva area, and osteomyelitis, characterized by bone infection and related symptoms.
Neisseria sicca is associated with endocarditis and meningitis. Symptoms comprise headache, fever, fatigue, vomiting, chest pain, and heart murmur. If not managed, endocarditis can lead to severe complications. Neisseria sicca has been identified through cerebrospinal fluid & blood cultures in patients.
Inflammation of the abdominal cavity lining, peritonitis, can result from Neisseria sicca infection. Indications involve abdominal pain, tenderness, swelling, fever, chills, and loss of appetite. This condition might arise due to organ rupture or wounds, allowing bacteria entry. Neisseria sicca has been detected in peritoneal fluid from peritonitis cases.
Culture method: Culture remains a fundamental and reliable method for Neisseria sicca detection. Patient samples like blood or cerebrospinal fluid are placed on specialized growth media; Thayer-Martin agar is commonly used for isolating Neisseria sicca. Incubation for 24 to 48 hours enables characteristic colonies to develop. These colonies exhibit distinct traits, typically appearing small, round, smooth, and grayish white. The oxidase-positive reaction, characterized by a blue or purple hue upon exposure to an oxidizing agent, further confirms the presence of Neisseria sicca.
Biochemical Tests: Biochemical assays assess Neisseria sicca‘s utilization and production of specific substances like sugars, amino acids, and enzymes. This aids differentiation from other Neisseria species or related bacteria. Neisseria sicca‘s ability to ferment glucose and maltose and its unique acid production patterns distinguish it. Likewise, its capacity to hydrolyze arginine and urea, not esculin or gelatin, is a discriminating trait in identifying the bacterium.
Distinguishing Neisseriamucosa, Neisseria sicca, and Neisseriasubflava biovar perflava through biochemical methods presents challenges. However, specific tests target the identification of Neisseria sicca. These tests encompass carbonic anhydrase, catalase, iodine test for polysaccharide synthesis from sucrose, nitrite reduction with gas production, oxidase (utilizing the Superoxol Test involving 30% hydrogen peroxide), and the enzyme-substrate test for prolyl aminopeptidase positivity. Together, this suite of tests forms a comprehensive toolkit for profiling, enabling the precise recognition of Neisseria sicca. Such identification is pivotal in comprehending its unique attributes and potential implications.
Molecular techniques: For Neisseria sicca identification, DNA-DNA hybridization (DDH) and phylogenetic analyses of the 16S ribosomal gene serve as additional molecular tools. However, relying solely on single loci like the 16S rRNA genes can be constrained by limited resolution and horizontal genetic transfer (HGT). To surmount this, implementing multi-locus sequence analysis (MLSA) has brought substantial differentiation enhancements.
MLSA methods, notably Multi Locus Sequence Typing (MLST) utilizing seven loci, ribosomal MLST (rMLST) encompassing 53 ribosomal genes, and the core genome MLST (cgMLST) engaging 246 loci across the Neisseria genus, have emerged as pivotal advancements. These methodologies markedly bolster classification accuracy, propelling the discrimination of Neisseria species to new heights. By incorporating a spectrum of genetic markers, MLSA techniques offer a more comprehensive and intricate understanding, effectively propelling the realm of Neisseria species distinction.
Encourage good hygiene habits, including frequent handwashing with water & soap, especially after sneezing, coughing, or touching surfaces. Proper hygiene helps limit the spread of bacteria from contaminated surfaces to the respiratory tract.
Immunization against other pathogens that can weaken the immune system, such as influenza and Streptococcus pneumoniae, can reduce the susceptibility to opportunistic infections, including those caused by Neisseria sicca.
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