Elizabethkingia meningoseptica is a remarkably resilient bacterium, with its presence spanning across diverse environments, including soil, water, and healthcare facilities. While its infection in humans is relatively rare, it poses a substantial threat, especially to neonates and individuals with compromised immune systems.
At the 2006 conference of the International Committee on Systematics of Prokaryotes, J.-F. Bernardet, and B. Bruun were designated as critical authorities for the taxonomy of this bacterium within the Flavobacterium and Cytophaga-like bacteria group. Among Elizabethkingia species, E. meningoseptica is the primary causative agent of the disease, followed by E. anophelis and the E. miricola cluster.
A retrospective study in China found that prevalence rates of E. meningoseptica infection were rapidly rising from 0 to 0.19 per 1,000 patients from 2011 to 2019. About 93.48% of Elizabethkingia meningoseptica isolates were multidrug-resistant and showed 100% resistance to carbapenem.The mortality rate associated with E. meningoseptica infections varies between 18.2% and 41%, contingent on the clinical manifestations and the patient’s underlying health condition.
These infections have been reported worldwide, yet they are more prevalent in Southeast Asia, particularly in regions like Taiwan, Singapore, and Malaysia. E. meningoseptica infections can manifest sporadically or as outbreaks within healthcare settings, frequently affecting neonatal intensive care units and adult intensive care units.
Classification and Structure:
Kingdom: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus: Elizabethkingia
Species: E. meningoseptica
E. meningoseptica presents a rod-shaped morphology with a subtle curve, imparting a comma-like appearance. It is notably larger than the average rod-shaped bacteria, with a diameter of approximately 0.7 μm and an extended length of around 5 μm.
E. meningoseptica contains a periplasmic space between the two membranes, pivotal in various cellular processes. Being gram-negative, it possesses a thin peptidoglycan layer ensconced by an outer membrane featuring lipopolysaccharides (LPS). This characteristic distinguishes it in terms of cell wall structure.
Elizabethkingia meningoseptica exhibits several notable characteristics:
Metallo-β-lactamases (MBLs): E. meningoseptica produces two types of MBLs, BlaB-1, and BlaB-3, which are enzymes capable of hydrolyzing β-lactam antibiotics, including penicillins, cephalosporins, and carbapenems. This enzymatic activity contributes to its resistance to these drugs.
Sialic Acid Transporters and Curli Synthesis Genes: The bacterium possesses genes responsible for the uptake and utilization of sialic acid, a sugar molecule found abundantly on the surface of human cells and tissues. E. meningoseptica can utilize sialic acid as a nutrient source, employing it as a camouflage mechanism to evade host recognition and clearance.
These characteristics, including its ability to resist various antibiotics and interact with host cells through sialic acid utilization, contribute to the pathogenicity of Elizabethkingia meningoseptica. Two well-known strains, ATCC 13253 and DSM 2800, are historically significant for their isolation and deposition, respectively.
Elizabethkingia meningoseptica‘s pathogenesis involves various transmission routes, including direct contact with contaminated sources like lipid stock bottles, venous catheter lines, nutritional solutions, and tap water.Additionally, person-to-person transmission can occur through respiratory droplets or contact with skin lesions. This bacterium primarily triggers meningitis outbreaks, particularly affecting premature newborns and infants within neonatal intensive care units, predominantly in underdeveloped countries.
However, it is not limited to this, as it can also lead to bacteremia, pneumonia, skin infections, and a range of other infections in individuals with compromised immunity, such as those battling cancer, diabetes, or recipients of organ transplants. The bacterium’s resilience is underscored by its ability to survive in moist environments and water sources, such as tap water, where it can persist for extended periods and form biofilms on various surfaces.
These primary defenses, including the skin and mucous membranes, act as a physical blockade against the entry of E. meningoseptica. The skin’s low pH, high salt concentration, and antimicrobial peptides inhibit bacterial growth. Mucous membranes feature protective elements such as cilia, mucus, and lysozyme, which trap and eliminate E. meningoseptica.
Comprising a group of circulating proteins, the complement system enhances the immune response against E. meningoseptica. It opsonizes (coats) pathogens for phagocytosis, lyses bacterial cells, and recruits inflammatory cells. Activation occurs through three pathways: the classical pathway (triggered by antibodies bound to E. meningoseptica), the alternative pathway (triggered by bacterial surface molecules), and the lectin pathway (triggered by carbohydrate-binding proteins).
The most abundant neutrophils rapidly kill bacteria with granules containing enzymes and peptides. Macrophages, residing in various tissues, eliminate bacteria by producing ROS, NO, and cytokines, while dendritic cells capture and present bacterial antigens to T cells. NK cells identify infected or abnormal cells by detecting alterations in major histocompatibility complex (MHC) class I molecules, typically expressed in healthy cells.
Elizabethkingia meningoseptica infection can manifest in various clinical presentations.
Neonatal Meningitis: This bacterial infection predominantly manifests as neonatal meningitis, especially in infants. It is characterized by fever, irritability, lethargy, poor feeding, vomiting, seizures, and a bulging fontanelle. Tragically, neonatal meningitis caused by E. meningoseptica carries a high mortality rate and may result in long-term neurological sequelae.
Bacteremia and Sepsis: Elizabethkingia meningoseptica can enter the bloodstream, leading to bacteremia. This condition is often a precursor to sepsis, a life-threatening state. Symptoms of bacteremia include fever, chills, low blood pressure, rapid heart rate, and potential organ failure.
Pneumonia: E. meningoseptica infections can also give rise to pneumonia involving the lungs. Clinical signs include cough, chest pain, shortness of breath, wheezing, and frothy or bloody sputum.
Skin Infections: Skin infections attributed to this bacterium include cellulitis, wound infections, necrotizing fasciitis, and abscesses. These infections are marked by local redness, swelling, pain, warmth, pus formation, and the potential for tissue necrosis.
In addition to these primary clinical presentations, E. meningoseptica infections can affect various other parts of the body, including the urinary tract, eye, heart, brain, and reproductive organs. The specific symptoms in these cases vary according to the site of infection. These may encompass pain, discharge, inflammation, vision loss, heart murmurs, hydrocephalus, and epididymo-orchitis.
Culture-Based Diagnosis: Culture is a fundamental method for identifying E. meningoseptica. The bacterium grows well on blood agar and chocolate agar plates. Its colonies on these media appear pale yellow and may not be readily discernible within the first 24 hours of incubation. Notably, strains of E. meningoseptica that grow better at 40 °C are often associated with invasive meningitis.
A distinct greyish discoloration around the blood agar colonies indicates the presence of proteases and gelatinase. While E. meningoseptica thrives on these specific agar types, it generally grows poorly on MacConkey agar, and it’s considered a glucose oxidizer. The colonies on blood agar or chocolate agar plates exhibit a characteristic smell, and it’s important to note that they may not always display a yellow color.
Biochemical Tests: Biochemical tests play a crucial role in identifying E. meningoseptica. Several vital tests are employed, including catalase, oxidase, indole, urease, and nitrate reductase tests. E. meningoseptica typically tests positive for catalase, oxidase, and indole, while it tests negative for urease and nitrate reductase. It’s worth mentioning that, in some cases, certain strains of E. meningoseptica may exhibit positive results for nitrate reductase.
Molecular Methods: Molecular diagnostic techniques offer a rapid & highly accurate means of detecting & differentiating E. meningoseptica from other related bacteria. Polymerase chain reaction and 16S rRNA sequencing are two common molecular methods used for this purpose. PCR is a sensitive technique that detects specific DNA sequences unique to E. meningoseptica, while 16S rRNA sequencing provides a detailed genetic profile. These molecular methods are invaluable for precise identification, although their availability may vary depending on the clinical setting.
Water Management: Use water-free patient rooms or minimize the use of tap water for patient care activities, including handwashing and medical device rinsing. Disinfect water systems and equipment regularly to ensure water quality.
Infection Control Practices: Implement rigorous infection control practices, such as hand hygiene, isolation precautions, and cohorting of patients and staff. Use splash guards on sinks to prevent water droplet splashing.
Store respiratory therapy supplies away from water sources and use sterile water for humidifiers or nebulizers. Regularly clean and disinfect shower facilities and equipment and use disposable or dedicated items for each patient.
»
Home » Pathogen » Elizabethkingia meningoseptica
Elizabethkingia meningoseptica
Updated :
November 10, 2023
Elizabethkingia meningoseptica is a remarkably resilient bacterium, with its presence spanning across diverse environments, including soil, water, and healthcare facilities. While its infection in humans is relatively rare, it poses a substantial threat, especially to neonates and individuals with compromised immune systems.
At the 2006 conference of the International Committee on Systematics of Prokaryotes, J.-F. Bernardet, and B. Bruun were designated as critical authorities for the taxonomy of this bacterium within the Flavobacterium and Cytophaga-like bacteria group. Among Elizabethkingia species, E. meningoseptica is the primary causative agent of the disease, followed by E. anophelis and the E. miricola cluster.
A retrospective study in China found that prevalence rates of E. meningoseptica infection were rapidly rising from 0 to 0.19 per 1,000 patients from 2011 to 2019. About 93.48% of Elizabethkingia meningoseptica isolates were multidrug-resistant and showed 100% resistance to carbapenem.The mortality rate associated with E. meningoseptica infections varies between 18.2% and 41%, contingent on the clinical manifestations and the patient’s underlying health condition.
These infections have been reported worldwide, yet they are more prevalent in Southeast Asia, particularly in regions like Taiwan, Singapore, and Malaysia. E. meningoseptica infections can manifest sporadically or as outbreaks within healthcare settings, frequently affecting neonatal intensive care units and adult intensive care units.
Classification and Structure:
Kingdom: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus: Elizabethkingia
Species: E. meningoseptica
E. meningoseptica presents a rod-shaped morphology with a subtle curve, imparting a comma-like appearance. It is notably larger than the average rod-shaped bacteria, with a diameter of approximately 0.7 μm and an extended length of around 5 μm.
E. meningoseptica contains a periplasmic space between the two membranes, pivotal in various cellular processes. Being gram-negative, it possesses a thin peptidoglycan layer ensconced by an outer membrane featuring lipopolysaccharides (LPS). This characteristic distinguishes it in terms of cell wall structure.
Elizabethkingia meningoseptica exhibits several notable characteristics:
Metallo-β-lactamases (MBLs): E. meningoseptica produces two types of MBLs, BlaB-1, and BlaB-3, which are enzymes capable of hydrolyzing β-lactam antibiotics, including penicillins, cephalosporins, and carbapenems. This enzymatic activity contributes to its resistance to these drugs.
Sialic Acid Transporters and Curli Synthesis Genes: The bacterium possesses genes responsible for the uptake and utilization of sialic acid, a sugar molecule found abundantly on the surface of human cells and tissues. E. meningoseptica can utilize sialic acid as a nutrient source, employing it as a camouflage mechanism to evade host recognition and clearance.
These characteristics, including its ability to resist various antibiotics and interact with host cells through sialic acid utilization, contribute to the pathogenicity of Elizabethkingia meningoseptica. Two well-known strains, ATCC 13253 and DSM 2800, are historically significant for their isolation and deposition, respectively.
Elizabethkingia meningoseptica‘s pathogenesis involves various transmission routes, including direct contact with contaminated sources like lipid stock bottles, venous catheter lines, nutritional solutions, and tap water.Additionally, person-to-person transmission can occur through respiratory droplets or contact with skin lesions. This bacterium primarily triggers meningitis outbreaks, particularly affecting premature newborns and infants within neonatal intensive care units, predominantly in underdeveloped countries.
However, it is not limited to this, as it can also lead to bacteremia, pneumonia, skin infections, and a range of other infections in individuals with compromised immunity, such as those battling cancer, diabetes, or recipients of organ transplants. The bacterium’s resilience is underscored by its ability to survive in moist environments and water sources, such as tap water, where it can persist for extended periods and form biofilms on various surfaces.
These primary defenses, including the skin and mucous membranes, act as a physical blockade against the entry of E. meningoseptica. The skin’s low pH, high salt concentration, and antimicrobial peptides inhibit bacterial growth. Mucous membranes feature protective elements such as cilia, mucus, and lysozyme, which trap and eliminate E. meningoseptica.
Comprising a group of circulating proteins, the complement system enhances the immune response against E. meningoseptica. It opsonizes (coats) pathogens for phagocytosis, lyses bacterial cells, and recruits inflammatory cells. Activation occurs through three pathways: the classical pathway (triggered by antibodies bound to E. meningoseptica), the alternative pathway (triggered by bacterial surface molecules), and the lectin pathway (triggered by carbohydrate-binding proteins).
The most abundant neutrophils rapidly kill bacteria with granules containing enzymes and peptides. Macrophages, residing in various tissues, eliminate bacteria by producing ROS, NO, and cytokines, while dendritic cells capture and present bacterial antigens to T cells. NK cells identify infected or abnormal cells by detecting alterations in major histocompatibility complex (MHC) class I molecules, typically expressed in healthy cells.
Elizabethkingia meningoseptica infection can manifest in various clinical presentations.
Neonatal Meningitis: This bacterial infection predominantly manifests as neonatal meningitis, especially in infants. It is characterized by fever, irritability, lethargy, poor feeding, vomiting, seizures, and a bulging fontanelle. Tragically, neonatal meningitis caused by E. meningoseptica carries a high mortality rate and may result in long-term neurological sequelae.
Bacteremia and Sepsis: Elizabethkingia meningoseptica can enter the bloodstream, leading to bacteremia. This condition is often a precursor to sepsis, a life-threatening state. Symptoms of bacteremia include fever, chills, low blood pressure, rapid heart rate, and potential organ failure.
Pneumonia: E. meningoseptica infections can also give rise to pneumonia involving the lungs. Clinical signs include cough, chest pain, shortness of breath, wheezing, and frothy or bloody sputum.
Skin Infections: Skin infections attributed to this bacterium include cellulitis, wound infections, necrotizing fasciitis, and abscesses. These infections are marked by local redness, swelling, pain, warmth, pus formation, and the potential for tissue necrosis.
In addition to these primary clinical presentations, E. meningoseptica infections can affect various other parts of the body, including the urinary tract, eye, heart, brain, and reproductive organs. The specific symptoms in these cases vary according to the site of infection. These may encompass pain, discharge, inflammation, vision loss, heart murmurs, hydrocephalus, and epididymo-orchitis.
Culture-Based Diagnosis: Culture is a fundamental method for identifying E. meningoseptica. The bacterium grows well on blood agar and chocolate agar plates. Its colonies on these media appear pale yellow and may not be readily discernible within the first 24 hours of incubation. Notably, strains of E. meningoseptica that grow better at 40 °C are often associated with invasive meningitis.
A distinct greyish discoloration around the blood agar colonies indicates the presence of proteases and gelatinase. While E. meningoseptica thrives on these specific agar types, it generally grows poorly on MacConkey agar, and it’s considered a glucose oxidizer. The colonies on blood agar or chocolate agar plates exhibit a characteristic smell, and it’s important to note that they may not always display a yellow color.
Biochemical Tests: Biochemical tests play a crucial role in identifying E. meningoseptica. Several vital tests are employed, including catalase, oxidase, indole, urease, and nitrate reductase tests. E. meningoseptica typically tests positive for catalase, oxidase, and indole, while it tests negative for urease and nitrate reductase. It’s worth mentioning that, in some cases, certain strains of E. meningoseptica may exhibit positive results for nitrate reductase.
Molecular Methods: Molecular diagnostic techniques offer a rapid & highly accurate means of detecting & differentiating E. meningoseptica from other related bacteria. Polymerase chain reaction and 16S rRNA sequencing are two common molecular methods used for this purpose. PCR is a sensitive technique that detects specific DNA sequences unique to E. meningoseptica, while 16S rRNA sequencing provides a detailed genetic profile. These molecular methods are invaluable for precise identification, although their availability may vary depending on the clinical setting.
Water Management: Use water-free patient rooms or minimize the use of tap water for patient care activities, including handwashing and medical device rinsing. Disinfect water systems and equipment regularly to ensure water quality.
Infection Control Practices: Implement rigorous infection control practices, such as hand hygiene, isolation precautions, and cohorting of patients and staff. Use splash guards on sinks to prevent water droplet splashing.
Store respiratory therapy supplies away from water sources and use sterile water for humidifiers or nebulizers. Regularly clean and disinfect shower facilities and equipment and use disposable or dedicated items for each patient.
Elizabethkingia meningoseptica is a remarkably resilient bacterium, with its presence spanning across diverse environments, including soil, water, and healthcare facilities. While its infection in humans is relatively rare, it poses a substantial threat, especially to neonates and individuals with compromised immune systems.
At the 2006 conference of the International Committee on Systematics of Prokaryotes, J.-F. Bernardet, and B. Bruun were designated as critical authorities for the taxonomy of this bacterium within the Flavobacterium and Cytophaga-like bacteria group. Among Elizabethkingia species, E. meningoseptica is the primary causative agent of the disease, followed by E. anophelis and the E. miricola cluster.
A retrospective study in China found that prevalence rates of E. meningoseptica infection were rapidly rising from 0 to 0.19 per 1,000 patients from 2011 to 2019. About 93.48% of Elizabethkingia meningoseptica isolates were multidrug-resistant and showed 100% resistance to carbapenem.The mortality rate associated with E. meningoseptica infections varies between 18.2% and 41%, contingent on the clinical manifestations and the patient’s underlying health condition.
These infections have been reported worldwide, yet they are more prevalent in Southeast Asia, particularly in regions like Taiwan, Singapore, and Malaysia. E. meningoseptica infections can manifest sporadically or as outbreaks within healthcare settings, frequently affecting neonatal intensive care units and adult intensive care units.
Classification and Structure:
Kingdom: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus: Elizabethkingia
Species: E. meningoseptica
E. meningoseptica presents a rod-shaped morphology with a subtle curve, imparting a comma-like appearance. It is notably larger than the average rod-shaped bacteria, with a diameter of approximately 0.7 μm and an extended length of around 5 μm.
E. meningoseptica contains a periplasmic space between the two membranes, pivotal in various cellular processes. Being gram-negative, it possesses a thin peptidoglycan layer ensconced by an outer membrane featuring lipopolysaccharides (LPS). This characteristic distinguishes it in terms of cell wall structure.
Elizabethkingia meningoseptica exhibits several notable characteristics:
Metallo-β-lactamases (MBLs): E. meningoseptica produces two types of MBLs, BlaB-1, and BlaB-3, which are enzymes capable of hydrolyzing β-lactam antibiotics, including penicillins, cephalosporins, and carbapenems. This enzymatic activity contributes to its resistance to these drugs.
Sialic Acid Transporters and Curli Synthesis Genes: The bacterium possesses genes responsible for the uptake and utilization of sialic acid, a sugar molecule found abundantly on the surface of human cells and tissues. E. meningoseptica can utilize sialic acid as a nutrient source, employing it as a camouflage mechanism to evade host recognition and clearance.
These characteristics, including its ability to resist various antibiotics and interact with host cells through sialic acid utilization, contribute to the pathogenicity of Elizabethkingia meningoseptica. Two well-known strains, ATCC 13253 and DSM 2800, are historically significant for their isolation and deposition, respectively.
Elizabethkingia meningoseptica‘s pathogenesis involves various transmission routes, including direct contact with contaminated sources like lipid stock bottles, venous catheter lines, nutritional solutions, and tap water.Additionally, person-to-person transmission can occur through respiratory droplets or contact with skin lesions. This bacterium primarily triggers meningitis outbreaks, particularly affecting premature newborns and infants within neonatal intensive care units, predominantly in underdeveloped countries.
However, it is not limited to this, as it can also lead to bacteremia, pneumonia, skin infections, and a range of other infections in individuals with compromised immunity, such as those battling cancer, diabetes, or recipients of organ transplants. The bacterium’s resilience is underscored by its ability to survive in moist environments and water sources, such as tap water, where it can persist for extended periods and form biofilms on various surfaces.
These primary defenses, including the skin and mucous membranes, act as a physical blockade against the entry of E. meningoseptica. The skin’s low pH, high salt concentration, and antimicrobial peptides inhibit bacterial growth. Mucous membranes feature protective elements such as cilia, mucus, and lysozyme, which trap and eliminate E. meningoseptica.
Comprising a group of circulating proteins, the complement system enhances the immune response against E. meningoseptica. It opsonizes (coats) pathogens for phagocytosis, lyses bacterial cells, and recruits inflammatory cells. Activation occurs through three pathways: the classical pathway (triggered by antibodies bound to E. meningoseptica), the alternative pathway (triggered by bacterial surface molecules), and the lectin pathway (triggered by carbohydrate-binding proteins).
The most abundant neutrophils rapidly kill bacteria with granules containing enzymes and peptides. Macrophages, residing in various tissues, eliminate bacteria by producing ROS, NO, and cytokines, while dendritic cells capture and present bacterial antigens to T cells. NK cells identify infected or abnormal cells by detecting alterations in major histocompatibility complex (MHC) class I molecules, typically expressed in healthy cells.
Elizabethkingia meningoseptica infection can manifest in various clinical presentations.
Neonatal Meningitis: This bacterial infection predominantly manifests as neonatal meningitis, especially in infants. It is characterized by fever, irritability, lethargy, poor feeding, vomiting, seizures, and a bulging fontanelle. Tragically, neonatal meningitis caused by E. meningoseptica carries a high mortality rate and may result in long-term neurological sequelae.
Bacteremia and Sepsis: Elizabethkingia meningoseptica can enter the bloodstream, leading to bacteremia. This condition is often a precursor to sepsis, a life-threatening state. Symptoms of bacteremia include fever, chills, low blood pressure, rapid heart rate, and potential organ failure.
Pneumonia: E. meningoseptica infections can also give rise to pneumonia involving the lungs. Clinical signs include cough, chest pain, shortness of breath, wheezing, and frothy or bloody sputum.
Skin Infections: Skin infections attributed to this bacterium include cellulitis, wound infections, necrotizing fasciitis, and abscesses. These infections are marked by local redness, swelling, pain, warmth, pus formation, and the potential for tissue necrosis.
In addition to these primary clinical presentations, E. meningoseptica infections can affect various other parts of the body, including the urinary tract, eye, heart, brain, and reproductive organs. The specific symptoms in these cases vary according to the site of infection. These may encompass pain, discharge, inflammation, vision loss, heart murmurs, hydrocephalus, and epididymo-orchitis.
Culture-Based Diagnosis: Culture is a fundamental method for identifying E. meningoseptica. The bacterium grows well on blood agar and chocolate agar plates. Its colonies on these media appear pale yellow and may not be readily discernible within the first 24 hours of incubation. Notably, strains of E. meningoseptica that grow better at 40 °C are often associated with invasive meningitis.
A distinct greyish discoloration around the blood agar colonies indicates the presence of proteases and gelatinase. While E. meningoseptica thrives on these specific agar types, it generally grows poorly on MacConkey agar, and it’s considered a glucose oxidizer. The colonies on blood agar or chocolate agar plates exhibit a characteristic smell, and it’s important to note that they may not always display a yellow color.
Biochemical Tests: Biochemical tests play a crucial role in identifying E. meningoseptica. Several vital tests are employed, including catalase, oxidase, indole, urease, and nitrate reductase tests. E. meningoseptica typically tests positive for catalase, oxidase, and indole, while it tests negative for urease and nitrate reductase. It’s worth mentioning that, in some cases, certain strains of E. meningoseptica may exhibit positive results for nitrate reductase.
Molecular Methods: Molecular diagnostic techniques offer a rapid & highly accurate means of detecting & differentiating E. meningoseptica from other related bacteria. Polymerase chain reaction and 16S rRNA sequencing are two common molecular methods used for this purpose. PCR is a sensitive technique that detects specific DNA sequences unique to E. meningoseptica, while 16S rRNA sequencing provides a detailed genetic profile. These molecular methods are invaluable for precise identification, although their availability may vary depending on the clinical setting.
Water Management: Use water-free patient rooms or minimize the use of tap water for patient care activities, including handwashing and medical device rinsing. Disinfect water systems and equipment regularly to ensure water quality.
Infection Control Practices: Implement rigorous infection control practices, such as hand hygiene, isolation precautions, and cohorting of patients and staff. Use splash guards on sinks to prevent water droplet splashing.
Store respiratory therapy supplies away from water sources and use sterile water for humidifiers or nebulizers. Regularly clean and disinfect shower facilities and equipment and use disposable or dedicated items for each patient.
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