Elizabethkingia miricola is a bacterium that gained notoriety through its isolation from condensation water in Space Station Mir, demonstrating its adaptability to unique environments. This bacterium is closely related to Elizabethkingia anophelis, which caused a significant outbreak of human infections in Wisconsin in 2016.
The genus Elizabethkingia pays homage to Elizabeth O. King, a prominent microbiologist at the United States Centers for Disease Control. The species epithet, “miricola,” is derived from the Russian name “Mir” for the space station and the Latin term “incola,” signifying “inhabitant,” collectively forming “inhabitant of the Mir space station.” Infections with E. miricola are notably more prevalent in Asia, particularly in regions like Taiwan, Singapore, and Malaysia.
E. miricola infections exhibit a wide range, affecting various anatomical sites and systems in the human body, including the oral cavity, respiratory tract, urinary tract, eyes, heart, bones, joints, skin, and blood. A considerable risk marks these infections, as they are associated with high mortality rates, which can vary from 18.2% to 41%, contingent on the site and severity of the infection.
One of the challenges in addressing E. miricola infections is their unusual antibiotic resistance pattern for a Gram-negative bacterium. The bacterium inherently displays resistance to many commonly used antibiotics, such as beta-lactams, aminoglycosides, and tetracyclines.
Furthermore, in 2016, there were multiregional outbreaks of a meningitis-like disease attributed to Elizabethkingia miricola in black-spotted frog farms in China. Whole-genome sequencing indicated a close relationship between these strains and those isolated from humans. It suggests that E. miricola can be epizootic & may pose a health threat to humans, reinforcing its significance in epidemiology.
Classification and Structure:
Kingdom: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus:Elizabethkingia
Species:E. miricola
Elizabethkingia miricola is characterized as a gram-negative bacterium with an elongated and slightly curved rod shape. It exhibits non-budding, non-fermenting, and non-motile characteristics.
In terms of size, E. miricola cells typically measure between 0.5 and 1.5 μm in width and 1.5 to 4.0 μm in length, reflecting its structural features in the microbial world.
The cell wall of E. miricola is primarily composed of peptidoglycan and lipopolysaccharide, while its cytoplasmic membrane houses various respiratory enzymes. Notably, this bacterium may possess a capsule or slime layer, contributing to its virulence and antibiotic resistance.
E. miricola is characterized by its lipopolysaccharide layer, featuring O-antigens that can trigger an immune response. It is classified into distinct antigenic types based on serological reactions of its O-antigens. Notably, strains like miricola FL160902 belong to antigenic type 1, while E. miricola 12–002 is classified as antigenic type 2.
The type strain of Elizabethkingia miricola, known initially as Chryseobacterium miricola and later reclassified under the new genus Elizabethkingia, in 2005, is represented by DSM 14571. Additionally, strain EM798-26 is another documented strain of this bacterium.
Furthermore, E. miricola possesses specific genes, namely blaB and gob genes, responsible for encoding metallo-beta-lactamases (MBLs) BlaB and GOB. These genes are located on the bacterium’s chromosome and have the potential for horizontal gene transfer to other bacteria, impacting their antibiotic resistance profile.
The pathogenesis of Elizabethkingia miricola in humans remains a subject of limited understanding, primarily due to its rarity and its tendency to affect immunocompromised individuals. E. miricola can establish colonization in the oral cavity, particularly in patients with humoral immunodeficiency and deficiencies in immunoglobulins IgA and IgG.
This colonization can lead to severe periodontitis and, in some cases, bacterial translocation, potentially resulting in systemic infection.One of the features contributing to E. miricola‘s pathogenicity is the presence of a capsule or slime layer, which acts as a protective shieldagainst phagocytosis and complement-mediated killing.
This layer also plays a role in antibiotic resistance and biofilm formation. Additionally, E. miricola is capable of producing various enzymes, including lipases, proteases, and hemolysins, which can cause damage to host tissues and cells, leading to necrosis, inflammation, and hemorrhage.
E. miricola possesses specific adhesins and invasins that enable it to attach to and invade host cells, like endothelial cells, epithelial cells, and macrophages. This ability promotes its dissemination within the host and allows it to evade the immune system’s defenses.
Furthermore, E. miricola can modulate the host immune response by inducing processes like cytokine production, apoptosis, and oxidative stress. These alterations can result in tissue damage, septic shock, and organ failure, further complicating the clinical outcomes of E. miricola infections.
The human host defense mechanisms against Elizabethkingia miricola are multifaceted. In the innate immune system, E. miricola may be recognized as a foreign invader, prompting the activation of the complement system. This activation flags the bacterium for phagocytosis by neutrophils and macrophages, critical players in the immune response
Concurrently, the adaptive immune system responds by generating antibodies against various E. miricola antigens, including the capsule,enzymes, and adhesins. These antibodies can neutralize or opsonize the bacterium, rendering it susceptible to phagocytosis or lysis. Moreover, the immune response involves the production of cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).
However, E. miricola has evolved mechanisms to evade and suppress host defenses. It can resist neutrophil-mediated killing by producing catalase, an enzyme that degrades hydrogen peroxide, a significant component of reactive oxygen species (ROS). Additionally, E. miricola can survive within macrophages by inhibiting their acidification and maturation, further complicating the host’s immune response.
Elizabethkingia miricola is a relatively rare bacterium known to cause opportunistic infections, particularly in individuals with compromised immune systems. Clinical manifestations of E. miricola infection encompass a broad spectrum of conditions, which may include severe periodontitis and oral ulcers.
Additionally, infections can lead to more severe and potentially life-threatening outcomes, such as brain abscesses & meningoencephalitis. This bacterium has also been associated with necrotic spondylitis and retinitis, as well as septicemia and bacteremia. These infections may further progress to conditions like osteomyelitis and endocarditis.
Additionally, E. miricola has been implicated in endogenous endophthalmitis and epididymo-orchitis. In some cases, pulmonary abscesses and necrotizing fasciitis can develop, and the bacterium has been found in patients with cystic fibrosis and hydrocephalus. It’s essential to note that E. miricola infections can manifest differently in various individuals, with the severity of clinical outcomes often dependent on the patient’s overall health and immune status.
Culture of Body Fluids: Traditional culture techniques involve the inoculation of body fluids, such as blood, cerebrospinal fluid, urine, or pus, onto selective media, such as blood agar or chocolate agar. The appearance of the bacterium’s growth on these media can aid in its identification, which may appear as small, smooth, convex, and greyish-white colonies. However, this method is time-consuming and may offer low specificity, often requiring several days to produce results.
MALDI-TOF MS Biotyper System: A more advanced and reliable approach for E. miricola identification is the use of the MALDI-TOF MS Biotyper system. This system can accurately differentiate E. miricola from other Elizabethkingia species and similar bacteria such as Flavobacterium or Chryseobacterium. It is known for its speed and precision, making it a preferred choice over conventional culture methods.
Molecular Techniques: Molecular methods, including polymerase chain reaction and sequencing, are another option for diagnosing E. miricola infections. These techniques involve the amplification and analysis of E. miricola‘s DNA or RNA. They are more sensitive and specific than culture-based methods but may necessitate specialized equipment and expertise.
Implementing infection control policies and protocols is essential. These may include contact precautions, isolation of infected patients, cohorting of staff and equipment, and surveillance to detect and manage potential outbreaks. These measures collectively contribute to reducing the spread of E. miricola in healthcare settings.
Using water-free patient rooms is essential, as E. miricola can thrive in water sources within healthcare settings, including sinks, showers, and respiratory therapy equipment. Preventing its presence in such environments can reduce the risk of transmission.
Strict adherence to hygiene and disinfection practices is vital. This includes thorough hand washing, proper glove use, and regular cleaning and disinfection of medical devices and surfaces with appropriate agents. These measures help minimize the potential sources of infection.
Elizabethkingia miricola is a bacterium that gained notoriety through its isolation from condensation water in Space Station Mir, demonstrating its adaptability to unique environments. This bacterium is closely related to Elizabethkingia anophelis, which caused a significant outbreak of human infections in Wisconsin in 2016.
The genus Elizabethkingia pays homage to Elizabeth O. King, a prominent microbiologist at the United States Centers for Disease Control. The species epithet, “miricola,” is derived from the Russian name “Mir” for the space station and the Latin term “incola,” signifying “inhabitant,” collectively forming “inhabitant of the Mir space station.” Infections with E. miricola are notably more prevalent in Asia, particularly in regions like Taiwan, Singapore, and Malaysia.
E. miricola infections exhibit a wide range, affecting various anatomical sites and systems in the human body, including the oral cavity, respiratory tract, urinary tract, eyes, heart, bones, joints, skin, and blood. A considerable risk marks these infections, as they are associated with high mortality rates, which can vary from 18.2% to 41%, contingent on the site and severity of the infection.
One of the challenges in addressing E. miricola infections is their unusual antibiotic resistance pattern for a Gram-negative bacterium. The bacterium inherently displays resistance to many commonly used antibiotics, such as beta-lactams, aminoglycosides, and tetracyclines.
Furthermore, in 2016, there were multiregional outbreaks of a meningitis-like disease attributed to Elizabethkingia miricola in black-spotted frog farms in China. Whole-genome sequencing indicated a close relationship between these strains and those isolated from humans. It suggests that E. miricola can be epizootic & may pose a health threat to humans, reinforcing its significance in epidemiology.
Classification and Structure:
Kingdom: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus:Elizabethkingia
Species:E. miricola
Elizabethkingia miricola is characterized as a gram-negative bacterium with an elongated and slightly curved rod shape. It exhibits non-budding, non-fermenting, and non-motile characteristics.
In terms of size, E. miricola cells typically measure between 0.5 and 1.5 μm in width and 1.5 to 4.0 μm in length, reflecting its structural features in the microbial world.
The cell wall of E. miricola is primarily composed of peptidoglycan and lipopolysaccharide, while its cytoplasmic membrane houses various respiratory enzymes. Notably, this bacterium may possess a capsule or slime layer, contributing to its virulence and antibiotic resistance.
E. miricola is characterized by its lipopolysaccharide layer, featuring O-antigens that can trigger an immune response. It is classified into distinct antigenic types based on serological reactions of its O-antigens. Notably, strains like miricola FL160902 belong to antigenic type 1, while E. miricola 12–002 is classified as antigenic type 2.
The type strain of Elizabethkingia miricola, known initially as Chryseobacterium miricola and later reclassified under the new genus Elizabethkingia, in 2005, is represented by DSM 14571. Additionally, strain EM798-26 is another documented strain of this bacterium.
Furthermore, E. miricola possesses specific genes, namely blaB and gob genes, responsible for encoding metallo-beta-lactamases (MBLs) BlaB and GOB. These genes are located on the bacterium’s chromosome and have the potential for horizontal gene transfer to other bacteria, impacting their antibiotic resistance profile.
The pathogenesis of Elizabethkingia miricola in humans remains a subject of limited understanding, primarily due to its rarity and its tendency to affect immunocompromised individuals. E. miricola can establish colonization in the oral cavity, particularly in patients with humoral immunodeficiency and deficiencies in immunoglobulins IgA and IgG.
This colonization can lead to severe periodontitis and, in some cases, bacterial translocation, potentially resulting in systemic infection.One of the features contributing to E. miricola‘s pathogenicity is the presence of a capsule or slime layer, which acts as a protective shieldagainst phagocytosis and complement-mediated killing.
This layer also plays a role in antibiotic resistance and biofilm formation. Additionally, E. miricola is capable of producing various enzymes, including lipases, proteases, and hemolysins, which can cause damage to host tissues and cells, leading to necrosis, inflammation, and hemorrhage.
E. miricola possesses specific adhesins and invasins that enable it to attach to and invade host cells, like endothelial cells, epithelial cells, and macrophages. This ability promotes its dissemination within the host and allows it to evade the immune system’s defenses.
Furthermore, E. miricola can modulate the host immune response by inducing processes like cytokine production, apoptosis, and oxidative stress. These alterations can result in tissue damage, septic shock, and organ failure, further complicating the clinical outcomes of E. miricola infections.
The human host defense mechanisms against Elizabethkingia miricola are multifaceted. In the innate immune system, E. miricola may be recognized as a foreign invader, prompting the activation of the complement system. This activation flags the bacterium for phagocytosis by neutrophils and macrophages, critical players in the immune response
Concurrently, the adaptive immune system responds by generating antibodies against various E. miricola antigens, including the capsule,enzymes, and adhesins. These antibodies can neutralize or opsonize the bacterium, rendering it susceptible to phagocytosis or lysis. Moreover, the immune response involves the production of cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).
However, E. miricola has evolved mechanisms to evade and suppress host defenses. It can resist neutrophil-mediated killing by producing catalase, an enzyme that degrades hydrogen peroxide, a significant component of reactive oxygen species (ROS). Additionally, E. miricola can survive within macrophages by inhibiting their acidification and maturation, further complicating the host’s immune response.
Elizabethkingia miricola is a relatively rare bacterium known to cause opportunistic infections, particularly in individuals with compromised immune systems. Clinical manifestations of E. miricola infection encompass a broad spectrum of conditions, which may include severe periodontitis and oral ulcers.
Additionally, infections can lead to more severe and potentially life-threatening outcomes, such as brain abscesses & meningoencephalitis. This bacterium has also been associated with necrotic spondylitis and retinitis, as well as septicemia and bacteremia. These infections may further progress to conditions like osteomyelitis and endocarditis.
Additionally, E. miricola has been implicated in endogenous endophthalmitis and epididymo-orchitis. In some cases, pulmonary abscesses and necrotizing fasciitis can develop, and the bacterium has been found in patients with cystic fibrosis and hydrocephalus. It’s essential to note that E. miricola infections can manifest differently in various individuals, with the severity of clinical outcomes often dependent on the patient’s overall health and immune status.
Culture of Body Fluids: Traditional culture techniques involve the inoculation of body fluids, such as blood, cerebrospinal fluid, urine, or pus, onto selective media, such as blood agar or chocolate agar. The appearance of the bacterium’s growth on these media can aid in its identification, which may appear as small, smooth, convex, and greyish-white colonies. However, this method is time-consuming and may offer low specificity, often requiring several days to produce results.
MALDI-TOF MS Biotyper System: A more advanced and reliable approach for E. miricola identification is the use of the MALDI-TOF MS Biotyper system. This system can accurately differentiate E. miricola from other Elizabethkingia species and similar bacteria such as Flavobacterium or Chryseobacterium. It is known for its speed and precision, making it a preferred choice over conventional culture methods.
Molecular Techniques: Molecular methods, including polymerase chain reaction and sequencing, are another option for diagnosing E. miricola infections. These techniques involve the amplification and analysis of E. miricola‘s DNA or RNA. They are more sensitive and specific than culture-based methods but may necessitate specialized equipment and expertise.
Implementing infection control policies and protocols is essential. These may include contact precautions, isolation of infected patients, cohorting of staff and equipment, and surveillance to detect and manage potential outbreaks. These measures collectively contribute to reducing the spread of E. miricola in healthcare settings.
Using water-free patient rooms is essential, as E. miricola can thrive in water sources within healthcare settings, including sinks, showers, and respiratory therapy equipment. Preventing its presence in such environments can reduce the risk of transmission.
Strict adherence to hygiene and disinfection practices is vital. This includes thorough hand washing, proper glove use, and regular cleaning and disinfection of medical devices and surfaces with appropriate agents. These measures help minimize the potential sources of infection.
Elizabethkingia miricola is a bacterium that gained notoriety through its isolation from condensation water in Space Station Mir, demonstrating its adaptability to unique environments. This bacterium is closely related to Elizabethkingia anophelis, which caused a significant outbreak of human infections in Wisconsin in 2016.
The genus Elizabethkingia pays homage to Elizabeth O. King, a prominent microbiologist at the United States Centers for Disease Control. The species epithet, “miricola,” is derived from the Russian name “Mir” for the space station and the Latin term “incola,” signifying “inhabitant,” collectively forming “inhabitant of the Mir space station.” Infections with E. miricola are notably more prevalent in Asia, particularly in regions like Taiwan, Singapore, and Malaysia.
E. miricola infections exhibit a wide range, affecting various anatomical sites and systems in the human body, including the oral cavity, respiratory tract, urinary tract, eyes, heart, bones, joints, skin, and blood. A considerable risk marks these infections, as they are associated with high mortality rates, which can vary from 18.2% to 41%, contingent on the site and severity of the infection.
One of the challenges in addressing E. miricola infections is their unusual antibiotic resistance pattern for a Gram-negative bacterium. The bacterium inherently displays resistance to many commonly used antibiotics, such as beta-lactams, aminoglycosides, and tetracyclines.
Furthermore, in 2016, there were multiregional outbreaks of a meningitis-like disease attributed to Elizabethkingia miricola in black-spotted frog farms in China. Whole-genome sequencing indicated a close relationship between these strains and those isolated from humans. It suggests that E. miricola can be epizootic & may pose a health threat to humans, reinforcing its significance in epidemiology.
Classification and Structure:
Kingdom: Bacteria
Phylum: Bacteroidota
Class: Flavobacteriia
Order: Flavobacteriales
Family: Weeksellaceae
Genus:Elizabethkingia
Species:E. miricola
Elizabethkingia miricola is characterized as a gram-negative bacterium with an elongated and slightly curved rod shape. It exhibits non-budding, non-fermenting, and non-motile characteristics.
In terms of size, E. miricola cells typically measure between 0.5 and 1.5 μm in width and 1.5 to 4.0 μm in length, reflecting its structural features in the microbial world.
The cell wall of E. miricola is primarily composed of peptidoglycan and lipopolysaccharide, while its cytoplasmic membrane houses various respiratory enzymes. Notably, this bacterium may possess a capsule or slime layer, contributing to its virulence and antibiotic resistance.
E. miricola is characterized by its lipopolysaccharide layer, featuring O-antigens that can trigger an immune response. It is classified into distinct antigenic types based on serological reactions of its O-antigens. Notably, strains like miricola FL160902 belong to antigenic type 1, while E. miricola 12–002 is classified as antigenic type 2.
The type strain of Elizabethkingia miricola, known initially as Chryseobacterium miricola and later reclassified under the new genus Elizabethkingia, in 2005, is represented by DSM 14571. Additionally, strain EM798-26 is another documented strain of this bacterium.
Furthermore, E. miricola possesses specific genes, namely blaB and gob genes, responsible for encoding metallo-beta-lactamases (MBLs) BlaB and GOB. These genes are located on the bacterium’s chromosome and have the potential for horizontal gene transfer to other bacteria, impacting their antibiotic resistance profile.
The pathogenesis of Elizabethkingia miricola in humans remains a subject of limited understanding, primarily due to its rarity and its tendency to affect immunocompromised individuals. E. miricola can establish colonization in the oral cavity, particularly in patients with humoral immunodeficiency and deficiencies in immunoglobulins IgA and IgG.
This colonization can lead to severe periodontitis and, in some cases, bacterial translocation, potentially resulting in systemic infection.One of the features contributing to E. miricola‘s pathogenicity is the presence of a capsule or slime layer, which acts as a protective shieldagainst phagocytosis and complement-mediated killing.
This layer also plays a role in antibiotic resistance and biofilm formation. Additionally, E. miricola is capable of producing various enzymes, including lipases, proteases, and hemolysins, which can cause damage to host tissues and cells, leading to necrosis, inflammation, and hemorrhage.
E. miricola possesses specific adhesins and invasins that enable it to attach to and invade host cells, like endothelial cells, epithelial cells, and macrophages. This ability promotes its dissemination within the host and allows it to evade the immune system’s defenses.
Furthermore, E. miricola can modulate the host immune response by inducing processes like cytokine production, apoptosis, and oxidative stress. These alterations can result in tissue damage, septic shock, and organ failure, further complicating the clinical outcomes of E. miricola infections.
The human host defense mechanisms against Elizabethkingia miricola are multifaceted. In the innate immune system, E. miricola may be recognized as a foreign invader, prompting the activation of the complement system. This activation flags the bacterium for phagocytosis by neutrophils and macrophages, critical players in the immune response
Concurrently, the adaptive immune system responds by generating antibodies against various E. miricola antigens, including the capsule,enzymes, and adhesins. These antibodies can neutralize or opsonize the bacterium, rendering it susceptible to phagocytosis or lysis. Moreover, the immune response involves the production of cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).
However, E. miricola has evolved mechanisms to evade and suppress host defenses. It can resist neutrophil-mediated killing by producing catalase, an enzyme that degrades hydrogen peroxide, a significant component of reactive oxygen species (ROS). Additionally, E. miricola can survive within macrophages by inhibiting their acidification and maturation, further complicating the host’s immune response.
Elizabethkingia miricola is a relatively rare bacterium known to cause opportunistic infections, particularly in individuals with compromised immune systems. Clinical manifestations of E. miricola infection encompass a broad spectrum of conditions, which may include severe periodontitis and oral ulcers.
Additionally, infections can lead to more severe and potentially life-threatening outcomes, such as brain abscesses & meningoencephalitis. This bacterium has also been associated with necrotic spondylitis and retinitis, as well as septicemia and bacteremia. These infections may further progress to conditions like osteomyelitis and endocarditis.
Additionally, E. miricola has been implicated in endogenous endophthalmitis and epididymo-orchitis. In some cases, pulmonary abscesses and necrotizing fasciitis can develop, and the bacterium has been found in patients with cystic fibrosis and hydrocephalus. It’s essential to note that E. miricola infections can manifest differently in various individuals, with the severity of clinical outcomes often dependent on the patient’s overall health and immune status.
Culture of Body Fluids: Traditional culture techniques involve the inoculation of body fluids, such as blood, cerebrospinal fluid, urine, or pus, onto selective media, such as blood agar or chocolate agar. The appearance of the bacterium’s growth on these media can aid in its identification, which may appear as small, smooth, convex, and greyish-white colonies. However, this method is time-consuming and may offer low specificity, often requiring several days to produce results.
MALDI-TOF MS Biotyper System: A more advanced and reliable approach for E. miricola identification is the use of the MALDI-TOF MS Biotyper system. This system can accurately differentiate E. miricola from other Elizabethkingia species and similar bacteria such as Flavobacterium or Chryseobacterium. It is known for its speed and precision, making it a preferred choice over conventional culture methods.
Molecular Techniques: Molecular methods, including polymerase chain reaction and sequencing, are another option for diagnosing E. miricola infections. These techniques involve the amplification and analysis of E. miricola‘s DNA or RNA. They are more sensitive and specific than culture-based methods but may necessitate specialized equipment and expertise.
Implementing infection control policies and protocols is essential. These may include contact precautions, isolation of infected patients, cohorting of staff and equipment, and surveillance to detect and manage potential outbreaks. These measures collectively contribute to reducing the spread of E. miricola in healthcare settings.
Using water-free patient rooms is essential, as E. miricola can thrive in water sources within healthcare settings, including sinks, showers, and respiratory therapy equipment. Preventing its presence in such environments can reduce the risk of transmission.
Strict adherence to hygiene and disinfection practices is vital. This includes thorough hand washing, proper glove use, and regular cleaning and disinfection of medical devices and surfaces with appropriate agents. These measures help minimize the potential sources of infection.
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