Kosakonia cowanii is primarily recognized as a pathogen that affects various crops, leading to ailments like wilt and dieback. Nevertheless, it has emerged as a rare cause of human infections, particularly among individuals with compromised immune systems or those experiencing traumatic plant-related injuries.
The prevalence of Kosakonia cowanii in clinical specimens from human infections remains exceptionally low, typically ranging from 0.01% to 0.1%. Notably, this bacterium is more frequently encountered in plant samples, with soybean crops being a common source.
The epidemiology of K. cowanii in human infections needs to be more studied, mainly due to challenges in its identification using conventional methods, often resulting in misclassification as other members of the Enterobacteriaceae family. A comprehensive literature review reveals that between 2000 and 2020, only a scant 14 cases of human infections attributed to K. cowanii have been reported worldwide.
Classification and Structure:
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Kosakonia
Species: K. cowanii
Kosakonia cowanii is a rod-shaped bacterium with a facultatively anaerobic metabolism. It typically measures about 0.5–1.0 µm in width and 1.5–3.0 µm in length.
This bacterium is motile, facilitated by a single polar flagellum. The flagellum allows Kosakonia cowanii to move through its environment, which is vital for its survival and ability to colonize various niches.
Kosakonia cowanii has a cell wall composed of peptidoglycan and an outer membrane containing lipopolysaccharides. Notably, it also possesses a capsule, which may serve multiple functions.
Kosakonia cowanii Pa82, a bacterium known for its association with plant pathogenicity and rare human infections, possesses several virulence-related genes, including adhesins and those involved in endotoxin biosynthesis and modification. Adhesins play a crucial role in bacterial colonization, invasion, and the formation of biofilms. In the case of K. cowanii Pa82, these adhesins are predicted to contribute to its pathogenicity.
Furthermore, Kosakonia cowanii has been studied in various strains, with 888-76T as the type strain previously referred to as E. cowanii. Phylogenetically related strains, such as BCC 078, BCC 074, BCC 008, BCC 011, and BCC 009, have been identified through genetic sequencing using 16S rRNA and rpoB genes. These strains provide valuable insights into the diversity and genetic makeup of Kosakonia cowanii.
K. cowanii, primarily a plant pathogen, can access the human body through wounds caused by plant thorns or other sharp objects. This traumatic inoculation can lead to localized or systemic infections. In some cases, it has been associated with severe conditions like rhabdomyolysis and bacteremia, highlighting the potential for significant health consequences.
Evidence suggests that K. cowanii may be able to colonize the human gut, particularly in immune compromised individuals or those with alterations in their gut microbiota. This colonization can facilitate the translocation of the bacterium across the intestinal barrier, leading to infections in other organs, such as the gallbladder. This process underscores the opportunistic nature of K. cowanii infections.
K. cowanii possesses a protective capsule that may aid in adhesion to host tissues and protection from host defenses. Additionally, its flagellum enables motility and invasion, potentially contributing to its ability to cause infections. Furthermore, K. cowanii has resisted certain antibiotics, including ampicillin and cephalosporins. This antibiotic resistance can limit treatment options and increase the risk of complications associated with K. cowanii infections.
Human host defenses play a crucial role in protecting against Kosakonia cowanii infections through various mechanisms:
The skin is a formidable barrier, preventing Kosakonia cowanii from entering the body through wounds or cuts caused by plant thorns or similar objects. Additionally, mucous membranes in the respiratory, genitourinary, and gastrointestinal tracts can trap and expel the bacterium.
Several chemical defenses are employed against Kosakonia cowanii. Lysozyme, an enzyme, can damage the bacterium’s cell wall by breaking down the muramic acid linkage. Immunoglobulins, including antibodies, can hinder K. cowanii‘s attachment to host cells or facilitate their opsonization for phagocytosis.
Antimicrobial peptides disrupt the bacterial membrane or interfere with DNA synthesis. Iron-binding proteins limit Kosakonia cowanii‘s access to essential iron. Cytokines, signaling molecules, can activate or recruit other immune cells to combat the infection.
Both granulocytes and agranulocytes contribute as a cellular defense against Kosakonia cowanii. These immune cells can phagocytose and subsequently kill the bacterium using various mechanisms, including producing reactive oxygen species, nitric oxide, lysosomal enzymes, or defensins.
Lymphocytes, another essential immune system component, generate antibodies that bind to K. cowanii, neutralizing it or enhancing its phagocytosis. Additionally, lymphocytes can produce cytotoxic molecules that induce apoptosis in infected cells or secrete cytokines that regulate the immune response.
Clinical manifestations of Kosakonia cowanii infections in humans are rare but have been reported, typically associated with traumatic inoculation from plant sources. One case involved a patient who developed rhabdomyolysis and bacteremia after being pricked by a rose thorn contaminated with K. cowanii.
This incident underscores the potential of K. cowanii to act as an opportunistic pathogen, particularly in individuals with compromised immune systems. Another case involved acute cholecystitis caused by K. cowanii, with the bacterium isolated from the patient’s gall bladder and bile. Clinical presentations of K. cowanii infections can vary depending on the infection site and severity.
Still, they may encompass symptoms such as fever, pain, inflammation, tissue necrosis, and affected organ dysfunction. These cases highlight considering K. cowanii as a potential pathogen in specific clinical contexts, particularly when there is a history of traumatic plant-related injuries.
Diagnosing Kosakonia cowanii infections typically involves a combination of laboratory techniques to identify the bacterium accurately.
MALDI-TOF Mass Spectrometry: MALDI-TOF is a powerful technique that analyzes the molecular weight of bacteria. It ionizes bacterial molecules with a laser and measures their time to reach a detector. By comparing the resulting mass spectrum to a database, healthcare professionals can rapidly and accurately identify K. cowanii.
VITEK 2 GN ID Card: The VITEK 2 system employs biochemical reactions to identify Gram-negative bacteria based on their metabolic profiles. This system provides valuable information about the bacterium’s metabolic activity, aiding in its identification.
16S rRNA Sequencing: 16S rRNA sequencing is a molecular method that compares the genetic sequence of a specific region of bacterial ribosomal RNA to known sequences in a database. This technique is highly accurate and can confirm the specific species of bacteria, including K. cowanii.
Biolog Gen III: Biolog Gen III utilizes 96-well microplates containing different substrates and indicators to assess the metabolic activity of bacteria. The pattern of color changes in the wells can be compared to a database, assisting in bacterial species identification.
16S rDNA and gyrB Sequencing: Molecular methods such as 16S rDNA and gyrB sequencing followed by polymerase chain reaction (PCR) to amplify and sequence specific regions of the bacterial genome. These sequences can be compared to reference databases to pinpoint the bacterial species accurately.
Kosakonia cowanii is primarily recognized as a pathogen that affects various crops, leading to ailments like wilt and dieback. Nevertheless, it has emerged as a rare cause of human infections, particularly among individuals with compromised immune systems or those experiencing traumatic plant-related injuries.
The prevalence of Kosakonia cowanii in clinical specimens from human infections remains exceptionally low, typically ranging from 0.01% to 0.1%. Notably, this bacterium is more frequently encountered in plant samples, with soybean crops being a common source.
The epidemiology of K. cowanii in human infections needs to be more studied, mainly due to challenges in its identification using conventional methods, often resulting in misclassification as other members of the Enterobacteriaceae family. A comprehensive literature review reveals that between 2000 and 2020, only a scant 14 cases of human infections attributed to K. cowanii have been reported worldwide.
Classification and Structure:
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Kosakonia
Species: K. cowanii
Kosakonia cowanii is a rod-shaped bacterium with a facultatively anaerobic metabolism. It typically measures about 0.5–1.0 µm in width and 1.5–3.0 µm in length.
This bacterium is motile, facilitated by a single polar flagellum. The flagellum allows Kosakonia cowanii to move through its environment, which is vital for its survival and ability to colonize various niches.
Kosakonia cowanii has a cell wall composed of peptidoglycan and an outer membrane containing lipopolysaccharides. Notably, it also possesses a capsule, which may serve multiple functions.
Kosakonia cowanii Pa82, a bacterium known for its association with plant pathogenicity and rare human infections, possesses several virulence-related genes, including adhesins and those involved in endotoxin biosynthesis and modification. Adhesins play a crucial role in bacterial colonization, invasion, and the formation of biofilms. In the case of K. cowanii Pa82, these adhesins are predicted to contribute to its pathogenicity.
Furthermore, Kosakonia cowanii has been studied in various strains, with 888-76T as the type strain previously referred to as E. cowanii. Phylogenetically related strains, such as BCC 078, BCC 074, BCC 008, BCC 011, and BCC 009, have been identified through genetic sequencing using 16S rRNA and rpoB genes. These strains provide valuable insights into the diversity and genetic makeup of Kosakonia cowanii.
K. cowanii, primarily a plant pathogen, can access the human body through wounds caused by plant thorns or other sharp objects. This traumatic inoculation can lead to localized or systemic infections. In some cases, it has been associated with severe conditions like rhabdomyolysis and bacteremia, highlighting the potential for significant health consequences.
Evidence suggests that K. cowanii may be able to colonize the human gut, particularly in immune compromised individuals or those with alterations in their gut microbiota. This colonization can facilitate the translocation of the bacterium across the intestinal barrier, leading to infections in other organs, such as the gallbladder. This process underscores the opportunistic nature of K. cowanii infections.
K. cowanii possesses a protective capsule that may aid in adhesion to host tissues and protection from host defenses. Additionally, its flagellum enables motility and invasion, potentially contributing to its ability to cause infections. Furthermore, K. cowanii has resisted certain antibiotics, including ampicillin and cephalosporins. This antibiotic resistance can limit treatment options and increase the risk of complications associated with K. cowanii infections.
Human host defenses play a crucial role in protecting against Kosakonia cowanii infections through various mechanisms:
The skin is a formidable barrier, preventing Kosakonia cowanii from entering the body through wounds or cuts caused by plant thorns or similar objects. Additionally, mucous membranes in the respiratory, genitourinary, and gastrointestinal tracts can trap and expel the bacterium.
Several chemical defenses are employed against Kosakonia cowanii. Lysozyme, an enzyme, can damage the bacterium’s cell wall by breaking down the muramic acid linkage. Immunoglobulins, including antibodies, can hinder K. cowanii‘s attachment to host cells or facilitate their opsonization for phagocytosis.
Antimicrobial peptides disrupt the bacterial membrane or interfere with DNA synthesis. Iron-binding proteins limit Kosakonia cowanii‘s access to essential iron. Cytokines, signaling molecules, can activate or recruit other immune cells to combat the infection.
Both granulocytes and agranulocytes contribute as a cellular defense against Kosakonia cowanii. These immune cells can phagocytose and subsequently kill the bacterium using various mechanisms, including producing reactive oxygen species, nitric oxide, lysosomal enzymes, or defensins.
Lymphocytes, another essential immune system component, generate antibodies that bind to K. cowanii, neutralizing it or enhancing its phagocytosis. Additionally, lymphocytes can produce cytotoxic molecules that induce apoptosis in infected cells or secrete cytokines that regulate the immune response.
Clinical manifestations of Kosakonia cowanii infections in humans are rare but have been reported, typically associated with traumatic inoculation from plant sources. One case involved a patient who developed rhabdomyolysis and bacteremia after being pricked by a rose thorn contaminated with K. cowanii.
This incident underscores the potential of K. cowanii to act as an opportunistic pathogen, particularly in individuals with compromised immune systems. Another case involved acute cholecystitis caused by K. cowanii, with the bacterium isolated from the patient’s gall bladder and bile. Clinical presentations of K. cowanii infections can vary depending on the infection site and severity.
Still, they may encompass symptoms such as fever, pain, inflammation, tissue necrosis, and affected organ dysfunction. These cases highlight considering K. cowanii as a potential pathogen in specific clinical contexts, particularly when there is a history of traumatic plant-related injuries.
Diagnosing Kosakonia cowanii infections typically involves a combination of laboratory techniques to identify the bacterium accurately.
MALDI-TOF Mass Spectrometry: MALDI-TOF is a powerful technique that analyzes the molecular weight of bacteria. It ionizes bacterial molecules with a laser and measures their time to reach a detector. By comparing the resulting mass spectrum to a database, healthcare professionals can rapidly and accurately identify K. cowanii.
VITEK 2 GN ID Card: The VITEK 2 system employs biochemical reactions to identify Gram-negative bacteria based on their metabolic profiles. This system provides valuable information about the bacterium’s metabolic activity, aiding in its identification.
16S rRNA Sequencing: 16S rRNA sequencing is a molecular method that compares the genetic sequence of a specific region of bacterial ribosomal RNA to known sequences in a database. This technique is highly accurate and can confirm the specific species of bacteria, including K. cowanii.
Biolog Gen III: Biolog Gen III utilizes 96-well microplates containing different substrates and indicators to assess the metabolic activity of bacteria. The pattern of color changes in the wells can be compared to a database, assisting in bacterial species identification.
16S rDNA and gyrB Sequencing: Molecular methods such as 16S rDNA and gyrB sequencing followed by polymerase chain reaction (PCR) to amplify and sequence specific regions of the bacterial genome. These sequences can be compared to reference databases to pinpoint the bacterial species accurately.
Kosakonia cowanii is primarily recognized as a pathogen that affects various crops, leading to ailments like wilt and dieback. Nevertheless, it has emerged as a rare cause of human infections, particularly among individuals with compromised immune systems or those experiencing traumatic plant-related injuries.
The prevalence of Kosakonia cowanii in clinical specimens from human infections remains exceptionally low, typically ranging from 0.01% to 0.1%. Notably, this bacterium is more frequently encountered in plant samples, with soybean crops being a common source.
The epidemiology of K. cowanii in human infections needs to be more studied, mainly due to challenges in its identification using conventional methods, often resulting in misclassification as other members of the Enterobacteriaceae family. A comprehensive literature review reveals that between 2000 and 2020, only a scant 14 cases of human infections attributed to K. cowanii have been reported worldwide.
Classification and Structure:
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Gammaproteobacteria
Order: Enterobacterales
Family: Enterobacteriaceae
Genus: Kosakonia
Species: K. cowanii
Kosakonia cowanii is a rod-shaped bacterium with a facultatively anaerobic metabolism. It typically measures about 0.5–1.0 µm in width and 1.5–3.0 µm in length.
This bacterium is motile, facilitated by a single polar flagellum. The flagellum allows Kosakonia cowanii to move through its environment, which is vital for its survival and ability to colonize various niches.
Kosakonia cowanii has a cell wall composed of peptidoglycan and an outer membrane containing lipopolysaccharides. Notably, it also possesses a capsule, which may serve multiple functions.
Kosakonia cowanii Pa82, a bacterium known for its association with plant pathogenicity and rare human infections, possesses several virulence-related genes, including adhesins and those involved in endotoxin biosynthesis and modification. Adhesins play a crucial role in bacterial colonization, invasion, and the formation of biofilms. In the case of K. cowanii Pa82, these adhesins are predicted to contribute to its pathogenicity.
Furthermore, Kosakonia cowanii has been studied in various strains, with 888-76T as the type strain previously referred to as E. cowanii. Phylogenetically related strains, such as BCC 078, BCC 074, BCC 008, BCC 011, and BCC 009, have been identified through genetic sequencing using 16S rRNA and rpoB genes. These strains provide valuable insights into the diversity and genetic makeup of Kosakonia cowanii.
K. cowanii, primarily a plant pathogen, can access the human body through wounds caused by plant thorns or other sharp objects. This traumatic inoculation can lead to localized or systemic infections. In some cases, it has been associated with severe conditions like rhabdomyolysis and bacteremia, highlighting the potential for significant health consequences.
Evidence suggests that K. cowanii may be able to colonize the human gut, particularly in immune compromised individuals or those with alterations in their gut microbiota. This colonization can facilitate the translocation of the bacterium across the intestinal barrier, leading to infections in other organs, such as the gallbladder. This process underscores the opportunistic nature of K. cowanii infections.
K. cowanii possesses a protective capsule that may aid in adhesion to host tissues and protection from host defenses. Additionally, its flagellum enables motility and invasion, potentially contributing to its ability to cause infections. Furthermore, K. cowanii has resisted certain antibiotics, including ampicillin and cephalosporins. This antibiotic resistance can limit treatment options and increase the risk of complications associated with K. cowanii infections.
Human host defenses play a crucial role in protecting against Kosakonia cowanii infections through various mechanisms:
The skin is a formidable barrier, preventing Kosakonia cowanii from entering the body through wounds or cuts caused by plant thorns or similar objects. Additionally, mucous membranes in the respiratory, genitourinary, and gastrointestinal tracts can trap and expel the bacterium.
Several chemical defenses are employed against Kosakonia cowanii. Lysozyme, an enzyme, can damage the bacterium’s cell wall by breaking down the muramic acid linkage. Immunoglobulins, including antibodies, can hinder K. cowanii‘s attachment to host cells or facilitate their opsonization for phagocytosis.
Antimicrobial peptides disrupt the bacterial membrane or interfere with DNA synthesis. Iron-binding proteins limit Kosakonia cowanii‘s access to essential iron. Cytokines, signaling molecules, can activate or recruit other immune cells to combat the infection.
Both granulocytes and agranulocytes contribute as a cellular defense against Kosakonia cowanii. These immune cells can phagocytose and subsequently kill the bacterium using various mechanisms, including producing reactive oxygen species, nitric oxide, lysosomal enzymes, or defensins.
Lymphocytes, another essential immune system component, generate antibodies that bind to K. cowanii, neutralizing it or enhancing its phagocytosis. Additionally, lymphocytes can produce cytotoxic molecules that induce apoptosis in infected cells or secrete cytokines that regulate the immune response.
Clinical manifestations of Kosakonia cowanii infections in humans are rare but have been reported, typically associated with traumatic inoculation from plant sources. One case involved a patient who developed rhabdomyolysis and bacteremia after being pricked by a rose thorn contaminated with K. cowanii.
This incident underscores the potential of K. cowanii to act as an opportunistic pathogen, particularly in individuals with compromised immune systems. Another case involved acute cholecystitis caused by K. cowanii, with the bacterium isolated from the patient’s gall bladder and bile. Clinical presentations of K. cowanii infections can vary depending on the infection site and severity.
Still, they may encompass symptoms such as fever, pain, inflammation, tissue necrosis, and affected organ dysfunction. These cases highlight considering K. cowanii as a potential pathogen in specific clinical contexts, particularly when there is a history of traumatic plant-related injuries.
Diagnosing Kosakonia cowanii infections typically involves a combination of laboratory techniques to identify the bacterium accurately.
MALDI-TOF Mass Spectrometry: MALDI-TOF is a powerful technique that analyzes the molecular weight of bacteria. It ionizes bacterial molecules with a laser and measures their time to reach a detector. By comparing the resulting mass spectrum to a database, healthcare professionals can rapidly and accurately identify K. cowanii.
VITEK 2 GN ID Card: The VITEK 2 system employs biochemical reactions to identify Gram-negative bacteria based on their metabolic profiles. This system provides valuable information about the bacterium’s metabolic activity, aiding in its identification.
16S rRNA Sequencing: 16S rRNA sequencing is a molecular method that compares the genetic sequence of a specific region of bacterial ribosomal RNA to known sequences in a database. This technique is highly accurate and can confirm the specific species of bacteria, including K. cowanii.
Biolog Gen III: Biolog Gen III utilizes 96-well microplates containing different substrates and indicators to assess the metabolic activity of bacteria. The pattern of color changes in the wells can be compared to a database, assisting in bacterial species identification.
16S rDNA and gyrB Sequencing: Molecular methods such as 16S rDNA and gyrB sequencing followed by polymerase chain reaction (PCR) to amplify and sequence specific regions of the bacterial genome. These sequences can be compared to reference databases to pinpoint the bacterial species accurately.

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