Staphylococcus pettenkoferi is a bacterium named in honor of Max von Pettenkofer, a prominent German physician and hygienist who lived from 1818 to 1901. Max von Pettenkofer made significant advancements in the study of hygiene and infectious diseases, particularly concerning water sanitation and the transmission of diseases.
According to a retrospective study review, S. pettenkoferi was found in traditional cultures in 25 cases. Among these cases, 12 were blood cultures, and 13 were from other sources. In most cases, S. pettenkoferi was found alongside commensal flora and was considered clinically insignificant. However, the significance of S. pettenkoferi in two cases with non-healing, deep foot wounds remained uncertain.
The mean age of the reported cases was 65 ± 16 years, indicating that the infection tends to affect older individuals. Furthermore, one-third of the cases had immunosuppressing conditions, suggesting that individuals with weakened immune systems may be more susceptible to S. pettenkoferi infections. Based on one study, 10 case reports of S pettenkoferi infection were documented in various regions worldwide. From 2015 – 2019, samples of S. pettenkoferi were isolated in the serum of 80 patients at American Healthcare. 90% of the isolates were found to be impure, with the rest, or 10%, labeled as inconclusive. None of them fit their criteria for genuine bacteremia, implying that S. pettenkoferi‘s pathogenicity continues to be disputed.
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: Staphylococcus pettenkoferi
Staphylococcus pettenkoferi belongs to the genus Staphylococcus, encompassing spherical, nonmotile, Gram-positive, non-spore-forming, facultative anaerobic bacteria.
The cell wall is composed of peptidoglycan, which gives it the characteristic Gram-positive staining property.
Size varies from 0.5 to 1.5 µm in diameter. It is coagulase-negative & is most likely a commensal organism on human skin.
S. pettenkoferi may also produce a slimy extracellular matrix called glycocalyx or biofilm.
The antigenic types of Staphylococcipettenkoferi have not been extensively characterized or classified.
S. pettenkoferi can produce various virulence factors, such as toxins and enzymes, contributing to tissue damage and immune evasion. These virulence factors can include hemolysins, proteases, and lipases. Hemolysins can cause the destruction of red blood cells, while proteases and lipases can degrade host proteins and lipids, respectively, leading to tissue damage and inflammation.
S. pettenkoferi can evade the immune system through mechanisms like antigenic drift, where the bacterial surface proteins, including adhesins, undergo constant changes. This antigenic variation helps the bacteria evade recognition and clearance by the host immune response, making it challenging to develop effective vaccines against S. pettenkoferi.
Genomic analysis of Staphylococcus pettenkoferi has identified several virulence factors contributing to its pathogenicity. These include biofilm-encoding genes such as icaABCD and rsbUVW. In addition to biofilm-encoding genes, the genomic analysis has revealed regulator-encoding genes associated with virulence. These genes include agr, mgrA, sarA, and saeS, which are involved in regulating various virulence factors and coordinating bacterial responses to environmental cues.
Fibronectin-binding proteins allow the bacterium to adhere to host cells and extracellular matrix components, promoting colonization and the formation of biofilms.
Glycocalyx-associated proteins contribute to the formation of the bacterial glycocalyx, a protective extracellular matrix that helps the bacterium evade host immune defenses and resist antimicrobial agents. The glycocalyx can enhance the ability of S. pettenkoferi to adhere to surfaces, form biofilms, and cause persistent infections.
Together, these virulence factors contribute to the pathogenicity of Staphylococcus pettenkoferi by promoting adhesion, colonization, immune evasion, and the establishment of chronic infections.
The mobilization of secretory vesicles within the immune cells leads to the upregulation of specific cell surface receptors, such as CD11b/CD18; it is also known as Mac-1 or complement receptor 3 (CR3), a vital receptor found on the surface of phagocytes, including neutrophils and macrophages. It plays a crucial role in recognizing and engulfing pathogens, including Staphylococcus pettenkoferi.
Up-regulation of CD11b/CD18 on the surface of phagocytes enhances their ability to bind to and engulf Staphylococcus pettenkoferi bacteria. It promotes the formation of phagocytic cups and the subsequent bacteria internalization into phagosomes. Once inside the phagosome, the bacteria undergo various antimicrobial mechanisms, such as reactive oxygen species production, lysosomal degradation, and antimicrobial peptide release.
Neutrophils employ extracellular molecules like group IIA phospholipase A2 (gIIA-PLA2), a small cationic antimicrobial protein in extracellular fluids. The antimicrobial activity of gIIA-PLA2 is mediated by its ability to target and hydrolyze bacterial phospholipids, disrupting bacterial cell membranes.
This action affects the structural integrity of the bacterial cells and exposes them to the bactericidal action of ROS generated by the neutrophil NADPH oxidase. gIIA-PLA2 can synergize with the neutrophil NADPH oxidase, an enzyme complex that generates reactive oxygen species (ROS).
Together, gIIA-PLA2 and NADPH oxidase promote the digestion of phospholipids present in the membrane of S. pettenkoferi; the collective action of gIIA-PLA2 and NADPH oxidase results in the enhanced killing of Staphylococcus pettenkoferi by neutrophils. The digestion of phospholipids by gIIA-PLA2 weakens the bacterial membrane, making it more susceptible to ROS-mediated damage.
Staphylococcus pettenkoferi is implicated in osteomyelitis associated with a diabetic foot infection; it can lead to specific clinical manifestations. Pus or fluid may accumulate in the infected area, leading to a draining sinus or an abscess.
Inflammation and swelling can occur around the infected area. The skin may appear red, warm, and tender to the touch. Patients may develop systemic symptoms such as fever, chills, and malaise in more severe cases.
S. pettenkoferi can enter the bloodstream, leading to bacteremia and potentially causing systemic infections. Symptoms include fever, chills, hypotension, and signs of organ involvement.
Culture method: The specimen, such as blood, wound swab, or tissue sample, is collected and inoculated onto appropriate culture media, such as blood or nutrient agar. The plates are then incubated at an appropriate temperature, typically 37°C, for 24 to 48 hours. Staphylococcus pettenkoferi typically forms small, circular colonies 1-2 mm in size. The colonies appear as smooth, opaque, and creamy in texture.
Biochemical tests are commonly used for the diagnosis of S. pettenkoferi. These tests help to identify specific metabolic characteristics of the bacterium. Some critical tests include catalase, coagulase, oxidase, and various sugar fermentation tests. S. pettenkoferi typically exhibits positive results for catalase, meaning it produces the enzyme catalase, and negative results for coagulase, indicating it does not produce the coagulase enzyme. Additionally, it may show negative results for oxidase, as it lacks the oxidase enzyme. Sugar fermentation tests can determine the ability of the bacterium to ferment different sugars, providing further insights into its metabolic profile.
Practicing regular handwashing with soap and water or using alcohol-based hand sanitizers.
Implement strict infection control protocols, including proper sterilization and disinfection procedures, adherence to standard and isolation precautions in healthcare settings.
Promoting appropriate and judicious use of antibiotics to prevent the emergence of antibiotic-resistant strains.
Staphylococcus pettenkoferi is a bacterium named in honor of Max von Pettenkofer, a prominent German physician and hygienist who lived from 1818 to 1901. Max von Pettenkofer made significant advancements in the study of hygiene and infectious diseases, particularly concerning water sanitation and the transmission of diseases.
According to a retrospective study review, S. pettenkoferi was found in traditional cultures in 25 cases. Among these cases, 12 were blood cultures, and 13 were from other sources. In most cases, S. pettenkoferi was found alongside commensal flora and was considered clinically insignificant. However, the significance of S. pettenkoferi in two cases with non-healing, deep foot wounds remained uncertain.
The mean age of the reported cases was 65 ± 16 years, indicating that the infection tends to affect older individuals. Furthermore, one-third of the cases had immunosuppressing conditions, suggesting that individuals with weakened immune systems may be more susceptible to S. pettenkoferi infections. Based on one study, 10 case reports of S pettenkoferi infection were documented in various regions worldwide. From 2015 – 2019, samples of S. pettenkoferi were isolated in the serum of 80 patients at American Healthcare. 90% of the isolates were found to be impure, with the rest, or 10%, labeled as inconclusive. None of them fit their criteria for genuine bacteremia, implying that S. pettenkoferi‘s pathogenicity continues to be disputed.
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: Staphylococcus pettenkoferi
Staphylococcus pettenkoferi belongs to the genus Staphylococcus, encompassing spherical, nonmotile, Gram-positive, non-spore-forming, facultative anaerobic bacteria.
The cell wall is composed of peptidoglycan, which gives it the characteristic Gram-positive staining property.
Size varies from 0.5 to 1.5 µm in diameter. It is coagulase-negative & is most likely a commensal organism on human skin.
S. pettenkoferi may also produce a slimy extracellular matrix called glycocalyx or biofilm.
The antigenic types of Staphylococcipettenkoferi have not been extensively characterized or classified.
S. pettenkoferi can produce various virulence factors, such as toxins and enzymes, contributing to tissue damage and immune evasion. These virulence factors can include hemolysins, proteases, and lipases. Hemolysins can cause the destruction of red blood cells, while proteases and lipases can degrade host proteins and lipids, respectively, leading to tissue damage and inflammation.
S. pettenkoferi can evade the immune system through mechanisms like antigenic drift, where the bacterial surface proteins, including adhesins, undergo constant changes. This antigenic variation helps the bacteria evade recognition and clearance by the host immune response, making it challenging to develop effective vaccines against S. pettenkoferi.
Genomic analysis of Staphylococcus pettenkoferi has identified several virulence factors contributing to its pathogenicity. These include biofilm-encoding genes such as icaABCD and rsbUVW. In addition to biofilm-encoding genes, the genomic analysis has revealed regulator-encoding genes associated with virulence. These genes include agr, mgrA, sarA, and saeS, which are involved in regulating various virulence factors and coordinating bacterial responses to environmental cues.
Fibronectin-binding proteins allow the bacterium to adhere to host cells and extracellular matrix components, promoting colonization and the formation of biofilms.
Glycocalyx-associated proteins contribute to the formation of the bacterial glycocalyx, a protective extracellular matrix that helps the bacterium evade host immune defenses and resist antimicrobial agents. The glycocalyx can enhance the ability of S. pettenkoferi to adhere to surfaces, form biofilms, and cause persistent infections.
Together, these virulence factors contribute to the pathogenicity of Staphylococcus pettenkoferi by promoting adhesion, colonization, immune evasion, and the establishment of chronic infections.
The mobilization of secretory vesicles within the immune cells leads to the upregulation of specific cell surface receptors, such as CD11b/CD18; it is also known as Mac-1 or complement receptor 3 (CR3), a vital receptor found on the surface of phagocytes, including neutrophils and macrophages. It plays a crucial role in recognizing and engulfing pathogens, including Staphylococcus pettenkoferi.
Up-regulation of CD11b/CD18 on the surface of phagocytes enhances their ability to bind to and engulf Staphylococcus pettenkoferi bacteria. It promotes the formation of phagocytic cups and the subsequent bacteria internalization into phagosomes. Once inside the phagosome, the bacteria undergo various antimicrobial mechanisms, such as reactive oxygen species production, lysosomal degradation, and antimicrobial peptide release.
Neutrophils employ extracellular molecules like group IIA phospholipase A2 (gIIA-PLA2), a small cationic antimicrobial protein in extracellular fluids. The antimicrobial activity of gIIA-PLA2 is mediated by its ability to target and hydrolyze bacterial phospholipids, disrupting bacterial cell membranes.
This action affects the structural integrity of the bacterial cells and exposes them to the bactericidal action of ROS generated by the neutrophil NADPH oxidase. gIIA-PLA2 can synergize with the neutrophil NADPH oxidase, an enzyme complex that generates reactive oxygen species (ROS).
Together, gIIA-PLA2 and NADPH oxidase promote the digestion of phospholipids present in the membrane of S. pettenkoferi; the collective action of gIIA-PLA2 and NADPH oxidase results in the enhanced killing of Staphylococcus pettenkoferi by neutrophils. The digestion of phospholipids by gIIA-PLA2 weakens the bacterial membrane, making it more susceptible to ROS-mediated damage.
Staphylococcus pettenkoferi is implicated in osteomyelitis associated with a diabetic foot infection; it can lead to specific clinical manifestations. Pus or fluid may accumulate in the infected area, leading to a draining sinus or an abscess.
Inflammation and swelling can occur around the infected area. The skin may appear red, warm, and tender to the touch. Patients may develop systemic symptoms such as fever, chills, and malaise in more severe cases.
S. pettenkoferi can enter the bloodstream, leading to bacteremia and potentially causing systemic infections. Symptoms include fever, chills, hypotension, and signs of organ involvement.
Culture method: The specimen, such as blood, wound swab, or tissue sample, is collected and inoculated onto appropriate culture media, such as blood or nutrient agar. The plates are then incubated at an appropriate temperature, typically 37°C, for 24 to 48 hours. Staphylococcus pettenkoferi typically forms small, circular colonies 1-2 mm in size. The colonies appear as smooth, opaque, and creamy in texture.
Biochemical tests are commonly used for the diagnosis of S. pettenkoferi. These tests help to identify specific metabolic characteristics of the bacterium. Some critical tests include catalase, coagulase, oxidase, and various sugar fermentation tests. S. pettenkoferi typically exhibits positive results for catalase, meaning it produces the enzyme catalase, and negative results for coagulase, indicating it does not produce the coagulase enzyme. Additionally, it may show negative results for oxidase, as it lacks the oxidase enzyme. Sugar fermentation tests can determine the ability of the bacterium to ferment different sugars, providing further insights into its metabolic profile.
Practicing regular handwashing with soap and water or using alcohol-based hand sanitizers.
Implement strict infection control protocols, including proper sterilization and disinfection procedures, adherence to standard and isolation precautions in healthcare settings.
Promoting appropriate and judicious use of antibiotics to prevent the emergence of antibiotic-resistant strains.
Staphylococcus pettenkoferi is a bacterium named in honor of Max von Pettenkofer, a prominent German physician and hygienist who lived from 1818 to 1901. Max von Pettenkofer made significant advancements in the study of hygiene and infectious diseases, particularly concerning water sanitation and the transmission of diseases.
According to a retrospective study review, S. pettenkoferi was found in traditional cultures in 25 cases. Among these cases, 12 were blood cultures, and 13 were from other sources. In most cases, S. pettenkoferi was found alongside commensal flora and was considered clinically insignificant. However, the significance of S. pettenkoferi in two cases with non-healing, deep foot wounds remained uncertain.
The mean age of the reported cases was 65 ± 16 years, indicating that the infection tends to affect older individuals. Furthermore, one-third of the cases had immunosuppressing conditions, suggesting that individuals with weakened immune systems may be more susceptible to S. pettenkoferi infections. Based on one study, 10 case reports of S pettenkoferi infection were documented in various regions worldwide. From 2015 – 2019, samples of S. pettenkoferi were isolated in the serum of 80 patients at American Healthcare. 90% of the isolates were found to be impure, with the rest, or 10%, labeled as inconclusive. None of them fit their criteria for genuine bacteremia, implying that S. pettenkoferi‘s pathogenicity continues to be disputed.
Kingdom: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: Staphylococcus pettenkoferi
Staphylococcus pettenkoferi belongs to the genus Staphylococcus, encompassing spherical, nonmotile, Gram-positive, non-spore-forming, facultative anaerobic bacteria.
The cell wall is composed of peptidoglycan, which gives it the characteristic Gram-positive staining property.
Size varies from 0.5 to 1.5 µm in diameter. It is coagulase-negative & is most likely a commensal organism on human skin.
S. pettenkoferi may also produce a slimy extracellular matrix called glycocalyx or biofilm.
The antigenic types of Staphylococcipettenkoferi have not been extensively characterized or classified.
S. pettenkoferi can produce various virulence factors, such as toxins and enzymes, contributing to tissue damage and immune evasion. These virulence factors can include hemolysins, proteases, and lipases. Hemolysins can cause the destruction of red blood cells, while proteases and lipases can degrade host proteins and lipids, respectively, leading to tissue damage and inflammation.
S. pettenkoferi can evade the immune system through mechanisms like antigenic drift, where the bacterial surface proteins, including adhesins, undergo constant changes. This antigenic variation helps the bacteria evade recognition and clearance by the host immune response, making it challenging to develop effective vaccines against S. pettenkoferi.
Genomic analysis of Staphylococcus pettenkoferi has identified several virulence factors contributing to its pathogenicity. These include biofilm-encoding genes such as icaABCD and rsbUVW. In addition to biofilm-encoding genes, the genomic analysis has revealed regulator-encoding genes associated with virulence. These genes include agr, mgrA, sarA, and saeS, which are involved in regulating various virulence factors and coordinating bacterial responses to environmental cues.
Fibronectin-binding proteins allow the bacterium to adhere to host cells and extracellular matrix components, promoting colonization and the formation of biofilms.
Glycocalyx-associated proteins contribute to the formation of the bacterial glycocalyx, a protective extracellular matrix that helps the bacterium evade host immune defenses and resist antimicrobial agents. The glycocalyx can enhance the ability of S. pettenkoferi to adhere to surfaces, form biofilms, and cause persistent infections.
Together, these virulence factors contribute to the pathogenicity of Staphylococcus pettenkoferi by promoting adhesion, colonization, immune evasion, and the establishment of chronic infections.
The mobilization of secretory vesicles within the immune cells leads to the upregulation of specific cell surface receptors, such as CD11b/CD18; it is also known as Mac-1 or complement receptor 3 (CR3), a vital receptor found on the surface of phagocytes, including neutrophils and macrophages. It plays a crucial role in recognizing and engulfing pathogens, including Staphylococcus pettenkoferi.
Up-regulation of CD11b/CD18 on the surface of phagocytes enhances their ability to bind to and engulf Staphylococcus pettenkoferi bacteria. It promotes the formation of phagocytic cups and the subsequent bacteria internalization into phagosomes. Once inside the phagosome, the bacteria undergo various antimicrobial mechanisms, such as reactive oxygen species production, lysosomal degradation, and antimicrobial peptide release.
Neutrophils employ extracellular molecules like group IIA phospholipase A2 (gIIA-PLA2), a small cationic antimicrobial protein in extracellular fluids. The antimicrobial activity of gIIA-PLA2 is mediated by its ability to target and hydrolyze bacterial phospholipids, disrupting bacterial cell membranes.
This action affects the structural integrity of the bacterial cells and exposes them to the bactericidal action of ROS generated by the neutrophil NADPH oxidase. gIIA-PLA2 can synergize with the neutrophil NADPH oxidase, an enzyme complex that generates reactive oxygen species (ROS).
Together, gIIA-PLA2 and NADPH oxidase promote the digestion of phospholipids present in the membrane of S. pettenkoferi; the collective action of gIIA-PLA2 and NADPH oxidase results in the enhanced killing of Staphylococcus pettenkoferi by neutrophils. The digestion of phospholipids by gIIA-PLA2 weakens the bacterial membrane, making it more susceptible to ROS-mediated damage.
Staphylococcus pettenkoferi is implicated in osteomyelitis associated with a diabetic foot infection; it can lead to specific clinical manifestations. Pus or fluid may accumulate in the infected area, leading to a draining sinus or an abscess.
Inflammation and swelling can occur around the infected area. The skin may appear red, warm, and tender to the touch. Patients may develop systemic symptoms such as fever, chills, and malaise in more severe cases.
S. pettenkoferi can enter the bloodstream, leading to bacteremia and potentially causing systemic infections. Symptoms include fever, chills, hypotension, and signs of organ involvement.
Culture method: The specimen, such as blood, wound swab, or tissue sample, is collected and inoculated onto appropriate culture media, such as blood or nutrient agar. The plates are then incubated at an appropriate temperature, typically 37°C, for 24 to 48 hours. Staphylococcus pettenkoferi typically forms small, circular colonies 1-2 mm in size. The colonies appear as smooth, opaque, and creamy in texture.
Biochemical tests are commonly used for the diagnosis of S. pettenkoferi. These tests help to identify specific metabolic characteristics of the bacterium. Some critical tests include catalase, coagulase, oxidase, and various sugar fermentation tests. S. pettenkoferi typically exhibits positive results for catalase, meaning it produces the enzyme catalase, and negative results for coagulase, indicating it does not produce the coagulase enzyme. Additionally, it may show negative results for oxidase, as it lacks the oxidase enzyme. Sugar fermentation tests can determine the ability of the bacterium to ferment different sugars, providing further insights into its metabolic profile.
Practicing regular handwashing with soap and water or using alcohol-based hand sanitizers.
Implement strict infection control protocols, including proper sterilization and disinfection procedures, adherence to standard and isolation precautions in healthcare settings.
Promoting appropriate and judicious use of antibiotics to prevent the emergence of antibiotic-resistant strains.
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