Williamsia deligens

Updated : January 9, 2024

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The epidemiology of Williamsia deligens infection remains relatively understudied, given its rarity as an emerging pathogen. Initial documentation of this bacterium dates back to 2001, when it was isolated from the blood of a 65-year-old woman with a history of chronic obstructive pulmonary disease. The infection followed a bronchoscopy, and successful treatment was achieved with a regimen of vancomycin and rifampicin.    

Subsequent reports have highlighted the infrequent occurrence of Williamsia deligens infections, primarily manifesting as bacteremia. However, a broader spectrum of infection sites has been noted in isolated cases, including peritoneal dialysis fluid, pleural fluid, and wound infections. The optimal treatment strategy for W. deligens infections remains uncertain, and susceptibility to antibiotics like vancomycin, linezolid, and rifampicin is suggested. However, reported cases of resistance or relapse emphasize the potential necessity for prolonged or combination therapy. 

  

Kingdom: Bacteria  

Phylum: Actinobacteria  

Class: Actinomycetia  

Order: Corynebacteriales  

Family: Nocardiaceae  

Genus: Williamsia  

Species: W. deligens  

Williamsia deligens, characterized as a non-spore-forming and non-motile organism, displays an aerobic lifestyle. The bacterium features short rods without branching, with dimensions typically ranging from 0.5-0.8 x 1.0-2.0 µm. Its unique cell wall structure includes mycolic acid components, classifying it as an actinomycete—a distinctive trait among bacterial species.  

Within the peptidoglycan layer of the cell wall, Williamsia deligens incorporates meso-2,6-diaminoheptanedioate as the diagnostic diamino acid, contributing to its structural composition. Additionally, the bacterium utilizes dihydrogenated menaquinone with eight isoprene units as the primary respiratory quinone, reflecting its respiratory characteristics.

Williamsia deligens possesses distinctive characteristics that contribute to its identity and potential pathogenicity. The bacterium has a cell wall structure containing mycolic acid components, known for their antigenic nature that can trigger immune reactions in the host. This feature suggests that the cell wall composition of W. deligens may play a role in interactions with the host immune system.  

Examining the virulence factors within its genome, W. deligens harbors a genome of 5.4 Mb, featuring 4,885 protein-coding genes & 50 RNA genes. Among these, genes encoding lipases, proteases, and peptidases are notable, indicating potential roles in the bacterium’s pathogenicity.

The high similarity (96.8%) in the 16S rRNA gene sequence with Williamsia muralis, the type species of the genus, emphasizes its taxonomic affiliation within the Williamsia genus. Unique features of W. deligens further include the presence of N-glycolyl muramic acid as a primary polar lipid, a distinctive trait that may contribute to its pathogenic properties.

Additionally, the diagnostic diamino acid meso-2,6-diaminoheptanedioate in the peptidoglycan layer is a common characteristic of actinomycetes and could influence the host immune response. The type strain, IMMIB RIV-956T, isolated from human blood in 2001, is recognized by various designations such as DSM 44902T, CCUG 50873T, CIP 109147, JCM 13662, and IFM 10667, highlighting its identification across different culture collections. 

 

Williamsia deligens possess multiple entry points into the human body, with potential routes including inhalation, ingestion, or skin contact with contaminated soil, water, or air, owing to its presence as an actinomycete in these diverse environments. This bacterium’s ability to colonize these habitats underscores the varied ways in which individuals may come into contact with W. deligens.  

The pathogenicity of W. deligens is further amplified by its capacity to evade the host immune system through the formation of biofilms. These biofilms, intricate communities of bacteria adhering to surfaces and shielded by a matrix of extracellular polymeric substances, contribute to the organism’s ability to resist antibiotics, and enhance its virulence.

This mechanism may pose a particular threat to individuals who are elderly or immunocompromised, especially those with underlying conditions like chronic lung disease, making them more susceptible to Williamsia deligens infection. Once established within the host, Williamsia deligens employs an arsenal of enzymes, including lipases, proteases, and esterases.

These enzymes play a crucial role in degrading host cell membranes and extracellular matrix components, enabling the bacterium to invade host tissues and organs. Additionally, these enzymes facilitate the dissemination of W. deligens through the bloodstream and lymphatic system, contributing to the pathogenicity and potential systemic impact of the infection.  

  

The human innate immune system employs a multifaceted defense mechanism against Williamsia deligens, recognizing specific cell wall components like mycolic acids and lipopolysaccharides (LPS). These antigens bind to pattern recognition receptors (PRRs) on immune cells, including macrophages, dendritic cells, and natural killer cells. This recognition can stimulate the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), contributing to the elimination or inhibition of W. deligens. 

In response to W. deligens, the adaptive immune system activates, generating antibodies and cytokines. These molecules are crucial in neutralizing or opsonizing the bacterium and orchestrating the activation of other immune cells, notably T cells and B cells. This orchestrated immune response may lead to the formation of granulomas, organized structures of immune cells designed to isolate and contain the infection.  

 

Williamsia deligens, a rarely encountered pathogen in human infections, has been identified from blood cultures of patients with bacteremia. The clinical manifestations of W. deligens infections are not extensively documented, but typical symptoms include fever, chills, malaise, and, in severe cases, septic shock. 

  • Culture test: Culturing the bacterium from clinical specimens is a primary diagnostic method. Williamsia deligens can be isolated using various media such as trypticase soy broth agar, brain heart infusion medium, or ISP media. Distinctive orange colonies with pigment production are indicative of its presence. However, the growth is slow, requiring 10-14 days for colonies to appear, emphasizing the need for patience in diagnostic procedures.
  • Molecular Tests: Molecular techniques play a crucial role in accurate identification. Sequencing the 16S rRNA gene and comparing it with reference sequences is a reliable method. The 16S rRNA gene sequence of the type strain is accessible at NCBI. Additional molecular methods, including PCR, MALDI-TOF MS, or DNA-DNA hybridization, can be utilized for confirmation. These advanced molecular approaches enhance the specificity and precision of the diagnostic process. 
  • Biochemical Analysis: Williamsia deligens can be characterized by its unique fatty acid profile, featuring hexadecenoic acid, oleic acid, palmitic acid, and tuberculostearic acid. Mycolic acid components with a chain length of C50-C56 further contribute to its biochemical fingerprint. Various biochemical tests, such as catalase, oxidase, urease, nitrate reduction, and sugar fermentation, can be employed to differentiate W. deligens from closely related bacteria.  

 

  • Avoiding exposure to contaminated soil, water, and air is crucial in preventing Williamsia infections. As an actinomycete found in these habitats, individuals must be cautious when engaging in activities that involve contact with potentially contaminated environments. Adhering to hygiene practices, such as wearing protective clothing & practicing proper hand hygiene, can contribute to minimizing the risk of exposure. 
  • Practicing good hygiene and meticulous wound care is imperative in preventing W. deligens infections through skin contact or trauma. Individuals should prioritize cleanliness and promptly attend to any wounds or skin injuries, employing proper cleaning and disinfection measures. 
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Williamsia deligens

Updated : January 9, 2024

Mail Whatsapp PDF Image



The epidemiology of Williamsia deligens infection remains relatively understudied, given its rarity as an emerging pathogen. Initial documentation of this bacterium dates back to 2001, when it was isolated from the blood of a 65-year-old woman with a history of chronic obstructive pulmonary disease. The infection followed a bronchoscopy, and successful treatment was achieved with a regimen of vancomycin and rifampicin.    

Subsequent reports have highlighted the infrequent occurrence of Williamsia deligens infections, primarily manifesting as bacteremia. However, a broader spectrum of infection sites has been noted in isolated cases, including peritoneal dialysis fluid, pleural fluid, and wound infections. The optimal treatment strategy for W. deligens infections remains uncertain, and susceptibility to antibiotics like vancomycin, linezolid, and rifampicin is suggested. However, reported cases of resistance or relapse emphasize the potential necessity for prolonged or combination therapy. 

  

Kingdom: Bacteria  

Phylum: Actinobacteria  

Class: Actinomycetia  

Order: Corynebacteriales  

Family: Nocardiaceae  

Genus: Williamsia  

Species: W. deligens  

Williamsia deligens, characterized as a non-spore-forming and non-motile organism, displays an aerobic lifestyle. The bacterium features short rods without branching, with dimensions typically ranging from 0.5-0.8 x 1.0-2.0 µm. Its unique cell wall structure includes mycolic acid components, classifying it as an actinomycete—a distinctive trait among bacterial species.  

Within the peptidoglycan layer of the cell wall, Williamsia deligens incorporates meso-2,6-diaminoheptanedioate as the diagnostic diamino acid, contributing to its structural composition. Additionally, the bacterium utilizes dihydrogenated menaquinone with eight isoprene units as the primary respiratory quinone, reflecting its respiratory characteristics.

Williamsia deligens possesses distinctive characteristics that contribute to its identity and potential pathogenicity. The bacterium has a cell wall structure containing mycolic acid components, known for their antigenic nature that can trigger immune reactions in the host. This feature suggests that the cell wall composition of W. deligens may play a role in interactions with the host immune system.  

Examining the virulence factors within its genome, W. deligens harbors a genome of 5.4 Mb, featuring 4,885 protein-coding genes & 50 RNA genes. Among these, genes encoding lipases, proteases, and peptidases are notable, indicating potential roles in the bacterium’s pathogenicity.

The high similarity (96.8%) in the 16S rRNA gene sequence with Williamsia muralis, the type species of the genus, emphasizes its taxonomic affiliation within the Williamsia genus. Unique features of W. deligens further include the presence of N-glycolyl muramic acid as a primary polar lipid, a distinctive trait that may contribute to its pathogenic properties.

Additionally, the diagnostic diamino acid meso-2,6-diaminoheptanedioate in the peptidoglycan layer is a common characteristic of actinomycetes and could influence the host immune response. The type strain, IMMIB RIV-956T, isolated from human blood in 2001, is recognized by various designations such as DSM 44902T, CCUG 50873T, CIP 109147, JCM 13662, and IFM 10667, highlighting its identification across different culture collections. 

 

Williamsia deligens possess multiple entry points into the human body, with potential routes including inhalation, ingestion, or skin contact with contaminated soil, water, or air, owing to its presence as an actinomycete in these diverse environments. This bacterium’s ability to colonize these habitats underscores the varied ways in which individuals may come into contact with W. deligens.  

The pathogenicity of W. deligens is further amplified by its capacity to evade the host immune system through the formation of biofilms. These biofilms, intricate communities of bacteria adhering to surfaces and shielded by a matrix of extracellular polymeric substances, contribute to the organism’s ability to resist antibiotics, and enhance its virulence.

This mechanism may pose a particular threat to individuals who are elderly or immunocompromised, especially those with underlying conditions like chronic lung disease, making them more susceptible to Williamsia deligens infection. Once established within the host, Williamsia deligens employs an arsenal of enzymes, including lipases, proteases, and esterases.

These enzymes play a crucial role in degrading host cell membranes and extracellular matrix components, enabling the bacterium to invade host tissues and organs. Additionally, these enzymes facilitate the dissemination of W. deligens through the bloodstream and lymphatic system, contributing to the pathogenicity and potential systemic impact of the infection.  

  

The human innate immune system employs a multifaceted defense mechanism against Williamsia deligens, recognizing specific cell wall components like mycolic acids and lipopolysaccharides (LPS). These antigens bind to pattern recognition receptors (PRRs) on immune cells, including macrophages, dendritic cells, and natural killer cells. This recognition can stimulate the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), contributing to the elimination or inhibition of W. deligens. 

In response to W. deligens, the adaptive immune system activates, generating antibodies and cytokines. These molecules are crucial in neutralizing or opsonizing the bacterium and orchestrating the activation of other immune cells, notably T cells and B cells. This orchestrated immune response may lead to the formation of granulomas, organized structures of immune cells designed to isolate and contain the infection.  

 

Williamsia deligens, a rarely encountered pathogen in human infections, has been identified from blood cultures of patients with bacteremia. The clinical manifestations of W. deligens infections are not extensively documented, but typical symptoms include fever, chills, malaise, and, in severe cases, septic shock. 

  • Culture test: Culturing the bacterium from clinical specimens is a primary diagnostic method. Williamsia deligens can be isolated using various media such as trypticase soy broth agar, brain heart infusion medium, or ISP media. Distinctive orange colonies with pigment production are indicative of its presence. However, the growth is slow, requiring 10-14 days for colonies to appear, emphasizing the need for patience in diagnostic procedures.
  • Molecular Tests: Molecular techniques play a crucial role in accurate identification. Sequencing the 16S rRNA gene and comparing it with reference sequences is a reliable method. The 16S rRNA gene sequence of the type strain is accessible at NCBI. Additional molecular methods, including PCR, MALDI-TOF MS, or DNA-DNA hybridization, can be utilized for confirmation. These advanced molecular approaches enhance the specificity and precision of the diagnostic process. 
  • Biochemical Analysis: Williamsia deligens can be characterized by its unique fatty acid profile, featuring hexadecenoic acid, oleic acid, palmitic acid, and tuberculostearic acid. Mycolic acid components with a chain length of C50-C56 further contribute to its biochemical fingerprint. Various biochemical tests, such as catalase, oxidase, urease, nitrate reduction, and sugar fermentation, can be employed to differentiate W. deligens from closely related bacteria.  

 

  • Avoiding exposure to contaminated soil, water, and air is crucial in preventing Williamsia infections. As an actinomycete found in these habitats, individuals must be cautious when engaging in activities that involve contact with potentially contaminated environments. Adhering to hygiene practices, such as wearing protective clothing & practicing proper hand hygiene, can contribute to minimizing the risk of exposure. 
  • Practicing good hygiene and meticulous wound care is imperative in preventing W. deligens infections through skin contact or trauma. Individuals should prioritize cleanliness and promptly attend to any wounds or skin injuries, employing proper cleaning and disinfection measures. 

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