Staphylococcus hominis is a coagulase-negative member of the bacterial genus Staphylococcus, consisting of Gram-positive, spherical cells in clusters. It occurs very commonly as a generally harmless commensal on human and animal skin and is known for producing thioalcohol compounds that contribute to body odour. Like many other coagulase-negative staphylococci, S. hominis may occasionally cause infection in patients whose immune systems are compromised, for example by chemotherapy or predisposing illness.

Description

Colonies of S. hominis are small, usually 1–2 mm in diameter after 24 hours' incubation at 35 °C, and white or tan in colour. Occasionally, strains are resistant to novobiocin and may be confused with other resistant species (e.g. S. saprophyticus).

Resistance

Based on a total of 240 strains, all were resistant to lysozyme, some were slightly resistant to lysostaphin, 77% were susceptible to penicillin G, 97% to streptomycin, 93% to erythromycin, 64% to tetracycline, and 99% to novobiocin.

The SHN is so similar to the original S. hominis, now called S. hominis subsp. hominis, that in 2010, a MicroScan system that clinical microbiology laboratories used, identified 7 of 31 S. hominis novobiosepticus cultures as S. hominis hominis. The relationship between the two was unknown, but antibiotic-resistant isolates of S. hominis belonged only to SHN.

SHN strains seems to have thickened cell walls, which can be the result of a genetic background that also allows for vancomycin resistance. The thickened cell walls exist in subspecies with and without vancomycin resistance which suggests this subspecies did not originate from the acquiring of resistance genes.

Origin

The combined resistance to novobiocin and oxacillin is hypothesized to have originated from a simultaneous introduction of genes controlling the resistance to the two. These genes were believed to have been acquired originally through heterologous DNA from a methicillin-resistant strain of one of the novobiocin-resistant species belonging to the S. sciuri or the S. saprophyticus groups. The larger genome size of the SHN compared to that of S. hominis hominis may be the result of the acquiring of heterologous DNA. This new, divergent strain was first described in 1998, and was first implicated in causing bacteremia in 2002.

Another hypothesis is the insertion of the mec A gene and its flanking sequence into the chromosome of SHN might have affected the expression of a closely linked gene, which converted the host to become novobiocin-resistant.

SHN has also been responsible for nosocomial outbreaks elsewhere. SHN strains have been causing bloodstream infections, but have still been classified as vancomycin-susceptible.

References

Further reading

  • Type strain of Staphylococcus hominis at BacDive - the Bacterial Diversity Metadatabase