Introduction: The distribution of Staphylococcus aureus and Staphylococcus epidermidis
among Malaysian healthy adults and their capability to produce enzyme hyaluronidase are less
reported. Hyaluronidase degrade hyaluronic acid in animal connective tissue and facilitate
bacterial spreading in host body. This study aims to identify the distribution of both
Staphylococci species in healthy subject, the hyaluronidase producer among the isolates and
the association of the latter with site of isolation (palm skin and anterior nares) and gender of
the host. Methods: A total of 108 swab samples were collected from anterior nares and palm
of 54 healthy subjects. The bacteria were identified through microscopic and biochemical tests,
before screened for hyaluronidase production using hyaluronic acid diffusion rapid plate
method. Results: Total of 139 bacterial isolates were identified; 68 isolates are S. aureus, 63
S. epidermidis and 8 other bacterial species. Staphylococcus aureus was highly isolated from
palm (57%) than anterior nares (47%). On the contrary for S. epidermidis was highly isolated
from anterior nares (53%) than from palm skin (43%). Equal proportion was found for both
species in male and female subject. A total of 77 (59%) isolates produced hyaluronidase; 55%
are S. aureus and 45% are S. epidermidis. Hyaluronidase-producer isolates are equally found
between anterior nares (56%) and palm skin (61%) or male (57%) and female subject (60%)
regardless of Staphylococcal species. No significant value was recorded for any analysis.
Conclusion: Capability of commensal S. aureus and S. epidermidis isolated from healthy
subject to produce hyaluronidase may indicate their potential as opportunistic pathogen
whenever the opportunity arises in any way.
Streptococcus pneumoniae (S. pneumoniae) is a gram-positive diplococci belonging to the genus Streptococcus and it is a well-studied pathogenic bacterium. Pneumococcal diseases such as otitis media, pneumonia, sepsis and meningitis caused by pathogenic strains of S. pneumoniae still brought significant mortality and morbidity worldwide. The pathogenicity of S. pneumoniae is exerted by various virulence factors and one of it is the enzyme hyaluronate lyase. Hyaluronate lyase plays a major role in
the invasive capability of S. pneumoniae. Its mechanism of action and crystallographic
structure have been determinedbut its regulatory mechanism is still poorly understood.
Drawing connections between the nutritional behaviour and invasive property of S.
pneumoniae, CodY regulator is hypothesized as a potential hyaluronate lyase regulator.
This work was aimed to construct CodY deficient mutant of S. pneumoniae to form
foundational work for the study of CodY regulatory effect on hyaluronate lyase.