How Staphylococci become a foe from a friend?

How Staphylococci become a foe from a friend?

-Nisha Paudel | Feb 01, 2018

How Staphylococci become a foe from a friend?


Staphylococci is one of the major normal flora ( bacteria which are found in or on our bodies living without causing disease) usually colonizing the skin surface and upper respiratory system. It helps our body from pathogens by competing with invaders for space and nutrients and helps to build immune system but the bacteria is also pathogenic in some conditions.

Staphylococci can cause many forms of infection.( Timothy Foster, Medical Microbiology, 4th edition)

 (1) S aureus causes superficial skin lesions (boils, styes) and localized abscesses in other sites.

(2) S aureus causes deep-seated infections, such as osteomyelitis and endocarditis and more serious skin infections (furunculosis).

(3) S aureus is a major cause of hospital-acquired (nosocomial) infection of surgical wounds and, with S epidermidis, causes infections associated with indwelling medical devices.

(4) S aureus causes food poisoning by releasing enterotoxins into food.

(5) S aureus causes toxic shock syndrome by release of superantigens into the bloodstream.

(6) S saprophiticus causes urinary tract infections, especially in girls.

(7) Other species of staphylococci (S lugdunensis, S haemolyticus, S warneri, S schleiferi, S intermedius) are infrequent pathogens.

Virulence factors of Staphylococcus aurues ( Kennth Todar, Online textbook of bacteriology)

 (1) surface proteins that promote colonization of host tissues;

(2) invasions that promote bacterial spread in tissues (leukocidin, kinases, hyaluronidase);

(3) surface factors that inhibit phagocytic engulfment (capsule, Protein A);

 (4) biochemical properties that enhance their survival in phagocytes (carotenoids, catalase production);

 (5) immunological disguises (Protein A, coagulase);

(6) membrane-damaging toxins that lyse eucaryotic cell membranes (hemolysins, leukotoxin, leukocidin;

 (7) exotoxins that damage host tissues or otherwise provoke symptoms of disease (SEA-G, TSST, ET); and

(8) inherent and acquired resistance to antimicrobial agents. 

Genetic introspect

Due to different nutrient limitations and stress conditions encountered in vivo for adaptation, they use regulatory loci. This allows them to survive and/or thrive in different compartments during colonization and infection processes(Konstanze et al. 2009). The in vitro expression of most virulence factors is tightly related to the growth phase. For instance protein A (encoded by spa), fibronectin-binding proteins (encoded by fnbA and fnbB), and coagulase (encoded by coa) are expressed during the exponential growth phase, whereas most secreted proteins (e.g., hemolysins, enterotoxins, and proteases) and the capsule (enzymes encoded by the capA-capP operon) are expressed mainly during the postexponential phase (Goerke et al. 2004). Upon passing a critical concentration threshold, the autoinducers activate specific transcriptional regulators, leading to the differential expression of target genes. The agr locus of S. aureus is a prototypic quorum-sensing system mainly involved in the regulation of virulence genes (Norvik et al. 2003). At high cell densities, the regulatory RNAIII is expressed, leading to the inhibition of spa, for instance, and to the activation of genes encoding secreted virulence factors and the capsular polysaccharide. Besides quorum sensing, additional mechanisms have to be triggered for the growth phase transition in S. aureus since the expression of certain virulence factors remains growth phase dependent in agr mutants ( Saravia-Otten et al. 1997; Vandenesch et al. 1991).