TABLE 3.

Carriage rates of genes that encode toxins and adhesins in S. aureus strains that colonize only the nose and those that colonize the gut or both the gut and nose^a

Virulence trait	Gene	Carriage rate (% of strains)
		Only nose (n = 32)	Gut (n = 100)	P value
				Fisher’s	Corrected
Bone sialoprotein-binding protein	bsp	41	19	0.018	0.16
Collagen-binding protein	cbp	59	64
Elastin-binding protein	ebp	80	68
Fibrinogen-binding protein	fib	55	58
Fibronectin-binding protein A	fnbA	50	80	0.002	0.027
Fibronectin-binding protein B	fnbB	81	93
Superantigens
Enterotoxin A	sea	6	6
Enterotoxin C	sec	19	29
Enterotoxin H	seh	31	9	0.003	0.043
Enterotoxin K	selk	3	8
Enterotoxin L	sell	31	37
Enterotoxin M	selm	56	63
Enterotoxin O	selo	71	71
Enterotoxin P	selp	0	12
Enterotoxin R	selr	9	7
Toxic shock syndrome toxin TSST-1	tst	41	15	0.005	0.055
No superantigen		12	13
Other toxins
Beta-hemolysin	hlb	44	64
Epidermal cell differentiation inhibitor toxin	edin	3	10
agr alleles
agr1		50	56
agr2		10	20
agr3		40	15	0.008	0.09
agr4		0	8

^aSubjects were infants who were monitored from 3 days to 3 years of age. Rates of virulence gene carriage by S. aureus strains that were found exclusively in the nose (n = 32) or in the gut (either only in the gut or in both the nose and gut, n = 100), isolated from 54 Swedish infants, are shown. Proportions were compared using Fisher’s exact test. The column heading P value corrected refers to the P values derived after correction for multiple inferences using the Westfall-Young permutation method. No superantigen refers to a lack of carriage of all the screened superantigen genes. The following toxin genes were identified in <5% of the strains: sed (enterotoxin D), eta, etb, and etd (exfoliative toxins A, B and D), pvl (Panton-Valentine leukocidin), and lukM (leukotoxin M). No strain carried the toxin gene seb or selq. The following adhesin genes were carried by ≥98% of the strains: clfA and clfB (clumping factors A and B, respectively) and lbp (laminin-binding protein).