Table 1. Overview of 16 studies on molecular typing of T. pallidum clinical strains.

First author, publication year	Country, location, study populationa	Specimen collection period	Clinical stage of syphilisb	Specimen typec	Gene for T. pallidum detectiond	No. of specimens					No. of subtypes identified
						All	DNA +	arp +	tpr +	Full typee
Pillay A, 1998 [11] f	U.S., 10 cities, GUD patients; Madagascar, primary syphilis; South Africa, 3 cities, GUD patients	N/A	P	PU	tpp47	N/A	55	55	38	38	7; 8; 3
Sutton MY, 2001 [24]	U.S., Arizona, SP	03/1998–10/1999	P, S, L	PU, WB	polA	85	56	N/A	N/A	45	10
Pope V, 2005 [25]	U.S., North and South Carolina, SP	11/1999–01/2003	P, S	PU, SL	polA	61	27	N/A	N/A	23	7
Katz KA, 2010 [12] g	U.S., San Francisco, SP	11/2004–11/2007	P, S	PU, SL	polA	74	71	69	70	69	8
Marra CM, 2010 [13] h	U.S., Seattle, 87% MSM; Madagascar; U.S., San Francisco; U.S., Baltimore; China, Nanjing; Ireland, Dublin	1999–2008; 2003–2008; 2001–2007; 1999–2001; 2006–2007; 2002	P, S, L	PU, SL, WB, CSF	N/A	N/A	N/A	N/A	N/A	84; 20; 19; 15; 10; 10	8; 6; 4; 5; 2; 4
Martin IE, 2010 [18]	Canada, Alberta and Northwest territories, SP	02/2007–04/2009	P, S, C	PU, SL, WB, PSi, SSi, CSFi, VEFi	bmp, tpp47 and polA	449	43	43	36	36	4
Cruz AR, 2010 [26]	Colombia, Cali, from a network of public sector primary health care providers	2003–2009	S	SL, WB	polA	38	20	6	8	6	4
Zeng TB, 2004 [27]	China, Hengyang and Jiangmen, SP	02/2002–01/2004	P	PU	polA	85	69	57	63	57	8
Zhan LS, 2005 [28]	China, South Hunan Province, SP	02/2002–08/2004	P	PU	polA	52	43	43	41	38	10
Zheng HP, 2005 [29]	China, Guangzhou, MSP	2002–2004	P	PU	bmp	62	54	47	49	47	7
Martin IE, 2009 [17]	China, Shanghai, GUD patients	12/2007–05/2008	P	PU, WBi	bmp, tpp47 and polA	57	38	36	38	36	4
Pillay A, 2002 [16]	South Africa, 5 cities, MSP	1996–2000	P	PU	tpp47 or polA	1954	201	161	175	161	35
Molepo J, 2007 [19]	South Africa, Pretoria, patients in neurology ward	06/1999–09/2000	LN	CSF	tpp47	50	28	13	15	13	4
Florindo C, 2008 [14]	Portugal, Lisbon, SP	2004–2007	P, S	PU, SL, WB	bmp and polA	N/A	86	N/A	N/A	42	3
Castro R, 2009 [15]	Portugal, Lisbon, SP	06/2003–07/2005	P, S, L	PU, SL, WB, PS, ELS	polA	212	90	N/A	N/A	62	5
Cole MJ, 2009 [30]	U.K., Scotland, MSM	08/2006–12/2007	P, S	GU, AU, OU	polA	N/A	75	61	64	58	6

^aStudy population: GUD-genital ulcer disease, SP-STD patients, including males and females, MSP-male STD patients, and MSM-men who have sex with men.

^bClinical stage of syphilis: P-primary syphilis, S-secondary syphilis, L-latent syphilis, C-congenital syphilis, and LN-late neurosyphilis.

^cSpecimen type: PU-primary ulcer, WB-whole blood, SL-secondary lesion, including secondary skin lesion and/or mucosal lesion, CSF-cerebrospinal fluid, PS-plasma specimen, SS-serum specimen, VEF-vitreous eye fluid, ELS-ear lobe scraping, GU-genital ulcer, AU-anal ulcer, and OU-oral ulcer.

^dGene for T. pallidum detection: tpp47-47 kDa protein gene, bmp-basic membrane protein gene, and polA-DNA polymerase I gene.

^eFull type was based on two genes (arp and tpr) or three genes (arp, tpr, and rpsA or tp0548).

^fEight laboratory strains were excluded, remaining 55 clinical strains were included for analysis.

^gIntroducing a third gene, rpsA.

^hIntroducing a third gene, tp0548. Laboratory strains were excluded.

ⁱ T. pallidum DNA was not amplified successfully by screening PCR assay.