ACTA BIOLOGICA SLOVENICA 
 LJUBLJANA 2008           Vol. 51, [t. 1: 21–31
Sprejeto (accepted): 27.10.2008
Prevalence, distribution and genetic association of adhesin gene sequences 
of Escherichia coli isolates from urinary tract infections in Slovenia
Prevalenca, porazdelitev in genetska asociacija zapisov za adhezine v izolatih 
bakterije Escherichia coli iz okužb sečil v Sloveniji
Marjanca STARČIČ-ERJAVEC, Darja ŽGUR-BERTOK
Department of Biology, Biotechnical Faculty, University of Ljubljana, Večna pot 111, 
SI-1000 Ljubljana; E-mail: marjanca.starcic.erjavec@bf.uni-lj.si, darja.zgur@bf.uni-lj.si
Abstract. 110 uropathogenic Escherichia coli (UPEC) strains obtained from the Institute 
of Microbiology and Immunology of the Medical Faculty in Ljubljana, Slovenia were screened 
with molecular biology methods for the well characterized adhesin gene sequences: fimH (Type 1 
fimbriae), papC, papGII and papGIII (P-fimbriae), sfa (S-fimbriae) and afa/dra (Afa/Dr adhesins). 
The fimH gene nucleotide sequences were detected in 97% of the isolates, papC in 49%, papGII 
in 34%, papGIII in 13%, sfa/foc in 24% and afa/dra sequences were harbored by 2% of the tested 
isolates. FimH sequences were found with similar prevalence in E. coli strains of all four phylo-
genetic groups A, B1, B2 and D. papC sequences were also found in all phylogenetic groups, but 
they were the most prevalent (64%) in the B2 group. The papGII showed the highest prevalence 
in the D group (48%), but papGIII adhesin sequences were exclusively found in the B2 group. A 
very high prevalence of S-fimbriae in the B2 group was detected. The analysis of co-associations 
of adhesin gene sequences and some other traits revealed that papC gene sequences were co-
associated with P-fimbriae adhesin gene sequences papGII and papGIII and with S-fimbriae sfa/
foc sequences. A negative association was found between papGIII and traT and between papGIII 
and RepFIB sequence. Interestingly, a negative association was also visible between integrons 
and P- and S-fimbriae, albeit the association was not statistically significant. 
Key words. uropathogenic Escherichia coli, UPEC, adhesin, fimbriae
Izvleček. 110 uropatogenih sevov Escherichia coli, ki so jih na Inštitutu za mikrobiologijo 
in imunologijo Medicinske fakultete v Ljubljani osamili iz diagnostičnih vzorcev urina, smo 
z molekularnobiološkimi metodami analizirali z namenom določiti gene, ki imajo zapise za 
adhezine: fimH (fimbrije tipa 1), papC, papGII in papGIII (fimbrije P), sfa (fimbrije S) in afa/
dra (adhezini Afa/Dr). Nukleotidno zaporedje gena fimH smo odkrili v 97 % izolatov, papC v 
49 %, papGII v 34 %, papGIII v 13 %, sfa/foc v 24% in zaporedja afa/dra smo našli v 2 % vseh 
preučevanih izolatih. Prevalenca zaporedja fimH po posameznih filogenetskih skupinah A, B1, B2 
in D je primerljiva. V vseh štirih filogenetskih skupinah smo našli tudi zaporedja papC, največja 
prevalenca je bila v skupini B2, kjer je kar 64 % izolatov vsebovalo to zaporedje. Zaporedje 
papGII je imelo največjo prevalenco v skupini D. Zaporedje papGIII smo našli izključno v 
skupini B2. V skupini B2 smo odkrili tudi veliko prevalenco fimbrij S (45 %). Analiza asociacij 
zapisov za adhezine z drugimi zapisi je pokazala, da je zaporedje papC asociirano z zaporedji 
papGII in papGIII ter zaporedji sfa/foc. Negativno povezavo smo našli med papGIII in traT ter 
med papGIII in zaporedji RepFIB. Med integroni in fimbrijami P in S smo tudi našli negativno 
povezavo, a le ta ni bila statistično značilna. 
Ključne besede. uropatogena Escherichia coli, UPEC, adhezin, fimbrija
22 Acta Biologica Slovenica, 51 (1), 2008
Introduction
Escherichia coli (E. coli) is a very diverse bacterial species found naturally in the intestinal tract 
of all humans and many other animal species. Even though E. coli is known to be part of the normal 
gut flora, some strains – that are pathogenic – cause a wide variety of different intestinal and extrain-
testinal diseases (Marrs & al. 2005). Typical extraintestinal infections due to E. coli include urinary 
tract infections (UTI) (russo & Johnson 2006).
Any component of a microbe that is required for, or potentiates its ability to cause disease is 
called a virulence factor. The best known virulence factors are adhesins, toxins, polysaccharide coat-
ings, invasins and iron uptake systems. Among the first virulence factors that come into play during 
establishment of an infection are adhesins. Besides their primary role as adhesin molecules, they can 
also function as invasins, promoters of biofilm formation and transmitors of signals to epithelial cells 
resulting in inflammation. 
Type 1 fimbriae are the most common adhesive organelles of E. coli strains. They are encoded by 
the vast majority of uropathogenic E. coli (UPEC) isolates and many other pathogenic and commensal 
isolates (Bower & al. 2005). They are also found in other bacteria, such as Salmonella typhimurium, 
Pseudomonas putida and Klebsiella pneumoniae (Capitani & al. 2006). Receptors for type 1 fimbriae 
are present on erythrocytes, buccal epithelial cells, intestinal cells, vaginal cells and uroepithelial cells 
(Johnson 1991). The fimH gene encodes the minor subunit protein FimH that mediates binding to the 
receptor. FimH has several variants: UPEC strains have a FimH that binds both monomannose and 
trimannose containing gycoprotein receptors, while commensal E. coli isolates typically show high 
affinity binding to only trimannose residues (Bower & al. 2005). Type 1 fimbriae function not just as 
adhesins, but also as invasins for bladder epithelial cells (Martinez & al. 2000). 
P fimbriae are among the best studied fimbrial adhesive fibres of UPEC strains. The P fimbrial 
adhesin molecule (PapG) recognizes globoseries of glycolipids as receptors (zhang & FoxMan 2003). 
The papC gene encodes the outer membrane usher protein that is required for ordered P fimbriae 
assembl y (thanassi & al. 1998). Many studies showed that P fimbriae occur more frequently among 
UPEC than fecal isolates. It was estimated, that about 80% of E. coli isolates from patients with 
pyelonephritis possess P-fimbriae. Based on binding specificities, P fimbriae are grouped into three 
major classes (I, II and III); class II (papGII) is more often found in pyelonephritic strains and class 
III (papGIII) in cystitis strains (zhang & FoxMan 2003).
S fimbriae bind to sialyl galactosides. Studies showed that E. coli UTI isolates were at least two 
times more likely to carry S fimbriae genes (sfa operon) than fecal strains (zhang & FoxMan 2003).
The 13 known adhesins of the Afa/Dr family all bind to the Dra blood group antigen present on 
the complement regulatory molecule CD55, also known as decay-accelerating factor (DAF) (Bower 
& al. 2005). The E. coli strains harboring these adhesins have been found to be associated with UTIs 
and also with various enteric infections (servin 2005).
The subunit proteins of adhesins are seriously considered as possible vaccines against E. coli infec-
tions (oelsChlaeger & al. 2002). Since UTIs and other extraintestinal infections due to E. coli cause 
considerable costs to the health system vaccines against E. coli are searched for (russo & Johnson 
2006). To evaluate the potential of different adhesins as vaccines it is necessary to investigate the pres-
ence of individual adhesins among pathogenic strains. To our knowledge, no such data are available 
for Slovenian uropathogenic E. coli (UPEC) strains. We therefore, analyzed a collection of 110 UPEC 
strains, that were previously screened for antibiotic resistance and horizontal gene transfer elements 
(riJaveC & al. 2006), for the presence of the following adhesin gene sequences: fimH (Type 1 fimbriae), 
papC, papGII and papGIII (P fimbriae), sfa (S-fimbriae) and afa/dra (afimbrial adhesin).
23M. Starčič-Erjavec, D. Žgur-Bertok: Prevalence, distribution and genetic association of adhesin gene …
Table 1:  Oligonucleotide primers and PCR conditions to detect adhesin genes
Tabela 1: Oligonukleotidni začetniki in pogoji PCR za ugotavljanje genskih zapisov za adehezine
Gene Oligonucleotide sequence 
(5’ to 3’)
Size of  
product (bp)
PCR conditions Reference
fimH tgcagaacggataagccgtgg
gcagtcacctgccctccggta
508 95°C    2,5 min     1×   
94°C 0,5 min
60°C 0,5 min     30×
72°C      1 min        
72°C   10 min     1× 
Johnson & 
stell, 2000
papC gacggctgtactgcagggtgtggcg
atatcctttctgcagggatgcaata
328 94°C       3 min     1×   
94°C       2 min
65°C             1 min     25×
72°C       2 min        
72°C           10 min     1× 
le BougueneC 
& al., 1992
papGII gggatgagcgggcctttgat
cgggcccccaagtaactcg
190 95°C          2,5 min     1×    
94°C          0,5 min
55°C             1 min     25×
72°C          0,5 min             
 
72°C             7 min     1× 
Johnson & 
Brown, 1996
papGIII ggcctgcaatggatttacctgg
ccaccaaatgaccatgccagac
258 94°C          2,5 min     1×   
94°C          0,5 min
63°C          0,5 min     25×
72°C             3 min        
72°C           10 min     1× 
Johnson & 
Brown, 1996
sfa/foc ctccggagaactgggtgcatcttac
cggaggagtaattacaaacctggca
410 94°C             3 min     1×   
94°C             2 min
65°C             1 min     25×
72°C             2 min        
72°C           10 min     1× 
le BougueneC 
& al., 1992
afa/dra gctgggcagcaaactgataactctc
catcaagctgtttgttcgtccgccg
750 94°C             3 min     1×   
94°C             2 min
65°C             1 min     25×
72°C             2 min        
72°C           10 min     1× 
le BougueneC 
& al., 1992
Material and methods
Bacterial strains and media
A total of 110 E. coli isolates (DL strains) from humans with urinary tract infections collected in 
2002, at the Institute of Microbiology and Immunology, Medical Faculty, Ljubljana, Slovenia were 
studied. Only one isolate from each patient was analyzed. Ninety-four (86%) of the patients were 
women. The strains had already been examined for prevalence of antibiotic resistances further, the 
serotype and phylogenetic groups were assigned and traits typical of horizontal gene transfer (traT, 
integrons, rep) were searched for (riJaveC & al. 2006). For cultivation of strains Luria Bertani medium 
or agar were used.
24 Acta Biologica Slovenica, 51 (1), 2008
Detection of adhesin genes
The primers and PCR conditions used to amplify adhesin genes with polymerase chain reaction 
(PCR) are listed in Table 1. DNA to be amplified was released from whole organisms by boiling accord-
ing to Le Bouguenec et al. (le BougueneC & al. 1992). Amplification was performed in an automated 
thermal cycler (UNOII, Biometra, Göttingen, Germany) in a 50 µl reaction mixture containing template 
DNA (10 µl of boiled lysate), 20 pmol of forward and reverse primer, 0,2 mM of dNTP mixture, 1,25 U 
Taq DNA polymerase and 2,5 mM MgCl2 in 1× PCR buffer (Fermentas, Vilnius, Lithuania). 
Dot blot hybridization experiments using the DIG DNA labelling and detection kit (Roche, Man-
nheim, Germany) were performed to validate the PCR assays. Probes were prepared using the same 
primers as for the PCR experiments and labelled with digoxigenin. The template DNA samples were 
the same as in the PCR experiments. 
Statistical analysis 
The significance of the results was established using the Fisher’s exact test (2-tailed) available 
on-line on the web site http://www.matforsk.no/ola/fisher.htm and the level of significance was set 
at a P value < 0.05. 
Results
Prevalence of adhesin genes
The presence of adhesin genes in the genomes of DL strains was screened by PCR and validated 
in the hybridization experiments. Figure 1 gives an example for papGIII detection. Among the tested 
adhesive organelles, the type 1 fimbriae were the most prevalent – the fimH gene nucleotide sequences 
were detected in 107 strains (97%). The P-fimbriae were also abundant, in 54 strains (49%) papC 
encod ing gene sequence was found, 37 strains (34%) harbored the class II papG adhesin sequence 
and 14 strains (13%) harbored the class III papG adhesin. 26 (24%) possessed the S fimbriae typical 
gene sequence sfa/foc. Only 2 strains (2%) harbored afa/dra sequences (Figure 2).
Distribution of adhesin genes among phylogenetic groups
E. coli isolates can be divided into four main phylogenetic groups A, B1, B2 and D (herzer & 
al. 1990). Analysis of the distribution of adhesin gene sequences among the previously determined 
phylogenetic groups of DL strains (riJaveC & al. 2006) revealed that different adhesin gene sequences 
were differently distributed (Table 2). FimH sequences were found with similar prevalence in strains 
of all four phylogenetic groups, papC sequences were found in all phylogenetic groups, but they 
were most prevalent (64%) among B2 group strains. The association of papC with the B2 group was 
statistically significant. The distribution of the P-fimbriae adhesins papGII and papGIII, however, 
differed. papGII sequences showed the highest prevalence in the D group (48%), albeit the associa-
tion was not statistically significant. In contrast, papGIII adhesin sequences were exclusively found 
among strains of the B2 group. Further, a very high, statistically significant, prevalence of S-fimbriae 
in the B2 group was detected.
Co-associations of adhesin genes
The analysis of co-associations of adhesin gene sequences and some other traits revealed (Table 
3) that the P-fimbriae usher papC gene sequences were 100% co-associated with P-fimbriae adhesin 
25M. Starčič-Erjavec, D. Žgur-Bertok: Prevalence, distribution and genetic association of adhesin gene …
Figure 1: An example of detection of adhesin genes – detection of the papGIII gene
 (A) Visualization of PCR products obtained in PCR reactions on lysates of DL strains with primers 
specific for the papGIII gene (1% agarose gel, stained with ethidium bromide). 
 M: marker – 1 kb DNA ladder (Fermentas, Vilnius, Lithuania); 1: strain DL1 (papGIII+); 2: strain DL9 
(papGIII-); 3: strain DL12 (papGIII+); 4: strain DL23 (papGIII-); 5: strain DL30 (papGIII+); 6: strain 
DL49 (papGIII-); 7: strain DL59 (papGIII+); 8: strain DL62 (papGIII+); 9: strain DL89 (papGIII-); 10: 
strain DL90 (papGIII-); 11: laboratory strain DH5α (papGIII-) and 12: negative control – a PCR reaction 
with sterile water instead of a lysate.
 (B) Validation of the PCR assay with DIG hybridization of a papGIII specific probe on papGIII PCR 
products (10 µl) bound to a nylone membrane.
 1: strain DL1 (papGIII+); 2: strain DL9 (papGIII-); 3: strain DL12 (papGIII+); 4: strain DL23 
(papGIII-); 5: strain DL30 (papGIII+); 6: strain DL 49 (papGIII-); 7: strain DL59 (papGIII+); 8: strain 
DL62 (papGIII+); 9: strain DL89 (papGIII-); 10: strain DL90 (papGIII-); 11: laboratory strain DH5α 
(papGIII-) and 12: negative control – a PCR reaction with sterile water instead of a lysate.
Slika 1: Primer detekcije genskega zapisa za adhezin – detekcija gena papGIII
 (A) Vizualizacija produktov PCR dobljenih v reakcijah PCR na lizatih sevov DL z začetnimi oligonuk-
leotidi specifičnimi za gen papGIII (1 % agarozni gel, obarvan z etidijevim bromidom).
 M: standard – 1 kb DNA-lestvica (Fermentas, Vilnius, Litva); 1: sev DL1 (papGIII+); 2: sev DL9 
(papGIII-); 3: sev DL12 (papGIII+); 4: sev DL23 (papGIII-); 5: sev DL30 (papGIII+); 6: sev DL49 
(papGIII-); 7: sev DL59 (papGIII+); 8: sev DL62 (papGIII+); 9: sev DL89 (papGIII-); 10: sev DL90 
(papGIII-); 11: laboratorijski sev DH5α (papGIII-) in 12: negativna kontrola – reakcija PCR s sterilno 
vodo namesto lizata.
 (B) Preverjanje PCR z DIG-hibridizacijo z vezavo sonde specifične za papGIII na produkte papGIII iz 
PCR (10 µl) vezane na nylonski membrani.
 1: sev DL1 (papGIII+); 2: sev DL9 (papGIII-); 3: sev DL12 (papGIII+); 4: sev DL23 (papGIII-); 5: 
sev DL30 (papGIII+); 6: sev DL 49 (papGIII-); 7: sev DL59 (papGIII+); 8: sev DL62 (papGIII+); 9: 
sev DL89 (papGIII-); 10: sev DL90 (papGIII-); 11: laboratorijski sev DH5α (papGIII-) in 12: negativna 
kontrola – reakcija PCR s sterilno vodo namesto lizata.
26 Acta Biologica Slovenica, 51 (1), 2008
gene sequences papGII and papGIII. Further, papC gene sequences were also statistically significantly 
co-associated with S-fimbriae sfa/foc sequence. The P-fimbriae adhesin gene sequences papGIII, but 
not papGII, were statistically significantly co-associated with S-fimbriae sfa/foc sequence. A statisti-
cally significant negative association was found between papGIII and traT and between papGIII and 
RepFIB sequences. Interestingly, a negative association was also visible between integrons and P- and 
S-fimbriae, albeit the association was not statistically significant. 
Co-associations of adhesin genes (Table 3) fimH and afa/dra were not analyzed, due to either very 
high or low prevalence, respectively.
Discussion
In the presented study 110 UTI E. coli strains isolated in Ljubljana, Slovenia, were characterized 
using PCR with primers specific for adhesin genes: fimH, papC, papGII, papGIII, sfa/foc and afa/dra.
Among the tested adhesin gene sequences the prevalence of fimH gene sequences was the highest, 
almost 100%. The high prevalence of fimH sequences found in our study assures a good possibility 
Figure 2: Prevalence (in % of the total 110 DL strains) of adhesin gene sequences
Slika 2:  Prevalenca (v % od 110 preučevanih sevov E. coli) genskih zapisov za adhezine
Table 2:  Distribution of adhesin gene sequences among E. coli phylogenetic groups
Tabela 2: Razporeditev genskih zapisov za adhezine po filogenetskih skupinah E. coli
Prevalence of trait (no. [%] of isolates) within phylogenetic groupa
Toxin gene A (n = 28) B1 (n = 6) B2 (n = 55) D (n = 21)
fimH 28 (100) 5 (83) 53 (96) 21 (100)
papC  8 (29)(*) 1 (17) 35 (64)** 10 (48)
papGII  5 (18) 1 (17) 21 (38) 10 (48)
papGIII  0 (0)(*) 0 (0) 14 (25)***  0 (0)
sfa/foc  1 (4)(**) 0 (0) 25 (45)***  0 (0)(**)
afa/dra  1 (4) 0 (0)  1 (2)  0 (0)
aP values (Fisher’s exact test) are indicated by asterisks where P is <0,05. Symbols: *, P<0,05; **, P≤0,01; ***, 
P≤0,001. Parentheses indicate negative associations. 
a vrednost P (Fisherjev eksaktni test) <0,05 je nakazana z zvezdicami: simboli *, P<0,05; **, P≤0,01; ***, P≤0,001. 
Negativne povezave so označene z oklepajem.
27M. Starčič-Erjavec, D. Žgur-Bertok: Prevalence, distribution and genetic association of adhesin gene …
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28 Acta Biologica Slovenica, 51 (1), 2008
for prevention of infection with the vaccine against the type 1 fimbriae that is already in phase II/III 
trial in theUS (russo & Johnson 2006). 
The P-fimbriae papC sequences were found in 49% of the tested DL strains. Comparison of our 
data with data on prevalences of papC or papA (encoding major fimbrial subunit PapA) from other 
studies (Table 4) showed a similar prevalence among UTI strains from Romania and cystitis strains 
from Israel and USA, but higher prevalence of papC/A among the pyelonephritis strains from USA 
and cystitis and pyelonephritis strains from Japan, compared to the prevalence in DL strains inves-
tigated in this study.
 The papC sequences were 100% co-associated with the adhesin genes papGII and papGIII. This 
was expected, since papGII and papGIII are alleles of P-fimbriae adhesins and each strain harboring 
either papGII or papGIII sequences also harbors papC sequences. 
Interestingly, in our study, as well as, in the study of Johnson et al. (Johnson & al. 2005b), papGII 
exhibited the highest prevalence among strains of the D group. This is in contrast to the results of papC 
and papGIII for which the highest prevalence was found among strains belonging to the B2 group, 
which is known to exhibit the highest prevalence of virulence traits.
Further, papC sequences were also strongly co-associated with sfa/foc sequences. This is surprising, 
as to our knowledge no previous study reported such a correlation. Co-association of virulence factors 
are expected, when they are physically joined, and it is well known that uropathogenic strains carry 
large chromosomal regions, termed pathogenicity islands (PAI) that encode several virulence factors. 
A number of PAIs have been identified in uropathogenic strains (oelsChlaeger & al. 2002), however 
to our knowledge no PAI harboring S-fimbriae and P-fimbriae has ever been described.
A negative association of P and S fimbriae with integrons is, even though not statistically signifi-
cant, evident. Integrons are known to carry resistance genes for different/multiple antibiotics (Mazel 
2006). Further, it is well known, that antibiotic-sensitive isolates possess more virulence factors than 
antibiotic-resistant isolates (Johnson & al. 2003, Starčič ErjavEc & al. 2007). Therefore, it is reason-
able that in strains with virulence associated adhesins, the prevalence of integrons is smaller.
It is worth to be noted, that not all studies (Table 4) support the assumption, that the papGIII al-
lele is associated with cystitis isolates and papGII with pyelonephritis (zhang & FoxMan 2003). For 
example the study on Israelian cystitis isolates showed, that cystitis isolates have a higher prevalence 
of the papGII allele than the papGIII allele. 
Further studies on different cystitis/pyelonephritis isolates are needed to clarify the importance of 
different papG alleles and to clarify the basis of the correlation between P and S fimbriae.
Table 4:  Comparison of results from different studies of UTI adhesin genes
Tabela 4: Primerjava rezultatov različnih raziskav genskih zapisov za adhezine
Adhesin gene prevalence (%)
Study fimH papC/A papGII papGIII sfa/foc afa/dra Ref.
76 pyelonephritis strains (Japan) na 78 na na 42 12 KanaMaru & al. 2003, 
YaMaMoto & al. 2001
74 cystitis strains (USA) na 35  5 31 36  4 Johnson & al. 2001
170 pyelonephritis strains (USA) 99 68 60  9 na 17 Johnson & al. 2005b
194 cystitis strains (Japan) na 64 na na 37  9 KanaMaru & al. 2003, 
YaMaMoto & al. 2001
100 cystitis strains (Israel) na 46 31 17 37 14 Johnson & al. 2005a
78 UTI strains (Romunia) 86 36 na na 23 14 usein & al. 2001
110 UTI strains (Slovenia) 97 49 34 13 24  2 this study
29M. Starčič-Erjavec, D. Žgur-Bertok: Prevalence, distribution and genetic association of adhesin gene …
Conclusions
To summarise and conclude: 
1. 110 uropathogenic Escherichia coli (UPEC) strains were screened with molecular biology methods 
for the well characterized adhesin gene sequences: fimH (Type 1 fimbriae), papC, papGII and 
papGIII (P-fimbriae), sfa (S-fimbriae) and afa/dra (Afa/Dr adhesins); 
2. the prevalence, the distribution and the genetic associations of the tested adhesin gene sequences 
were determined;
3. the fimH gene nucleotide sequences were detected in 97% of the isolates, papC in 49%, papGII 
in 34%, papGIII in 13%, sfa/foc in 24% and afa/dra sequences were harbored by 2% of the tested 
isolates;
4. fimH, papC, papGII were found in all four E. coli phylogenetic groups, sfa/foc and afa/dra in A 
and B2 group and the papGIII was found only in the B2 group;
5. papC gene sequences were co-associated with P-fimbriae adhesin gene sequences papGII and 
papGIII and with S-fimbriae sfa/foc sequence.
Acknowledgements
The authors thank Veronika Križan-Hergouth, M.D., M.Sc. from the Institute of Microbiology 
and Immunology, Medical Faculty, University of Ljubljana for providing the investigated strains, as 
well as Darja Lončar and Matija Rijavec from Biotechnical Faculty, University of Ljubljana for their 
help in performing some testing of the UPEC strains. This research was supported by Grant PO-0508-
0487 of the Ministry of Education, Science and Technology, Slovenia and by a personal donation from 
Farmadent, d.o.o., Maribor, Slovenia.
Povzetek
Bakterija Escherichia coli (E. coli) je del normalne flore prebavila človeka in toplokrvnih živali. 
A obstajajo sevi E. coli, ki imajo virulentne dejavnike (toksine, adhezine, kapsule, ...) in lahko pov-
zročijo okužbe (driska, vnetje sečil, pljučnica, vnetje možganskih ovojnic, okužbe ran, ...). Okužba 
sečil je ena izmed najpogostejših bakterijskih infekcij in E. coli povzroča veliko večino teh okužb. 
Zaradi pogostnosti pojavljanja teh okužb so virulentni dejavniki sevov E. coli, ki povzročajo te okužbe 
(UPEC – uropatogena E. coli) za preučevanje zelo zanimivi. Kar nekaj adhezinov in fimbrij (fimbrije 
tipa 1, P-fimbrije, S-fimbrije, Afa/Dr-adheizini) povezujejo s patogenimi sevi UPEC. 110 uropatogenih 
sevov Escherichia coli, ki so jih na Inštitutu za mikrobiologijo in imunologijo Medicinske fakultete v 
Ljubljani osamili iz diagnostičnih vzorcev urina, smo z molekularnobiološkimi metodami analizirali z 
namenom določiti gene, ki imajo zapise za adhezine: fimH (fimbrije tipa 1), papC, papGII in papGIII 
(fimbrije P), sfa (fimbrije S) in afa/dra (adhezini Afa/Dr). Nukleotidno zaporedje gena fimH smo odkrili 
v 97 % izolatov, papC v 49 %, papGII v 34 %, papGIII v 13%, sfa/foc v 24% in zaporedja afa/dra 
smo našli v 2 % vseh preučevanih izolatih. Prevalenca zaporedja fimH po posameznih filogenetskih 
skupinah A, B1, B2 in D je primerljiva – je več kot 80 %. V vseh štirih filogenetskih skupinah smo 
našli tudi zaporedja papC, največ v skupini B2 (64 % izolatov). Zaporedje papGII je imelo največjo 
prevalenco v skupini D (48 %). Zaporedje papGIII smo našli izključno v skupini B2 (25 %). V skupini 
B2 smo odkrili tudi veliko prevalenco fimbrij S (45 %). Analiza asociacij zapisov za adhezine z drugimi 
zapisi je pokazala, da je zaporedje papC asociirano z zaporedji papGII in papGIII ter zaporedji sfa/
foc. Negativno povezavo smo našli med papGIII in traT ter med papGIII in zaporedji RepFIB. Med 
integroni in fimbrijami P in S smo tudi našli negativno povezavo, a le ta ni bila statistično značilna. 
Zbrane informacije o pogostnosti zapisov za adhezine bi lahko bile osnova za načrtovanje cepiv proti 
patogenim sevom E. coli.
30 Acta Biologica Slovenica, 51 (1), 2008
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