Background & objectives: Uropathogenic Esclierichia coli have virulence properties, that are absent in non pathogenic E. coli. The distribution of these markers can vary according to patient populations. Hence, a study was undertaken to describe the presence of virulence factors like P-fimbriae, type 1 fimbriae and haemolysin in E.coli causing urinary infections in three groups of patients. Antibiogram was also recorded to determine differences, if any, between the groups.

Methods: E. coli isolated from three groups of subjects, in counts of ≥10^sup 5^ CFU/ml and in pure growth were tested for mannose resistant haeniagglutination (MRHA) to indicate P fimbriae and mannose sensitive haeniagglutination (MSHA) to indicate type 1 fimbriae. Haemolysin production and antimicrobial susceptibility patterns were also recorded.

Results: Significantly more isolates from antenatal and postnatal women possessed P fimbriae compared to groups with urologie abnormalities (P=0.05). Haemolysin production was also significantly higher (P

Key words Adherance - antibiogram - E. coli - fimbriae - mannose resistant haemagglutination - urinary tract infection uropathogenic - virulence

Urinary tract infections (UTI) are probably the most common bacterial infections. Bacteria responsible for UTI, often originate from the faecal and perineal flora1,2. Under normal circumstances, these bacteria are cleared from the urinary system by effective protective mechanisms. If, however, they overcome these mechanisms, they can colonize the lower urinary tract. Subsequent progress is determined by the host susceptibility and bacterial virulence factors1,2. Manifestations can vary from asymptomatic bacteriuriato symptomatic cystitis, pyelonephritis and blood stream infection1,2.

A single bacterial species, Escherichiacoli, causes majority of UTI. Subsets identifiable using O, K. and H antigens were shown to have increased ability to cause symptomatic urinary infections1·2. Thus arose the concept of uropathogenic E, coll clones. Recent studies confirm that uropathogenic E. coli have several attributes that are lacking in the commensal E. coli. They carry chromosomal gene clusters on 'pathogenicity islands'1,2, encoding adhesins and other virulence factors. The most important amongst these, probably, are the adhesins that help them to adhere to uroepithelium3 and this property was recognized decades ago4. These include type 1, S and P fimbriae, and adhesins like Dr1,2. The type 1 fimbriae are widely prevalent and are probably involved in colonization of lower urinary tract1,2. Mannose-sensitive haemagglutination (MSHA) denotes presence of these fimbriae5,6.

The role of P fimbriae in upper UTI is well documented1,2. These are encoded by the pap operon and are present in 20 per cent of faecal, 60 per cent of cystitis causing, and 80 per cent of pyelonehritis causing E. coli isolates2. It is shown that some pap positive isolates, especially those isolated form asymptomatic infections, do not express P fimbriae2. Phenotypic expression of P fimbriae can be detected by mannose-resistant haemagglutination (MRHA) of human erythrocytes2. Attachment of P fimbriae is also associated with increased host inflammatory response2.

Other factors associated with uropathogenic E. coli include production of haemolysin, serum resistance and release of aerobactin1,2. Haemolysin provides E. coli with possible selective advantage by releasing iron from lysed erythrocytes and enhances pathogenicity by destroying phagocytic and epithelial cells1,2.

Measuring a phenotype in vitro does not always correlate with in vivo expression and may underestimate the presence of a virulence factor in vivo1,2. Identifying a genotype, on the other hand, does not mean that it is expressed in the body. However, MRHA can be used for presumptive identification of virulence factors in E. coli7. The distribution of virulence properties can also vary depending on host characteristics and type of infection3,8-12. There are however, very few reports in the literature, where, phenotypic expression of virulence factors in E. coli and antibiogram have been compared in isolates from different patient groups. The present study was therefore undertaken to determine differences if any, in the presence of phenotypically expressed virulence factors like P-fimbriae, type 1 fimbriae and haemolysin among E. coli causing urinary infections in three different groups of patients. Antibiogram was also recorded to determine differences, if any, between the groups.  Medical Supplies.