1. Serum bactericidal activity against the homologous organism was determined in patients with urinary tract infections and has been related to the site of infection and to serum antibody titres. 2. A significantly higher number of patients with upper compared to lower urinary infections were found to have either a specific defect in bactericidal activity against the homologous organism or to be infected with organisms inherently resistant to normal serum bactericidal activity. 3. It is suggested that these factors may be important in determining the site of urinary tract infections.
I N the majority of cases of symptomatic urinary-tract idection occurring in non-pregnant women in domiciliary practice, the Escherichia coli 0-serogroup causing the infection is also present in the patient's faecal flora (Turck, Petersdorf and Fournier, 1962;Vosti et al., 1964; Griineberg, Leigh and Brumfitt, 1968). This correspondence between urinary and faecal 0-groups is likely to occur by chance in only a small proportion of patients. It is therefore implied that the source of the organism infecting the urine is the patient's own faecal flora, which does not change with respect to the urinary 0-group from the time the infection becomes established until it is detected. If a significant proportion of these symptomatic infections in non-pregnant women arises from preexisting asymptomatic bacteriuria, as is the case in pregnancy (see Beard and Roberts, 1968), correspondence between urinary and faecal 0-groups should also be found in non-pregnant women with asymptomatic bacteriuria. The previous studies, however, have either dealt exclusively with symptomatic patients (Turck et al., 1962; Gruneberg et al., 1968) or have not considered asymptomatic patients separately (Vosti et al., 1964). In the present study, the correspondence between urinary and Eaecal E. coli 0-groups has therefore been assessed in non-pregnant women with either symptomatic urinary-tract infection or asymptomatic bacteriuria. MATERIALS AND METHODS Patients.Initially, women attending an out-patient clinic for urinary-tract infections were studied. Patients attending the clinic for the first time and those known to have been free of bacteriuria at their previous visit to the clinic 1 month to 1 year earlier, were included. None of the patients had been in hospital during the previous 6 months, nor had they received antibiotics during the previous month. Subsequently, in order to see if the results were more generally applicable, women presenting with symptomatic urinary-tract infection in a general practice and patients found to have asymptomatic bacteriuria during a screening programme at " well woman " clinics were also studied.Urine was obtained by suprapubic aspiration as described by Beard et al. (1965) or as a midstream specimen after vulva1 cleansing with sterile water (Roberts, Robinson and Beard, 1967). From the patients attending the urinary-infection clinic, a rectal swab was taken followed by a suprapubic aspirate of urine if the patient was symptomatic, or a midstream specimen of urine if the patient had no symptoms. When the results from a midstream-urine
Twenty-six urinary strains of Escherichia coli belonging to O-sero-groups commonly associated with urinary infection but differeing in serum sensitivity and K antigen content were examined for their ability to survive in the kidneys following inoculation into the bladder of male Wistar rats. Reproducibility studies showed that some strains consistently caused kidney infection whereas others were consistently unable to do so. However, the ability to infect the kidneys was not correlated with serum resistance or K antigen content. Some evidence for the nature of the factors responsible for kidney infection came from a study of various mutants derived from E.coli LP729 (serotype 09), which produces negligible amounts of K antigen and is rapidly killed by serum after a delay of one hour. Both LP729 and a serum-resistant mutant derived from it caused kidney infections, but two rough variants derived from the serum-resistant mutant were unable to infect the rat kidneys. One variant was devoid of lipopolysaccharide O-side chains; the other showed the delayed serum-killing effect characteristic of LP729 and retained 09 specificity with a full complement of O-side chains, suggesting that loss of surface components unrelated to O or K specificity may be responsible for failure to invade the kidneys.
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