Urinary tract infection: current status.

VN Acharya, SK Jadav 
 

Correspondence Address:
V N Acharya

Full Text



Human urine can support the bacterial growth due to its favourable chemical composition.[4], [5], [8] Though urinary antibodies have been demonstrated[14] there has been no specific study indicating a role for urinary antibodies as a defence mechanism against infection. Thus, infections of the urinary tract (U.T.I.) are a common source of morbidity and mortality. Moreover, even in the absence of any detectable urinary tract malformations making way for infections, many patient have repeated episodes of UTI, which are often asymptomatic.[7] It has been observed that 7 per cent of children with UTI develop renal scarring.[18] U.T.I. in pregnancy may be associated with an increased neonatal mortality [17] and it can also be a source of gram negative septicaemia which so frequently proves fatal. Recently, it was found that about 20% of patients had pyelonephritis as the cause of primary renal disease.[19] All this literature on U.T.I. concludes that these infections leave their mark from cradle to the grave and are responsible for many complications such as premature babies, hypertension and renal failure. Hence it would seem important to diagnose and treat LM before it produces symptoms since this would offer the prospect of reducing morbidity and decreasing the work load of costly dialysis and transplant units.

In our country there is no co-ordinated data available on the prevalence, incidence and morbidity of UTI. Obviously the answer to the question-What is the true prevalence and incidence of UTI depends on

(1) the method of evaluation

(2) number and type of samples collected and

(3) the group selected for study.

[Tag:2]Method of Evaluation[/Tag:2]

Any method of evaluation for establishing a definitive diagnosis of LM must aim at doing quantitative culture examination of urine for the presence of significant bacteriuria in a mid-stream urine sample.[13]

At the nephrology division of the K.E.M. Hospital, Bombay, the dip slide inoculum method was simplified[10] by using two 1" x 3" standard glass slides. One of them is coated with nutrient agar and the other with MacConkey's agar. These slides are preserved under sterile conditions and dipped in the urine sample freshly collected in a sterile bottle. The slides are then incubated at 37°C overnight and inspected thereafter; and the bacterial growth is compared with standard reference photographs. By this method, a colony count of over 105/ml was significant and any growth of less than 104/ml was not considered as urinary infection. Those samples showing a colony count of 104-105/ml. required special scrutiny for (a) pH of urine at the time the sample was collected, (b) history of previous fluid consumption and (c) previous antibacterial therapy, to decide whether UTI was really present.

[Tag:2]Method and type of urine sample collection[/Tag:2]

By further critical observation the authors have established8 that significant bacteriuria in a single mid-stream urine (MSU) sample was adequate for initial diagnostic scrutiny and would be accurate to the tune of 85%. With two consecutive MSU and 3 consecutive MSU samples, the accuracy rose to 97% and 99% respectively as compared to a sample obtained by suprapubic bladder aspiration. However, for research purposes the best method is to establish the presence of any growth of micro-organisms in a bladder sample obtained by suprapubic bladder aspiration done with all aseptic precautions.

[Tag:2]Group selected for the study[/Tag:2]

After application of stringent criteria mentioned above, one can look at the problem of prevalence and incidence of UTI. This would vary widely with the group selected for study. In a study involving 1000 school children between the ages of 5 and 10 years, the overall prevalence of asymptomatic bacteriuria of 1.1% was reported by a group of workers from K.E.M. Hospital, Bombay.[9] In the above study, 2.1% of school girls and 0.8% of school boys showed asymptomatic bacteriuria. A study of 1000 pregnant women from National Medical College, Calcutta has revealed the prevalence of bacteriuria to be 10.2%.[9] This included 8% cases of symptomatic bacteriuria and 2.2% of asymptomatic bacteriuria. We studied bacteriuria in a randomised outpatient diabetic population and found asymptomatic bacteriuria to be present in 3.4% of the population.[2] Amongst the group of 596 adult subjects studied for suspected urinary tract infection,[16] it was noted that urinary infection was found in 36.3% of the hospitalised group and 15.9% of the non-hospitalised subjects. In the most vulnerable group of patients with acute and chronic renal failure undergoing dialysis, the prevalence of urinary infection was found to be 73.0% and 57.5% respectively.[11] Though a small number of additional subjects with recurrent UTI may be harbouring the L forms of bacteria which would add to the above prevalence and incidence, it is self evident that prevalence and incidence of UTI would be much lower than is clinically suspected and corroborated with the use of diagnostic methods dependent on the presence of pus cells in the urine and routinely done urine cultures without colony count. Thus the quantitative culture examination would help to overcome the problem of over-diagnosis and unnecessary antibacterial therapy of symptomatic cases and also help in early diagnosis of asymptomatic bacteriuria in a vulnerable population like diabetics, pregnant women and school girls.

[Tag:2]Urinary pathogens and their antibacterial sensitivity[/Tag:2]

In a study done by the authors between May 1972 and September 1973, it was noted that E. coli were responsible for only 30% of all recurrent urinary infections.[1] Klebsiella, Pseudomonas aeruginosa and Proteus organisms were responsible for 18.8%, 15.4% and 14.4% of all urinary infections respectively. Other gram negative organisms caused 15.3% and gram positive organisms 6.2% of urinary infections., On a yearly break up of six years' data (1973-1978), it was revealed that there was a gradual change in the bacterial flora.[12] It was noted that Klebsiella group of organisms (28.9%) have become the leading urinary pathogen as a whole. Statistically significant difference was observed amongst all urinary pathogens except for Pseudomonas aeruginosa and Proteus groups which remained constant at about 10% and 15% respectively. In contrast to these observations the percentage incidence of E. coli and Klebsiella groups was reported by another Indian Centre as 68.69% and 13.04% respectively.[15] This may be so because of difference in the group of the patients studied. It was noted in our previous report that E. coli was the predominant urinary pathogen in outpatient group while Klebsiella was the predominant urinary pathogen amongst hospitalised group.[16] In a -study of antibacterial sensitivity pattern, it was noted that frequency of bacterial resistance was rather alarming. On the basis of sensitivity pattern the chemotherapeutic agents could be divided into 4 groups. Those manifesting overall sensitivity of less than 25% formed the largest group consisting of most of the routinely used antibiotics like penicillin, ampicillin, cloxacillin, streptomycin, tetracycline, chloramphenicol, carbenicillin and sulphonamides. Gentamicin sulphate leads the whole group with 85% group sensitivity. It must, however, be noted that since gentamicin sulphate was made freely available in this country over the last 4 years sensitivity to it has gradually declined from 99% to 80%.[12] Proteus and Klebsiella organisms have been particularly noted to have developed resistance to it rapidly. This probably exemplifies the emergence of R factor transfer resistant bacteria due to improper and excessive usage of antibacterial agents for various infections.

[Tag:2]Significance of serum-antibody titres in UTI[/Tag:2]

The most perplexing question is "How does urinary tract infection produce pyelonephritis?" The factors in the host such as (a) obstruction, (b) vesico-ureteric reflux and (c) hydrokinetic and mucosal defence factors have long been well established. In recent years attention has been turned towards the role of antigenicity of urinary pathogens. Our own communication in 1979 showed that patients with recurrent UTI and patients with chronic pyelonephritis continued to show elevated antibody titres against the standard strains of E. coli even when they had no bacteriuria. [3] In that study, 34.3% of subjects with proven UTI continued to manifest high antibody titres in their serum against their own previous bacteria long after bacterial infection cleared. From this study it was concluded that immunological mechanisms are likely to be involved in the development of chronic pyelonephritis following UTI. This has thrown considerable light on the perplexing problem of absence of bacteria noticed in subjects with chronic pyelonephritis. These 34.3% of subjects of UTI are likely to be vulnerable to this kind of chronic disability which develops very slowly and silently without any indications of its existence. Whether the progression into this malady following UTI is preventable by adequate early therapy is a question yet unanswered. Continued research on this front in future would be rewarding.

References