Some cases of UTI caused by bacteria happen to be bacteria coming from the gastrointestinal tract and entering the urinary tract via faeces. As a matter of fact, E.coli which is known to be the most common uropathogen usually enters the urinary tract as a faecal contaminant especially in women (short distance between the anus and urethral meatus)[11]. The Shigella and of course the E. coli we have in this case report most likely entered the urinary tract as faecal contaminants. Unfortunately, stool culture was not done to confirm this. However, the question here is: Did the “faecal contaminant” succeed in establishing itself as a uropathogen in the urinary tract? Not every bacterial growth from urine culture is considered as a UTI or as a uropathogen. Other parameters need to be taken into consideration in order to distinguish between contamination and infection. These include direct WBC count, nitrate reduction, proteinuria (evidence of inflammation from the urinary tract) leucocyte esterase, colony count of bacterial growth etc [12–14] . We considered all of this (as seen in table 2) before arriving at the fact that Shigella was a causative agent of the UTI episode.
Shigella and Escherichia are closely related phenotypically [15] and their genetic makeup is about 80-90% similar [16]. These similarities may also be reflected in their virulence factors as some studies have shown that Shigella flexneri also possesses the sat gene [17–20] found in uropathogenic Escherichia coli (UPEC) and known to code for a secreted autotransporter toxin that elicits cytopathic effect on bladder and kidney cells in the course of a urinary tract infection [21]. This may explain why a UTI initially caused by Shigella flexneri could easily undergo a swift and unnoticeable change in uropathogen to Escherichia coli as both bacteria probably affect the urinary tract in a similar way due to some similarities in their pathogenicity and virulence. If both bacterial isolates do not share the same antimicrobial sensitivity profile, treatment with an antibiotic that can eliminate the initial causative agent but not the “successor” would most probably give rise to a recurrent infection.
A recurrent infection is usually associated with unresolved bacteriuria, bacterial persistence or reinfection [22]. The clinical findings and laboratory diagnosis of this patient presents a rare case of reinfection which apparently looks like bacterial persistence. The fact that the patient’s condition presented an unexpected prognosis with a complete and abrupt change in uropathogen species during the same UTI episode made it quite difficult to distinguish bacterial persistence from reinfection. Although the initial treatment with ofloxacin following the first urine culture was effective (it eliminated the Shigella flexneri), it also gave room for ofloxacin resistant Escherichia coli to swiftly proliferate and colonize the urinary tract. As such, the overall outcome revealed an apparent treatment failure and it boils down to this question: What are the steps to consider when a treatment failure is recorded even after administering the appropriate antibiotics as determined by urine culture and sensitivity?
Treatment failure after urine culture and sensitivity is often linked to obstructive pyelonephritis (requiring a renal ultrasound) or misdiagnosis [23, 24]. As such, some common ways of addressing this in clinical practice is usually to also consider different conditions that mimic the signs and symptoms of UTI. Some of these conditions may include kidney stone [25], painful bladder syndrome (interstitial cystitis)[26], possible renal tract malignancy, renal tuberculosis, urethritis and some sexually transmitted infections [27]. Since most of these conditions are seldom found in children [28–31], we still required more evidence to exclude a UTI for this patient, thus the need for a second urine culture. The second urine culture was quite necessary in this context as it helped to eliminate the possibilities of misdiagnosis and presented an unusual, rapid reinfection of the urinary tract by a completely different bacteria species. Although a second urine culture is recommended for treatment failure [27], urinalysis is what is commonly done to exclude or include a possible on-going UTI episode despite treatment [32] especially in resource limited settings like ours. In addition to the fact that it is less specific and does not directly guide the choice of antibiotics as compared to urine culture, urinalysis on its own cannot identify a short-term reinfection (especially in the case of our patient) nor detect a polymicrobial UTI episode.
Polymicrobial infections often lead to dramatic and unexpected outcomes in the aptitude of antibiotics to eliminate bacteria [33]. Based on the fact that we isolated pure colonies from the first two meticulously done urine cultures, this case report apparently looks like a non-polymicrobial UTI episode which lead to a dramatic and unexpected outcome following therapy. However, this may have been a polymicrobial infection which initially had a Shigella dominance.
In conclusion, antibiotics tailored towards the elimination of a particular bacterial species may as well provide a favourable environment for other bacterial species that are resistant to it in the course of treating a UTI episode. This can indicate an overall treatment failure and may first of all require a second urine culture for confirmation rather than considering the possibilities of a misdiagnosis.