Discussion
Community-acquired E. coli  meningitis in adults is a severe disease, often with poor outcome and high case fatality rate even with appropriate antimicrobial treatment. In addition to systemic complications that are an important cause of death in these patients, multi-organ failure and sepsis appear to be a major cause.Compared to general population with bacterial meningitis due to other pathogens, patients with GNB meningitis like E. coli , more often had comorbid conditions [5].
Microbiological studies indicated a majority of wild-type E. coliand other items included quinolone resistant or trimethoprim–sulfamethoxazole resistant, ESBLs and penicillinase producer [1].
Enterobacteriaceae are not a frequent cause of meningitis in adults andE. coli is a rare etiology in community-acquired adult meningitis and recent reports of this entity is a challenging issue. In a study by Bodilsen et al. one of the most differences in clinical presentation of patients with E. coli meningitis was a low incidence (41%) of fever and classic meningitis triad including fever, neck stiffness and altered mental status. Also this study showed that patients with GNB meningitis were older and more often had comorbid conditions with a mortality rate of 36% [2]. Zafar et al. described a case of meningitis due to E. coli , presented with complaints of vomiting, severe headache, altered level of consciousness and fever. In this case urine and blood culture came out to be negative and no distant source of origin was identified [6]. Pomar et al. reported that the overall mortality rate for patients with spontaneous GNB meningitis was high (53%). The authors found that advanced age, positive blood cultures, inappropriate initial antibiotic therapy, and complications were associated with greater mortality in these patients [7]. In the study by Yang et al. 15 cases of adults with the diagnosis of E. colimeningitis were evaluated. Six cases were community acquired and diabetes mellitus was an important risk factor. The overall mortality reported in this study was 47% [8].
Cromlin et al. reported a case of O117:K52: H E. coli meningitis and multiple brain abscesses with the demonstration of acute pyelonephritis as the primary source. The patient died from complications [9]. Common risk factors for GNB meningitis include cirrhosis, alcoholism, malignancy, diabetes mellitus, immunosuppressive drugs and HIV infection [10]. The presented case was a known case of ITP, and was on prednisolone 5mg/d. Hence the patient was not an immunocompromised case according to the corticosteroid duration of use and doses, but she was a diabetic patient as the important risk factor.
In our 53-year-old patient acute meningitis was accompanied by an emphysematous pyelonephritis as the primary focus of infection in which the same organism was isolated from the blood, CSF and urine.
Emphysematous pyelonephritis is a life-threatening infection of the kidney that is characterized by an accumulation of gas in the renal parenchyma. The most common predisposing factor is diabetes mellitus. The management include antibiotic therapy alone, percutaneous drainage in addition to antibiotics or nephrectomy, if the patient has progressive disease or has unstable hemodynamic status. The most common pathogen is E. coli cultured from urine and blood [11]. In serial imaging our patient showed improvement for emphysematous pyelonephritis with antibiotic therapy.
According to the study by Bichon et al. up to 7% of community acquired infections with E. coli are ESBL producer and 9% are broad spectrum betalactamase producer with resistance to penicillin group [1]. Diabetes mellitus, previous hospital admission and older age in male patients have been described as risk factors for infection of ESBL producing E. coli [12].
It is important to say that the majority of E. coli meningitis develop as a result of hematogenous spread, but the underlying mechanism for E. coli penetration of the blood brain barrier (BBB) is not clear and is a challenging entity. In-vivo and in-vitro studies indicates that meningitic E. coli strains have the ability to invade the brain, and lead to BBB disruption [13]. Some studies revealed that crossing of the BBB by this bacteria requires a high degree of bacteremia for brain penetration but it is not enough for the pathogenesis. The important prerequisite for penetration of E. coli into the brain is binding and invasion of human brain microvascular endothelial cells. Traversal of the BBB as live bacteria is another critical factor for the development of meningitis by this organism [14].