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].