The development of a brain abscess owing to hematogenous spread of pathogens from a distant infectious focus, such as a lung abscess, empyema, skin infection, or intra-abdominal infection, is seen in 15–30% of cases [
1]. In patients with a cryptogenic brain abscess, examination for potential cardiovascular diseases may reveal congenital heart diseases, patent foramen ovale, or arteriovenous fistula that can permit pathogenic bacteria to bypass the lungs and enter the systemic circulation [
1]. Urinary tract infections may cause metastatic brain abscesses, and
Enterobacteriaceae and
Pseudomonas species have been reported as causative pathogens [
1,
2]. In general, however, aerobic and anaerobic streptococci are the most common pathogens in brain abscesses owing to contiguous and hematogenous spread of infection; the frequency of gram-negative bacterial infection is low [
1,
2]. Basically,
E. coli and Group B
Streptococcus are known to be common causative bacteria of neonatal meningitis [
3]. Moreover, to the best of our knowledge, only nine adults with
E. coli intracranial abscesses, including brain abscesses or subdural empyema, have been reported in the past 20 years (Table
1) [
4‐
12]. Additionally, only two cases of
E. coli brain abscess have been reported [
6,
9]. Interestingly, eight of the nine reported cases involved older men, implying that age and sex may be potent risk factors. Six patients died within 1 month after diagnosis [
4‐
6,
8,
10,
12]. In five cases, extracranial infection had been recognized prior to the onset, suggesting that the hematogenous spread of
E. coli might be a pivotal cause of intracranial abscess formation [
4,
5,
7,
9,
11]. Preceding urinary tract infection was reported in three cases [
4,
7,
11], and only one patient had a history of taking immunosuppressants (corticosteroids) [
6]. These reported patients include one with a history of splenectomy [
8], one with esophageal cancer undergoing radiochemotherapy [
11], and two with diabetes [
6,
10]. These findings suggest that in addition to sex and age, immunosuppression may be another risk factor for intracranial
E. coli infection. In our case, the
E. coli strains obtained from urine, blood, and aspirated pus from the infected renal cyst showed the same minimum inhibitory concentration, suggesting a strong involvement of hematogenous infection. However, one limitation of our report was the inability to determine the genetic identity of these
E. coli strains by analysis of restriction products after digestion of chromosomal deoxyribonucleic acid with restriction endonuclease.
Table 1
Reported adult cases of brain abscess or subdural empyema owing to
Escherichia coli
infection
| 1995 | 88 W | (−) | Column fracture | Orthopedic surgery (hip), UTI | SE | Drainage | Dead |
| 1995 | 86 M | (−) | Chronic cholecystitis | Cholecystitis | SE | Drainage | Dead |
| 2000 | 52 M | Cortico- steroids | DCM, DM | (−) | BA, Malaloplakia | Craniotomy | Dead |
| 2005 | 76 M | (−) | ADPKD | Renal cyst infection | SE | Drainage | Alive |
| 2005 | 55 M | (−) | Esophageal cancer | (−) | SE | (−) | Dead |
| 2006 | 67 M | (−) | PFO | Perianal abscess | BA | (−) | Alive |
| 2007 | 91 M | (−) | Chronic subdural hematoma, DM | Surgical aspiration of subdural hematoma | SE | Drainage | Dead |
| 2009 | 80 M | (−) | Post-gastrectomy and splenectomy | Orthopedic surgery (leg, spine), UTI | SE | Drainage | Alive |
| 2011 | 48 M | (−) | (−) | (−) | SE, Pneumo-cephalus | Craniotomy | Dead |
Recent experimental hematogenous meningitis models have indicated that the primary site of entry of circulating
E. coli into the CNS is the cerebral vasculature, not the choroid plexus [
3]. Nevertheless, hematogenous brain abscess formation owing to
E. coli infection is rare. Bakker
et al.[
4] reported that autopsy of a patient with
E. coli-induced subdural empyema showed no obvious inflammation in the brain parenchyma. In our reviewed cases, seven of nine patients showed subdural empyema. These findings suggest the presence of key mechanisms preventing
E. coli infection in the brain parenchyma. In an in vitro blood–brain barrier model using human brain microvascular endothelial cells (HBMECs),
E. coli was shown to invade and internalize the HBMECs as membrane-bound vacuoles with no changes in the integrity of the HBMEC monolayer [
3]. Moreover,
E. coli enters the CNS with no changes in the blood–brain barrier permeability and no concomitant presence of host inflammatory cells [
4]. Once
E. coli invades the brain parenchyma, microglia, the resident macrophage population in the CNS, may play a key role in recognizing and eliminating the microbes via Toll-like receptors or phagocytic receptors [
13]. Additionally, activated microglia produce various pro-inflammatory cytokines, leading to the activation and chemotaxis of peripheral immune cells; however, their phagocytic or killing activity toward microbes is less potent than that of polymorphonuclear leukocytes [
13]. A recent study showed that microglia and astrocytes are specifically activated soon after bacterial invasion into the CNS parenchyma [
13]. The above findings indicate that impaired glial cell function or an impaired immune response induced by glial cells may contribute to
E. coli infection in the CNS parenchyma.
Notably, a preceding
E. coli infection of a simple right renal cyst might have caused the bacteremia and subsequent brain abscess in the present case. Simple renal cysts are usually observed as unilateral and solitary lesions, and the prevalence rate ranges from 7 to 10%, increasing with age [
14]. Major complications of simple renal cysts, such as hemorrhage, infection, and rupture, are rare events seen in only 2–4% of affected patients [
14]. Suwabe
et al.[
15] showed that renal cysts with high intensity, a fluid–fluid level, or wall thickening on diffusion-weighted imaging suggest the presence of a cyst infection in patients with autosomal dominant polycystic kidney disease. A heterogeneous internal cyst density with no enhancement on CT also suggests a cyst infection [
15]. Symptoms of cyst infection are nonspecific. Especially in patients with autosomal-dominant polycystic kidney disease, the most conspicuous symptom is fever; in general, abdominal pain and frank hematuria are not observed [
15]. Cyst puncture and aspiration can be diagnostic and may circumvent the need for surgical procedures such as nephrectomy [
14]. Physicians should know that cyst infections may cause serious complications, even in patients with simple renal cysts.