Intracranial bleeding (ICB) as a catastrophic complication of Streptococcus gordonii infective endocarditis (IE) in an immunocompetent patient

Abstract

We present an interesting case of late-onset intracranial bleeding (ICB) as a complication of Streptococcus gordonii causing infective endocarditis. A previously healthy young woman was diagnosed with infective endocarditis. While she was already on treatment for 2 weeks, she had developed seizures with a localising neurological sign. An urgent non-contrasted CT brain showed massive left frontoparietal intraparenchymal bleeding. Although CT angiogram showed no evidence of active bleeding or contrast blush, massive ICB secondary to vascular complication of infective endocarditis was very likely. An urgent decompressive craniectomy with clot evacuation was done immediately to release the mass effect. She completed total 6 weeks of antibiotics and had postoperative uneventful hospital stay despite having a permanent global aphasia as a sequel of the ICB.

Background

Neurological complications may occur in about 15%–30% of patients with infective endocarditis (IE) which are mainly a consequence of embolism from vegetation. Intracranial bleeding (ICB), ischaemic stroke, brain abscess and transient ischaemic attack are the major neurological complications.¹ Intracranial haemorrhage alone contribute to 12%–30% of neurological complications in IE.² The pathogenesis of intracranial haemorrhages is attributed to transformation of ischaemic infarct from septic emboli and ruptured mycotic aneurysm leading to either intraparenchymal or subarachnoid bleeding.³ There are multiple well-recognised organism causing IE such as Staphylococcus aureus, Streptococcus viridans, Streptococcus bovis, coagulase negative staphylococcus, Streptococcus pneumoniae and other Streptococcal species. Streptococcus gordonii is a gram-positive coloniser in the periodontal area and have been rarely reported as a cause.⁴ We report an interesting case of immunocompetent patient with life-threatening ICB secondary to S. gordonii endocarditis.

Case presentation

A previously healthy 38-year-old Malay woman presented with 1 month history of fever associated with vomiting. She had significant loss of appetite and weight for the same duration. She also complained of dull aching right lumbar pain associated with dysuria. Otherwise, she had no headache, chronic cough, chest pain, alter bowel habit, limb weakness or bleeding tendency. She received two pints of packed cell transfusion in view of anaemia few weeks prior to current presentation. She denied high-risk behaviour, smoking or alcohol intake. She is a housewife and married to a lorry driver. She had poor social economic background.

On physical examination, she was febrile, pale and dehydrated. She had poor oral hygiene with multiple dental carries. She was not jaundice. There was no stigmata of IE. Her blood pressure was 98/50 mm Hg with pulse rate of 115 bpm. Cardiovascular examination revealed displaced apex beat with pansystolic murmur over mitral region, grade 4/6 and radiating to axillary. Her jugular venous pressure was not raised and there was no pedal oedema. Respiratory examination was normal. Abdomen examination was soft with no hepatosplenomegaly.

Investigations

Initial blood investigations showed leucocytosis with anaemia. Urinalysis revealed haematuria, proteinuria, nitrite+1 and leucocyte+1. Diagnosis of urosepsis with dehydration was made. Haemodynamically she improved with fluid resuscitation. Intravenous ceftriaxone 2 g daily was commenced. Echocardiogram of the heart showed the presence of vegetation at anterior mitral valve leaflet (AMVL) 0.9 cm² and posterior mitral valve leaflet (PMVL) 0.8 cm², severe mitral valve regurgitation with ejection fraction of 75%. Multiple blood culture revealed positive S. gordonii sensitive to penicillin and gentamicin. Urine culture was negative. The diagnosis of IE was made.

Differential diagnosis

1. Urosepsis.

2. Glomerulonephritis.

3. Chronic infection.

Treatment

Intravenous C-penicillin 4 Mu every 4 hours and gentamicin 120 mg daily were started. She responded to treatment of antibiotic. Clinically, she was afebrile and asymptomatic. She was able to tolerate orally well with no more vomiting. Biochemical septic parameters were improving. White blood cell count reduced from 17.8×10⁹/L on admission to 11.18×10⁹/L, while C-reactive protein from 183 mg/L to 108 mg/L after 2 weeks of treatment. The repeated echocardiogram at day 14 of antibiotic revealed reducing vegetation size (AMVL 0.4 cm² and PMVL 0.5 cm²). Intravenous antibiotic was continued as per standard IE protocol.

Outcome and follow-up

However, on day 17 of hospitalisation, she developed focal seizure on the right upper limb with secondary generalisation which was aborted by intravenous diazepam. Post-ictally, the conscious level did not improved. She had new localising neurological sign which was increased tone of both right upper and lower limb, limb weakness with positive Babinski sign. Non-contrast CT brain showed massive left frontoparietal bleeding with perilesional oedema (figure 1). CT angiogram (CTA) showed no evidence of arteriovenous malformation (AVM) or cerebral aneurysm (figure 2). Her blood pressure in the ward was normal. She underwent left decompressive hemicraniectomy on the same day. The intraoperative finding was left cerebral intraparenchymal bleed. Evacuation of clots was done. Postoperatively, she suffered from permanent global aphasia and became dependant in her activity of daily living.

Figure 1.

A CT scan of the brain showing large left frontoparietal intraparenchymal bleed size (4.3×5.9×6cm) with compression of the left lateral, third ventricle and midline shift to the right. It was associated with right temporal lobe infarct.

Figure 2.

CT angiography brain showing no evidence of arteriovenous malformation or cerebral aneurysm.

Discussion

Neurological complication occurs in about 12%–30% of patients with IE.⁵ ICB accounts for up to 30% of neurological complication and has negative impact on IE prognosis.²

Despite of prolong usage of antibiotic therapy, septic emboli may occur at any time causing injuries to cerebral wall or aneurysms which may lead to ICB when ruptured. García-Cabrera et al showed the temporal relationship between the onset of symptomatic ICB and duration of IE antimicrobial therapy in the cohort of 1545 patients. These resulted in 7% (prior to antibiotics), 14% (first week of treatment and subsequent gradual decrease during the following weeks), 2%, 0.6% and 0.3%.⁵ Our patient had massive ICB on day 17 (third week) of antibiotic in which septic parameter appeared improving. This supports that ICB can occur at any time despite effective antimicrobial treatment. Meshael et al highlighted that routine cerebral CT may resulted in changes in treatment plan in patients with IE even those without clinically evident neurological disease.⁶ They reviewed 81 patients with IE who have all undergone cerebral CT within 2 weeks of admission. Results of cerebral CT showed that 51 patients had evidence of cerebral embolisation, 17 of them were clinically silent.

Cerebral (CT) and MR angiogram (MRA) are reliable tools to detect infectious aneurysm; however, if both non-invasive techniques fail to identify the aneurysm, conventional angiography remain as gold standard.¹ Diagnostic performance of contrast-enhanced MRA does not significantly differ from CTA in patients presenting with intracranial aneurysms.⁷

As in this case, S. gordonii is an oral commensal synthesis cavity causing IE. Studies showed that S. gordonii also synthesis biofilm formation causing dental plague.⁴ Poor social support in our patient was reflected by her poor oral hygiene with multiple dental carries. This is a risk factor for her to get IE despite being immunocompetent.

Recent study revealed that S. gordonii interact with platelets to form clot.⁸ An interesting pathomechanism of S. gordonii is that it can mimic a damaged endothelium. The platelets roll on immobilised S. gordonii by a unique interaction which occurs via direct binding of platelet to the bacteria surface protein, namely Srr proteins SrpA, GspB/Has and platelet adherence protein A (Pad A). Pad A is a unique feature of S. gordonii. It plays an important role in platelet adhesion. Multistep of adhesion process will lead to thrombi formation. The unique character of having these proteins are that they may cause thrombus as well as being self-protected by biofilm. This might explain the virulence of the bacteria leading to IE even in immunocompetent patient.⁸ Our patient is an immunocompetent patient who developed IE which later complicated with devastating condition. The complexity of pathogenesis of S. gordonii to form thrombosis as well as synthesise biofilm supports the evidence that even in immunocompetent patient, the risk of developing IE is high. As postulated earlier, septic emboli can cause aneurysm which rupture at the time of aseptic condition.

To the best of our knowledge, this is the first reported case of massive ICB due to S. gordonii IE. We highlighted this case because this catastrophic event was a direct cause of S. gordonii which was regarded as coloniser in mouth cavity.

Learning points.

• Streptococcus gordonii, which colonised in mouth cavity may cause infective endocarditis due to its complex pathogenesis formation of thrombosis (septic vegetation).

• Infective endocarditis caused by S. gordonii may lead to life-threatening condition in immunocompetent patient.

• Neurological complication may occur despite being aseptic on timely and appropriate antibiotic.

• Careful and close monitoring of patients with infective endocarditis should be undertaken appropriately even though already on proper treatment.