Beta haemolytic streptococci, which include serogroups A, B, C and G, cause a wide variety of infections including cellulitis, necrotising fasciitis, bacteremia and infective endocarditis [4]. Although BHS endocarditis is relatively uncommon, it is very aggressive, with a high rate of cardiac valve destruction, cardiac abscess formation and systemic embolization [4].Of the different subgroups, group B streptococcus (S.agalactiae) is the most common cause   of BHS endocarditis. BHS Endocarditis due to groups C and G are less common, but presents similarly to that caused by group B BHS [4].It is noted that Group A β-hemolytic Streptococcus pyogenes is the least common cause of BHS endocarditis [4].Forty cases of endocarditis caused by Streptococcus pyogenes in children and adults have been reported since 1940, with a median age of 32 years, ages ranging from four months to 80 years. The mortality rate was 24% (62.5% before 1990 and 15.4% after 1990) and was mainly due to cardiac failure and/or septic shock; most patients recovered after antibiotic therapy [50].In our case, the outcome was dramatic, due to a neurologic complication, namely, intracranial haemorrhage. Intracranial Mycotic aneurysm, which results from the septic embolism of vegetation in the cerebral circulation, has been reported secondary to infective endocarditis, with an estimated range between 2% and 10%, The most common causative organisms being Streptococcus viridans, Streptococcus group D and Staphyl ococcusaureus species [6].The clinical presentation of unruptured ICMAs is variable and lacks specificity: Fever, headache, convulsions and focal deficit. Ruptured ICMAs are responsible of a clinical profile of cerebral or subarachnoid haemorrhage: headache, loss of consciousness, intracranial hypertension and focal deficit[7].The diagnosis of ICMAs is possible on brain CT scan that visualises the indirect signs. Cerebral angiography, cerebral MRI and/or cerebral angio MRI have a 95% sensitivity in diagnosing ICMAs greater than 5mm. CT angiography may not be sufficient to detect small aneurysms at the base of the skull[7].Brain angiography remains the benchmark examination, in particular for the diagnosis of small ICMA[7].In our case, cerebral CT angiography gave evidence of two aneurysms.Mortality associated with rupture of intracranial mycotic aneurysm, leading to subarachnoid haemorrhage or intracerebral haemorrhage, is reported to be as high as 80%[6].There are, however, no published reports of S.Pyogenes causing intracerebral mycotic aneurysms.Treatment of intracranial mycotic aneurysms is challenging and to date, there are no standard guidelines. Antibiotic therapy is an essential component of the treatment and studies have reported variable rates of resolution in response to antimicrobial therapy [6]. Taking into consideration the variable response to antibiotics and the high rate of mortality associated with rupture of intracranial mycotic aneurysms, some authors have advocated more aggressive treatment, using endovascular or open surgical treatment, to permit securing of aneurysms and timely cardiac valve replacement [6]. Furthermore, timing of cardiac surgery is difficult to determine, owing to the cerebral damage thatmaybeamplifiedbyheparinizationandhypotensionduringthe cardiopulmonary bypass or postoperative anticoagulant therapy. Therecent European society of cardiology guidelines recommend, that after ICH, surgery should be postponed for more than one month [3].In our case, the clinical presentation has deteriorated rapidly, even after the decompressive craniectomy.