Scientonline.org



STREPTOCOCCUS AGALACTIAE INFECTIVE ENDOCARDITIS MASQUERADING AS POSTERIOR CIRCULATION INFARCT IN AN OTHERWISE HEALTHY ADULT Low Jia Zhen, Lee Pei Hua, Gerard Yeo Kheng Leong, Kristine Teoh Leok Kheng, Christopher Seet Ying Hao IntroductionTime remains a critical factor in patients with acute ischemic stroke due to the availability of hyperacute stroke therapies such as thrombolysis and endovascular therapy. The American Heart Association recommends a primary goal of achieving door-to-needle timing within sixty minutes. Unfortunately stroke mimics are still frequently treated with thrombolysis in clinical practice and thrombolytic trials due to the time sensitive nature of stroke activations. In this case report, we describe a patient with initial clinical suspicion of posterior circulation infarct who was treated with intravenous rTPA but eventually was diagnosed with Streptococcus agalactiae infective endocarditis with meningoencephalitis. Case report We describe a case of a 61-year-old male, previously healthy, who was admitted to the Neurology department with a clinical suspicion of posterior circulation infarct. He was noted to be well at 430pm after returning from work. He was subsequently noted to have global aphasia with left hemiparesis at 7pm the same day. The patient had no significant medical history with no risk factors of steroid use, dental visits, intravenous drug abuse, high risk sexual behaviour or immunosuppression. On review in the Emergency Department, he was afebrile with a blood pressure 135/61 but was tachycardic at 112bpm with normal oxygen saturation of 98% on room air. He was noted to be aphasic with a Glasgow Coma Scale (GCS) of E4V1M5 and NIH Stroke Scale (NIHSS) of 16. There was left gaze preference, downbeat nystagmus with torsional component on vertical gaze and left hemiplegia with left sided muscle strength of MRC grade of 1 and 3 in the right upper and lower limb. There was no murmur on auscultation of the heart and Kernig’s sign was negative. An urgent computed tomography (CT) of the brain and angiogram was performed which did not show any acute intracranial haemorrhage or territorial infarct. CT angiogram also showed normal opacification of the anterior and posterior circulation with no large vessel occlusion or stenosis. In view of the acuity of his neurological deficits coupled with the normal brain imaging, he was treated as for posterior circulation infarct and given rTPA at 2042 hours the same day. Unfortunately, his clinical condition deteriorated in the high dependency unit and he required inotropic support to maintain his blood pressure. He also developed right daze deviation with features of meningism (Kernig’s sign). There was one episode of right complex partial seizures which was aborted with benzodiazepines.Marker Value haemoglobin (Hb)11g/dLwhites (TW)16.4 x109/Lneutrophils15 x109/Lplatelets199 x109/LAPTT38.9 secondsPT14.9 secondsINR1.2Na140K3.6Cr 282 umol/LHCO3 17 mmol/L C-reactive protein199 mg/LProcalcitonin16.16 ug/LFerritin587 ug/LFibrinogen6.5 g/LLaboratory investigations reviewed high inflammatory markers. Ferritin was 587 ug/L with cholestasis ALT 24 U/L ALP 295 U/L AST 27 U/L and bilirubin 43 umol/L. Fibrinogen was elevated at 6.5 g/L. Peripheral blood film showed mild polychromasia and a few large platelets but no schistocytes. The clinical suspicion of a possible meningoencephalitis was heightened in view of acute encephalopathy, elevated inflammatory markers with meningism on physical examination. Magnetic Resonance Imaging (MRI) of the brain imaging showed multiple small foci of diffusion restriction scattered in the frontal parietal cortices, with additional punctate foci in the left centrum semiovale, right occipital lobe and a focus in the cerebellar vermis. There was also diffusion restriction layering in the occipital horns of the lateral ventricles suggestive of pus. Lumbar puncture revealed turbid and yellowish cerebrospinal fluid (CSF) with nucleated cells of 1005 cells/uL with a differential count of 51% neutrophils, 34% lymphocytes and 11% monocytes. Protein was >2.00 g/L and glucose 1.9 mmol/L. Capillary blood glucose was 4.9 and CSF/serum glucose ratio was less than 0.5. Meningitis multiplex PCR assay of the CSF was positive for streptococcus agalactiae a few days later. He received intravenous meningitis doses of meropenem, vancomycin and acyclovir while awaiting blood and lumbar puncture culture resultsTrans-thoracic echocardiogram revealed new onset atrial fibrillation, severe aortic regurgitation, multiple vegetations on aortic leaflets with largest being 11mm in diameter, and aortic leaflet perforation (see Figure 1 and 2).Figure 1 &2. Parasternal Long-Axis View (PLAX) showing Aortic valve vegetation and perforationHe was subsequently transferred under the care of Cardiothoracic Surgery for urgent aortic valve replacement with a 25mm Avalus bioprosthesis. Histology of the native damaged valve leaflet showed myxoid degeneration with focal fibrinous exudate and necrotic debris admixed with clusters of bacteria cocci. DiscussionStroke mimics receiving thrombolysis in the emergency room is inevitable due to the time sensitive nature of acute ischemic stroke treatment1,4,5. There is a prevalence of 5-30% 1, 4 of stroke mimics receiving thrombolysis. It was also found that patients with stroke mimics had fewer clinical findings of gaze palsy, loss of visual field, facial paresis, limb motor deficit, aphasia, dysarthria and neglect1. There were less reports of occlusion of arteries seen on CT angiography. In our patient, CT angiography did not show any large vessel occlusion and hence he was initially planned for an MRI brain. However, in view of this chest X-ray findings of pneumonia and in light of precautions that have to be taken during COVID-19, this could not be performed until the patient was proven to not have a coronavirus infection. Great care must be taken in excluding stroke mimics prior to rTPA administration. Streptococcus agalactiae is a gram-negative coccus that can cause serious invasive diseases in newborns, immunocompromised patients (e.g. pregnant women, elderly) and also adults without predisposing conditions2. Our patient worked as a coffee supplier distributor at a neighbourhood shop with little contact with raw food and no history of raw food consumption. It is of note that in 2015, an outbreak of group B streptococcal (GBS) infection caused by Streptococcus agalactiae Serotype III, multilocus sequence type 283, related to consuming infected raw freshwater fish affected more than 200 patients in Singapore3. As such, constant vigilance is essential for public health surveillance. References 1 Christopher Elnan Kvistad et al. Safety and predictors of stroke mimics in The Norwegian Tenecteplase Stroke Trial (NOR-TEST). International Journal of Stroke 2019, Vol. 14(5) 508–5162 H. Fujita et al. Severe infective endocarditis in a healthy adult due to Streptococcus agalactiae. International Journal of Infectious Diseases 38 (2015) 43–45 453 Kevin Tan et. al. Diffusion-Weighted MRI Abnormalities in an Outbreak of Streptococcusagalactiae Serotype III, MultilocusSequence Type 283 Meningitis. J. MAGN. RESON. IMAGING 2017;45:507–5144 Merino JG, Luby M, Benson RT, et al. Predictors of acute stroke mimics in 8187 patients referred to a stroke service. J Stroke Cerebrovasc Dis 2013; 22: e397–e403.5 Tsivgoulis G, Zand R, Katsanos AH, et al. Safety of intravenous thrombolysis in stroke mimics: prospective 5-year study and comprehensive meta-analysis. Stroke 2015; 46: 1281–1217.6 Winkler DT, Fluri F, Fuhr P, et al. Thrombolysis in stroke mimics: frequency, clinical characteristics, and outcome. Stroke 2009; 40: 1522–1525 ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download