Consider the following medical report that includes the patient's historical health records. Use it to predict the disease that the patient is high likely exposed to. 

 Medical Report: allergies: penicillins attending: chief complaint: left sided weakness major surgical or invasive procedure: transesophageal echocardiogram history of present illness: hpi; 35 yo m with history of htn presenting with acute onset of left face and arm weakness at 9:50 pm while eating dinner. he was noted to have water spill out the side of his mouth and have slurred speech. he was sitting and was unsure if his leg was involved. the episode lasted five minutes and resolved spontaneously. shortly after he had another episode and continued to have intermittent episodes lasting 5-10 minutes at a time with last one lasting up to an hour. he was taken to an osh and upon presentation bp 168/116, ct head was reported to be unremarkable, inr 1.04, plts 115, and fs was normal. his symptoms continued to wax and wane. at midnight records indicate he had no deficits and then again developed left face and arm weakness at 00:05. he was noted to have a nihss of 12 and given iv tpa prior to transfer to for further care. of note at 0118 he was noted to "grip equally, moving all extremities" prior to transfer. he was noted by ems to have recurrence of his symptoms five minutes after his tpa infusion ended and minutes prior to arrival at . he currently denies headache, nausea, or vomiting. ros otherwise negative. past medical history: htn social history: lives with his girlfriend in . works as a construction worker. no history of smoking or illicits. family history: grandmother with a history of stroke. physical exam: vs; t 178/98 rr 13 p 80 98% ra general: awake, cooperative, nad. heent: nc/at, no scleral icterus noted, mmm, no lesions noted in oropharynx neck: supple, no carotid bruits appreciated. no nuchal rigidity pulmonary: lungs cta bilaterally cardiac: rrr, nl. s1s2 abdomen: soft, nt/nd, normoactive bowel sounds extremities: no c/c/e bilaterally skin: no rashes or lesions noted. neurologic: -mental status: alert, oriented x 3. able to relate history without difficulty. language is fluent with intact repetition and comprehension. normal prosody. there were no paraphasic errors. able to read without difficulty. speech was not dysarthric. able to follow both midline and appendicular commands. there was no evidence of apraxia or neglect. -cranial nerves: i: olfaction not tested. ii: perrl 3 to 2mm and brisk. vff to confrontation. iii, iv, vi: eomi without nystagmus. normal saccades. v: decreased sensation to light touch v1-v3 on left vii: left facial droop viii: hearing intact to finger-rub bilaterally. ix, x: palate elevates symmetrically. : 5/5 strength in trapezii and scm bilaterally. xii: tongue protrudes in midline. -motor: normal bulk, tone throughout. no adventitious movements, such as tremor, noted. no asterixis noted. delt bic tri wre ffl fe io ip quad ham ta edb l 0 0 0 0 0 0 0 0 0 0 0 0 0 0 r 5 5 5 5 5 5 5 5 5 5 5 5 5 5 -sensory: decreased to light touch and pinprick on left. extinguishes to dss but inconsistently. -dtrs: tri pat ach l 2 2 2 2 1 r 2 2 2 2 1 plantar response was flexor bilaterally. -coordination: no dysmetria on right. unable to assess on left -gait: deferred pertinent results: admission labs: 140 | 103 | 21 ---------------< 106 3.5 | 26 | 1.0 ca: 8.9 mg: 2.3 po4: 4.2 14.9 10.8 >-----< 254 42.6 ck: 87 trop: <0.01 multiple hypercoagulatibility and secondary hypertension studies were performed to assess the underlying etiology: -normal complement levels - negative -anca negative -tox screen negative -lupus anticoagulant - neg -aldosterone < 1 pending results requiring follow up: -anticardiolipin antibodies -protein c/s -at iii -factor v leiden -metanephrines, plasma -prothrombin mutation -renin imaging: non-contrast ct head: there has been no significant interval evolution over approximately a 3/2 hour time interval of the ill-defined hypodensities within the right centrum semiovale, right lentiform nucleus, and right subinsular cortex. the remaining -white matter differentiation is otherwise preserved. there is mild hypoattenuation of the periventricular and deep subcortical white matter. the ventricles and cortical sulci are normal in size and configuration without evidence of mass effect or shift of the normally midline structures. there is no evidence of intra- or extra-axial hemorrhage. there are mucus retention cysts or polyps within both maxillary sinuses. there is opacification involving multiple bilateral ethmoid air cells, the sphenoid sinuses, and the frontal sinuses. the mastoid air cells and middle ear cavities are well aerated. cta head: the right vertebral artery is dominant. the right posterior communicating artery is hypoplastic. the left posterior communicating artery is visualized. there is mild narrowing involving the mid-to-distal m1 segment of the right mca. the remaining intracranial arterial vasculature is within normal limits. there is no evidence of aneurysm or arteriovenous malformation. ct perfusion: the perfusion images are nondiagnostic secondary to technical failure. cta neck: the great vessel origins at the level of the aortic arch are within normal limits. the vertebral artery origins are patent. the paired vertebral arteries are normal in course and caliber without evidence of occlusion, flow-limiting stenosis, or dissection. the common, internal, and external carotid arteries are normal in course and caliber without evidence of occlusion, flow-limiting stenosis, or dissection. cross-sectional analysis of the internal carotid arteries is as follows: on the right: proximal dmin 7.0 mm; distal dmin 4.2 mm. on the left: proximal dmin 5.8 mm; distal dmin 4.0 mm. the lung apices are clear. the airway is patent. the thyroid gland demonstrates homogeneous attenuation. there are no osseous lytic or blastic lesions identified. impression: 1. hypodensities of indeterminate age in the right centrum semiovale, right subinsular cortex, and right lentiform nucleus with mild narrowing of the mid to distal right m1 segment, which may be secondary to intrinsic disease or thrombus. recommend mri for further evaluation of acute infarction. 2. pansinus disease as described above, the activity of which is to be determined clinically. 3. no ct evidence of aneurysm, dissection, or arteriovenous malformation. mri: findings: increased flair signal of the posterior limb of the right internal capsule extending to involve the posterior caudate nucleus and putamen with corresponding diffusion restriction is consistent with acute to early subacute infarct. there is no intracranial hemorrhage, edema, or shift of midline structures. the ventricles and cerebral sulci are normal in size and configuration. basal cisterns are preserved. there is a mucous retention cyst of the right anterior maxillary sinus, and mucosal thickening of the ethmoid air cells, frontal sinuses and fluid levels in the sphenoid sinuses. the mastoid air cells are clear. impression: 1. acute to early subacute infarct of the posterior limb of the right internal capsule, extending into the posterior caudate nucleus and putamen. discussed by dr. with dr. on at 3 p.m. 2. pansinus disease. carotid dopplars: findings: duplex evaluation was performed of bilateral carotid arteries. on the right and the left there is no plaque seen. on the right systolic/end diastolic velocities of the ica proximal, mid and distal respectively are 69/30, 51/23, 51/23 cm/sec. cca peak systolic velocity is 86 cm/sec. eca peak systolic velocity is 74 cm/sec. the ica/cca ratio is .8. these findings are consistent with no stenosis. on the left systolic/end diastolic velocities of the ica proximal, mid and distal respectively are 83/28, 58/27, 57/28 cm/sec. cca peak systolic velocity is 109 cm/sec. eca peak systolic velocity is 100 cm/sec. the ica/cca ratio is .76. these findings are consistent with no stenosis. right vertebral antegrade artery flow. left vertebral antegrade artery flow. impression: right ica no stenosis. left ica no stenosis. multiple hypercoagulatibility and secondary hypertension studies were performed to assess the underlying etiology: -normal complement levels - negative -anca negative -tox screen negative -lupus anticoagulant - neg -aldosterone < 1 pending results requiring follow up: -anticardiolipin antibodies -protein c/s -at iii -factor v leiden -metanephrines, plasma -prothrombin mutation -renin carotid series : impression: right ica no stenosis. left ica no stenosis. renal ultrasound : impression: 1. no evidence of hydronephrosis, or renal stone. 2. no evidence of renal artery stenosis bilaterally. tte : conclusions the left atrium is normal in size. no atrial septal defect or patent foramen ovale is seen by 2d, color doppler or saline contrast with maneuvers. there is mild symmetric left ventricular hypertrophy. the left ventricular cavity size is normal. overall left ventricular systolic function is normal (lvef 60%). right ventricular chamber size and free wall motion are normal. the aortic root is mildly dilated at the sinus level. the aortic valve leaflets (3) appear structurally normal with good leaflet excursion and no aortic regurgitation. the mitral valve appears structurally normal with trivial mitral regurgitation. there is no mitral valve prolapse. the estimated pulmonary artery systolic pressure is normal. there is no pericardial effusion tee : the left atrium and right atrium are normal in cavity size. no spontaneous echo contrast or thrombus is seen in the body of the left atrium/left atrial appendage or the body of the right atrium/right atrial appendage. no atrial septal defect or patent foramen ovale is seen by 2d, color doppler or saline contrast with maneuvers (though prominent inflow from the inferior vena cava directed towards the interatrial septum by the eustachian valve seems to blunt the amount of superior vena caval inflow that comes in contact with the interatrial septum). there is mild symmetric left ventricular hypertrophy with normal cavity size and global systolic function (lvef>55%). right ventricular chamber size and free wall motion are normal. the ascending, transverse and descending thoracic aorta are normal in diameter and free of atherosclerotic plaque to 40 cm from the incisors. the aortic valve leaflets (3) appear structurally normal with good leaflet excursion and no aortic stenosis. no masses or vegetations are seen on the aortic valve. no aortic regurgitation is seen. the mitral valve appears structurally normal with trivial mitral regurgitation. no mass or vegetation is seen on the mitral valve. no vegetation/mass is seen on the pulmonic valve. impression: no cardiac source of embolism. no evidence of atrial septal defect or patent foramen ovale with saline contrast and maneuvers. no significant valvular abnormality. normal thoracic aorta to 40 cm from the incisors. if exclusion of a pfo is a clinical necessity, injection of saline via a femoral vein might help to completely exclude a pfo. brief hospital course: 35 yo m with history of htn presenting with acute onset of left face and arm weakness at 9:50 pm while eating dinner. symptoms have had a stuttering course and he was given iv tpa for nihss 12 prior to transfer. he was called as a code stroke for recurrence of his deficits shortly after infusion of tpa and minutes prior to arrival to . his examination is notable for a dense left hemiplegia as well as decreased sensation on the left. #neuro: he received iv tpa prior to transfer, so was initially admitted to the neuro icu. he underwent an mri which confirmed the presence of a posterior limb of the right internal capsule infarct, extending into the posterior caudate nucleus and putamen. he had a carotid dopplers, as well as a cta of the head and neck which showed no signs of vascular occlusion. tte and tee were peformed (see above) which failed to show a pfo, asd, right to left shunt or a source of an embolism. echocardiograms were notable for mild symmetric left ventricular hypertrophy with normal cavity size and global systolic function (lvef>55%) suggestive of prior hypertension. the ascending, transverse and descending thoracic aorta were normal in diameter and free of atherosclerotic plaque. fasting lipids showed ldl of 121 and an a1c was 5.1. patient was started on simvastatin. it was thought that his infarct was secondary to hypertension, however possibility of an embolic infarction (though no clear source was identified) which can occur in up to many patients with this presentation could not be ruled out. given his risk of stroke recurrence (3-5% per year) and age, he was started on coumadin daily (goal inr ) with asa bridge until therapeutic. he will require further monitoring of inr, at time of discharge was 1.1 (coumadin initiated on at 5mg daily and may need adjustment). he will require follow up with dr. of neurology at which was arranged. #cv: the patient was hypertensive on admission, and reported that this was a problem his pcp had been following for several years, recommended dietary changes at this time. given his relatively young age, he underwent an evaluation for secondary causes of hypertension, including a renal ultrasound which showed no signs of renal artery stenosis, and plasma renin, aldosterone and metanephrines which are pending at time of discharge. given persistently elevated sbps (150-170s) mmhg even 4 days after the cva, he was started on lisinopril 10mg daily. no significant response was noted after 2 days of therapy, thus dose was increased to 20mg daily on . no change in cr was observed after tx initiation. this will require follow up. his eventual goal of bp is 130/80 and should be achieved within 1-2 months after his cva. due to ldl of 127 and cva, he was started on simvastatin to control the rfs. the following studies will require follow up (pending at ): -anticardiolipin antibodies -protein c/s -at iii -factor v leiden -metanephrines, plasma -prothrombin mutation -renin level neurological exam notable for: alert, oriented to time, place person. language intact. cns: l facial droop, mild leftward tongue deviation (due to facial) motor: rue and rle full in strength. lue flaccid. lle: ip, hamstring, quadriceps, remainder is 0/5. tone: flacid in lue, lle mildly increased relative to lue. dtrs 3+ at l biceps, triceps, patella. toes: extensor bilaterally. sensory: intact lt, proprioception. extinction on the left with dss. medications on admission: none discharge medications: 1. acetaminophen 325 mg tablet sig: two (2) tablet po q6h (every 6 hours) as needed for pain. 2. docusate sodium 100 mg capsule sig: one (1) capsule po bid (2 times a day). 3. senna 8.6 mg tablet sig: one (1) tablet po bid (2 times a day) as needed for constipation. 4. aspirin 325 mg tablet sig: one (1) tablet po daily (daily). 5. heparin (porcine) 5,000 unit/ml solution sig: one (1) injection tid (3 times a day). 6. miconazole nitrate 2 % powder sig: one (1) appl topical (2 times a day) as needed for rash in armpit. 7. simvastatin 10 mg tablet sig: two (2) tablet po daily (daily). 8. warfarin 5 mg tablet sig: one (1) tablet po once daily at 4 pm. 9. lisinopril 20 mg tablet sig: one (1) tablet po daily (daily). 10. sodium chloride 0.9% flush 3 ml iv q8h:prn line flush peripheral line: flush with 3 ml normal saline every 8 hours and prn. 11. hydralazine 10 mg iv q6h:prn sbp>180 discharge disposition: extended care facility: rehab in discharge diagnosis: primary: right anterior choroidal artery secondary: hypertension, hyperlipidemia discharge condition: neurological exam notable for: alert, oriented to time, place person. language intact. cns: l facial droop, mild leftward tongue deviation (due to facial) motor: rue and rle full in strength. lue flaccid. lle: ip, hamstring, quadriceps, remainder is 0/5. tone: flacid in lue, lle mildly increased relative to lue. dtrs 3+ at l biceps, triceps, patella. toes: extensor bilaterally. discharge instructions: you were admitted to the hospital after sudden onset left sided weakness. you were found to have a significant stroke in the right side of your brain. you underwent a thorough evaluation for the source of this stroke (detailed in discharge summary). after a thorough evaluation, we were unable to identify a definite source of the stroke, however, it was felt that it was due to hypertension and a possible embolic source. because of this, you were started on the following medications: - coumadin 5mg daily - asa 325mg until coumadin is therapeutic range (inr ) - simvastatin 20mg - lisinopril 20mg - bowel regimen, pain regimen as per your rehabilitation physician because of the aftermath from your stroke, you will require extensive rehabilitation. you were discharged to such a facility there are still tests pending that will require follow up: followup instructions: please follow up with the following providers: provider: , .d. phone: date/time: 1:00 please call the pcp's office to arrange for a follow up appointment in 1month from your discharge: name: , address: , , phone: fax: md, procedure: diagnostic ultrasound of heart diagnoses: unspecified essential hypertension other and unspecified hyperlipidemia cerebral embolism with cerebral infarction cerebral artery occlusion, unspecified with cerebral infarction status post administration of tpa (rtpa) in a different facility within the last 24 hours prior to admission to current facility 

Answer: The patient is high likely exposed to