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: patient recorded as having no known allergies to drugs attending: chief complaint: unresponsive major surgical or invasive procedure: ventricular drain angiography s/p tpa and balloon angioplasty history of present illness: pt is a 33 yo male with no sig pmh except for chronic abdominal pain that he has had for 13 years who presents as transfer from osh for "bilateral occipital lobe infarcts." he was intubated and sedated on arrival, and family was not initially at the bedside to obtain history regarding last known well time or precipitating events. per history obtained later, he had been in usoh until the weekend before admission when he had his "usual" episodes of severe abdominal pain. his wife remembers seeing him at 11pm on sunday, and talking with him on the phone at 2:30 pm monday (day of admission). at 5pm, his wife came home to find him in the bed, unresponsive and unconscious. she called ems, and he was taken to an outside hospital; he had normal glucose at the scene. narcan given en route without relief; pinpoint pupils were noted at the time per ems notes. en route to osh, he reportedly had minute convulsive seizure of which further details are unknown, and for which he was given valium 5 mg with cessation of seizure. he then had an episode of vomiting post-ictally with a report of significant aspiration per ems. upon arrival to the osh, he was intubated and received ceftriaxone, ativan, versed and paralytics; head ct was obtained and was reported as "bilateral occipital strokes." there is no documented exam at osh but by verbal report to ed resident, he had been posturing; he received more propofol. he was medflighted to and arrived after 10pm for further management. en route he received an additional 4mg of iv ativan. per ed neurology resident, he was noted to be hemodynamically stable but continues to be unresponsive. he was seen briefly off of propofol and did not respond to stimuli. past medical history: chronic abdominal pain x 13 years, episodic per wife social history: pt is married and lives with his wife; he does not smoke, drink alcohol or use any drugs including iv drugs. family history: there is no family history of strokes or coagulopathies. physical exam: exam:100.2(rectally), 68, 137/66, 16, 100% on vent gen:intubated and sedated heent:mm dry. sclera clear with corneal edema. mild proptosis neck: no carotid bruits on right. left unable due to c-collar cv: rrr, nl s1 and s2, no murmurs/gallops/rubs lung: clear to auscultation bilaterally abd:soft. nd. nabs neurologic examination: mental status: intubated and sedated cranial nerves: i: not tested ii: pupils 1mm bilaterally and not responsive to light. unable to visualize fundi. unable to doll's eye due to c-collar. v, vii: face symmetric weak corneals bilaterally right<left no cough/gag motor: no tremor. withdraws/postures to painful stim in all ext. flexes legs to this and extends arms. reflexes: b t br pa pl right 2 2 2 2 1 left 2 2 2 2 1 toes were downgoing bilaterally pertinent results: |105|14/161 ---------- 4.2|23|0.9\ 21.0\9.8/478 /34.1\ n:86.8 l:7.9 m:4.9 e:0.4 bas:0.1 pt: 13.5 ptt: 19.6 inr: 1.2 ua neg utox neg etoh neg lfts at osh: alt=38, ast=25, ap=108, bili=0.3, alb=4.8, trop<0.01 12:58am lactate-3.1* admission cxr: ap supine portable view of the chest: the endotracheal tube terminates 2.7 cm above the carina and nasogastric tube terminates with tip in the stomach and side port near the gastroesophageal junction. lungs are clear. heart size is borderline. no definite pleural fluid is seen. no evidence of pneumothorax. impression: 1. endotracheal tube 2.7 cm above the carina. 2. ng tube with side port near the expected location of the ge junction. recommend advancement to ensure placement of the side port within the stomach. mri/a/v upon arrival to 4:16 am: findings: the diffusion-weighted imaging shows slow diffusion throughout the entire cerebellum, brainstem as well as within the posterior medial left temporal lobes and both occipital lobes. there is also extension of slow diffusion up into the left thalamus. these findings are consistent with posterior circulation infarct with an acute posterior circulation infarct along the basilar artery territory into both posterior cerebral artery territories, left greater than right. no areas of significant magnetic susceptibility are identified to indicate an acute hemorrhage. the cerebellar tonsils appear slightly low which is likely a sign of mass effect in the posterior fossa. the lateral ventricles are enlarged, indicating obstructive hydrocephalus. the axial t1 fat saturated images through the neck do not demonstrate evidence of a dissection. the anterior circulation including the internal carotid arteries are normal bilaterally. the anterior middle cerebral arteries are normal and symmetric. the posterior cerebral arteries demonstrate flow distally on the source images. there is also flow within the distal vertebral arteries and small amount of the proximal basilar, but no flow signal is identified within the mid-to-distal basilar artery as well as very proximal posterior cerebral arteries. the mrv demonstrates no evidence of sinus thrombosis. impression: large posterior circulation territory infarct involving the basilar and both posterior cerebral arteries. please see above. developing obstructive hydrocephalus. edema and mass effect in the posterior fossa. no evidence of dissection or venous sinus thrombosis. cerebral angiography : procedure: following informed consent from the patient's wife, the patient was positioned supine on the angiography table. a preprocedure timeout was performed to confirm patient, procedure and site. standard sterile prep and drape of the inguinal regions. local anesthesia with 7 cc of 1% lidocaine subcutaneously. using a combination of palpatory and fluoroscopic guidance, a single wall puncture of the right common femoral artery was performed with a 19-gauge needle. a 0.035-inch guidewire was advanced through the needle into the abdominal aorta. the needle was exchanged for a 6-french vascular sheath. the sheath was attached to continuous heparinized saline flush. using a 4-french berenstein ii catheter and a 0.035-inch glidewire, the left vertebral artery was selected. left vertebral arteriography was performed. based on the findings of the diagnostic angiogram it was determined that the patient may benefit from and was a suitable candidate for thrombolysis. the berenstein catheter was removed and a 6-french envoy guiding catheter was used to select the left vertebral artery with the aid of the glidewire. through the guiding catheter, a prowler plus microcatheter was advanced into the basilar artery. a solution of tpa of 1 mg/ml was then administered in divided doses of 1 mg each. total of 7 mg was administered into the basilar artery and left posterior cerebral artery. the catheter was then repositioned into the right posterior cerebral artery and 4 mg of tpa was administered in divided doses of 1 mg each. the catheter was then withdrawn into the basilar artery and 8 mg of tpa were administered in divided doses of 1 mg each. angiography through the microcatheter was performed at various intervals during the administration of thrombolytic to assess for progress of thrombolysis and for any residual thrombus. after pharmacologic thrombolysis was performed, mechanical thrombolysis was performed using the 0.014-inch guidewire. angiography was repeated through the microcatheter in the basilar artery. findings of this angiogram demonstrated that the patient was a suitable candidate for and may benefit from angioplasty. angioplasty of the area of thrombus in the distal basilar artery was performed with a 4-mm diameter x 10 mm long hyperglide balloon. angiography post-angioplasty was performed. at this stage based on the findings of the angiogram and on discussion with the neurology and neurosurgical services, it was decided to stop treatment. all catheters and wires were removed. the sheath was sewn in place with 0 silk suture. the sheath was left in place for the administration of tpa and because the clinical service required invasive arterial monitoring for blood pressure. the patient was transferred to the pacu for further observation. findings: left vertebral arteriography with imaging from the c6-7 vertebral level to the confluence of the vertebral arteries. this demonstrates patency of the left vertebral artery. there is an area of minor irregularity of the left vertebral artery at the occiput-c1 vertebral level. the opacified portion of the right vertebral artery above the level of c1 is patent. the confluence of the vertebral arteries is patent. left vertebral arteriography with imaging focused on the cranium in the frontal and lateral projections: this demonstrates total occlusion of the basilar artery in its mid portion. post-procedure left vertebral artery arteriography in the frontal and lateral projections demonstrated the vertebral arteries to remain patent in their visualized portions. again, minor irregularity of the left vertebral artery in the level of the occipital condyles was visualized. the basilar artery is now patent. the right posterior cerebral artery is now patent. the proximal aspects of the superior cerebellar arteries are now patent bilaterally. the left posterior cerebral artery is occluded. based on the findings of this post-procedure angiogram and discussion with the neurology and neurosurgical services and review of the preprocedure mri, it was decided that further transcatheter therapy was not indicated and thus the procedure was stopped. impression: complete occlusion of the mid basilar artery extending to the basilar tip was treated with a combination of pharmacologic and mechanical thrombolysis (a total of 19 mg of tpa was utilized). in addition, a 4-mm diameter x 10-mm long angioplasty of the distal basilar artery was performed. the basilar artery and right posterior cerebral arteries were patent post procedure. the left posterior cerebral artery was patent proximally and then occluded. the proximal superior cerebellar arteries were patent bilaterally at the end of the procedure. dr. dr. post-angio ct : non-contrast head ct. findings: today's examination demonstrates decompressed lateral ventricles due to a right frontal ventriculostomy catheter. there is extensive hypoattenuation throughout the entire cerebellum and most of the brainstem extending into the both occipital lobes and the left posterior medial temporal lobe. these findings are consistent with the documented posterior circulation infarct (please see the mri from earlier in the day). on this exam, there is increased attenuation material within the suprasellar cistern and large rounded area of density within the left portion of the pons. there is also high-density material posteriorly within the fourth ventricle. while the patient did receive a significant amount of contrast during the angiogram, in all likelihood this dense material represents subarachnoid blood. this could be due to hemorrhagic conversion of the infarct or vessel rupture. dr. is aware of these findings as of 11 a.m. on . there is no shift of the normally midline structures. impression: large posterior circulation territory infarct. high-density material along the right portion of the pons and into the fourth ventricle and the suprasellar cistern. while contrast was administered and this may represent some enhancement, the high-density nature of this material is very suspicious for a hemorrhage. brief hospital course: 33 yo male with no sig pmh except some chronic abdominal pain (13 hr history) presented as a transfer from osh after being found unresponsive, head ct showing "bilateral occipital lobe infarcts" and cerebellar infarcts. he had an mri/a upon arrival which showed a clot in the basilar artery, as well as multiple areas of acute infarction - cerebellar, occipital, brainstem, l basal ganglia. neurosurgery and neurology agreed that he needed an emergent intervention. he underwent placement of a ventricular drain for obstructing hydrocephalus by the neurosurgical team. at 7am on , he underwent cerebral angiography and received 19 mg tpa to the site of the clot as well as balloon angio, with recanalization of basilar artery, but persistent occlusion of left pca. stat head ct performed just following the procedure showed extravasation of contrast/blood, subarachnoid blood around brainstem into 4th ventricle, and swelling of posterior fossa. following the procedure, exam off propofol and paralytics showed absent brainstem reflexes with pupils 5-6 mm and unreactive, no corneals, no gag, no nasal tickle, could not assess ocr because hard collar in place; there was trace tripleflexion versus withdrawal to nox stim in lower extremities, absent movement to noxious stimulation in the upper extremities, trace dtrs and mute toes. he was evaluated further by neurosurgery who felt he was not a surgical candidate as exam suggested brain death (though with recent propofol and paralytics, he could not definitively be considered brain dead at this time). he was not overbreathing the vent. mannitol was continued, with close monitoring of electrolytes and osms. at 1600 on , the patient had an episode of bradycardia and hypotension requiring epinephrine, atropine and neosynephrine gtt. the family was made aware of this and the question was posed regarding code status; in accordance with the family's wishes, the patient continued to be full code. by sicu recommendation, the organ bank was called. the following morning, off all sedating medications, the patient's exam remained unchanged with regards to absent brainstem reflexes, trace dtrs, with occasional trace tripleflexion of the lower extremitites to nailbed pressure. at 11am, in accordance with the patient's family's wishes, brain death exam was performed and confirmed brain death via absent brainstem reflexes, including absent response to cold calorics, failed apnea test with rise in pco2 from 35 to 69 within just 5 minutes of no ventillation (with 100%fio2 supplementation). a family meeting was held to let them know of the results, and they had further discussion with neob regarding organ donation, which they agreed to. per neob recommendations, time of death recorded as "legal brain death" at 11:00am on 3/22pm. medical examiner contact and declined case despite age, due to fact that family requested full autopsy at to work up underlying cause. he was continued on the ventillator for harvest of organs in the or, until time of apnea and asystole following organ harvest. medications on admission: prilosec discharge medications: none discharge disposition: expired discharge diagnosis: expired - cause of death - apnea due to basilar artery thrombosis and multiple cerebral infarctions discharge condition: expired discharge instructions: expired followup instructions: expired md procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours insertion of endotracheal tube injection or infusion of thrombolytic agent arteriography of cerebral arteries intravascular imaging of intrathoracic vessels percutaneous angioplasty of extracranial vessel(s) procedure on single vessel diagnoses: obstructive hydrocephalus other convulsions occlusion and stenosis of basilar artery with cerebral infarction cerebral thrombosis with cerebral infarction 

Answer: The patient is high likely exposed to