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: seizure and hemorrhage major surgical or invasive procedure: intubation arterial line placement bilaterally. history of present illness: 50 year-old man with a history of htn, chol, right parietal infarct , s/p r cea (stenosis 80%) , admitted to hospital with status epilepticus and worsening left hemiparesis ( vs new stroke), then with decreasing alertness and repeat ct with parieto-occipital hemorrhage. pt presented in with left hemiparesis, had right parietal infarct, and recovered well with only mild residual hemiparesis. workup revealed an 80% r ica stenosis. he was discharged on asa, lipitor and coumadin. he then underwent r cea on , without complications and was discharged on . on , family observed clonic movements of left arm followed by a generalized tonic-clonic seizure at home. no h/o headache or head injury. ems arrived and en route to hospital he had another gtc lasting 2.5 minutes, and was given valium 5mg imx1, and he became combative and restless. he was intubated for airway protection, given morphine, ativan and 1gm fosphenytoin with good effect and resolution of seziures. etiology of seizures was unclear. ct at that time showed only old right parietal stroke. bilateral carotid ultrasound without stenosis. on exam, he had worsened left hemiparesis, unclear if due to vs new right-sided stroke. head ct unchanged, and cta neck without carotid disease. pt was never stable enough for mri. on , motor exam was uncahnged but he was increasingly lethargic. sedation was discontinued, and by the evening of he was agitated and combative. on morning of he started to become more lethargic, and this progressed over the day despite lack of sedation. he also had worsening hypertension that was refractory to labetalol, enalaprilat, and metoprolol. he was started on nipride with increased doses of enalaprilat and metoprolol with sbp 170s (goal). due to increased lethargy, neurology consultant recommended repeat head ct which showed large right temporo-occipital bleed with extension into right ambient cistern, 5x4x1.8 cm. ct also showed diffuse edema r>l and narrowing of the ambient cistern concerning for early herniation so pt started on decadron and mannitol. exam prior to transfer with no purposeful movement, some movement of bilateral limbs with deep sternal rub, increased tone on left, equal and reactive pupil's with +oculocephalic reflex. ros: unable past medical history: 1. right parietal stroke , residual mild left hemiparesis. per records, had multiple tias involving left arm and leg and then had stroke high right parietal lobe. carotid us with >805 r ica stenosis, echo with lvh but no siurce of embolus, no afib on tele. rx'd acutely with heparin, then with asa/coumadin while awaiting cea. workup also with normal factor v, atiii, protein c and s, homocysteine . 2. hypertension 3. hypercholesterolemia 4. r ica stenosis (80%), s/p r cea 5. copd 6. chronic lbp 7. chronic eczema 8. s/p bilateral inguinal hernia repair , vasectomy 9. hepatitis b social history: lives at home with family. works in automotive and motorcycle repair. quit smoking a few years ago. h/o alcoholism, sober x6yrs. no other drug use. family history: no h/o seizures, early stroke or mi physical exam: t 97.8 bp 194/108 hr 119 ac fio2 1.0 650x16 peep 5 o2 sat 99% general: appears stated age, intubated heent: nc/at sclera anicteric neck: supple. r cea incision c/d/i, stapled lungs: clear to auscultation anterolaterally cv: rrr, nl s1, s2, no murmur. abd: soft, nontender, normoactive bowel sounds extr: no edema, good dorsalis pedis pulses neurologic examination: mental status: awake, agitated, bucking vent, vigorously moving right arm and leg, responding to noxious stimulus of a-line placement. does not follow commands. no obvious neglect cranial nerves: pupils equally round and reactive to light, 4 to 3 mm bilaterally, brisk. does turn head to both sides, unable to assess vor as pt too awake but does not look right or left to command. corneal reflexes normal bilaterally. no upper face droop with grimace to noxious, difficult to assess lower face given intubation. motor: normal bulk. decreased tone left arm and leg. no fasiculations. no tremor. vigorously moves right arm and leg to noxious/spontaneously with full strength. some flexion of left arm in response to arterial stick but otherwise minimal, no spontaneous movement left leg. sensation: withdraws right arm/leg. minimal, near absent posturing of left leg and arm to noxious. reflexes: dtrs brisker left vs right. toes were up on right, mute on left. unable to assess coordination and gait given mental status. pertinent results: admission labs: 02:38am blood wbc-27.2* rbc-4.43* hgb-13.7* hct-39.4* mcv-89 mch-31.0 mchc-34.9 rdw-13.3 plt ct-403 02:38am blood pt-14.1* ptt-30.2 inr(pt)-1.3 03:36pm blood ret aut-0.5* 02:38am blood glucose-150* urean-16 creat-0.7 na-138 k-3.5 cl-100 hco3-23 angap-19 02:38am blood alt-17 ast-21 alkphos-105 amylase-21 totbili-0.7 03:36pm blood ld(ldh)-328* 02:38am blood calcium-9.8 phos-4.4 mg-2.3 03:36pm blood caltibc-221* vitb12-427 folate-8.3 hapto-pnd ferritn-468* trf-170* 02:38am blood phenyto-14.9 ---- discharge labs: 06:15am blood wbc-16.8* rbc-3.47* hgb-11.0* hct-31.4* mcv-90 mch-31.8 mchc-35.2* rdw-13.7 plt ct-617* 06:15am blood pt-13.6* ptt-29.0 inr(pt)-1.2 06:15am blood glucose-101 urean-17 creat-0.8 na-140 k-4.0 cl-103 hco3-23 angap-18 06:15am blood alt-46* ast-24 ck(cpk)-32* alkphos-170* totbili-0.4 06:15am blood totprot-7.5 albumin-4.0 globuln-3.5 calcium-10.0 phos-4.6* mg-1.9 ---- studies: head mri: evolving right parietal hematoma with extension into the adjacent lateral ventricle and basal csf cisterns, with much associated vasogenic edema. in this clinical setting, intracerebral hemorrhage secondary to hyperperfusion post carotid endarterectomy remains a distinct possibility. hemorrhage into a pre-existing vascular malformation is possible. other etiologies, such as hemorrhage secondary to amyloid angiopathy, overcoagulation, or pre-existing tumor, either primary or secondary, are thought to be less likely. followup mra or cta will provide further information, to exclude underlying vascular malformation. ---- head ct:large area of parietal occipital intraparenchymal hemorrhage which extends into the ambient cistern and quadrigeminal plate cistern all the way to the foramen magnum in the subarachnoid space. no or minimal shift of midline structures to the left. normal-sized ventricles without evidence of hydrocephalus. the pattern of white matter hypodensity is not characteristic for infarction, and a white matter process, including a tumor and a multifocal vascular process, should be considered as a cause for this hemorrhage. an mri/mra is recommended. this was discussed with dr. at 9:40am on . ---- cta:fetal type posterior communicating arteries bilaterally as described. no definite evidence of aneurysm. ---- mr :anterolisthesis with posterior disc bulge at l4-l5 with associated bilateral pars defect. increased l4-l5 disc t2-signal, which may reflect spinal degeneration, although possible infection cannot be excluded. recommend clinical correlation and followup radiographs to monitor for interval change. ---- mr :mild-to-moderate cervical spondylosis at c5-c6 level with central shallow disc protrusion. moderate-to-severe narrowing of the right foramen at that level probably impinging on the right exiting c6 nerve root. minor cervical spondylosis and annular bulge at c6-c7 level. small central disc protrusion of the upper thoracic disc at t3-t4 level. ---- repeat head ct:: interval decrease in size of right parietal/occipital intraparenchymal hemorrhage with continued surrounding edema and subcortical white matter hypodensity. no new intracranial hemorrhage or mass effect demonstrated. ---- eeg:abnormal portable eeg due to the slow and disorganized background and bursts of generalized slowing. these indicate a widespread encephalopathic condition. the record did not appear much changed from the earlier encephalopathic record except that suppressive bursts were no longer as evident. this might be related to discontinuation of prpofol. there were still occasional focal isolated sharp waves, possibly slightly fewer than on the previous recording, but there were no electrographic seizures. ---- cxr:9/30:1. malpositioning of feeding tube, which coils within the thoracic esophagus. 2. new patchy bibasilar opacities, which may reflect aspiration or atelectasis. brief hospital course: pt was transferred to icu with his parieto-occiptal intracranial hemorrhage on and was treated initially with decadron, mannitol, and hyperventilation. the decadron was stopped on . he continued to do well so mannitol stopped several days later. an initial eeg showed a slow background, ~2hz, with frequent fronto-central discharges, but no seizure activity. he was loaded with dilantin, but had difficulty maintaining adequate levels, so he was switched to keppra and titrated up to his current dose. a repeat eeg was essentially unchanged, but showed him to be somewhat more awake. his bleed is felt to be the result of carotid hyperperfusion syndrome, but the time course is odd as he did not have hemorrhage for several days after his seizure, and 6 full days after his cea. this still appears to be the most likely etiology. he should continue keppra until neuro follow-up. the patient was extubated on and became more awake and conversational. while in the icu, his elevated blood pressure was difficult to control. he was thought to have developed a right hilar pneumonia in the setting of fevers and an elevated white count and sputum culture growing coag positive staph. he therefore completed 10 days of levofloxacin/vancomycin and defervesced by . pt complained of worsenign of his chronic low back pain and mri l-spine showed anterolisthesis at l4-5 with possible nerve root compression. this is believed to be old and did not seem greatly changed from a prior film. this back pain resolved during his stay. patient was transferred to floor on with stable blood pressure and heart rate. this was acheived using metoprolol, norvasc, and enalapril(initially required much more acutely in the icu). he did well with this. he did have 1-2 episodes of bradycardia to the high 30s while sleeping that were not symptomatic. these were sinus brady. his hospital course on the floor was notable for right arm (triceps and deltoid) and right hand (finger extensor) weakness as well as decreased r arm reflexes that could not be explained by his intracranial hemorrhage. his wife believes that these deficits were not present prior to his seizure on . repeat head ct on did not show new or worsening hemorrhage or evidnce of any left sided stroke. an mri of the c-spine on showed moderate to severe compression of c6 nerve root, which is not entirely consistent with his motor deficits. etiology of his r arm weakness is not entirely understood and we have strongly recommended that he follow-up with a neurogist as an outpatient for further evaluation. we recommnded an lp to evaluate for possible infection such as lyme, or evidence of malignancy/paraneoplastic syndrome. a plexopathy is also a possiblity. he refused this despite our strong insistence. at this time, we are unsure why he has developed arm weakness, but given the wasting in his muscles, it appears to be a more chronic process. this is not in agreement with his wife's thoughts. it is possible that he has more than one process contributing. this does not appear to be an acute issue though and he will need to follow up in neurology clinic for further work-up whether this resolves or not. an emg may be a next step to assess for whether this is a peripheral problem or not. pt was also seen by hematology on for eval of leukocytosis and increased platelets. heme believes these findings are most consistent with a reactive process, but spep, upep, lap, esr, crp, hep b viral load pending at time of discharge to rule out a myelodysplastic syndrome. these will need to be followed by his pcp or mds. during their evaluation, they also noted burr cells on his smear and became concerned about liver disease, given his history of hep b and alcoholism. a hep b viral load was checked and is pending. an abd ultrasound showed an essentially normal iver(non-specific heterogeneity only) and a slightly small spleen. patient's mental status has gradually improved, although he remains quite inattentive. he also continues to have unchanged right arm weakness as above in a pattern not typical for a particualr pathology, but is closer to an upper motor neuron pattern than anything else. his left arm is also weak in an upper motor neuron pattern since his stroke. both legs remain slightly weak as well, with his left weaker than his right. he was discharged on an 81 mg asa for secondary ischemic stroke prevention. his plavix was not restarted. he will possibly need additional antiplatelet agents in the future, but needs to be further from his hemorrhage before starting these. medications on admission: asa 81 mg po qd plavix lipitor 40 mg po qd discharge disposition: extended care facility: - discharge diagnosis: right-sided parieto-occipital hemorrhage with generalized tonic-clonic seizure thought to be secondary to carotid hyperperfusion syndrome. -- htn h/o stroke leukocytosis discharge condition: stable. continued right arm weakness, left arm weakness and leg weakness bilaterally. mild confusion at times discharge instructions: please tell the doctors at rehab if you have any change in your symptoms, chest pain, shortness of breath, or new weakness/numbness. take your medications. please follow up with a neurologist after you leave rehab. followup instructions: please call to schedule a follow-up appointment with dr. , dr or dr in the neurology clinic. please follow up with your pcp after you leave rehab. procedure: venous catheterization, not elsewhere classified continuous invasive mechanical ventilation for 96 consecutive hours or more enteral infusion of concentrated nutritional substances diagnoses: pneumonia, organism unspecified pure hypercholesterolemia unspecified essential hypertension chronic airway obstruction, not elsewhere classified other convulsions intracerebral hemorrhage hypopotassemia personal history of other diseases of circulatory system other vascular complications of medical care, not elsewhere classified lumbago other specified anemias other specified disease of white blood cells unspecified diseases of blood and blood-forming organs other musculoskeletal symptoms referable to limbs 

Answer: The patient is high likely exposed to