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: no known allergies / adverse drug reactions attending: chief complaint: peg tube malfunction, seizure while in ed major surgical or invasive procedure: - reprogramming of vp shunt history of present illness: 42y f bed-bound, non-verbal woman seen previously for gtc seizures by our neurology service; followed in clinic by dr. for recent-onset seizure disorder thought to be in general secondary to severe traumatic brain injury suffered in mvc (car-on-pedestrian) in . please see prior notes from myself (), dr. (mid-), and dr. ( clinic follow-up) for detailed information. pt has a vp-shunt in her l-lat ventricle (placed earlier this year). she is on keppra (currently 1500mg/d) and valproate (started earlier this year, and subsequently increased to 2250mg/d as 750mg tid dosing). in other recent events, she had a tracheostomy revision here at earlier this month, apparently without complication. i have no information that she has been infected or ill in any way recently. the last known report of seizure activity, mentioned in dr. clinic note, was at her nursing home and was prolonged and generalized, treated there (without hospital evaluation) using benzodiazepine medication. her seizure onset is unclear, but may be secondary/generalized and is likely a right-frontal onset consistent with her right-frontal encephalomalacia and her presentation with lue twitching. ********** she was transferred to our ed today from her nursing home due to malfunction of her peg feeding tube. by verbal report, it is unclear whether she actually missed any doses of medications; no missed doses are charted, but she was brought because of leakage and difficulty pushing fluids through the peg, so this seems to be the case although it is unclear how long it has been a problem (to be clarified in the am if possible). shortly after arrival in our ed, she exhibited clonic seizure activity. i do not have information regarding the onset or exact semiology, but dr. thinks that convulsions involved primarily her left arm and possibly leg, and that she had left- eye deviation at that time. an iv hadn't been placed yet, so i.m. ativan was given without seizure resolution initially, so i.v. ativan was added, up to a total dose of 6mg by combined routes (?2 im + ?4 iv) before her movements stopped over a period of roughly 40 minutes total (i was not present and did not observe the duration of any individual bouts). on our recommendation, she was then loaded with a dose each of iv vpa and iv lev (1 gram each). review of systems: unable (non-verbal pt) past medical history: 1. traumatic brain injury (struck by motor vehicle on ) causing right sdh, right frontal sah and iph, left subfalcine herniation and uncal herniation; status post right-sided hemicraniectomy, right sdh evacuation, right frontal lobectomy and right temporal lobectomy and vp shunt. 2. status post revision of vp shunt with placement of a programmable valve on . 3. history of seizure in and second seizure in . 4. remote history of oxycontin abuse, alcohol abuse, and question heroin abuse. 5. history of hypothyroidism without need for present treatment 6. remote history of anxiety and back pain. social history: nursing home resident @ hn. father is the guardian, , 87yo, his phone number is . her sister is , phone number is . pcp . has a remote history of opioid abuse prior to mva in . family history: unknown physical exam: admission physical exam: vital signs: see ed vs sheet (initially mild tachycardia resolved; no other pertinent abnormalities, afebrile and normotensive) general exam: lying in bed in nad. trach with 15l o2 running, balloon with appropriate pressure. awakens to voice, appears displeased or angry. non-verbal, does not follow any commands. heent: depressed r frontal/supraorbital ridge, as before. anicteric. mucous membranes are moist. neck: supple. trach, cdi. no gross cervical lymphadenopathy. pulmonary: good air movement bilaterally. no wheezes or loud crackles. non-labored breathing. cardiac: rrr, no loud m/r/g appreciated. abdomen: soft, non-distended. pt moves r arm on palpation, but not exquisitely tender. peg site non-tender and mildly erythematous. extremities: rue and rle withdraw to pain and move spontaneously to resist some aspects of exam (but not on command). warm and well-perfused x4. intact radial, dp pulses bilaterally. skin: rue in restraint (mitt). on removal of mitt, hand and mitt are mildly malodorous. lateral dorsum of wrist has erythematous abrasions, seems mildly tender to palpation. mild rash on chest, similar to appearance in (see note from that time). ***************** neurologic examination: mental status: opens eyes to voice. mildly lethargic, but by end of exam maintains eyes open. does not follow commands, but does resist exam intermittently with angry facial expression, rue/rle movements (swats at me with mitt/rue external rotation, withdraws and arm/leg, kicks rle). seems to attempt vocalization on two occasions, with mouth movements and attendant respiratory changes. -cranial nerves: ii: perrl, 4 to 3mm and brisk. blinks to threat in both eyes, possibly only from the right side of each visual field (also closes eyes and resists exam frequently, limiting conclusions). not cooperative with fundoscopy. iii, iv, vi: eoms conjugate with spontaneous saccades. no spontaneous nystagmus. does not track. reliably looks to right, not to left on my exam. suppresses ocrs and closes eyes, so cannot examine smooth pursuits. v: facial sensation intact and subjectively symmetric to eyelash stimulation (blinks) and nasopharyngeal stimulation (grimaces). bites tongue depressor and will not open mouth on command. vii: no ptosis. have mild facial assymetry (left edge of lips slightly less elevation than right), but this is subtle. does not smile or raise brows on command. symmetric eye closure. viii: hearing grossly intact (opens eyes to voice). suppresses ocrs and closes eyes, limits vestibular testing. no nystagmus observed. ix, x: does not open mouth or swallow on command. : cannot assess. xii: cannot assess. -motor: increased tone in rue>lle (i cannot extend rue past 90deg at elbow) and rle (hyperextended), with easily evoked non-sutstained clonus at r knee (also intermittently @ l ankle). tone in lle is low vs. normal. spontaneous/purposeful movements observed in rue (swats at me, withdraws briskly) and rle (withdraws) only, not in lue or lle at this time. r wrist held in pronation with thumb adducted. no tremor. does not comply with power testing; rue and rle seem grossly strong, but limited exam (lift at delt, pull at biceps, ip, hams). -sensory: grimaces and increases activity to mild pinch x4. withdraws on r, not on l. -reflexes (left; right): biceps (++;++) brisker on l (tone already increased on r) triceps (++;++) brachioradialis (++;++) quadriceps / patellar (++++;+) gastroc-soleus / achilles (++;++++) intermittently evokes clonus on l plantar response was withdraw on r and upgoing with clonus on l. -coordination & gait: cannot assess. discharge physical exam: unchanged pertinent results: 03:50pm blood wbc-7.9 rbc-4.66 hgb-14.5 hct-41.8 mcv-90 mch-31.2 mchc-34.8 rdw-13.1 plt ct-208 03:50pm blood neuts-71.1* lymphs-17.0* monos-9.5 eos-2.0 baso-0.3 03:50pm blood pt-10.6 ptt-37.5* inr(pt)-1.0 03:50pm blood glucose-97 urean-9 creat-0.4 na-136 k-4.0 cl-97 hco3-28 angap-15 03:50pm blood alt-89* ast-88* alkphos-82 totbili-0.3 03:50pm blood calcium-9.1 phos-4.2 mg-1.9 03:50pm blood valproa-29* 03:50pm blood asa-neg acetmnp-neg bnzodzp-neg barbitr-neg tricycl-neg 07:05pm blood tsh-2.9 anti-epileptic drug levels: 03:50pm blood valproate-29* 07:05pm blood valproate-58 04:15am blood valproate-103* 04:20am blood valproate-105* 06:10pm blood levetiracetam (keppra)-21.1 mcg/ml anti-epileptic drug levels on discharge: 04:20am blood valproate-113* 04:20am blood lamotrigine-pnd 04:20am blood levetiracetam (keppra)-pnd nchct (): 1. acute-on-chronic left subdural hematoma, as described above with some effacement of underlying sulci and decrease in size of the left lateral ventricle. 2. stable in position left frontal approach ventriculostomy catheter which again terminates in the third ventricle. vp shunt series (): 1. left-sided vp shunt without evidence of discontinuity or sharp kink, from a left frontal approach continues over the left neck, left hemithorax, into the left upper quadrant and terminates in the right lower quadrant. 2. patchy right base opacity new since , partially obscured by overlying leads, may be due to atelectasis or consolidation from infection and/or aspiration. dedicated pa and lateral views of the chest would be helpful for further evaluation. ap chest x-ray (): a tracheostomy tube is in place, 4.8 cm from the carina. a vp shunt catheter is seen overlying the left chest, unchanged from prior exams. the lung volumes are low. a linear opacity at the right base and mild volume loss is consistent with atelectasis. left basilar atelectasis is also present. this is similar in appearance to the prior chest radiograph in . there is no pulmonary edema, pleural effusion, or pneumothorax. the cardiomediastinal silhouette is normal. impression: bibasilar atelectasis. eeg (): at baseline, the recording showed periodic lateralized epileptiform discharges (pleds) especially in the right frontal central area. in addition, there were three electrographic seizures with very rapid, rhythmic hz sharp wave activity just posterior to the frontal sharp waves on the right side. the seizures lasted about a minute. on video, there was no clear or major change in behavior. there was a bit of blinking. in one, in the right hand quivered a bit of the left was patent by blankets. there was no convulsion. abnormality #2: background activity was of very low voltage broadly over the left side. hyperventilation: could not be performed. intermittent photic stimulation: could not be performed. sleep: the patient appeared to be awake between seizures, but no normal waking or sleep patterns were evident. cardiac monitor: showed a generally regular rhythm. impression: abnormal eeg due to the rightsided pleds, especially frontally, with the three electrographic seizures described above, with minimal clinical signs. eeg (): began just after midnight on the night of the 31st and continued through 9:00 the next morning. throughout the record, it showed extremely frequent sharp wave and following slow wave discharges widely over the right hemisphere and particularly in frontal regions, but the periodic appearance had diminished. the electrographic seizures, on the other hand, increased in frequency. bursts of spikes and sharp waves were frequent sometimes for just two to three seconds but often in longer runs constituting electrographic seizures. these seizures occurred about three times an hour and were not diminishing by the time of the end of the recording. they usually remained restricted to the right hemisphere. on video, there was usually no movement evident but, on one occasion, there was turning of her eyes to the left. spike detection programs: showed extremely frequent rightsided spikes and sharp waves. seizure detection programs: showed the same electrographic seizures described above. pushbutton activations: there were none. sleep: no normal waking or sleep patterns were evident. cardiac monitor: showed a generally regular rhythm. impression: this telemetry showed a disorganized background throughout with extremely frequent epileptiform discharges broadly over the right hemisphere. periodic discharges were no longer evident, but there were extremely frequent bursts of more rapid epileptiform discharges for a few seconds at a time and also electrographic seizures lasting a minute or more, about three times an hour, possibly increasing toward the end of the record. eeg (): began at 7:01 on the morning of and showed a low voltage fast pattern in all areas, likely reflecting medication use. there continued somewhat periodic polysharp wave discharges broadly over the right hemisphere, appearing every three seconds or so. on the first morning, the sharp waves progressed to rapid, hz sharp and spike activity especially in the right temporal region, spreading more broadly over the right hemisphere and becoming seizures lasting three to four minutes at a time. typically, on video, there was no motor phenomena. the seizures occurred about three times an hour in the morning. by the afternoon, seizures were occurring a bit more than once an hour and, after 2:00, there were three seizures until the end of the recording at 7:00. spike detection programs: showed the same innumerable right hemisphere spikes and sharp waves. seizure detection programs: showed the same seizures described above. pushbutton activations: there were none. sleep: no normal waking or sleep patterns were evident. cardiac monitor: showed a generally regular rhythm. impression: this telemetry showed continued right hemisphere periodic sharp wave discharges throughout, often at about one every two seconds. there were also very frequent three to four minute long electrographic seizures beginning in the same area and spreading through most of the right hemisphere but usually with no motor findings on video. over the course of the recording, seizures decreased markedly in frequency. eeg (): began at 7:01 on the morning of and continued until 8 the next morning. for much of the record, it showed less frequent blood rate hemisphere sharp waves with some following slowing than it had shown on earlier recordings. these sharp waves did not appear periodically. there were 13 electrographic seizures recorded. the first was at 7:29 on the first morning. it began in the same area as the right temporal sharp waves, maximal at t4-t6, with a "pleds plus" onset and rapid sharp activity following the larger sharp wave. this rhythmic sharp activity remained restricted to the right temporal region for about 12 seconds, and then there was sharp and very irregular hz activity in all areas for about one minute. on video, there was no clear left facial twitching or other movement. very similar seizures occurred later. they were somewhat less frequent beginning on the evening of the 23rd. a few were associated with facial twitching. spike detection programs: showed the same very frequent right hemisphere discharges. seizure detection programs: showed the same seizures described above. pushbutton activations: there were none. sleep: no normal waking or sleep patterns were evident. cardiac monitor: showed a generally regular rhythm. impression: this telemetry showed a disorganized background throughout with very frequent right hemisphere sharp and slow wave discharges, maximal in the right anterior to mid temporal region. these discharges occurred at least every few seconds but were not rhythmic or periodic. the same area was associated with the onset of all the electrographic and clinical seizures described above. seizures lasted for a minute or so and often had no clinical correlate. they were far less frequent than they were a few days earlier. eeg (): began at 7:01 on the morning of and continued for 24 hours. at the onset, it showed a very low voltage background in all areas. frequencies were generally faster, but there was widespread slowing over the right hemisphere, and there were area frequent moderate voltage polymorphic sharp waves seen broadly over the right side particularly in central and temporal areas. these sharp waves were not rhythmic or periodic. the record also showed three electrographic seizures, all beginning in the same area as the sharp waves just described. typically, the sharp waves became more periodic, at about 1 hz, four minutes before the seizure. on video, there was no facial twitching or other clear motor sign of the seizure. they lasted about a minute. spike detection programs: showed the same very frequent right hemisphere especially central temporal, polymorphic sharp wave discharges. overall, they became less frequent over the course of the recording and gave way to irregular slowing. there were exceptions with more rapid and periodic discharges for short periods. seizure detection programs: showed the same seizures described above at other periods of more rhythmic rightsided sharp waves. pushbutton activations: there was a single activation for movement or technical reasons, likely a mistake in activation. there were none for clinical events. sleep: no normal waking or sleep patterns were evident. cardiac monitor: showed a generally regular rhythm. impression: this telemetry showed a lower voltage fast background, likely indicative of medication effect. there continued to be prominent slowing broadly over the right side, and there were very frequent right central temporal sharp wave discharges. these are far less rhythmic than on earlier recordings. in the same area was involved three clinical seizures, around noon, at 7 in the evening, and just before midnight. the seizure frequency was markedly reduced from that on earlier days. brief hospital course: ms. is a 42 yo bed-bound, non-verbal f with seizure disorder tbi () s/p r hemicraniectomy and sdh evacuation, r frontal lobectomy and vp shunt who initially presented to ed on with malfunctioning peg tube. # neuro: while in the ed, patient had a witnessed seizure, semiology apparently convulsions of lle and ?lue with possible l eye deviation, requiring ativan 6mg iv. vpa level was found to be 29 despite recent dose increase to 750mg tid, so most likely reason for her seizure was suspected missed doses of aeds (vpa + keppra) secondary to blocked peg tube. she was loaded with iv vpa and keppra in the ed. nchct also showed acute on chronic l sdh and of l lateral ventricle, so vps causing sdh could have been contributing. toxic-metabolic workup was otherwise negative. 20-minute eeg subsequently showed multiple right-sided pleds and 3 electrographic seizures, so patient was admitted to the epilepsy monitoring unit for closer monitoring. in the hospital, patient remained on bedside eeg for five days. on eeg she initially was found to be having extremely frequent epileptiform discharges and electrographic seizures located over the right hemisphere with few clinical correlates (except for occasional left facial twitching and left hand twitching): diagnosis was non-convulsive status epilepticus. accordingly, her anti-epileptics were aggressively uptitrated. first her keppra was increased to 2000mg iv bid. then she was started on standing lorazepam. next, she was started on trial of lacosamide for non-convulsive status. her seizure frequency improved greatly after uptitration of these meds, and her mental status seemed to improve slightly in that she was more responsive to examiners with fewer nystagmoid eye movements on day of discharge. her discharge aed regimen is as follows: vpa 750mg tid (home dose), keppra 2000mg , lacosamide 150mg , and lorazepam 0.5mg tid. plan is for her to taper the lorazepam to off over the next 15 days: 0.5mg tid x5 days, then 0.5mg x5 days (starting ), then 0.5mg daily x5 days (starting ), then stop. # vp shunt: nchct in the ed revealed vps , vps was reprogrammed by neurosurgery. patient will follow up with neurosurgery (dr. in 2 weeks for repeat nchct and evaluation of vps. # gi: on hd #2 patient's damaged peg tube was replaced under flouroscopy by interventional radiology. after this it functioned without any further issues. she will follow up with ir q3 months for routine replacement of peg tube (to be scheduled by ir). # id: no active issues during hospitalization. # cv: continued home metoprolol for htn. # chronic problems - s/p tbi: continued home baclofen (for muscle contractures) and amantadine (for arousal) + percocet prn pain - depression: continued home sertraline - s/p tracheostomy: continued home albuterol + ipratropium nebs prn - gi ppx: continue home ranitidine - dvt ppx: sc heparin, pneumoboots - precautions: seizures and falls ================================= transitions of care: - patient should taper lorazepam on the following schedule: 0.5mg tid x5 days, then 0.5mg x5 days (starting ), then 0.5mg daily x5 days (starting ), then stop. - if patient has behavioral issues in the future, should consider tapering keppra as she is currently on high dose (2000mg ). - studies pending on discharge = lacosamide level and levetiracetam level from medications on admission: the preadmission medication list is accurate and complete. 1. albuterol 0.083% neb soln 1 neb ih q6h:prn dyspnea 2. amantadine 100 mg po tid 3. baclofen 10 mg po tid:prn muscle spasm 4. ipratropium bromide neb 1 neb ih q6h:prn dyspnea 5. levetiracetam oral solution 750 mg po bid per g tube 6. metoprolol tartrate 12.5 mg po bid 7. endocet *nf* (oxycodone-acetaminophen) 5-325 mg oral q4 hrs: prn pain 8. ranitidine (liquid) 150 mg po bid 9. valproic acid (as sodium salt) *nf* 250mg/5ml (15 ml total) ml oral tid take 15 ml (750mg) three times daily per g tube 10. acetaminophen (liquid) 650 mg po q6h:prn pain 11. bisacodyl 10 mg pr every other day 12. docusate sodium (liquid) 100 mg po bid 13. polysorbate 80-glycerin *nf* dosage unknown ou unknown 14. loperamide 2 mg po bid:prn loose stools 15. psyllium 1 pkt po frequency is unknown 16. sodium chloride nasal spry nu 17. sertraline 50 mg po daily discharge medications: 1. acetaminophen (liquid) 650 mg po q6h:prn pain 2. albuterol 0.083% neb soln 1 neb ih q6h:prn dyspnea 3. amantadine 100 mg po tid 4. baclofen 10 mg po tid:prn muscle spasm 5. bisacodyl 10 mg pr every other day 6. docusate sodium (liquid) 100 mg po bid 7. ipratropium bromide neb 1 neb ih q6h:prn dyspnea 8. metoprolol tartrate 12.5 mg po bid 9. ranitidine (liquid) 150 mg po bid 10. sodium chloride nasal spry nu 11. endocet *nf* (oxycodone-acetaminophen) 5-325 mg oral q4 hrs: prn pain 12. loperamide 2 mg po bid:prn loose stools 13. polysorbate 80-glycerin *nf* 1 application ou frequency is unknown 14. psyllium 1 pkt po bid:prn constipation 15. sertraline 50 mg po daily 16. levetiracetam oral solution mg po bid rx *levetiracetam 500 mg/5 ml (5 ml) 20 ml by mouth twice a day disp #*1 bottle refills:*3 17. valproic acid (as sodium salt) *nf* 750 mg oral tid reason for ordering: wish to maintain preadmission medication while hospitalized, as there is no acceptable substitute drug product available on formulary. 18. lacosamide 150 mg ng rx *lacosamide 10 mg/ml 15 ml by mouth twice a day disp #*1 bottle refills:*3 19. lorazepam 0.5 mg ng q8h rx *lorazepam 0.5 mg 1 tablet(s) by mouth as directed disp #*50 tablet refills:*0 20. outpatient lab work please check valproate (depakote) level and liver function tests (ast, alt, tbili, alkaline phosphatase) in one week and fax results to dr. (fax #). discharge disposition: extended care facility: discharge diagnosis: acute problems: 1. nonconvulsive status epilepticus 2. blocked peg tube 3. vp shunt over-drainage chronic problems: 1. status-post traumatic brain injury discharge condition: mental status: confused - sometimes. level of consciousness: lethargic but arousable. activity status: bedbound. neuro exam: eyes open spontaneously. nystagmus on leftward gaze, eyes move in all directions but left gaze preference. right arm contracted, left arm and leg extensor posturing. toes upgoing bilaterally. discharge instructions: dear ms. , you were brought to the hospital after developing a blockage in your peg tube. in the emergency department, you had a seizure which was likely caused by missing doses of your anti-epileptic medications. you received ativan and and extra iv dose of keppra and depakote in the ed and your seizure stopped. you also had a vp shunt study which showed that your shunt was probably draining too much, so neurosurgery reprogrammed the shunt so it would drain less. you were then admitted to the hospital, where your peg tube was replaced by interventional radiology. however, an eeg then revealed that you were having very frequent, long seizures on the right side of your brain (not associated with actually physical . therefore you were started on long-term eeg monitoring and your anti-epileptic drugs were increased to treat the seizures. over time, the frequency of the seizures decreased. you are being discharged back to your long-term care facility and will follow up with neurology to make sure your seizures have continued to improve. . please attend the outpatient appointments listed below with neurosurgery (to follow up on your vp shunt adjustment) and neurology (to follow up on your seizures). . we made the following changes to your medications: 1. increased keppra (levetiracetam) from 750mg twice daily per g-tube to 2000mg twice daily per g-tube 2. started vimpat (lacosamide) 150mg twice daily per g-tube 3. started ativan (lorazepam) 0.5mg three times daily per g-tube. lorazepam should be tapered as follows: -- decrease to 0.5mg twice daily starting in five days () -- decrease to 0.5mg once daily five days after that () followup instructions: check liver function tests and valproate level 1 week after discharge. you will be contact by interventional radiology to schedule routine peg tube replacement in the next 3 months. department: neurology when: friday at 1 pm with: , md building: sc clinical ctr campus: east best parking: garage department: neurology when: friday at 1 pm with: , md building: sc clinical ctr campus: east best parking: garage department: radiology when: wednesday at 8:45 am with: cat scan building: cc campus: west best parking: garage department: neurosurgery when: wednesday at 9:30 am with: , md building: lm campus: west best parking: garage procedure: replacement of gastrostomy tube diagnoses: depressive disorder, not elsewhere classified grand mal status surgical operation with implant of artificial internal device causing abnormal patient reaction, or later complication,without mention of misadventure at time of operation subdural hemorrhage tracheostomy status mechanical complication of gastrostomy mechanical complication of nervous system device, implant, and graft late effects of motor vehicle accident other conditions of brain late effect of intracranial injury without mention of skull fracture surgical operation with formation of external stoma causing abnormal patient reaction, or later complication, without mention of misadventure at time of operation 

Answer: The patient is high likely exposed to