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: fioricet attending: chief complaint: language and behavioral changes major surgical or invasive procedure: none history of present illness: 53 rhw with poorly controlled dm, anemia, hearing loss s/p cochlear implant on the right was brought to the ed from osh. she lives alone and works as a teacher in school. she was noted to have gradual onset progressive personality change in the school for last 4-5 days. she was noted to be more irritable and was noted to be "not her self." today the problems got worse and when she was teaching she wrote things on the blackboard which didnt make any sense at all. she was noted to have speech problems and would not answer questions in the correct way. she was not weak or didnt have any other neuro symptoms. she was taken to ed where vitals : 97.9, 18, 154/83, 62 reg, 99 ra. she was noted to say "i dont know why i am here" and said that her dob was though she wrote on paper. she underwent labs which were not available in chart. she underwent ct head which showed a hypodense lesion in left temporal parietal area. she was transfered to ed for further eval. past medical history: hypertension, dm type 2 on insulin recently, mitochondrial myopathy (as shown by muscle biopsy report in from ) asthma hearing loss, with cochlear implant hereps genitalis social history: works as a teacher. ex smoker, social alcohol use. no drugs. lives alone. family history: maternal uncle with hearing loss, father had a stroke in the setting a head injury at ? age physical exam: admission physical exam: vitals: 98.8 60 149/90 18 100% gen: nad, non cooperative; no dysmorphic features heent: mmm neck: no lad; no carotid bruits; full range neck movements lungs: clear to auscultation bilaterally heart: regular rate and rhythm, normal s1 and s2, no murmurs, gallops and rubs. abdomen: normal bowel sounds, soft, nontender, nondistended extremities: no clubbing, cyanosis, ecchymosis, or edema skull: no bruits. mental status: awake and alert, indifferent affect, very inattentive and answers either : i dont know or i am fine to any questions. says some spontaneus speech without any meaning. exam extremely difficult owing to deafness. when given pen and paper, said ( her sisters name), wrote k on the papar and then stopped and said "i dont know". other parts of exam not possible to test. cranial nerves: i: not tested ii: pupils . fundi : no papilledema. blinks to threat on both sides. iii, iv, vi: extraocular movements intact without nystagmus. no ptosis. v: facial sensation intact to light touch and pinprick. vii: facial movement symmetrical; no facial droop. viii: hearing severely impaired. has cochlear implant. ix: palate elevates in midline. xii: tongue protrudes in midline, no fasciculations. : sternocleidomastoid and trapezius normal bilaterally. motor system: bulk normal. tone normal bilaterally. mild right pronator drift. gives good effort and resistance, but formal power exam was difficult to obtain owing to inattention reflexes: dtr : 2 plus and normal. toes: downgoing on left, up on right sensory system: withdrawas to pain on both sides. coordination: difficult to test. gait: defd. _____________________________ discharge exam: physical examination: vs t: 98.5/97.9 hr: 65 bp: 102/62 (100-150s) rr: 13 sao2: 98% ra general: awake, nad, lying in bed comfortably / head: nc/at, no conjunctival icterus / neck: supple / cardiovascular: rrr, no m/r/g / pulmonary: poor cooperation, no crackles or wheezes / abdomen: soft, nt, nd, +bs, no guarding / extremities: no edema, palpable radial pulses / skin: no rashes or lesions neurologic examination: - mental status - lethargic, opens eyes spontaneously. verbalizes "i'm fine" and "that's fine, that's ok" to orientation questions and written questions. can write appropriate answers to written questions. partially intact written comprehension. attends to examiner. inattentive, does not read whole sentences reliably. follows single step written commands but not two steps. slowed responses. no left right agnosia. no acalculia. - cranial nerves - perrl 2->1.5. no blink to threat. crosses midline bilaterally. no facial asymmetry. severe hearing loss bilaterally, even with hearing aid. does not protrude tongue. - motor - can rearrange herself in bed. spontaneous bue, can hold pen and write with rh. bilateral drift but not full effort, inattentive. 5/5 strength in all four extremities - sensory - localizes to noxious in all four extremities - reflexes = ] l 1 1 1 1 1 r 1 1 1 1+ 1 plantar response extensor on r, mute on l. gait: able to walk slowly without taking steps to catch herself, tandem was not attempted pertinent results: admission labs: 04:55pm blood esr-10 02:35pm blood ck(cpk)-269* 02:35pm blood ck-mb-9 ctropnt-<0.01 04:10pm blood %hba1c-6.5* eag-140* 02:35pm blood triglyc-77 hdl-87 chol/hd-2.4 ldlcalc-108 02:35pm blood hcg-<5 07:20am blood tsh-1.3 12:40pm blood osmolal-274* 12:12am blood asa-neg ethanol-neg acetmnp-neg bnzodzp-neg barbitr-neg tricycl-neg wbc 10.7, hgb 12, plt 380, na 133, k 4.3, cl 101, hco3 19, bun 12, cr 0.5, glu 138, ca 8.9, mg 2.0, phos 3.4 eeg impression: this is an abnormal portable eeg because of a slow and disorganized background reaching up to a maximum of 7 hz posteriorly indicative of mild encephalopathy. additionally occasional left temporal slowing was seen indicative of subcortical dysfunction. no clear epileptiform discharges or electrographic seizures were seen. imaging: ct head : impression: limited study given significant streak artifacts from right-sided cochlear implant. however, there is hypodensity of the left temporal lobe extending into the parietal lobe with corresponding sulcal effacement. there is no acute hemorrhage. differential includes infarct, encephalitis, or less likely underlying mass with edema. cta : impression: 1. unchanged cytotoxic edema in the left temporal lobe, sparing its medial portion, and in the inferior left parietal lobe. the sparing of the medial temporal lobe makes an infarction slightly more likely than encephalitis. 2. unremarkable neck cta. 3. no evidence of intracranial arterial occlusion or hemodynamically significant stenosis. 4. arterial and venous enlargement in the area of left temporal and parietal cytotoxic edema, most likely due to hyperemia, since no definite abnormal vascular nidus is seen to clearly suggest a pathologic arteriovenous connection. a follow-up cta is suggested for reassessment when the clinical grounds for hyperemia resolve. if this appearance persists, then a conventional cerebral angiogram could be considered for further evaluation. an addendum to this report may be issued when the curved reformatted and volume-rendered three-dimensional images are finalized by the imaging lab. eeg : impression: this is an abnormal routine eeg because of the bursts of left temporal slowing indicative of subcortical dysfunction. in addition, throughout the recording, the background was very slow at 4 hz with bursts of generalized slowing indicative of a moderate to severe encephalopathy which is etiologically non-specific. no clear epileptiform discharges or electrographic seizures were seen. eeg : impression: abnormal eeg due to the slow and disorganized low voltage background with infrequent generalized slowing. this indicates a widespread encephalopathy. medications, metabolic disturbances, and infection are among the most common causes. excessive drowsiness is also a possible explanation of the background patterns, but this might also indicate an encephalopathy. there were no areas of prominent focal slowing, and there were no clearly epileptiform features. ct head : impression: stable appearance of cytotoxic edema in the left temporal and parietal lobes, compatible with a recent infarction in the left middle cerebral artery territory. no acute hemorrhage or increased mass effect. no evidence of other new intracranial abnormalities. microbiology: 3:40 am urine source: catheter. **final report ** urine culture (final ): klebsiella pneumoniae. >100,000 organisms/ml.. piperacillin/tazobactam sensitivity testing available on request. sensitivities: mic expressed in mcg/ml _________________________________________________________ klebsiella pneumoniae | ampicillin/sulbactam-- 4 s cefazolin------------- <=4 s cefepime-------------- <=1 s ceftazidime----------- <=1 s ceftriaxone----------- <=1 s ciprofloxacin---------<=0.25 s gentamicin------------ <=1 s meropenem-------------<=0.25 s nitrofurantoin-------- 64 i tobramycin------------ <=1 s trimethoprim/sulfa---- <=1 s ___________________________________________________ brief hospital course: is a 53 yo woman with diabetes, hearing loss w/ a cochlear implant, anemia and presumed melas who presented with personality changes and speech difficulty x4-5 days found to have a l parietotemporal hypodensity on ct scan, that given her post-infarct sx was not c/w a vascular territory, with hospital course c/b apneic episode from presumed seizure activity and increasing intermittent somnolence. . # neuro: when patient presented her ct showed a hypodensity that could be c/w an inferior mca territory, but this did not fit with her sx, given that she had fluent and appropriate language on our exam. this type of patchy stroke-like episode would be c/w melas. on admission, we were told that pt had an unknown myopathy, hearing loss (with a maternal uncle also with hearing loss), diabetes, and small stature. we started to consider that she may have melas at that time point. we found out from her family that she had a muscle biopsy done at this year, and that report was diagnostic of a mitochondrial disorder. the muscle biopsy showed ragged red fibers on gomori trichrome staining. there were patchy areas of cytochrome oxidase deficiency. this, and her history, with the recent stroke made us feel that she likely has melas although she is much older than the usual presentation. she has an unknown psychiatric history that we were unable to get more information on, but it is possible that she had prior "stroke-like" episodes in the past that were misdiagnosed as psychiatric symptoms. she was started on creatine, coenzyme q10, l-carnitine, and l-arginine which are the only known treatments for melas that have been shown to be somewhat effective. on the morning of she was found in her room apneic, but quickly regained spontaneous respirations, and was sent to the icu for airway protection, but did not require intubation. her sodium was found to be 117 (it had been trending down, see below), and it was presumed that she had had a seizure. while in the icu, she was intermittently somnolent and then agitated. we had ltm placed, but this showed only diffuse slowing and no seizure activity to explain her behavior. she was started on a full dose aspirin. she was initially on acyclovir until her hsv pcr returned negative given her hx of herpes genitalis, temporal lobe hypodensity on ct and behavior changes. she was given hypertonic saline to correct her sodium, and when stabilized, was started on nd, then was sent back to the neurology floor. over the next few days, her level of consciousness gradually improved to the point that she was readily awake and arousable and could converse and follow commands (primarily written commands due to her hearing loss and somewhat dysfunctional hearing aid). she was slightly weaker in her right arm and leg compared to her left, although confrontational strength testing was not able to be performed reliably due to difficulty with communication, fatigue, and inattention. # cards: because her apneic episode was unwitnessed, and from an unclear cause, we got an echo which was unremarkable, and she had repeated cardiac enzymes that were negative. she did have an ekg 1 hour after the apneic episode that showed some mild deepening of her previously noted v1-v6 st depressions. these changes then resolved on a repeat ekg. it was felt that because her cardiac enzymes were negative the ekg changes were likely demand related in the setting of another process that was most likely seizure. this did not recur and her slightly elevated ckmb trended down. . # pulm: she did not require any intubation throughout her stay here. she has a hx of asthma, but this is exercise induced. she did not require nebulizer treatments while inpatient. . # renal: pt with hyponatremia that developed after her stroke, so it was presumed to be siadh. it seemed to worsen with ivf, so she was fluid restricted. however, when she was in the icu with her na at 117, an ij was placed and her cvp's were noted to be . she was given hypertonic saline and her sodium improved, but given her low cvp's it was felt that her hyponatremia was likey hypovolemic hyponatremia. she was started on ns ivf after we stopped her hypertonic saline and her sodium continued to improve, making siadh very unlikely as the cause. this resolved with normal saline and remained stable by discharge. # endo: pt with known dm, but should not take metformin (which she had been on) with melas. we put her on an iss while an inpatient. her medication regimen will need to be adjusted as an outpatient so her sugars are controlled but not on metformin. . # id: patient had a u/a that showed elevated wbcs and rbcs that was felt to be because of a difficulty foley placement. however, when pt's ucx grew >100,000 klebseilla that was ceftriaxone sensitive, we put her on a 7 day course of ceftriaxone starting on . . # code/contact: full /sister- - ng labs: melas mutational analysis anticardiolipin antibodies beta 2 glycoprotein antibodies transtional care issues: recheck serum electrolytes (chem-10) in 7 days and 14 days after discharge continue supplements for melas (coenzyme q10, l-carnitine, creatine, l-arginine) the patient has followup with dr. in the clinic and dr. in the clinic. please make the family aware of these appointments. medications on admission: (confirmed with pcp after pt was admitted): 1)metformin 500mg qd 2)citalopram 10mg qd 3)glimipride 10mg qd 4)advair 1 puff 5)ventalin 2 puffs q6h prn discharge medications: 1. heparin (porcine) 5,000 unit/ml solution sig: one (1) injection three times a day. 2. coenzyme q10 400 mg capsule sig: one (1) capsule po daily (daily): for melas. 3. levocarnitine 330 mg tablet sig: three (3) tablet po qam (once a day (in the morning)): for melas. 4. aspirin 81 mg tablet, chewable sig: one (1) tablet, chewable po daily (daily). 5. omega-3 fatty acids capsule sig: one (1) capsule po daily (daily). 6. multivitamin tablet sig: one (1) tablet po daily (daily). 7. lisinopril 5 mg tablet sig: one (1) tablet po daily (daily): hold for sbp < 100. 8. albuterol sulfate 90 mcg/actuation hfa aerosol inhaler sig: inhalation every four (4) hours as needed for shortness of breath or wheezing. 9. cefpodoxime 200 mg tablet sig: one (1) tablet po twice a day for 4 days: for treatment of klebsiella urinary tract infection. 10. creatine monohydrate 1.5 gram/15 ml liquid sig: 4800 (4800) mg po tid (3 times a day). 11. arginine (l-arginine) 500 mg tablet sig: twenty (20) tablet po daily () as needed for melas. discharge disposition: extended care facility: - discharge diagnosis: primary: melas secondary: mitochondrial myopathy, diabetes mellitus, sensorineural/conduction hearing loss s/p cochlear implant, hyponatremia, hypomagnesemia, hypophosphatemia discharge condition: mental status: confused - sometimes. level of consciousness: lethargic but arousable. activity status: out of bed with assistance to chair or wheelchair. neurologic: arousable, sometimes inattentive but at other times attends to the examiner, verbalizes but sometimes inappropriately (due to very poor hearing, even with hearing aid), responds appropriately to written questions and follows written commands. mild right arm and right leg weakness compared to her left, but provides at least antigravity strength with some resistance in all four limbs. discharge instructions: dear ms. , it was a pleasure taking care of you during your stay at . you were transferred to our hospital for language problems and were found to have had a stroke. we think that you have a genetic disorder called melas that caused you to have a stroke-like episode. we started you on enzyme supplementation that may help improve the symptoms of melas (which stands for mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes). you were also treated for a urinary tract infection, hyponatremia, hypomagnesemia, and hypophosphatemia. we made the following changes to your medications: 1) we stopped your metformin (you can no longer take this medication) 2) we started you on coenzyme q10 3) we started you on l-carnitine 4) we started you on creatine monophosphate 5) we started you on l-arginine 6) we started you on fish oil 7) we started you on a multivitamin because of your mitochondrial disease, you can never use the following medications: valproic acid (and derivatives), metformin, barbiturates, tetracyclines, aminoglycosies, chloramphenicol. it you experience any of the below listed danger signs, please contact your doctor or go to the nearest emergency room. followup instructions: provider: , , md -, phone: date/time: 10:00 provider: , md phone: date/time: 2:30 provider: . & phone: date/time: 2:30 procedure: venous catheterization, not elsewhere classified spinal tap incision of lung enteral infusion of concentrated nutritional substances diagnoses: urinary tract infection, site not specified unspecified essential hypertension diabetes mellitus without mention of complication, type ii or unspecified type, not stated as uncontrolled hyposmolality and/or hyponatremia asthma, unspecified type, unspecified disorders of phosphorus metabolism long-term (current) use of insulin encephalopathy, unspecified cerebral artery occlusion, unspecified with cerebral infarction disorders of magnesium metabolism disorders of mitochondrial metabolism 

Answer: The patient is high likely exposed to