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: oxycodone / opioid analgesics attending: chief complaint: found down major surgical or invasive procedure: lumbar puncture. history of present illness: 70 yo ho hep c, dm2, cad s/p cabg, ppm, hyperchol, htn and polysubstance abuse including etoh and narcotics brought in by ems after being found at home confused with a clonidine patch on by his vna. neurology was consulted upon presentation to the ed and their exam at that time was notable for severe inattention and word finding difficulty with phonemic paraphrasias but exam was otherwise nonfocal and there were no signs of aphasia. additional assessment of patient's mental status was confounded by his severe inattention. there was no ophthalmoplegia to suggest a wernicke's encephalopathy however patient did seem to confabulate at times suggesting possible korsakoff's syndrome. he was noted to have bilateral dysmetria likely associated with chronic alcohol use. neuro impression at that time was that deficits were most c/w a delirium related to a toxic metabolic infectious etiology, but could not exclude seizure activity or post-ictal confusion. . ct was obtained in the ed on which showed no bleed nor edema, but neuro felt that, given his vascular risk factors, it would be reasonable to evaluate for interval change after 3 days with a noncontrast head ct. . because of severe agitation, he required 4 point leather restraints he received 6mg ativan and 15mg of haldol in ed and was transferred to the micu. past medical history: -coronary artery disease status post coronary artery bypass graft , status post failed percutaneous transluminal coronary angioplasty in secondary to tortuous vessels-->1. native two vessel coronary artery disease. 2. unsuccessful attempt at intervention on mid-rca stenosis. -status post pacer placement for bradycardia -status post atrial flutter ablation in -hypertension. -hyperlipidemia. -anemia. -dyspepsia. -syncope. -cirrhosis with a positive hepatitis c virus. -type ii diabetes mellitus. -80% vertebral artery stenosis. -severe restless legs. -depression and bipolar disorder. -hypothyroidism. social history: lives in a senior housing project. long h/o etoh dependence but sober for "many years" after aa, although endorses occasional beer, last drink he reports a few months ago. has experienced one withdrawal seizure in past. heavy use of amphetamines in . h/o abusing morphone, dissolved it and injected it. off narcotics after several detoxs. quit tob in . family history: father died at age 69 from a myocardial infarction and patient's mother died at age 86 and did have cardiac arrhythmias. physical exam: t-95.4 bp-97/40 hr-62 rr- o2sat 95%ra gen: elderly gentleman in nad, requesting sleeping pill. alert and oriented to person, place and date although thinks it's the 5th. heent: eomi, no nystagmus appreciated, moist oral mucosa, perrl neck: supple, no carotid or vertebral bruit. cv: rrr, nl s1 and s2, no murmurs/gallops/rubs although distant heart sounds lung: fine bibasilar rales l>r abd: obese, +bs soft, non tender not distended, no rebound, unable to appreciated ascites nor hsm but difficult given habitus ext: trace edema, no asterixis neuro: not displaying confabulation currently. cn ii-xii intact. ms . toes downgoing. + dyetria b/l w/ finger to nose and heel to shin. pertinent results: admission labs: ================ 14.4 3.7 >-------< 100 41.6 mcv 90 neuts 63.8 lymphs 24.9 monos 7.4 eos 3.5 baso 0.2 pt 13.4 ptt 27.3 inr 1.2 lactate 1.7 138 102 21 ----|----|-----< 224 5.0 23 1.4 . ca 9.9 phosphate 4.6 mg 1.7 alt 44 ast 75 alk phos 71 amylase 35 total bili 1.0 lipase 18 alb 4.5 serum tox: negative ua: 500 protein, 100 glucose . studies: ======== chest (pa & lat) impression: no acute cardiopulmonary disease. . ct head w/o contrast impression: 1. no evidence of intracranial hemorrhage or edema. 2. sinus mucosal disease with near complete interval opacification of the left side of the sphenoid sinus. of note, mri with diffusion-weighted imaging is most sensitive for acute ischemia. . ekg sinus rhythm. the p-r interval is prolonged. there are q waves in the inferior leads consistent with prior myocardial infarction. diffuse non-specific st-t wave changes. compared to the prior tracing st-t wave changes are more diffuse and atrial bigeminy is no longer present. . chest port. line placement portable ap chest radiograph compared to . the right subclavian line was inserted with its tip projecting at the level of low svc. there is no pneumothorax, apical hematoma or other complications. the heart size is mildly enlarged but unchanged as well as there is no change in the stable appearance of the mediastinum. the overall lung volumes have decreased compared to the previous study with subsequent increased _____ of the pulmonary vasculature with no pulmonary edema demonstrated. the pacemaker leads terminate in right atrium and right ventricle, unchanged. there is no pleural effusion or pneumothorax. . csf negative for malignant cells. . ct head w/o contrast impression: no acute intracranial process. no interval changes since . . eeg impression: this is an abnormal routine eeg due to the slow and disorganized background with bursts of generalized slowing suggestive of an encephalopathic process. infection, metabolic disturbances, and medications are among the most frequent causes of encephalopathy. no clear epileptiform features or electrographic seizures were seen during the recording. . ekg atrial fibrillation and ventricular paced rhythm. intermittent intrinsic a-v conduction. compared to the prior tracing of no diagnostic interim change. tracing #1 . video oropharyngeal swallow impression: 1. moderate oral and pharyngeal dysphagia, with mild delay in swallow initiation and reduced laryngeal valve closure. 2. silent aspiration with ineffective cued coughs . ekg atrial fibrillation and ventricular paced rhythm and more frequent intrinsic a-v conduction. compared to the prior tracing of no diagnostic interim change. tracing #2 . eeg impression: abnormal eeg due to the slow and disorganized background. this indicates a widespread encephalopathy. medications, metabolic disturbances, and infection are among the most common causes. there were no areas of persistent focal slowing, and there were no epileptiform features. . ct head w/o contrast impression: no significant change since with no acute intracranial abnormalities. . liver or gallbladder us (single organ) impression: no ascites. . ekg regular ventricular pacing with probable underlying atrial fibrillation. compared to tracing of all the beats are ventricular paced. . brief hospital course: mr. is a 70 y/o male with cad, dm, htn, hep c cirrhosis, p/w mental status change is setting of possible substance abuse at home, hospital course c/b prolonged delirium. . # delirium: the patient presented after initially found at home in a state of confusion by his vna. neurology was consulted upon presentation to the ed and their exam at that time was notable for severe inattention and word finding difficulty with phonemic paraphrasias but exam was otherwise nonfocal and there were no signs of aphasia. he was noted to have bilateral dysmetria likely associated with chronic alcohol use. neuro impression at that time was that deficits were most c/w a delirium related to a toxic metabolic infectious etiology. ct was obtained in the ed on which showed no bleed nor edema. pt received ativan and haldol in ed and transferred to the micu. in the micu, he was continued on ciwa protocol w/ standing valium out of concern for possible postictal state as well as etoh withdrawal. haldol was discontinued to prolonging qtc (reportedly 470s at longest). urine and serum tox were +only for benzos, which he had been receiving. infectious workup included cxr which did not reveal infiltrate, ua which showed rare bacteria, but no pyuria, and blood cultures which have shown ngtd. b12 and folate wnl. additionally, an lp was performed which had no rbcs nor wbcs, normal glucose, but did show elevated protein; gram stain of csf showed no pmns. rpr and vdrl were sent and were unrevealing. he was subsequently called out to the floor for further evaluation and management of his delirium. . on the floor () a repeat contrast ct was done which showed no change from the previous on , an eeg done showed no evidence of seizure activity. since that time, his neurologic status slowly began to improve. once patient able to communicate better, he admitted to taking valium at home. psychiatry also consulted and felt that the patients delirium was likely secondary to his valium overdose and that this would take time for the medication to clear his system. patient was started on standing haldol for agitation and had a 1:1 sitter for some time while on the floor. on he was persistantly agitated and we noted some resting hand tremor and rigidity as well as a concern for a wide based gait. this was felt to be secondary to the haldol. his medications were changed to zyprexa. given the delirium did not appear to be improving and was still waxing and ; neurology was re-consulted. neurology felt there was some concern for wernicke's encephalopathy that would take a long period of time to clear. he was started on iv thiamine x 5 daysof which he completed 4 before being changed to po thiamine, which was continued thoughout. also in the differential for the patient's presentation were stroke and ? silent mi. however, repeat head ct was unchanged, and numerous cardiac workups were unrevealing. given his history of hep c, the diagnosis of hepatic encephalopathy was considered as an etiology for his delirium. he was placed on standing tid lactulose. hepatology was consulted who felt that this clinical picture was unlikely due to hepatic encephalopathy, but they recommended continuing lactulose and starting rifaxamin. an abdominal u/s was negative for ascites or a cirrhotic liver. after being on lactulose and rifaximin for some time, these meds did not appear to be affecting his mental status, and they were discontinued. in terms of less likely diagnoses, an hiv test to rule out hiv encephalopathy was negative, and a urine porphobilinogen to rule out acute intermittent porphyria was also negative. psychiatry suggested the possibility of body dementia due to his mild parkinsonian features. an acetylcholinesterase inhibitor was added on the day of d/c. pre-aricept mini mental state exam was 17. . has continued to demonstrate marked improvement and awareness throughout his floor stay. we provided his with non-prescription glasses, as he does wear these at home. however, if possible his home prescription should be pursued as an outpatient. he did complain of insomnia and responded best to a combination of standing mirtazipine and prn ambien (needed often). his major concern was anxiety and a desire to go home to pay rent and take care of his cat. occupational therapy recommended rehab for continued cognitive therapy, and psychiatry confirmed his capacity to decide to go to rehab. . # cad: patient was initially found to have an elevation of his troponins which was concerning given known underlying cad (unable to intervene on mid rca lesion in ; pmibi in showed fixed, no reversible defects). troponin was elevated on presentation at 0.12, peaked at 0.20 on and was trending down to 0.16 on . cks were up, but mb was normal and mb index were negative throughout. ekgs were without significant st/tw changes from old dated . patient was markedly hypertensive on presentation and in the icu to 240s/120s per report so it was felt that the troponins may have risen secondary to subendocardial ischemia in the setting of hypertension. on the floor he had one episode of cp where an ekg was again done which showed a slight st depression. cardiac enzymes were negative at that time. the patient's blood pressure was elevated during this episode and again it was felt that this ekg change (which resolved 1 hour later on subsequent ekg) as likely secondary to subendocardial ischemia from hypertension. his blood pressure medications were uptitrated. his atenolol was increased to 100mg daily. he was continued on the aspirin. in addition, patient had several episodes of chest pain on the floor. it should be mentioned that they were highly inconsistent and occured during his delirium. once his ms cleared there were no complaints of cp. when his prior medical records were reviewed, it became clear that he has presented innumerably to the ed with cp, with numerous negative workups. a specific cp protocol was in effect per his outpatient cardiologist. this was to administer 0.5" of nitro paste or a nitro patch. this worked very well on the floor. he also responded to maalox or tums when it seemed that his cp was not of a cardiac etiology. . # rhythm: patient has a pacer. his ekg showed paced rhythm with underlying afib vs flutter. he would occasionally go from normal sinus rhythm to a.fibb/flutter. patient is s/p a.flutter ablation in past. electrophysiology saw the patient and felt he was paced appropriately. they recommended follow up in three months as an outpatient. . # htn: patient was hypertensive when he was on the floor (out of micu). his bp meds were intially held in the icu but restarted. he was continued on his verapamil, enalapril and hctz. his atenolol was titrated up as well as his verapamil. his lisinopril was also increased, and by the time of discharge he had excellent antihypertensive control with bps largely in the 120-130s. . # cirrhosis: patient has a history of +hep c and heavy etoh hx. not followed in our system for this so status largely unknown. a viral load was sent and was 77,000. no h/o gi bleed, no h/o ascites, no clear h/o hepatic encephalopathy. has stable, very mild transaminitis with a normal bilirubin. inr only mildly elevated to 1.2, albumin normal at 4.2. patient will need outpatient follow up with a hepatologist for further management. liver was consulted for possible hepatic encephalopathy as part of his delirium, who felt that this did not appear to be hepatic encephaloapthy. ammonia levels were checked and were not elevated. lactulose was started, but eventually d/c'ed due to ineffectiveness. . # pancytopenia: chronic. likely represents bm suppressive or infiltrative process and thrombocytopenia consistent with liver disease. it was felt that it may be direct etoh bone marrow toxicity. . # rash - developed a rash on his upper extremities while on a number of new medicines. the rash was felt to be a medication reaction, and began to improve after several meds were discontinued, including laculose/rifaximin/seroquel. it is non-prurutic and continues to clear at time of discharge. . # chronic kidney disease: no labs in our system since , last creatinine was isolated elevation to 1.3 (all those prior were normal). given time lapse since labs and known htn, it is unclear whether he has chronic renal insufficiency secondary to hypertension. patients creatinine increased while on the floor; felt to be secondary to dehdyration and a fena<1. pt received ivf with improvement in his creatinine. once mental status cleared, he was able to hydrate himself and eat accordingly and his renal function remained normal. . # positive urine culture: ua on admission with rare bacteria but 0 wbc, urine culture grew klebsiella pneumoniae. repeat again w/ neg nitrites, neg leukesterase, no wbcs, rare bacteria and 0-2squams. urine culture showed now growth. this was not treated with any antibiotics. a repeat urine culture was equivocal with moderate growth of enterococcus and he completed a 10-day course of ampicllin switched to amoxicillin with a negative confirmatory culture at the end of his treatment. . # dm: patient had refractory diabetes and required a large amount of insulin which was titrated upwards during his stay. at discharge, his requirements were 60 units qhs, 10 units humulog tid with meals, and a humulog sliding scale for extra coverage. the night prior to d/c his was mistakenly not administered, hence his am fsg was quite elevated at 400. he received his this am. throughout the day prior, fsgs were 99 to 116. on the night of discharge, please administer his at 3am and move backwards by 3 hour increments until it is once again administered at 9pm (usual hs). . # hypothyroidism: tsh slightly elevated to 6.2, but in setting of acute illness. ft4 wnl. a repeat tsh was within normal limits. he was continued on home synthroid. . # fen: patient had several video speech and swallow studies because there was a concern for aspiration risk. they suggested silent aspiration, but that that the patient could tolerate a honey thickened liquids and pureed solids.1:1 supervision during meals for feeding. pills were crushed with purees. no straws. . # ? heparin induced thrombocytopenia: his platelets dropped quite suddenly during the course of his hospital stay. his heparin was stopped and a hit antibody was quivocal. a serotonin release assay was sent and results were pending at time of discharge. he received no heparin products but was quite ambulatory ancd active during his floor stay. . # the patient was hypernatremic to 147 on occasion. 1/2 ns was given with resolution. . # was full code throughout medications on admission: 1. aspirin 325mg po daily 2. atenolol 50 mg daily 3. catapres-tts-3 0.3 mg/24hr; 1patch transdermal one time per week 4. enalapril 20mg po bid 5. hydrochlorothiazide 25 mg daily 6. unclear amount of units 7. humalog sliding scale 60-65 units per omr and note 8. lotrimin 1% 1 application as needed for prn itching 9. mirtazapine 60 mg po daily 10. neurontin 600 mg tid-qid prn:pain (total nte 2400 mg/day) 11. verapamil 80 mg po daily 12. desipramine 20 po qhs 13. levothyroxine 25 micrograms po daily 14. tramadol 50mg po q 8hrs 15. lunesta 25po q day 16. uroxatral 10mg po daily 17. actaplus met 15mg/850 discharge medications: 1. hexavitamin tablet sig: one (1) cap po daily (daily). 2. folic acid 1 mg tablet sig: one (1) tablet po daily (daily). 3. acetaminophen 325 mg tablet sig: two (2) tablet po q6h (every 6 hours) as needed for pain. 4. levothyroxine 25 mcg tablet sig: one (1) tablet po daily (daily). 5. aspirin 325 mg tablet sig: one (1) tablet po daily (daily). 6. bisacodyl 5 mg tablet, delayed release (e.c.) sig: two (2) tablet, delayed release (e.c.) po daily (daily) as needed for constipation. 7. atenolol 50 mg tablet sig: two (2) tablet po daily (daily). 8. thiamine hcl 100 mg tablet sig: one (1) tablet po daily (daily). 9. verapamil 120 mg tablet sig: one (1) tablet po q8h (every 8 hours). 10. lisinopril 20 mg tablet sig: one (1) tablet po daily (daily). 11. docusate sodium 100 mg tablet sig: one (1) tablet po bid (2 times a day) as needed for constipation. 12. senna 8.6 mg tablet sig: one (1) tablet po bid (2 times a day) as needed for constipation. 13. insulin glargine 100 unit/ml solution sig: sixty (60) units sc subcutaneous at bedtime. 14. humalog 100 unit/ml solution sig: ten (10) units sc subcutaneous with meals. 15. humalog 100 unit/ml solution sig: sliding scale per sliding scale subcutaneous four times a day. 16. mirtazapine 15 mg tablet sig: one (1) tablet po hs (at bedtime). 17. trazodone 50 mg tablet sig: 0.5 tablet po hs (at bedtime) as needed for insomnia. 18. zolpidem 5 mg tablet sig: one (1) tablet po hs (at bedtime) as needed for insomnia. 19. aricept 5 mg tablet sig: one (1) tablet po once a day. 20. aluminum-magnesium hydroxide 225-200 mg/5 ml suspension sig: 15-30 mls po qid (4 times a day) as needed. 21. nitroglycerin 0.3 mg tablet, sublingual sig: one (1) tablet, sublingual sublingual prn (as needed) as needed for chest pain. discharge disposition: extended care facility: - discharge diagnosis: delirium secondary to valium overdose enterococcal uti pancytopenia hepatitis c diabetes type ii cad htn discharge condition: stable. discharge instructions: you were admitted to the hospital because you were found to be confused and unresponsive by your visiting nurse. you were initially admitted to the icu. you received medications to control the agitation. . you also developed confusion while in the hospital and you had an extensive workup to determine the cause of this. we did not find any abnormalities on head ct or any evidence of a heart attack. it was felt that your confusion was likely multifactorial including an overdose of valium, dehydration and a urinary tract infection. . you were evaluated by neurology and psychiatry. there was concern that you might have some changes in your memory related to long term alcohol use. you were started on thiamine supplements. many of your medications were also stopped at is was felt that they may have been contributing to your confusion. . you should keep all your medical appointments. you should take all your medications as prescribed. if you have any of the following symptoms, please call your doctor or go to the nearest er: fever>101, chest pain, shortness of breath, abdominal pain, worst headaches of your life, black stools or any other concerning symptoms. followup instructions: please call and make an appointment with your pcp, . . please follow up with your psychiatrist. . you should follow up with behavioral neurology after discharge. an appointment has been set up for you with dr. phone: date/time: 9:00. he is located in , , . procedure: venous catheterization, not elsewhere classified spinal tap incision of lung diagnoses: coronary atherosclerosis of native coronary artery urinary tract infection, site not specified chronic hepatitis c without mention of hepatic coma acute kidney failure, unspecified unspecified protein-calorie malnutrition hypertensive chronic kidney disease, unspecified, with chronic kidney disease stage i through stage iv, or unspecified chronic kidney disease, unspecified poisoning by benzodiazepine-based tranquilizers accidental poisoning by benzodiazepine-based tranquilizers cardiac pacemaker in situ streptococcus infection in conditions classified elsewhere and of unspecified site, streptococcus, group d [enterococcus] hyperosmolality and/or hypernatremia 

Answer: The patient is high likely exposed to