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: unresponsiveness major surgical or invasive procedure: left thoracentesis history of present illness: 80 y.o. male with hx cad, s/p cabg, ischemic cm ef 20%, icd & pacemaker discharged 1 month ago after undergoing vt ablation. . his wife states she looked at him tonight while he was sleeping and noted he had a gasping, labored breathing. she tried to wake him up but he was unresponsive. there were no signs of t-c seizures or fecal incontinece. she called ems who arrived 20 minutes later. patient was alert but somnolent and diaphoretic at that time. patient is unsure whether pacemaker went off. . found to be hypokalemic and started repletion in ed. icd fired once night of admission and once later that morning (in ed) for vtach -> nsr. past medical history: 1. cad status post cabg and imi. catheterization in ' with 3 vd, 2+ mr, moderate systolic and diastolic dysfunction. ptca of svg to pda, mibi in ', severe fixed defect infero, post, and apical. partial reversible inferolateral defects. 2. esophageal stricture x2. 3. increased cholesterol. 4. colonic polyps. 5. abdominal aortic aneurysm s/p repair at in . 6. hypertension. 7. pacemaker placed prior to aaa repair - being checked monthly by dr. office. 8. status post bilateral cataract surgery. 9. ischemic cmy (echo ef 20% 1-2+ mr) 10. gout 11. chronic renal insufficiency (recent baseline unknown - no labs since ) social history: retired shipyard inspector. he quit smoking over 50 years ago. denies alcohol or drugs. lives with his wife and son. family history: non-contributory physical exam: t 96.7 bp 104/64 hr 70 rr 18 sat 97% on 2l gen: comfortable, elderly cachectic man in nad neck: jvp at clavicles while sitting at 30 degrees cv: reg rate, ii/vi systolic murmur at apex chest: faint crackles at both lung bases; clear in middle and at apices abd: soft, ntnd, no organomegaly extr: cool, no edema, 2+ dp and pt pulses pertinent results: 12:45am blood wbc-13.3* rbc-3.17* hgb-9.9* hct-29.0* mcv-91 mch-31.1 mchc-34.1 rdw-14.4 plt ct-321# 06:35am blood wbc-20.2* rbc-3.99* hgb-11.6* hct-37.0* mcv-93 mch-29.0 mchc-31.2 rdw-16.0* plt ct-240 12:45am blood neuts-75.8* lymphs-18.7 monos-3.4 eos-1.9 baso-0.2 06:25am blood neuts-89.7* lymphs-6.1* monos-3.5 eos-0.5 baso-0.2 12:45am blood pt-26.8* ptt-31.9 inr(pt)-2.7* 04:58pm blood pt-38.4* ptt-50.9* inr(pt)-6.0* 06:35am blood pt-21.4* ptt-35.7* inr(pt)-2.1* 12:45am blood glucose-186* urean-35* creat-2.5* na-139 k-2.7* cl-100 hco3-23 angap-19 12:35pm blood glucose-119* urean-97* creat-3.6* na-145 k-4.4 cl-109* hco3-21* angap-19 12:45am blood alt-37 ast-63* ck(cpk)-26* alkphos-288* amylase-50 totbili-1.0 06:35am blood alt-30 ast-55* alkphos-273* totbili-4.7* 12:45am blood ck-mb-notdone ctropnt-0.05* 07:40am blood ck-mb-2 ctropnt-.11* 03:24pm blood ck-mb-notdone ctropnt-0.08* 05:25am blood probnp-* . radiology ct abdomen: findings: the evaluation of the great vessels and mediastinum is somewhat limited due to lack of intravenous contrast . no significant mediastinal lymphadenopathy is noted. coronary arteries are calcified. the heart is enlarged in size. the patient is status post cabg with median sternotomy. note is made of bilateral pleural effusion, somewhat larger on the left, partially loculated. there is interlobar effusion on the left as well. in the lung window, note is made of diffuse ground-glass opacity with interlobular septal thickening predominantly in central distribution involving upper lobes, as well as lower lobes and middle lobes. there is somewhat focal patchy opacity in right middle lobe and lower lobes. mucous secretion in the trachea is seen, however, no central obstructing lesion is noted. ng tube is noted, with the tip terminating in the stomach. there is no suspicious lytic or blastic lesion. small bone islands are seen in lower thoracic vertebra. impression: 1. moderate amount of pleural effusion, larger on the left and somewhat loculated on the left, associated with basilar atelectasis. interlobar effusion on the left. 2. diffuse ground-glass opacity predominantly in central distribution, associated with smooth interlobular septal thickening bilaterally involving upper and lower lobes. the finding may represent pulmonary edema as mentioned in the report of prior chest radiograph, however, in the appropriate clinical setting, superimposed infection cannot be excluded. other possibility includes alveolar hemorrhage if the patient has hemoptysis. please correlate clinically. 3. patchy opacities in the right middle and lower lobes, which may be part of diffuse process mentioned in #2, however, please perform followup study after effusion and ground-glass opacities have resolved. 4. cardiomegaly, status post cabg and coronary artery calcification. . echocardiogram: conclusions: the left atrium is moderately dilated. the right atrium is moderately dilated. left ventricular wall thicknesses are normal. the left ventricular cavity is moderately dilated. there is severe global left ventricular hypokinesis (ejection fraction 20-30 percent). no masses or thrombi are seen in the left ventricle. there is no ventricular septal defect. right ventricular chamber size and free wall motion are normal. the aortic valve leaflets (3) are mildly thickened but aortic stenosis is not present. no aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. there is no mitral valve prolapse. moderate to severe (3+) mitral regurgitation is seen. there is no pericardial effusion. compared with the findings of the prior study (images reviewed) of , no major change is evident. brief hospital course: the patient expired on after a prolonged hospitalization. i will briefly outline his medical problems leading up to his death. . # syncope: patient came in to the hospital secondary to being found unresponsive by his wife. a head ct on admission ruled out an intracranial bleed and his potassium was closely monitored. in the emergency department they noted 15-20 beats of vtach and also a potassium of 2.7. it was thought that his vtach was the cause of his syncopal episode and his hypokalemia was the cause of his vtach. his potassium was repleted and he no longer experienced problems with pacing. . # chf: ef 20% - patient came in appearing euvolemic or even slightly dry. he was kept off his spironolactone, his lasix was initially held and his and bb were continued. his fluid status was monitored daily with serial exams and he had multiple chest xrays to monitor for fluid overload. he subsequently became fluid overload which prompted a visit to the medical icu. while in the icu, they tapped a pleural effusion on his left side which yielded 1.5l of transudative fluid. they also gave him gentle diuresis with lasix 10 mg iv. the patient subsequently became euvolemic and was transferred back to the floor. a day later, he became hypovolemic with a free water deficit of 3l. we replaced his fluid deficit appropriately but struggled with deteriorating respiratory status. . # cri: patient has had a baseline creatinine of 2.0 and had been increasing over the last month. his creatinine on admission was 2.5 and it climbed to 3.5 by the end of his stay. we initially held his and ace inhibitor and involved renal in his care. it was thought that his renal impairment was secondary to both atn from ischemic injury during his vtach but also from prerenal azotemia. we balanced his fluid status with his chf and attempted unsuccessfully to preserve his renal function. . # nutrition: patient had poor po intake during the admission so an ngt was placed for tube feeds. he tolerated the procedure well and was given low volume tube feeds with minimal flushing. once his sodium began to rise, we increased the flushing volumes in an attempt to correct his volume status. . # odynophagia: the etiology behind this wasn't clear. the patient developed throat pain in the middle of his admission. we sent multiple cultures and even had a biopsy performed of his posterior oropharynx. the cultures only yielded mssa and gnr which we treated with antibiotics. we had suspected hsv, , viral, bacterial and involved id, gi, and ent. the pain was resolving when patient expired. . # leukocytosis: present at admission without any fever or identifying source. initially thought to be secondary to inflammatory state. however, the differential showed 88% pmns. we began antibiotic treatment for coverage of the mssa and gnr described above yet his leukocytosis persisted. on the day of death, the patient had an even higher wbc. . # coagulopathy: patient had been taking coumadin at home and his inr rose during the beginning of his admission. initially it was 2.7 but gradually it rose to 6.4. we continued to hold his coumadin and encouraged patient to eat leafy vegetables. we believe that the significant rise of his inr was secondary to the increasing dosages of amiodarone the patient had received. it had returned to below 1.5 prior to thoracentesis but again climbed prior to his death. . # cardiovascular- coronaries: we continued the patient on bb, statin, aspirin and monitored for any signs or sx of chest pain. the patient had a workup for acs upon arrival which was negative. . ### events leading up to death: patient returned from the medical icu and was doing well on 60% o2. this was weaned over the next day and a half and the patient was oriented to person, place, situation, time. however, the patient gradually became more disoriented and his mental status was waxing and waining. we had considered infectious, medications, hypoxia, renal failure, hypercarbia, and hypernatremia in our differential. the patient was weaned from o2 so we thought hypoxia unlikely. additionally, we obtained a vbg which suggested he was not hypercarbic. we broadened his abx coverage for anaerobes with flagyl as he had developed abdominal pain the day prior to death. as he was clearly deteriorating, we had a family meeting the day prior to his death to discuss code status. at that time the family decided to change his code to dnr/dni with thoughts of cmo if he worsened. that night, he became hypotensive to the 60s systolic. aggressive fluid boluses were delivered (4 liters) without much improvement. the family was called and were present as the patient was undergoing fluid resuscitation. after attempts were seemingly unsuccessful, they decided to stop providing fluid and the patient expired shortly thereafter. no autopsy was requested. medications on admission: simvastatin 20mg daily allopurinol 100mg qod digoxin 0.125mg qod valsartan 40mg daily metoprolol 50mg warfarin 2.5mg daily niacin 500mg lasix 10mg qod amiodarone 200mg daily kayexelate discharge medications: none discharge disposition: home discharge diagnosis: chf respiratory failure acute renal failure delirium hypotension discharge condition: expired discharge instructions: none followup instructions: none procedure: enteral infusion of concentrated nutritional substances thoracentesis non-invasive mechanical ventilation pharyngeal biopsy diagnoses: mitral valve disorders acute kidney failure with lesion of tubular necrosis unspecified pleural effusion unspecified protein-calorie malnutrition chronic kidney disease, stage iv (severe) gout, unspecified aortocoronary bypass status hypopotassemia paroxysmal ventricular tachycardia acute respiratory failure cachexia hypovolemia hyperosmolality and/or hypernatremia acute on chronic systolic heart failure other and unspecified coagulation defects syncope and collapse delirium due to conditions classified elsewhere other specified disease of white blood cells fitting and adjustment of automatic implantable cardiac defibrillator 

Answer: The patient is high likely exposed to