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: heparin agents attending: chief complaint: hypoxia, shortness of breath, chest pain major surgical or invasive procedure: none history of present illness: 67 m with poorly controlled iddm, afib on coumadin, s/p partial right foot amputation p/w erythema, swelling, & wounds on rle. pt states that symptoms began 4 day ago with purulent drainage from foot lesions. endorses fevers at home yesterday. pt recently treated for cellulitis in rle 1 months ago with good resolution. no antecedent trauma but pt scratching legs vigorously. . also endorses decreased appetite with 20 lb weight loss in the past month. . vital signs in the ed: 98.0, 149/70, 80, 18, 98% 2l . in the , pt given iv vancomycin in ed. . review of systems: (+): as above (-): chest pain, sob, abdominal pain, nausea, vomiting, diarrea, headache. past medical history: -chf ef 45% () - on home oxygen 1-2l -cad s/p 4 mi's (, , ), s/p 3 vessel cabg and recent bms of d1 () -chronic atrial flutter -diabetes mellitus type ii c/b neuropathy, retinopathy, diabetic foot ulcer s/p amputations -pvd -hypertension -hyperlipidemia -gerd -depression -h/o alcoholism- stopped drinking 25 years ago -ischemic colitis -left subclavian stenosis (45 mmhg pressure drop across the stenotic lesion, cath ) . past surgical history: l 2nd toe amp r tma r partial colectomy for ischemic colitis 3 vessel cabg r fem-dp l fem- with stent bilaterally s/p aortoiliac stenting social history: patient lives in with 3 of his brothers. retired in his late 50s but he previously owned a radiator repiar business. no etoh x 25 years, but hx of heavy drinking x 15 years ("all day long"), hx of tobacco use (4ppd x 15 years), no ivdu. family history: -no cad, lung disease, or dm in the family -htn in father -breast cancer in mother physical exam: on admission: tcurrent: 37 ??????c (98.6 ??????f) hr: 94 (94 - 94) bpm bp: 121/32(53) {121/32(53) - 121/32(53)} mmhg rr: 21 (21 - 22) insp/min spo2: 98% heart rhythm: af (atrial fibrillation) general: nad. oriented x3. mood, affect appropriate. heent: ncat. muddy sclera. eomi. conjunctiva were pink, no pallor or cyanosis of the oral mucosa. no xanthalesma. neck: supple with jvp of in line with jaw line cardiac: rrr, normal s1, s2. no m/r/g. no thrills, lifts. no s3 or s4. lungs: crackles at bilateral bases, good air movement throughout abdomen: soft, ntnd. no hsm or tenderness. extremities: no c/c/e. missing front foot on r, missing toes and ulcerations on remaining on left, rle dressing c/d/i pulses: right: dp 1+ pt 1+ left: dp 1+ pt 1+ . at discharge: pertinent results: - ecg: lbbb at rate 90-112. greater than 5mm st elevations than previous, although hard to delineate st baseline. . - echo: : the left atrium is moderately dilated. there is mild symmetric left ventricular hypertrophy with normal cavity size. there is mild regional left ventricular systolic dysfunction with severe hypokinesis of the inferior, inferolateral and basal inferoseptal segments. the remaining segments contract normally (lvef = 40%). right ventricular chamber size and free wall motion are normal. the diameters of aorta at the sinus, ascending and arch levels 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. mild (1+) mitral regurgitation is seen. there is moderate pulmonary artery systolic hypertension. there is no pericardial effusion. impression: mild regional left ventricular systolic dysfunction, c/w cad. mild mitral regurgitation. moderate pulmonary hypertension. compared with the report of the prior study (images unavailable for review) of , the findings appear similar. . - cardiac cath: rhc : comments: 1. resting hemodynamics revealed normal right ventricular filling pressures with rvedp 7 mmhg and mildly elevated left sided filling pressures with pcwp 19 mmhg. there was pulmonary arterial hypertension with a mean pa pressures of 33 mmhg (pa prrresure 55/19 mmhg). the pulmonary vascular resistance was 157 dynes-sec/cm5. the cardiac index was normal at 3.26 l/min/m2. 2. treatment with 100% fio2 demonstrated lowering of the pulmonary artery resistance (97 dynes-sec/cm5) due to a rise in calculated cardiac index (5.27 l/min/m2) with a stable pcw of 19 mmhg. the mean pa pressure was measured at 33 mmhg. 3. treatment with inhaled no at 40 ppm in addition to 100% fio2 did not change the pulmonary pressures significantly with a mean pa pressure of 30mmhg. there was just a mild change in the mean pcwp measured at 17 mmhg. the pulmonary artery resistance was (107 dynes-sec/cm5) due to a rise in the calculated cardiac index (4.43 l/min/m2). final diagnosis: 1. pulmonary arterial hypertension at baseline with no improvement in mean pa pressures with 100% o2 and ino at 40ppm. 2. mildly elevated left ventricular filling pressures. . lhc : comments: 1. coronary angiography in this left-dominant system revealed diffuse coronary artery disease. the lmca was a small caliber vessel without disease. the lad had 60-70% calcified stenoses of the proximal section, as well as the diagonal branch, and was occluded after the mid-section. the lcx had sequential stenoses of the proximal and distal lcx, with occluded om1 and om2 branches, and total occlusion after the distal lcx. the rca was a non-dominant vessel with sequential 80% stenoses. 2. selective graft venography revealed a widely patent svg-pda and lpl graft. the svg-om1 graft had a 30-40% stenosis in the mid-svg, and was patent to the om1 branch. 3. selective graft arteriography revealed a widely patent lima-lad graft. 4. resting hemodynamics revealed elevated right- and left-sided filling pressures, with mean ra pressure of 15 mmhg, and mean pcw pressure of 30 mmhg. the wedge tracing was notable for a prominant v-wave with pressure of 51 mmhg, consistent with possible mitral regurgitation. there was mild pulmonary hypertension with mean pa pressure of 38 mmhg, and mild systemic hypertension, with sbp of 140mmhg. the cardiac output was normal at 5.1 l/min. there was no aortic stenosis detected by pullback technique. 5. nonselective left subclavian injection revealed a 70% stenosis of the proximal left subclavian artery, with a 45 mmhg pressure drop across the stenotic lesion. final diagnosis: 1. diffuse coronary artery disease. 2. elevated left- and right-sided filling pressures. 3. mild pulmonary and systemic hypertension. 4. subclavian stenosis. brief hospital course: patient expired as explained in omr death note summarized here: at approximately 12:30am, telemetry in the icu demonstrated ventricular tachycardia. dr. was present at bedside and the patient was found to be pulseless. code status was noted to be dnr and he became asystolic shortly thereafter. dr. called the time of death to be 12:36am on after listening for breath sounds bilaterally and not appreciating any. he also listened for heart sounds and did not appreciate any. he felt for peripheral pulses for 1 minute at both radial arteries, and did not appreciate any. he had absent corneal reflexes bilaterally. dr. has made several phone calls to patients brothers in attempt to inform them of grave situation. organ bank was also notified by dr. and they have declined. below is a brief summary of his hospital course: mr. is a 67 year old man with a past medical history significant for cabg, cad, schf, dm, pvd, originally admitted for rle cellulitis who was transferred to the ccu after developing acute pulmonary edema. his course was complicated by pulseless vt arrest on and respiratory failure and is now in the micu for further management . # hypoxemic respiratory failure: initially upon admission, mr. had an spo2 of 100% on 2l. given appearance of hypovolemia on exam, and concern for infection his home torsemide was held and he was given 1l ns. on the first night of admission, he became hypoxemic to spo2 in the 70s. cxr at the time demonstrated pulmonary edema. sbp was 150. hypoxemia initially improved with bipap and diuresis. he was transferred to the ccu for further management given concern for acs. on he was able to be weaned from bipap with lasix gtt and nitro gtt after 2l of diuresis, however on he removed his nrb mask and desaturated to the 60s, was obtunded and bradycardic in aflutter with variable block and he was intubated. abg initially demonstrated a moderate p/f ratio of ~250 suggestive of which has roughly remained constant. ct chest demonstrated bilateral ground glass opacities worsened in non-dependent areas since of unknown etiology. overall, non-resolving infiltrates were seen as likely secondary to flash pulmonary edema with component of alveolar hemorrhage given profound coagulopathy on admission. given spike to 102 on and cxr with worsening bilateral infiltrates, vap was seen as likely and broad spectrum abx (vanc, zosyn, and levofloxacin) were started. furthermore, swan on demonstrated wedge of 15-18 indicating a smaller component of l heart dysfunction than previously thought. furthermore pvr in 800s indicated that pulmonary hypertension occurred out of proportion to left heart dysfunction. after 1 week of intubation, his mental status had improved to the point where he could be safely extubated on . p/f ratio prior to extubation demonstrated a ratio of 250 which was similar to his baseline. for one day following extubation, he was able to maintain an spo2 of 97-99% on the high flow mask, but progressively became more tachypneic and demonstrated paradoxical respirations. bipap was initiated on . . he was transferred to the micu for further care . upon arrival his mental status was poor and appeared having significant difficulty on bipap. it was decided to re-intubate the patient. he was continued on vancomycin and meropenem. a bronchocsopy was performed which showed hemosiderin laden macrophages. his hypoxia was felt to be a combination of cardiogenic pulmonary edema given elevated v waves on swan plus intrinsic pulmonary process of undiagnosed etiology. a lung biopsy was considered. . # pulseless vt arrest: while mr. was being weaned from sedation on , he experienced an episode of pulseless vt. there was no evidence of cardiac ischemia, electrolytes were within normal limits, and qtc was 420. he had rosc after 1 shock and an amiodarone load. the etiology of this event was unclear, but was thought to occur secondary to catecholamine surge in the setting of sedation wean and profound agitation. in the micu, the patient had increased ectopy and nsvt. due to the increasing frequency, he was restarted on amiodarone with improved ectopy. . # ?????? with diuresis, mr. renal function progressively deteriorated to a peak bun/cr of 178/4.5 from a baseline of 34/1.7. after a peak cr of 4.5, mr. cr began to improve to a cr of 2.8 upon transfer to the micu. he continued to maintain good uop and followed closely by nephrology. he did not need renal replacement therapy while in the micu. . # hypernatremia: mr. became quite hypernatremic when his tube feeds were held following extubation. initial attempts to replete with 1/2 ns were unsuccessful, and his na was 157 on consistent with a 6.5 l free water deficit. d5w and free water flushes were started with good effect. . #ams ?????? a large component of mr. prolonged intubation was altered mental status. following initial sedation with fentanyl and midazolam he became quite sedated and would not follow commands. sedation was changed to propofol after inadequate sedation with precedex. given supratherapeutic inr, ct head was obtained which demonstrated atrophy but no acute changes. neuro consult was obtained, and their assessment was that his delerium was secondary to toxic metabolic causes (sedation, uremia, hypernatremia, and icu delerium). eeg shows metabolic encephalopathy, no epileptiform activity. as his renal function and hypernatremia improved, the patient's mental status slowly improved while on the vent. . # nutrition: upon transfer to the micu, mental status precluded po intake, and bipap precluded nasogastric tube feeds. tube feeds were initiated in the micu. . # dm ?????? blood sugars were difficult to control in the ccu, and an insulin drip was started. was consulted and saw the patient often for close monitoring of his blood sugars. . # fevers/infection: fever to 102 on with leukocytosis peak to 24 on . there existed concern for vap with prolonged intubation (no definite infiltrates for vap), as well as uti given prolonged foley catheterization (prior ua with wbcs but urine cx with only yeast). less likely was meningitis given ams, because time course/physical exam was inconsistent (he became altered before fevers started and no nuchal rigidity). initially vanc/zosyn/levofloxacin were started for vap on . levofloxacin was stopped on following vt arrest and concern for qt prolongation. he was broadened to vancomycin and upon transfer to the micu and his wbc improved. . # cad ?????? mr. experienced chest pain in setting of respiratory decompensation on admission without ekg changes from baseline, cardiac enzymes peaked on with mb of 21 and trop of 1.21. troponin was baseline and worsened with worsening ckd. overall his mb bump was seen as demand related to his hypoxemia and there was little concern for acs. he remained cp free since initial decompensation. # liver: lfts were elevated on admission to alt/ast in the 300s. etiology is likely secondary to congestive hepatopathy as ruq us ruled out abscess or reversal of flow, but was suggestive of chf and congestive hepatopathy. hcv ab was negative. hbv serologies negative. given downtrending lfts with diuresis, further workup was deferred. furthermore, inr improved dramatically with vit k administration c/w malnutrition. . #anemia. hematocrit slowly worsened from baseline of 29 on admission to a nadir of 22.1. he was transfused on due to low svo2 of 35%. cause of anemia has been thought to be secondary to ckd and/or anemia of chronic disease. hemolysis was ruled out with negative smear for schistocytes, elevated haptoglobin, and normal fibrinogen. in light of brown guiac positive stools, protonix was initiated. in the micu, he had a low hct of 20.6 and received two units of pbrcs with good effect. medications on admission: - aspirin 81 mg qd - trazodone 100 mg qhs prn - atorvastatin 80 mg qhs - sertraline 100 mg qd - clonazepam 0.5 mg tid prn anxiety - 10 mg qd - torsemide 20 mg qd - warfarin 1 mg qd - spironolactone 12.5 mg qd - isosorbide mononitrate 60 mg er qd - fluticasone-salmeterol 250-50 mcg/dose disk - metoprolol succinate 12.5 mg er qd - albuterol sulfate 90 mcg mdi inh q6h prn sob, wheeze - humulin-n 100 unit/ml suspension 20 units qam, 24 units qpm - humalog 100 unit/ml solution 10 units qam, 12 units qpm discharge medications: expired discharge disposition: expired discharge diagnosis: expired discharge condition: expired discharge instructions: expired followup instructions: expired procedure: continuous invasive mechanical ventilation for 96 consecutive hours or more continuous invasive mechanical ventilation for 96 consecutive hours or more insertion of endotracheal tube insertion of endotracheal tube enteral infusion of concentrated nutritional substances closed [endoscopic] biopsy of bronchus pulmonary artery wedge monitoring pulmonary artery wedge monitoring cardiopulmonary resuscitation, not otherwise specified central venous catheter placement with guidance diagnoses: pneumonia, organism unspecified acidosis thrombocytopenia, unspecified anemia in chronic kidney disease subendocardial infarction, initial episode of care congestive heart failure, unspecified acute kidney failure, unspecified candidiasis of other urogenital sites chronic kidney disease, stage iv (severe) hypertensive chronic kidney disease, unspecified, with chronic kidney disease stage i through stage iv, or unspecified atrial fibrillation coronary atherosclerosis of unspecified type of vessel, native or graft aortocoronary bypass status diabetes with neurological manifestations, type ii or unspecified type, not stated as uncontrolled peripheral vascular disease, unspecified depressive disorder, not elsewhere classified atrial flutter paroxysmal ventricular tachycardia ulcer of other part of foot acute respiratory failure cardiac arrest long-term (current) use of insulin postinflammatory pulmonary fibrosis other emphysema long-term (current) use of anticoagulants do not resuscitate status metabolic encephalopathy hyperosmolality and/or hypernatremia acute on chronic systolic heart failure other and unspecified coagulation defects asbestosis cellulitis and abscess of foot, except toes other dependence on machines, supplemental oxygen foot amputation status chronic passive congestion of liver physical restraints status 

Answer: The patient is high likely exposed to