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: aldomet / codeine phos/apap/caff/butalb / hydralazine / aldactone / effexor xr / lopid / ciprofloxacin / tricor / percocet / vicodin attending: chief complaint: nausea and shortness of breath major surgical or invasive procedure: none history of present illness: mr. is a 59 yar old man with a pmh significant for arf x 5, gib, and cholestatic jaundice during his last admit who was discharged 9 days prior to admission. he was in his usual state of health until about 3 days prior to arrival when he developed the onset of a headache, nausea, dry heaves. this is how he feels when he has renal failure. he also noted increasing pedal edema and thirst. he denies hematochezia, fevers, chills, diarrhea, chest pain, dysuria, or hematuria. he says that his sugars have been excellent lately. he has not taken lasix since his last admit. he states that he last took 2 tablets of alieve 2 nights ago. in the ed, he was found to be in acute renal failure with a creatinine of 5.2 up from 1.6 six days ago. lenis were negative for dvt. past medical history: dm, copd, "kidney failure" x 4, heart murmur since infancy, apnea, veins "stipped" varicose veins, appendectomy, "tendency to bleed" since childhood. social history: lives w/ wife. etoh: denies after . most prior to that would be "5 shots" on any one night. illicits: denies past/present. tobacco: denies past/present. family history: mother died at 36 years old. had dm, chf. father died at 50 years old; had cad. physical exam: 95.1 - 62 - 128/36 - 14 - 99%ra gen: morbidly obese body habitus; markedly jaundiced white male in nad lying flat on his back. communicates in full sentences and breathes comfortably. heent: nc/at. sclera markedly icteric bilaterally, perrl, eomi. nares patent. oropharynx: no erythema or exudate. dry mm. pulm: cta b. back: no cvat. cv: all heart sounds faint. rrr, s1, s2, ii/vi holosystolic murmur. unable to assess jvd due to obesity. pulses: bilateral radial. abd:+bs. enormously distended but soft obese abd. no organomegaly noted though exam limited by obesity. nontender.no guarding. extr: pitting edema of bilateral le. skin: violaceous discoloration of anterior tibial region bilaterally. rle had 4x2cm area of superficial ulceration that is non-erythematous and non-draining. 1 dressing on tibial aspect of right shin clean dry intact. pertinent results: 01:00am wbc-9.3 rbc-3.21* hgb-10.8* hct-33.3* mcv-104* mch-33.7* mchc-32.5 rdw-17.6* 01:00am neuts-86* bands-2 lymphs-2* monos-5 eos-1 basos-0 atyps-0 metas-3* myelos-1* 01:00am hypochrom-2+ anisocyt-1+ poikilocy-2+ macrocyt-2+ microcyt-normal polychrom-occasional target-1+ schistocy-occasional burr-occasional stippled-occasional teardrop-occasional 01:00am plt count-222 pltclm-1+ 01:00am pt-19.2* ptt-61.5* inr(pt)-2.6 12:14am glucose-150* urea n-101* creat-5.2*# sodium-132* potassium-4.3 chloride-101 total co2-11* anion gap-24* 12:14am alt(sgpt)-68* ast(sgot)-65* alk phos-251* amylase-60 tot bili-34.4* 12:14am lipase-61* 12:14am probnp-1472* 12:14am albumin-3.1* calcium-8.7 phosphate-7.5*# magnesium-2.0 . cxr: bilateral effusions consistent with pulmonary edema (my interpretation) . leni negative but limited by habitus . u/s impression: 1. sludge-filled gallbladder without evidence for cholecystitis. common duct dilatation to 2 cm, etiology indeterminate. 2. normal patency of the hepatic and portal venous vasculature. 3. fatty liver. 4. small ascites. . echo conclusions: the left atrium is markedly dilated. there is mild symmetric left ventricular hypertrophy. the left ventricular cavity is moderately dilated. overall left ventricular systolic function is normal (lvef 70 percent). no masses or thrombi are seen in the left ventricle. there is no ventricular septal defect. the aortic root is moderately dilated. the aortic valve leaflets (3) appear structurally normal with good leaflet excursion and no aortic regurgitation. the mitral valve leaflets are structurally normal. mitral regurgitation is present but cannot be quantified. tricuspid regurgitation is present but cannot be quantified. there is at least moderate pulmonary artery systolic hypertension. there is no pericardial effusion. . u/s with dopplers impression: 1. extremely limited study due to patient body habitus. 2. distended gallbladder with sludge. 3. fatty liver. main and right portal veins are patent. 4. increased ascites. brief hospital course: . # oliguric renal failure: initially patient was thought to be prerenal vs hrs, and fena was consistent with this. the patient was hydrated with nahco, cautiously, and was started on hepotorenal medications including octreotide, midodrine, and albumin. urine output transiently increased, but unclear if this was d/t hydration or hrs treatment, as both occurred simultaneously. additionally, foley was found to be in urethra on hd #2 and once this was replaced, urine output increased transiently. however, the patient continued to have poor urine output even in the setting of adequate bp. cvvh was started in setting of uremia. repeat fena suggested atn, but it was questionable how accurate this was in the setting of cvvh. there was some concern for right ventricular dysfunction in the face of pulmonary hypertension, and an echo was performed. this showed mod pulm htn based on tr gradient of 45, but right ventricle was not well visualized d/t patient's habitus. cxr demonstrated a widened mediastinum that was concerning for congestion. because the patient's fluid status was not completely clear and because there was some concern for hepatic congestion by renal and total body fluid overload, 50cc/hr was removed with cvvh. cr intermittently trended down with cvvh but then trended upwards. treatment for hrs was continued, but patient was unable to get midodrine for ~1day as he was aspirating meds and it was very difficult to pass an ngt. patient remained oliguric until death. . # transaminitis: pt had evidence of non-alcoholic steatohepatitis and presumed drug injury on previous biopsy and demonstrated continued worsening of synthetic funtion based upon inr and bilirubin. no clear etiology of acute liver decompensation was found. liver u/s from showed no thrombosis of portal or hepatic veins and little ascites, and this was repeated with no change. there may have been a small element of hepatic congestion, but this was not the cause of the acute decompensation as the lft's would have been more elevated. although the patient had already had a full workup for acute liver disease, repeat workup was performed with cmv, ebv, and hep serologies, all of which were negative. no cause for acute liver decompensation was determined, and the patient became progressively more encephalopathic. he was treated with lactulose for encephalopathy, but did not receive this for ~1 day d/t poor po access. an arterial ammonia level was obtained and was moderately elevated . # septicemia - the patient did not have fevers or a white count on presentation or for the majority of his icu stay. because his mental status was deteriorating and white count jumped up, blood cultures were taken on which showed gpc in clusters, which later grew out coagulase negative staph, and broad spectrum antibiotics were started. however, over the course of the following day he rapidly became hypotensive, febrile, and tachycardic. he was found to by hypoxic with pao2 78 and adidemic with ph 7.1 and was intubated. his lactate trended from 1.4 to 11.4 within 16 hours, and his hypotension progressed to the point or requiring 3 different pressors to maintain maps. a discussion was held with his wife and she made him in the face of rapid deterioration, overwhelming sepsis, acute worsening liver disease of unknown etiology, and renal failure. pressors were withdrawn and the patient expired shortly thereafter from cardiac and respiratory arrest. . # cardiology - last echo on record at with ef>50% in with dilated la and symmetric lvh, right heart not seen, and cardiac cath in with normal coronary arteries and mild pulmonary htn (pcwp 20, pap 20, ra 13). repeat echo with mod pulm htn, lvh, normal ef. after initial resuscitation with fluids, renal was consulted and started cvvh with goal to remove 50cc/hr in setting of ?right heart failure. . #fen - the patient was found to aspirate liquids and meds, and an ngt was placed and he was made npo. a speech and swallolw was planned but never obtained. . # sleep apnea: used cpap continuously, both at night and during the day, until intubation. . # type ii diabetes: continued on outpatient nph and sliding scale with fingersticks. . # htn: after fluid resuscitation remained normotensive until day of death. home dose of valsartan was held. . # psych: history of anxiety, depression. former alcoholic but had not had drink in many years. was continue lexapro 5 mg qpm. . medications on admission: 1. ursodiol 600 mg capsule qam 2. ursodiol 300 mg capsule qpm 3. albuterol-ipratropium 103-18 mcg/actuation aerosol sig: puffs inhalation q6h prn. 4. metoprolol tartrate 12.5 mg po bid 5. pantoprazole sodium 40 mg q24h 6. hydroxyzine hcl 25 mg tablet 1 q4-6h prn 7. morphine 30 mg prn 8. diovan 40 mg tablet sig: tablet po once a day. discharge medications: none discharge disposition: expired discharge diagnosis: septic shock discharge condition: deceased discharge instructions: none md procedure: enteral infusion of concentrated nutritional substances venous catheterization for renal dialysis non-invasive mechanical ventilation diagnoses: hypocalcemia congestive heart failure, unspecified diabetes mellitus without mention of complication, type ii or unspecified type, not stated as uncontrolled acute kidney failure, unspecified unspecified septicemia severe sepsis chronic airway obstruction, not elsewhere classified unspecified sleep apnea septic shock morbid obesity other chronic nonalcoholic liver disease 

Answer: The patient is high likely exposed to