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: aspirin attending: chief complaint: transfer from outside hospital for further management of acute alcohol-related hepatitis major surgical or invasive procedure: transcutaneous liver biopsy. ultrasound-guided paracentesis. history of present illness: mr. is a 39 year old male with a history of etoh abuse for the last 6 months who presented to an outside hospital on following a week of heavy binge drinking. the patient reports that he had been drinking at least a half liter of whiskey daily for the week leading up to admission and had noticed his skin becoming more jaundiced. he had been eating little during this time and noticed that he was very weak and could barely walk which prompted him to call an ambulance which took him to the osh. at the osh patient received serax for withdrawl at time of admission. he was initially admitted to the floor but transferred to the icu when he was noted to become increasingly somnolent. patient's hct noted to drop from 35 on admission to 26 on which prompted concern for an active bleed. patient was noted to be hypercoaguable with an inr of 4. he was given vitamin k on admission and also received ffp prior to an egd on for r/o ugib. on egd patient noted to have a duodenal ulcer with a clear base. he was started on a ppi. patient also had u/s with ? portal vein thrombosis. osh also concerned for sbp though no paracentesis was performed and it is unclear whether he was febrile. he was started on ceftriaxone which was switched to cipro. patient was transferred to for further management of his liver disease and ? pvt. past medical history: - etoh abuse: pt reports heavy drinking x 6 months. prior to this he would drink drinks with dinner. he was in detox at hospital for two weeks in . per osh records he has a hx of dts. - ? acute pancreatitis due to alcohol use - hypertension - ibs social history: patient is a graduate of with a degree in politics. heavy etoh use for the past 6 months. no smoking (quit 4 years ago). no history of illicit drug use. estranged from wife, has 1 year old son. family history: father: alcoholism family history of liver disease physical exam: vitals: t: 98.4 bp: 105/68 p:104 r: 18 o2: 98% ra general: alert, oriented, no acute distress heent: scleral icterus, mmm, oropharynx clear neck: supple, jvp not elevated, no lad lungs: clear to auscultation bilaterally, no wheezes, rales, ronchi cv: regular rate and rhythm, normal s1 + s2, no murmurs, rubs, gallops. + small spider on chest. abdomen: soft, non-tender, mildly distended and slightly tense, peripheral dullness ot percussion, bowel sounds present, no rebound tenderness or guarding, +hepatic enlargement by percussion. no fluid wave appreciated. ext: warm, well perfused, 2+ pulses, 2+ bilateral edema. neuro: +asterixis vs. tremor. pertinent results: admission labs: cbc: 11:00pm blood wbc-6.4 rbc-3.20* hgb-10.6* hct-32.3* mcv-101* mch-33.0* mchc-32.7 rdw-17.4* plt ct-171 11:00pm blood neuts-63 bands-1 lymphs-19 monos-16* eos-1 baso-0 atyps-0 metas-0 myelos-0 nrbc-1* coags: 11:00pm blood pt-16.5* ptt-42.2* inr(pt)-1.5* 11:00pm blood glucose-130* urean-2* creat-0.8 na-134 k-4.1 cl-102 hco3-22 angap-14 lfts: 11:00pm blood alt-192* ast-372* ld(ldh)-689* alkphos-145* totbili-24.2* iron studies: 11:00pm blood caltibc-137* ferritn-greater th trf-105* discharge labs: complete blood count wbc rbc hgb hct mcv mch mchc rdw plt ct 05:40am 10.0 2.75*# 9.3*# 27.2*# 99* 33.7* 34.1 21.4* 417 renal & glucose glucose urean creat na k cl hco3 angap 05:50am 88 7 0.4*1 138 3.8 104 26 12 enzymes alt ast ld(ldh) ck(cpk) alkphos amylase totbili dirbili 05:50am 43* 126* 313* 55 12.9* hemolytic workup ret man ret aut 05:50am 8.0* hematologic hapto 05:50am 38 microbiologic data: urine culture : negative blood cultures : negative x3 stool c dif : negative urine culture : negative peritoneal fluid culture : negative blood culture : negative x2 urine culture and : negative blood culture : negative x2 peritoneal fluid culture : negative blood culture : negative x2 stool c dif and : negative urine culture : negative imaging studies: cta abdomen/pelvis : 1. no evidence of venous thrombosis. 2. organizing fluid collection in the left anterior pararenal space from subacute pancreatitis, still active within the tail. 3. mild pancreatic duct dilation in the body and tail is likely related to the sequela of pancreatitis, although mrcp after the patient's symptoms have resolved can be obtained to evaluate . 4. diffusely fatty liver. no biliary pathology to explain hyperbilirubinemia. liver core biopsy liver, core needle biopsy: 1) severe macrovesicular steatosis with frequent ballooning degeneration; no definitive hyaline is seen. 2) portal and lobular predominantly neutrophilic infiltrate. 3) bile duct proliferation with associated neutrophils. 4) focal portal venous thrombosis with organization. 5) mild cholestasis. 6) mild portal fibrosis, no significant sinusoidal fibrosis (trichrome). 7) mild iron deposition seen predominantly in kupffer cells (iron stain). mra/mrv brain : findings: mra head: the arteries of anterior and posterior circulation demonstrate normal flow signal without stenosis or occlusion. no aneurysm greater than 3 mm in size is seen. impression: normal mra of the head. mrv of the head: the head mrv demonstrates normal flow in the superior sagittal and transverse sinuses as well as in the deep venous system. impression: normal mrv of the head. mri abdomen : 1. minimal decrease in size of left retroperitoneal hematoma. 2. decreased signal intensity in the pancreas, which may be due to pancreatitis. suspect a phlegmon adjacent to the tail (not significantly changed vs. prior). 3. fatty liver without evidence of biliary ductal dilatation. no evidence of gallstones or choledocholithiasis. cxr : the heart size is normal. mediastinal position, contour and width are unremarkable. the lung volumes are significantly better compared to the prior study with improvement of bibasal atelectasis. the current study demonstrates what appears to be a new opacity at the left lower lung in the left infrahilar area that might represent a focus of aspiration or developing infection. attention to this area on the subsequent studies is highly recommended. no pleural effusion or pneumothorax is demonstrated. bilateral lower extremity ultrasound : large amount of subcutaneous edema noted bilaterally in the calves. no evidence of dvt seen in either lower extremity. brief hospital course: a 39 year-old man with history of etoh abuse without known cirrhosis, who was originally admitted to osh with likely alcoholic hepatitis, now transferred for further management. # acute hepatitis he underwent a liver biopsy shortly after admission. pathology was consistent with acute alcoholic hepatitis (see full report above). there was no evidence of cirrhosis. cta at admission showed no portal vein thrombosis. his liver enzymes were followed daily and bilirubin rose to peak at 38. prednisone was started when he did not improve with supportive management. however, due to the development of fevers and infection, prednisone was stopped after only three days. as his liver function worsened, he developed symptoms of hepatic encephalopathy, abdominal distention, lower extremity swelling, and diffuse pruritis from hyperbilirubinemia. his encephalopathy was treated with lactulose and rifaximin, titrated to four bowel movements per day. pruritis was treated with ursodiol in addition to hydroxyzine and sarna lotion as needed. ascites and lower extremity edema were treated with paracenteses (therapeutic and diagnostic), lasix and spironolactone. with these interventions, his symptoms were well-controlled. his liver function has improved significantly, with mental status having returned to baseline, anasarca now resolved, and pruritis well-controlled on prn meds. at time of discharge we are continuing rifaximin for encephalopathy prophylaxis. lactulose was stopped due to stomach cramping and diarrhea. he should continue rifaximin until he follows up with dr. . he can continue on hydroxyzine and sarna as needed for pruritis. # acute renal failure his renal function worsened in tandem with worsening liver function. there was no improvement after fluid challenge or albumin infusion. we started midodrine and octreotide for treatment of hepatorenal syndrome when his creatinine rose to as high as 3.0 (from baseline <1.0). renal function improved and returned to baseline with this intervention. # history of etoh upon admission, he was started on thiamine, multivitamin, and folate. for alcohol withdrawal, we used a ciwa scale with valium given every six hours for scores >10. despite this, he was found a few days after admission to be non-responsive, with normal blood pressure and pulse. given that he was alert and fully oriented minutes before this event it was felt he could have been having a seizure. he was given intravenous ativan and transferred to the icu. he underwent mra/mrv of the head and head ct that were all normal. he was seen by the neurology team who agreed that this event could have been an alcohol withdrawl seizure. he was extubated 12 hours later and transferred back to the floors within one day. he was continued on valium prn, and there were no further withdrawal symptoms. social work has been involved in his care from the onset, and has provided him with multiple options for rehabilitation. he understands the serious danger of drinking again, and he will begin inpatient alcohol rehab after this admission. # fevers, leukocytosis, and lll infiltrate on cxr after prednisone was initiated for alcoholic hepatitis, he developed fevers to 101.7. we therefore stopped the prednisone and checked urine, blood, and peritoneal fluid for infection. all of these returned negative. however, he was noted on cxr to have a new left lower lobe infiltrate. this was treated with a five day course of levofloxacin. his symptoms and fever resolved after this treatment. the cxr should be followed up as outpatient to ensure resolution of the infiltrate. # left leg cellulitis as his hepatitis was improving, he was noted to have asymmetric edema with lle>rle. there was concern of dvt versus cellulitis. bilateral le doppler showed no venous clot. therefore we started iv nafcillin for empiric treatment of cellulitis. he received four days of nafcillin, after which the left leg redness and swelling improved substantially. the nafcillin was then switched to oral dicloxacillin. he should complete a 7-day course for left leg cellulitis. # llq organization/loculation this was seen on imaging at admission and felt to be consistent with a pancreatic pseudocyst. he had acute alcoholic pancreatitis in . this collection can be followed as outpatient. # question of sbp he was started on ceftriaxone which was transitioned to ciprofloxacin at outside hospital for concern of sbp. per osh records no paracentesis was performed. at radiology was unable to perform a diagnostic paracentesis at admission since ascitic fluid was not accessible even by u/s guidance. cipro was stopped. however, later in the admission, when he spiked a fever on prednisone, we again pursued ultrasound-guided paracentesis for diagnostic work-up. at that time, there was sufficient fluid for drainage. this fluid was negative by cell count analysis and culture for sbp. # diarrhea he has chronic diarrhea believed due to ibs (he has in the past declined colonoscopy as outpatient), which may have been exacerbated during this admission by lactulose. ttg during this admission was negative for celiac disease. we sent stool samples for pancreatic elastase and fat studies to evaluate for pancreatic insufficiency given his history of pancreatitis; these were both positive. we therefore started him on pancreatic enzyme supplements to be taken with meals. he should also continue on pantoprazole twice daily to enhance absorption of the enzymes. given that all infectious work-up for diarrhea was negative, we were comfortable starting loperamide for symptom treatment. # anemia his hematocrit was low throughout this admission, stabilizing in the mid 20s. iron level was 128, with ferritin greater than . his mcv was elevated, suggestive of anemia from underlying liver disease. b12 and folate levels were normal. there were no signs or symptoms of active bleeding. stool guiaic was negative. one day prior to discharge, he was transfused 2u prbcs for hematocrit of 22 with appropriate bump after the transfusion to 27. labs were sent for haptoglobin (38), ldh (313) and reticulocyte count (8.0). these were indicative of an appropriate marrow response to anemia; the normal haptoglobin makes hemolysis less likely; furthermore, his ldh is only mildly elevated and bilirubin has been downtrending, both not consistent with an active hemolytic process. he will likely need colonoscopy as outpatient, but we believe his anemia will continue to improve as his bone marrow responds from this severe acute illness. # duodenal ulcer this was noted on egd from osh. per their report there was a clean ulcer base with no signs of active bleeding. during this admission we started a ppi, and increased the dosing frequency to allow for better absorption of pancreatic enzyme supplements. # fen post-pyloric dobhoff tubes were placed during the admission for poor oral intake. he pulled these out on two separate occasions, and because his oral intake was improving when he pulled out the dobhoff for the second time, we were comfortable supplementing meals with ensure supplements. at time of discharge, he is tolerating pos with adequate caloric intake. his code status is full code. medications on admission: metoprolol 50 mg daily discharge medications: 1. folic acid 1 mg tablet sig: one (1) tablet po daily (daily). disp:*30 tablet(s)* refills:*2* 2. thiamine hcl 100 mg tablet sig: one (1) tablet po daily (daily). disp:*30 tablet(s)* refills:*2* 3. multivitamin tablet sig: one (1) tablet po daily (daily). disp:*30 tablet(s)* refills:*2* 4. loperamide 2 mg capsule sig: one (1) capsule po daily (daily) as needed for diarrhea. disp:*30 capsule(s)* refills:*2* 5. amylase-lipase-protease 20,000-4,500- 25,000 unit capsule, delayed release(e.c.) sig: two (2) cap po tid w/meals (3 times a day with meals). disp:*60 cap(s)* refills:*2* 6. pantoprazole 40 mg tablet, delayed release (e.c.) sig: one (1) tablet, delayed release (e.c.) po q12h (every 12 hours). disp:*60 tablet, delayed release (e.c.)(s)* refills:*2* 7. tramadol 50 mg tablet sig: one (1) tablet po bid (2 times a day) as needed for pain. disp:*30 tablet(s)* refills:*0* 8. rifaximin 200 mg tablet sig: two (2) tablet po tid (3 times a day). disp:*180 tablet(s)* refills:*2* 9. hydroxyzine hcl 25 mg tablet sig: one (1) tablet po q6h (every 6 hours) as needed for itching. disp:*30 tablet(s)* refills:*2* 10. camphor-menthol 0.5-0.5 % lotion sig: one (1) appl topical tid (3 times a day) as needed. disp:*1 qs* refills:*2* discharge disposition: extended care facility: treatment center - discharge diagnosis: primary diagnoses alcoholic hepatitis hepatorenal syndrome pneumonia cellulitis alcohol-withdrawal seizure discharge condition: vital signs stable. afebrile. mentating at baseline. discharge instructions: you were admitted to the hospital for treatment of alcoholic hepatitis. a biopsy taken of the liver showed changes consistent with acute hepatitis. there was no evidence of cirrhosis. if you continue to drink alcohol, it is very likely that the liver disease will progress to cirrhosis, which carries with it increased risk of infection, bleeding from the gastrointestinal tract, and fluid retention in the abdomen and legs. cirrhosis is irreversible. if you stop drinking alcohol altogether, it is likely that the changes in the liver seen during this admission will reverse themselves and you will return to your normal state of health. for this reason, it is very important that you seek help so that you do not drink alcohol again. . this hospital course was complicated by alcohol withdrawal seizures for which you received valium, and also by pneumonia and skin infection for which you were treated with antibiotics. there was also concern of kidney failure (hepatorenal syndrome), which reversed after treatment with medicines to increase blood flow to the kidneys. . there have been several changes to your medicines: 1. we added multivitamin, folate and thiamine. please continue to take these nutritional supplements. 2. we added pancreatic enzyme supplements to help decrease diarrhea. 3. we added pantoprazole for gastric acid suppression and protection against ulcers. 4. we added rifaximin, to be taken three times daily to prevent mental status change or confusion from the hepatitis. 5. we added tramadol to be taken up to two times daily as needed for abdominal pain related to the hepatitis. 6. we added hydoxyzine and sarna lotion, which can be taken as needed for itch. . please note your follow-up appointments below. . please call your doctor if you develop worsening abdominal pain, blood in stools, fevers, or other symptoms that are concerning to you. followup instructions: please note the appointments below that have been scheduled for you: 1. , md phone: date/time: 8:00 2. , md phone: date/time: 3:00 procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours insertion of endotracheal tube enteral infusion of concentrated nutritional substances closed (percutaneous) [needle] biopsy of liver percutaneous abdominal drainage transfusion of packed cells transfusion of other serum electroencephalogram diagnoses: pneumonia, organism unspecified anemia of other chronic disease abnormal coagulation profile unspecified essential hypertension hepatorenal syndrome other convulsions personal history of tobacco use cellulitis and abscess of leg, except foot other ascites hepatic encephalopathy acute pancreatitis cyst and pseudocyst of pancreas other and unspecified alcohol dependence, continuous acute alcoholic hepatitis alcohol withdrawal irritable bowel syndrome jaundice, unspecified, not of newborn nonspecific elevation of levels of transaminase or lactic acid dehydrogenase [ldh] alcoholic fatty liver acute kidney failure with other specified pathological lesion in kidney duodenal ulcer, unspecified as acute or chronic, without hemorrhage or perforation, without mention of obstruction other specified pruritic conditions 

Answer: The patient is high likely exposed to