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: linezolid attending: chief complaint: abdominal distension, lethargy major surgical or invasive procedure: paracentesis, perihepatic fluid collection drainage history of present illness: 44 yom with hx of hep c cirrhosis recently admitted for ccy on c/b bacterial peritonitis who now presents with increased lethargy, abdominal pain and jaundice. patient reports increasing lethargy over the last few days. he does not feel confused and is aaox3. he also reports increasing abdominal pain which is similar to when he was diagnosed with peritonitis on last admission. he has had poor po intake but has been taking lactulose at home. he has not been taking his linezolid since discharge as his pharamacy has not filled the medication. he denies any recent fevers but does report chills. +nausea but no vomiting. +diarrhea but is on lactulose, no brbpr, no melena. he denies any chest pain, sob, cough or dysuria . in the ed: temp 98.1, bp 117/56, hr 73, rr 18, 97% ra. ct scan done which showed no abcess at ccy site. transplant surgery consulted and believed no surgical issue at this time. liver fellow consulted and decided to admit to med. past medical history: hcv cirrhosis gall stone pancreatitis, s/p ercp , splenectomy ccy . home medications: (per last d/c summary) linezolid 600mg po q12h (not taking) levothyroxine 75mcg daily clotrimazole 10 troch prn 5 times daily oxycodone 5mg q4h prn pain lactulose 30mg po tid methadone 10mg daily docusate senna midodrine 5mg tid atenolol 50mg daily furosemide 40mg social history: married, lives in , has children. denied current etoh or iv drug use. family history: n/c physical exam: vs: temp 97.5, bp 114/60, hr 79, rr 20 97% ra gen: middle-aged man in nad, extremely jaundiced, lethargic, aaox3 heent: eomi, perrl, sclera icteric, op moist neck: supple, no jvd, no lad cv: reg rate, normal s1, s2. +sem ii/vi lusb chest: resp were unlabored, no accessory muscle use. ctab, no crackles, wheezes or rhonchi. abd: soft, +mild distension, +ttp of entire abdomen, no rebound, no guarding, +healing scar in ruq from site of ccy, no discharge from wound ext: +2 pitting edema of b/l le, +asterixis skin: +jaundice, +spider angiomata pertinent results: labs on admission: 09:20pm blood wbc-14.7*# rbc-unable to hgb-8.4* hct-27.5* mcv-unable to mch-unable to mchc-35.7* rdw-unable to plt ct-124* 09:20pm blood neuts-82.6* bands-0 lymphs-14.3* monos-2.2 eos-0.9 baso-0.1 10:53pm blood glucose-90 urean-62* creat-0.9 na-132* k-5.3* cl-102 hco3-20* angap-15 10:53pm blood alt-92* ast-141* alkphos-65 totbili-38.0* 10:53pm blood albumin-3.0* calcium-9.9 phos-5.0* mg-3.3* 07:20am blood albumin-4.1 calcium-11.7* phos-6.0* mg-4.1* 05:15am blood hapto-<20* 09:20pm blood ammonia-63* 01:37pm blood pth-29 09:57pm blood lactate-2.9* 07:14am blood lactate-12.9* 05:10am blood freeca-1.44* . labs prior to death: . 11:26am blood wbc-12.4* rbc-3.21* hgb-10.5* hct-29.0* mcv-90 mch-32.6* mchc-36.0* rdw-17.1* plt ct-37* 11:26am blood pt-36.7* ptt-59.9* inr(pt)-3.9* 11:26am blood glucose-114* urean-101* creat-3.5* na-151* k-4.1 cl-106 hco3-8* angap-41* 03:18am blood alt-231* ast-506* alkphos-58 totbili-47.3* 11:26am blood calcium-10.3* phos-8.8* mg-4.0* 11:51am blood type-art po2-118* pco2-25* ph-7.13* caltco2-9* base xs--19 intubat-intubated 11:51am blood glucose-102 lactate-18.8* k-3.9 . 01:16pm urine color-yellow appear-hazy sp -1.010 01:16pm urine blood-lg nitrite-neg protein-100 glucose-neg ketone-neg bilirub-mod urobiln-0.2 ph-5.0 leuks-neg 01:16pm urine rbc-282* wbc-0 bacteri-none yeast-many epi-3 01:16pm urine hours-random urean-87 creat-50 na-96 . microbiology: . bcx - negative, ascitic fluid negative, fluid collection showing vre, ucx initially negative, then growing yeast. sputum cx with budding yeast, 3+ 2 days prior to death. . imaging/studies: . ct abd/pelvis: . impression: 1. increased bibasilar consolidation/atelectasis. 2. interval removal of jp drain. the subhepatic collection is decreased in size, now measuring 5.4 cm in greatest dimension. 3. moderate ascites. this may represent reaccumulation of ascites in the setting of liver disease though bile leak not excluded given the provided history. if there is clinical concern for bile leak, consider mrcp with a hepatobiliary (gd-bopta or eovist) which may demonstrate a leak if present, although hepatic excretion may be reduced in the setting of cirrhoisis. 4. cirrhotic liver, unchanged. 5. mild bilateral hydronephrosis, unchanged. 6. interval decrease in size of right cardiophrenic lymph node, now 1.8 x 1.0 cm. . cxr : . chest, two views: band-like linear density of the left lung base corresponds to atelectasis seen on subsequent ct of the abdomen and pelvis. there is no evidence of pneumonia or pulmonary edema. cardiac size is normal. no subdiaphragmatic free air is identified. impression: bibasilar atelectasis . echo : . the left atrium is mildly dilated. left ventricular wall thicknesses and cavity size are normal. regional left ventricular wall motion is normal. left ventricular systolic function is hyperdynamic (ef>75%). transmitral doppler and tissue velocity imaging are consistent with normal lv diastolic function. right ventricular chamber size and free wall motion are normal. the aortic valve leaflets (3) appear structurally normal with good leaflet excursion and no aortic regurgitation. the mitral valve appears structurally normal with trivial mitral regurgitation. there is no mitral valve prolapse. no mass or vegetation is seen on the mitral valve. the tricuspid valve leaflets are mildly thickened. there is moderate pulmonary artery systolic hypertension. there is no pericardial effusion. impression: suboptimal image quality. hyperdynamic left ventricular function (ef>75%). no vegetations seen. if clinically suggested, the absence of a vegetation by 2d echocardiography does not exclude endocarditis. compared with the prior study (images reviewed) of , the ventricular rate is now faster, the ventricular function is now hyperdynamic and moderate pulmonary artery hypertension is now present. . cxr , micu transfer day: . there are bibasilar opacities partially retrocardiac, but also continuing towards the more lateral aspect of the chest that appears to be worsening atelectasis, although underlying infection cannot be excluded. small bilateral pleural effusion is demonstrated. upper lungs are clear. the cardiomediastinal silhouette is unchanged. . kub : . impression: no ileus, obstruction or free air. . cta abd/pelvis ; . impressions: 1. bibasilar consolidation slightly more than that seen on , likely representing atelectasis although infection cannot be excluded. 2. percutaneous transhepatic drain in place, with adjacent small bubble of gas. given history of recent procedures and perihepatic infection, multiple new small hypodensities in the liver are concerning for liver abscesses. 3. increasing ascites and anasarca. 4. diffuse colonic mucosal wall thickening and thumbprinting, non-specific, but infectious/inflammatory etiology such as c. difficile colitis is favored. no secondary or vascular findings to suggest ischemic colitis. . echo : . the left atrium is mildly dilated. left ventricular wall thicknesses and cavity size are normal. left ventricular systolic function is hyperdynamic (ef>75%). the estimated cardiac index is high (>4.0l/min/m2). right ventricular chamber size and free wall motion are normal. the aortic valve leaflets (3) appear structurally normal with good leaflet excursion and no aortic regurgitation. there is no valvular aortic stenosis. the increased transaortic velocity is likely related to high cardiac output. the mitral valve leaflets are structurally normal. no masses or vegetations are seen on the mitral valve, but cannot be fully excluded due to suboptimal image quality. trivial mitral regurgitation is seen. the pulmonary artery systolic pressure could not be determined. there is no pericardial effusion. impression: no vegetations seen. hyperdynamic systolic function, consistent with low systemic vascular resistance . cxr : . findings: as compared to the previous examination, there is no relevant change. the position of the monitoring and support devices is constant. there is unchanged moderate overhydration with minimally increasing bilateral areas of hypoventilation. no newly appeared focal parenchymal opacity suggestive of pneumonia, no evidence of pneumothorax brief hospital course: 44 yom with hx of hep c cirrhosis recently admitted for ccy on c/b bacterial peritonitis and perihepatic fluid collection who now presents with increased lethargy, abdominal pain, elevated wbc and jaundice after non-compliance with antibiotics at home. his bilirubin continued to rise during the admission. dx paracentesis was negative. fluid collection drain was placed under ir guidance and produced purulent material. patient was treated with broad spectrum antibiotics including linezolid for previous intraabdominal vre infection as well as zosyn. paracentesis was repeated on and was negative. pt. had decreasing hcts, requiring 2u daily for maitnenance at stable level of uncear source and was scheduled for egd the morning of icu transfer (please see below for icu course). . # abdominal pain/lethargy/wbc elevation/hyperbili. was felt to be most likely infection: source was unclear at time of icu transfer, but suspected intraabdominal fluid collection as the source. the bcx were pending at time of transfer to micu, ucx were negative to date, there was no sbp and fluid collection preliminary cultures were negative, however smear was with 4+ pmns. pt. was not tachycardic on admission, however, had progressively increasing hr which was felt to be due to either worsening infection vs. gib. patient was followed by id and surgery transplant team while on the floor. wbc was stable, patient was started on zosyn empirically for a presumed intraabdominal infection and restarted on linezolid. serial exams showed worsening ascites and increasing lethargy and weakness. echo was obtained to assess for cx negative endocarditis as a possible source due to worsening murmur on exam, no vegetations were noted. patient had a progressively increasing ag on chem 7 felt to be due to worsening acidosis and renal failure. he had a developing hypercalcemia. on day of micu transfer, patient was noted to be increasingly tachypneic, more lethargic and encephalopathic. his abg was 66* 34* 7.14*4 12, showing severe acidosis and hypoxemia. lactate was 12.4. patient received 2 amps of na hco3, ivf and was transferred to the micu for further care (see below). . # anemia. patient had a slowly dropping hct during first 3 days of admission, then continued to remain aroudn 22, despite 2u daily. baseline 27-30. no egd reports in omr, but per gi notes, egd from 8 did not show varices. concern for gib given sharp drop, eg. gastrophaty, vs. new varices. patient with chronic anemia at baseline so hemolysis less concerning and most of bili is direct, however difficult to assess given liver failure. stools guiac positive. he was treated with iv ppi . patient was scheduled for egd on morning of icu transfer. . # arf. baseline 0.6 - 0.8, na < 10 in urine. cr was 0.9 on admission, however increased to 1.5 by hd4. it improved to 1.0 w/ 2u prbcs and 50g albumin x2. etiology was felt to be pre-renal given suspected sepsis, but pt. was also hyperdynamic on exam, and did not respond to an initial fluids challenge, thus concern for hepatorenal. u/a was unremarkable. patient had slight hydronephrosis on ct . . # hep c cirrhosis: patient's home fursemide and atenolol were held in setting of infection. meld was 34 on . patient remained on transplant list prior to entering micu. he was continued on home midodrine, lactulose, rifaximiin, and cholestyramine for pruritis. . # hypothyroidism: patient was continued on home levothyroxine. . micu course: . the patient was transferred to the micu for hemodynamic instability and elevated lactate. during his initial survey and access placement he developed a lower gi bleed. central line was placed, the patient was intubated and blood rapidly transfused. he was stabilized with continually elevating lactate. surgery, gi, renal & infectious disease were consulted to provide recommendations to comment on refractory acidosis, pancolitis (c. diff), oliguric renal failure, worsening liver failure and persistant hypotension. fluid collection cultures eventually grew vre. bcx were negative and sputum and urine showed budding yeast. patient was treated with broad spectrum antibiotics. he was found to be a non-operative or endoscopic candidate and hemodialysis was not offered. he was maintained on levophed, neosynephrine and vasopressin while sedated and intubated. over his 3 days in the micu several family meetings were held and the patient was first made dnr/dnri then cmo. he passed on at approximately 6:30pm. medications on admission: linezolid 600mg po q12h (not taking) levothyroxine 75mcg daily clotrimazole 10 troch prn 5 times daily oxycodone 5mg q4h prn pain lactulose 30mg po tid methadone 10mg daily docusate senna midodrine 5mg tid atenolol 50mg daily furosemide 40mg discharge disposition: expired discharge diagnosis: death due to hemodynamic collapse and sepsis. discharge condition: death discharge instructions: none followup instructions: none procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours insertion of endotracheal tube percutaneous abdominal drainage transfusion of packed cells diagnoses: acidosis thrombocytopenia, unspecified abnormal coagulation profile anemia, unspecified other postoperative infection cirrhosis of liver without mention of alcohol chronic hepatitis c without mention of hepatic coma chronic hepatitis c with hepatic coma acute kidney failure, unspecified portal hypertension unspecified acquired hypothyroidism acute respiratory failure other ascites streptococcus infection in conditions classified elsewhere and of unspecified site, streptococcus, group d [enterococcus] hemorrhage of gastrointestinal tract, unspecified hyperosmolality and/or hypernatremia peritoneal abscess hypercalcemia 

Answer: The patient is high likely exposed to