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: no known allergies / adverse drug reactions attending: chief complaint: confusion major surgical or invasive procedure: intubation/mechanical ventilation arterial line lumbar puncture history of present illness: 61yom with hep c cirrhosis complicated with portal vein thrombosis on coumadin, known grade 1 varices, ascites on lasix 40mg, hepatic encephalopathy in past, on wait list for combined liver/kidney with meld 29, ckd from diabetic nephrosclerosis, and dm2 is admitted with confusion for 10 days and is transferred to the micu for unresponsiveness. according to the report, he reported taking less lactulose then normal, usualy takes 3 a day but has been taking 1 a day for the last 2 weeks. as a result, he has noticed he is more confused and sleepy than usual. has been oversleeping to 3pm daily. says he has been struggling to use phones lately, ataxic gait (uses cane at baseline). denies any fevers at home. does report 2 episodes of emesis (brown tinge) in the last 10 days, non-bloody non-bilious. last episode two days ago. no recent med changes. denies chills, cough, sob, chest pain, dysuria, no increase in abd girth. was seen by pcp at and subsequently referred in for assessment. . of note, pt admitted in for anemia and abdominal pain. he was managed conservatively with iv hydration and npo, and vanco/zosyn-->cipro/flagyl, continued on cipro for prophylaxis. transfused for hct goal 27. pt found to be pancytopenic due to hypersplenism. . in the ed, initial vs:97.2 62 136/63 18 100%. ammonia 85. lactate 2.1. bicarb 19. cr 2.2. wbc 2.9, hct 28.9, plt 66. inr 3.4. ptt 49. head ct, no acute process. cxr no acute process. bedside abd u/s scant ascites, not amenable to tap. given 500cc ivf. transfer vitals: 64 hr, 138/65, 98 on ra, temp 97.6, rr 18 . on arrival to the floor, he reported confusion but was a+o x3, knows he is at . he asked for narcotics and became angry when they were not given. he refused to take lactulose. at the time of 5am morning vitals, he was unresponsive to pain, loud voice or sternal rub vitals were 112/56 62 18 100% on nrb (nrb placed despite o2 sat >95% on ra). abg showed 7.50/28/91/23. he was then transferred to the micu for closer monitoring. past medical history: - hepatitis c cirrhosis genotype 1a (c/b h/o portal hypertension/ ascites/encephalopathy/sbp) awaiting combined liver/kidney , hepatitis c viral load : 401,000 iu/ml; meld 20 on . - esophageal varices: endoscopy : grade i varices - ckd (baseline cr = 1.4-1.5): diabetic nephrosclerosis by biopsy - diabetes (last hga1c 6%) with neuropathy - ribavirin-induced hemolytic anemia - history of spontaneous bacterial peritonitis - pancytopenia likely d/t hypersplenism - chronic hyperkalemia - hypertension - h/o ivdu with methadone maintenance, now off all therapy - dvt s/p ivc filter placement ()- spontaneous in setting of hepatic encephalopathy - hemmorhoids - hx of pv thrombosis, restarted on coumadin social history: works as a carpenter. lives with sister. recently quit smoking, 30 pack year history. sister is hpa. prior history of ivdu heroin and cocaine quit 7 years ago. on methadone until 2 years ago. denies alcohol, drugs recently. lives in alone. family history: father died at 55, no history of blood clots in family physical exam: vitals: t:97.6 bp:112/56 p:62 r: 18 o2: 100% nrb general: eyes closed mouth open, snoring. not responsive to pain or loud voice heent: pupils 5mm and reactive peerl sclera anicteric, mmm. edontulous neck: supple, jvp not elevated, no lad cv: regular rate and rhythm, normal s1 + s2, no murmurs, rubs, gallops lungs: clear to auscultation bilaterally, no wheezes, rales, ronchi abdomen: soft, non-tender, non-distended, bowel sounds present, no organomegaly gu: no foley ext: chronic venous stasis changes on lower extremities bl. warm, well perfused, no edema neuro: positive corneal reflex. flacid upper and lower extremities. . pertinent results: 02:06pm blood wbc-2.9* rbc-3.24* hgb-9.8* hct-28.9* mcv-89# mch-30.4 mchc-34.1 rdw-17.5* plt ct-66*# 02:06pm blood neuts-77.7* lymphs-11.2* monos-4.6 eos-5.8* baso-0.6 02:06pm blood hypochr-1+ anisocy-1+ poiklo-1+ macrocy-normal microcy-normal polychr-normal ovalocy-2+ 02:06pm blood pt-34.9* ptt-48.9* inr(pt)-3.4* 02:06pm blood glucose-315* urean-48* creat-2.2* na-141 k-3.9 cl-110* hco3-19* angap-16 02:06pm blood alt-23 ast-40 totbili-0.9 10:43am blood calcium-7.4* phos-2.3* mg-1.4* 02:11am blood hapto-24* 02:06pm blood ammonia-85* 02:11am blood hiv ab-negative 04:21am blood vanco-11.1 10:43am blood asa-neg ethanol-neg acetmnp-neg bnzodzp-neg barbitr-neg tricycl-neg 06:00am blood asa-neg ethanol-neg acetmnp-neg bnzodzp-neg barbitr-neg tricycl-neg 05:22am blood type-art po2-91 pco2-28* ph-7.50* caltco2-23 base xs-0 05:22am blood glucose-129* lactate-1.6 na-140 k-4.5 cl-113* 08:40pm blood freeca-1.23 ct head: impression: no acute intracranial process mri head: impression: predominantly cortical restricted diffusion. the most likely diagnosis would be diffuse hypoxic injury. other alternate possibilities include cjd but the distribution is contiguous and would be less typical. the appearances are also not typical for posterior reversible encephalopathy syndrome. cxr: the et tube tip is 3.2 cm above the carina. the ng tube tip is in the stomach. the heart size and mediastinum are unremarkable. there is interval development of widespread parenchymal opacities, with perihilar and basilar distribution, most likely representing edema, although interval development of infection is a possibility. reevaluation after diuresis is recommended if clinically warranted. there is no pleural effusion or pneumothorax. . mri head: impression: persistent areas of cortical restricted diffusion bilaterally, involving the frontal, temporal, parietal and insular regions as described above, persistent areas of restricted diffusion in the basal ganglia bilaterally. the possibility of diffuse hypoxic injury is a consideration, other causes cannot be completely excluded, including an infectious process. bilateral fluid levels at the occipital ventricular horns, suggesting intraventricular hemorrhage. there is no evidence of hydrocephalus or mass effect. . mr was performed at the level of the centrum semiovale. this demonstrates what appears to be increased choline and decreased naa. findings are nonspecific and can be seen in inflammatory disease or neoplasm. questionably increased lactate is noted in a few voxels impression: limited study due to motion. nonspecific findings on mr . . opacification of the left lung has increased, there is now a complete opacification of the left hemithorax. the left lung is normal and shows normal ventilation. unchanged course of the dobbhoff tube. a wet read was delivered at the time of image acquisition. brief hospital course: 61yom with hep c cirrhosis complicated with portal vein thrombosis on coumadin, known grade 1 varices, ascites, hepatic encephalopathy in past, previously on wait list for combined liver/kidney with meld 29, ckd from diabetic nephrosclerosis, and dm2 is admitted with confusion for 10 days now with persistent ams. # altered mental status: pt admitted initially with presumed hepatic encephalopathy as there was a history of decreased lactulose use. in the beginning of his admission he continued to refuse lactulose. later he was found unresponsive and transferred to the micu. his lactulose was restarted by ngt. his mental status improved however he was noted to have persistent confusion and significant moter deficits in non-vascular distribution and word finding difficulties. a lumbar puncture was performed which was unrevealing. multiple mris were performed which showed restricted diffusion in b/l cortices most consistent with hypoxic brain injury. neurology felt that this may still be hepatic encephalopathy though he had been stooling adequately for greater than two weeks without significant improvement in his mental status. a repeat lumbar was performed to rule out both cmv, in addition to prion disease. only a few millilters of fluid were obtained despite the fact that the procedure was done under fluoroscopy. due to the small volume only cmv pcr was sent which was negative. prognosis was felt to be extremely poor. after prolonged discussion with the family the patient was made dnr/dni. neurological status failed to improve and ultimately the passed passed away as below. . #seizure: he had a seizure during this hospitalization that was treated with iv ativan. per report he has a had a prior seizure eight years ago. his ciprofloxacin was stopped to avoid seizure threshold lowering and he was started on keppra. a video eeg did not show any seizure activity. initially his mental status was thought to be a post-ictal state, however as it did not improve with time this was not felt to be related. he was continued on keppra without further seizure activity. . # cirhosis: from hepatitis c, complicated by hepatic encephalopathy and h/o varices, portal vein thrombosis and ascites. he was presumptively treated for hepatic encephalopathy as this was felt to be a component of his ams. otherwise his liver was stable thoroughout this admission. however because of his mental deterioration he was de-activated and ultimately de-listed. . #hypernatremia: his course was complcated by hypernatremia. he was intermittently given small boluses of d5 with careful monitoring to avoid rapidly correcting his sodium levels. his free water flushes were increased and his lactulose was decreased to keep his volume adequate. . #portal vein thrombosis: he was initially on warfarin for anticoagulation. however, an showed patent portal veins and the decision was made that the risks of bleeding with continued anticoagulation outweighed the benfits and his warfarin was stopped. . # respiratory status- on the evening of the patient was noted to become acutely dyspneic. initial oxygen saturations remained stable in the high 90s. chest xray was suggestive of lung collapse which was attributed to mucous plugging. the patient's family was contact and once again expressed desire to avoid invasive procedure such as intubation. the patient's saturations began to decrease despite face oxygen. he ultimately expired. breath sounds and heart absent. pupils were non reactive and the patient was pronounced dead with family at bedside. medications on admission: propranolol 10 mg lactulose 10 gram/15 ml (15) ml po bid ciprofloxacin 250 mg daily calcitriol 0.25 mcg po mwf amlodipine 10 mg omeprazole 20 mg procrit 40,000 unit/ml solution once a week. gabapentin 300 mg qam gabapentin 600 mg qpm rifaximin 550 mg furosemide 40 mg daily coumadin 1 mg currently taking 5mg a day for last week, but was taking 3mg daily prior oxycodone mg q6h prn calcium 600 + d(3) 600 mg(1,500mg) -400 unit ferrous sulfate 325 mg (65 mg iron) ambien 5 mg risendronate 35 mg weekly fish oil 1,000 mg daily insulin glargine ten (10) units subcutaneous at bedtime. discharge disposition: expired discharge diagnosis: altered mental staus hepatic encephalopathy possible hypoxic brain injury . secondary diagnosis cirrhosis discharge condition: deceased procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours spinal tap incision of lung spinal tap incision of lung insertion of endotracheal tube enteral infusion of concentrated nutritional substances percutaneous abdominal drainage diagnoses: hyperpotassemia nephritis and nephropathy, not specified as acute or chronic, in diseases classified elsewhere cirrhosis of liver without mention of alcohol chronic hepatitis c with hepatic coma acute kidney failure, unspecified hepatorenal syndrome acquired coagulation factor deficiency portal hypertension other convulsions diabetes with neurological manifestations, type ii or unspecified type, not stated as uncontrolled polyneuropathy in diabetes candidiasis of mouth pulmonary collapse pneumonitis due to inhalation of food or vomitus anoxic brain damage cachexia long-term (current) use of insulin long-term (current) use of anticoagulants other sequelae of chronic liver disease other ascites awaiting organ transplant status urinary catheterization as the cause of abnormal reaction of patient, or of later complication, without mention of misadventure at time of procedure hyperosmolality and/or hypernatremia esophageal varices in diseases classified elsewhere, without mention of bleeding diabetes with renal manifestations, type ii or unspecified type, not stated as uncontrolled infection and inflammatory reaction due to indwelling urinary catheter mixed acid-base balance disorder other specified bacterial infections in conditions classified elsewhere and of unspecified site, other gram-negative organisms foreign body in larynx portal vein thrombosis inhalation and ingestion of other object causing obstruction of respiratory tract or suffocation infection with drug-resistant microorganisms, unspecified, with multiple drug resistance hypersplenism 

Answer: The patient is high likely exposed to