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: history of present illness: this is an 81-year-old with no significant past medical history who is transferred from hospital for anemia, melena, acute renal failure and rule in myocardial infarction. this is an 81-year-old with no medical history except for tophaceous gout who was in her usual state of excellent health until three days prior to admission when after lunch, she laid down because she did not feel well. she sleeps in a different room from her husband, with whom she lives. when he asked her later that evening how she was, she said she was fine. the next day, she continued to remain in bed. he offered her some juice, which she drank, but she was slowly becoming more confused and lethargic. on the third day, she was barely arousable and incoherent. he called ems who found her to be "incontinent of urine." she was taken to hospital where she was lethargic, oliguric and confused. she had a rectal temperature of 87 degrees. her pulse was 80 with a systolic blood pressure of 72-135. she was found to be guaiac positive with a fingerstick of 38. her white blood cell count was 17.1, 87% neutrophils, 14% bands, 4% lymphocytes and 2% monocytes. her hematocrit was found to be 16.1. he platelet count was 100,000. her chem-7 revealed a sodium of 148, potassium 4.8, chloride 118, bicarbonate 15, bun 83 and creatinine 2.5. her ck was 499 with an mb of 60 and an index of 12. her inr was 2.6. blood cultures times two were negative. a head ct was performed which showed enlarged ventricles, but was otherwise negative. she was resuscitated and given two units of packed red blood cells. she was warmed to a rectal temperature of 94 and transferred to for further care. on arrival, her temperature was 98 and she had a systolic blood pressure in the low 100s. she received more blood products and vitamin k and was admitted to the medical intensive care unit. past medical history: tophaceous gout. medications: advil 1 tablet q.d. allergies: no known drug allergies. social history: no tobacco or alcohol use. never visited a doctor. lives with her husband in . does the banking, and shopping and cooking. is very active at home, taking care of her husband of the past 60 years. family history: a sibling with diabetes. physical examination: this is an ill-appearing elderly woman who had a temperature of 98 rectally, a blood pressure of 106/50. pulse of 87. respiratory rate of 28 and an oxygen saturation of 100% on 100% nonrebreather. she was normocephalic, atraumatic with a 2 mm right pupil and a 1 mm sluggish left pupil. she had anicteric sclera. her mucous membranes were dry. she had upper dentures and dried blood on her upper palate above her dentures. her neck had no masses. her chest was clear except with good air movement except for decreased breath sounds at the right base. her heart was regular in rate and rhythm with no murmurs. her abdomen was moderately distended without rebound or guarding and good bowel sounds. her back had no overt lesions. she had a fluctuant mass along her right thorax extending from her axilla to her iliac crest without erythema. she had large gouty tophi and joint disease of bilateral hands and feet. she had 2+ anasarca. she had 2+ bilateral radial and dorsalis pedis pulses. she had ischemic discoloration of her right second finger, left second to fourth digits in all ten toes bilaterally. she had numerous ulcerations on her feet. her gout involved the small joints of her hands, as well as both her elbows and both her knees. on neurological exam, she was awake and responded to voice, but did not answer questions. her extraocular movements were intact and she was moving all her extremities, as well as withdrawing to pain. laboratory data on arrival: white blood cell count of 15.9, hematocrit of 24.9, a platelet count of 117,000, inr of 2.6, an arterial blood gas of 7.41, 28 and 114. a negative toxicology screen and a chem-7 consistent with that of the outside hospital. albumin is 3.1, ast of 749 with alt of 437. alkaline phosphatase of 269 and a total bilirubin of 1.9. her tsh was 6 with a free t4 of 0.7. her cortisol was 55. amylase and lipase revealed a 123 and 405. her ck was 485. it peaked at 1064 and then returned to . her troponin peaked at 1.4. electrocardiogram revealed normal sinus rhythm at 90 beats per minute with low voltage in the limb leads. she had normal axis, normal intervals and no acute st changes. chest x-ray showed low lung volumes and bilateral pleural effusions, right greater than the left, with associated collapse of her right lower lobe and right middle lobe. abdominal ct revealed a large right and a moderate left pleural effusion, as well as ascites. she also had a right subcutaneous fluid collection. she had a uterine fibroid. her bowels appeared normal as did her liver and gallbladder. she had atrophic kidneys with scattered cysts. she had normal pancreas, spleen and adrenals. hospital course: on admission to the medical intensive care unit, she was resuscitated with two units of ffp, 1 mg of intravenous vitamin k, intravenous fluids and she was started on antibiotics, mainly vancomycin, ceftriaxone and flagyl. she did not require pressors at any point during her stay. the main initial differential included ttp, although, her coags were abnormal and she had a negative lupus anticoagulant and anticardiolipin antibodies, so that diagnosis was excluded. the main concerns then were either sepsis leading to dic or massive gastrointestinal bleed leading to dic. she spent six days in the intensive care unit where she was persistently obtunded and guaiac positive. however, she was hemodynamically stable and was easily weaned off all supplemental oxygen and remained with a good blood pressure. multiple blood cultures were negative. she had a single urine culture on presentation that had 10-100,000 pansensitive e. coli, but all subsequent urine cultures were negative. her necrotic toes were cultures and grew out polymicrobial gram positive cocci and gram negative rods. she was given the diagnosis of sepsis of unknown etiology with complications of dic and multisystem organ failure, namely acute renal failure, shock liver, acute myocardial infarction, altered mental status and digital necrosis. she also had gross anasarca. given her altered mental status, mr of her head was performed which revealed chronic microvascular infarct, but was negative for anoxic brain injury or major infarct. an lumbar puncture was negative with normal protein and glucose and negative cultures. an electroencephalogram was consistent with toxic metabolic encephalopathy. her b12, folate and rpr were all normal. her arterial blood gases remained within normal limits. her white blood cell count fell to approximately 13. her inr improved with vitamin k and ffp. she initially had a lactate of 3.9 that dropped to 1.9. her hematocrit remained stable at about 26-28. her platelets remained low in the 80,000s. her creatinine peaked at 3.9 and then slowly dropped to approximately 1.4. her bicarbonate improved from 17 to 25. her transaminases returned to . her alkaline phosphatase stabilized in the 300-400 range. numerous consultations were obtained including a cardiology that stated that her myocardial infarction was likely in the setting of severe anemia and sepsis. an echocardiogram revealed severe apical hypokinesis with decreased systolic function and a small effusion with fiber and deposits on the cardiac surface. cardiology recommended no anticoagulation given her anemia and guaiac positive stools. they recommended keeping her hematocrit about 30 and the use of a beta-blocker if she became hypertensive or tachycardic, neither of which happened during her stay. hematology was also consulted regarding her coagulopathy. they felt it was consistent with dic and was not ttp. they recommended vitamin k supplementation which improved her inr. she did, however, have a persistently elevated ptt despite having a negative lupus anticoagulant and anticardiolipin antibody. the renal service was consulted and diagnosed her with atn with muddy brown casts. he creatinine slowly improved from a peak of 3.9 to 1.4. her anasarca improved with diuresis. she did not require hemodialysis. a rheumatology consult stated that she had chronic gout with no apparent acute flare of any joints. she was unable to receive colchicine or nsaids due to her acute renal failure and would not have benefited from allopurinol at that time. her right elbow was causing her some discomfort and was tapped twice during her stay. both times, it was negative for infectious arthritis, but did reveal crystals suggestive of gout. the vascular surgery service was consulted and continues to follow her throughout her stay with regard to the gangrene of her toes. her lower extremities were elevated and received wound care. amputations were recommended when she was medically stable. her toes were never a cause of her sepsis and never look infected. they were debrided as necessary. they became very well demarcated and healed nicely. the gastrointestinal service was consulted. they felt that she most likely had pancreatitis and were uncertain what the initial cause of her sepsis or her massive gastrointestinal bleed was. they recommended transfusions, following her guaiac and no ng suction. they stated that neither esophagogastroduodenoscopy nor colonoscopy could be done until six weeks after her myocardial infarction unless she demonstrated active bleeding. however, her hematocrit remained stable after her initial transfusion. after six days in the unit, she was transferred to the floor. there was a concern that her mental status were due to the morphine and ativan she was receiving because of her extreme pain during dressing changes. during her stay in the unit, she was nearly constantly crying or screaming. on the floor, she remained hypothermic with an alkaline phosphatase of about 500. her white blood cell count increased to about 26. her stool culture was negative for c. difficile times three. she was changed from ceftriaxone to ceftazidime and remained on broad spectrum coverage. she continued to have excellent saturations and blood pressures. her only focal sign remained abdominal pain. an ultrasound was unhelpful. a second ct was obtained which showed a large gallbladder that was not inflamed with a large gallstone. there was no pericholecystic fluid or biliary dilatation or obstruction. during this time, she had been started on tube feeds. however, she had an episode of nausea and vomiting with aspiration and so she was made npo and tpn was started via a picc. due to the concern for cholecystitis, a hida scan was performed which showed no uptake. this was consistent with acute cholecystitis and there was a potential that this could have been the triggers setting off her sepsis. a gallbladder drain was placed by interventional radiology as general surgery consulted and stated that she was far too ill to undergo surgery. her viral culture was negative. in the continued search for a source of her sepsis, her pleural effusion was tapped. it was transudate and the cultures were negative. her ascites was also tapped. her serum to ascites albumin gradient was 1.1. she had 1700 white blood cells with 60% polys and a negative gram stain and cultures. at that point, she had received adequate coverage for bacterial peritonitis with ceftriaxone and then ceftazidime. after the gallbladder drain was placed. her white blood cell and alkaline phosphatase started to decrease, but after a few days, her total bilirubin, white blood cell count and alkaline phosphatase once again started to rise for unclear reasons. a ggt was checked to insure that the alkaline phosphatase was of liver source and it was very elevated. she also had a mild lipase leak at this point from 45 to 71. there was a concern for gallstone pancreatitis or cholangitis. she continued to have melena throughout this time. a magnetic resonance cholangiopancreatography was performed which showed pancreatitis and no biliary dilatation, but raised the question of a mass in the head or uncinate process of the pancreas and also a question of duct disruption. as her alkaline phosphatase continued to rise, from the 500s to the 1000s and her total bilirubin increased to 2.2 and her lipase increased to 123, an endoscopic retrograde cholangiopancreatography consult was obtained. the endoscopic retrograde cholangiopancreatography fellow recommended a cholangiogram as an initial first step. this was done injecting dye through her gallbladder drain. this revealed a distal common bile duct obstruction, question stenosis versus stone with no duodenal filling and mild dilatation of her hepatic and common bile ducts. also during this time, other sources of infection were being sought and an mri of her feet were done, which were negative for infection. as above, her right elbow joint was also tapped and was negative for septic arthritis. after the cholangiogram revealed obstruction, an endoscopic retrograde cholangiopancreatography was performed which revealed no pus or masses but did reveal ampullary stenosis. a sphincterotomy was performed. on the floor, after her endoscopic retrograde cholangiopancreatography, she developed post endoscopic retrograde cholangiopancreatography pancreatitis and her lipase rose to 163. she had increasing abdominal tenderness and became slightly more confused. prior to the endoscopic retrograde cholangiopancreatography, her mental status had greatly improved, although, she still was not speaking, she was alert. after the endoscopic retrograde cholangiopancreatography, a third abdominal ct with intravenous contrast was obtained to evaluate for potential endoscopic retrograde cholangiopancreatography induced perforation of the intestine or for pancreatic mass given the question raised on the magnetic resonance cholangiopancreatography done earlier. abdominal ct number three revealed pancreatitis with no hemorrhage or significant necrosis and no pancreatic mass. she had no signs of perforation secondary to her endoscopic retrograde cholangiopancreatography and no bowel ischemia. after the endoscopic retrograde cholangiopancreatography, her total bilirubin dropped to normal, however, her alkaline phosphatase continued to increase from the 1100s to the 1700s. as she slowly recovered from her endoscopic retrograde cholangiopancreatography pancreatitis, not only did her alkaline phosphatase continue to rise, but she developed a direct hyperbilirubinemia again. at this point, she began growing from her blood and her urine. she received 24 days of broad spectrum antibiotics at this point. her antibiotics were stopped and her tpn was stopped as well. her picc line was removed. she was started on fluconazole. right around this time, she developed dysarthria and a facial droop that was unclear if it was new. a repeat mri with gadolinium was the same as her previous. the repeat was done on and it showed no changes from the mri on . a repeat electroencephalogram was normal. over a few days, her dysphonia improved. she remained on her fluconazole. surveillance blood cultures were negative. a repeat cholangiogram showed normal biliary tree and flow. this cholangiogram was performed as her alkaline phosphatase had continued to rise from the 1700s to the . a repeat bile culture grew yeast. her white blood cell count remained stable between 16 and 20,000 throughout this time. she was restarted on tube feeds as her post endoscopic retrograde cholangiopancreatography pancreatitis was improving. an ophthalmology consult was obtained to evaluate for fungal eye disease secondary to her candidemia. she had no evidence of fungal eye disease. after she developed candidemia and with her increasing alkaline phosphatase, her creatinine bumped from 1.4 to 1.6. despite her positive cultures, she continued to improve in terms of mental status, abdominal pain, and renal function. however, since her bile culture had grown out , her gallbladder drain was removed. after it was pulled, she had leakage of her ascites out of the cutaneous fistula tract that had led to her gallbladder. the ascitic fluid was tinged brown with concern for bile spillage into the peritoneal cavity. over the afternoon after her gallbladder drain was pulled, she demonstrated increasing abdominal tenderness and guarding that was new. this was discussed with the gastrointestinal and radiology services who stated that she should be started on broad spectrum antibiotics to cover potential secondary bacterial peritonitis, although, she was most likely suffering from a chemical peritonitis secondary to bile spillage. fluid was sent for gram stain culture and fungal culture. radiology stated that in the presence of ascites, the site of her gallbladder drain in the gallbladder wall was less likely to close off immediately after the catheter was pulled, but should close with time. they recommended supportive care through this peritonitis. later that evening, she was noted to be bradycardic on telemetry. a code was called. she underwent pea arrest and was transferred to the medical intensive care unit after she was resuscitated. , m.d. dictated by: medquist36 procedure: venous catheterization, not elsewhere classified continuous invasive mechanical ventilation for 96 consecutive hours or more parenteral infusion of concentrated nutritional substances diagnostic ultrasound of heart insertion of endotracheal tube enteral infusion of concentrated nutritional substances endoscopic sphincterotomy and papillotomy endoscopic dilation of ampulla and biliary duct other cholecystotomy diagnoses: acute kidney failure with lesion of tubular necrosis acute and subacute necrosis of liver unspecified septicemia acute respiratory failure defibrination syndrome disseminated candidiasis acute pancreatitis calculus of gallbladder with acute cholecystitis, without mention of obstruction gouty tophi of other sites, except ear 

Answer: The patient is high likely exposed to