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: keflex / percodan / duragesic / procardia / augmentin / iodine; iodine containing / fentanyl / amiodarone attending: chief complaint: melena, chest pain major surgical or invasive procedure: coronary catheterization history of present illness: 84 yo f w/ hx of cad s/p angioplasty (anatomy unknown), extensive pvd s/p aorto-bifem bypass, paf on coumadin, and h/o gi bleed in who is transferred from after reportedly presenting with hematemesis with a hct of 16 and cp. the pt denies any episodes of hematemesis and states that she presented to the hospital in the setting of increasing frequency and severity of non-radiating sscp. she has had "stable angina" for several years after her poba in ' but this has worsened over the past few months to the point that she will have these symptoms at rest. three weeks ago, she had episodes of melena. her pcp referred her for a egd/colonoscopy that showed minor gastritis without any gastric or duodenal ulcers and severe diverticulosis to the cecum. she did not undergo a capsule endoscopy. . four days prior to admission, she had a repeat episode of melena. she denies brbpr or hematemesis. this was accompanied with worsening ? pleuritic sscp with sob. she was then evaluated at the osh where she was found to have a hct of 16, inr 3.7, troponin i 2.10, and depressions in lead i, avl, v3-6. she was transfused a total of 5 units prbc and given ffp to a hct of 33.1 and inr 1.4 at the time of transfer. asa, coumadin, and cilostazil were held and a protonix gtt was started. gi was consulted and held off on scoping her in the setting of stuttering chest pain not completely relieved with a nitro gtt and iv morphine, worsening ekg st depressions on ekg, and a troponin i peak to 57.27, ck 711, and mbi 11.1. she was transferred to for further cardiac and gi evaluation. . on review of symptoms, she denies any prior history of stroke, tia, deep venous thrombosis, pulmonary embolism, bleeding at the time of surgery, myalgias, joint pains, cough, and hemoptysis. she denies recent fevers, chills or rigors. she does complain of rest calf pain for which she saw dr. in clinic on and the plan was for an angiogram via the l brachial approach with possible catheter based intervention. all of the other review of systems were negative. . cardiac review of systems is notable for absence of paroxysmal nocturnal dyspnea, orthopnea, palpitations, syncope or presyncope. + le edema, chest pain, sob as above. past medical history: # cad, s/p angioplasty (anatomy unknown), no h/o stents # paroxysmal afib - on coumadin # hypertension # gerd, on daily ppi 40mg # diverticulosis # chronic renal failure, baseline 1.3 # pvd, s/p left fem-at', and aortobifem bypass ' - rest pain at baseline # bilateral ras # sma stenosis # s/p bilateral carotid endarterectomies # cholecystitis # s/p thyroidectomy # s/p l hip orif # s/p hysterectomy social history: significant for previous tobacco use, approx. 20 pack-year hx, quit smoking >40 yrs ago. there is no history of alcohol abuse. family history: significant for mi in brother age 35, mi in another brother 46, another brother in his 80s, one sister at age 60. one brother had a stroke at age 60. several members with diabetes. physical exam: (on admission) vs: t 98.7, bp 149/60, hr 88, rr 24, o2 98% on 10l vm gen: elderly woman sitting in hosp bed in nad wearing face mask. oriented x3. mood, affect appropriate. pleasant. heent: sclera anicteric. perrl, eomi. conjunctiva were pink, no pallor or cyanosis of the oral mucosa. neck: cv: pmi located in 5th intercostal space, midclavicular line. rr, normal s1, s2. no s4, no s3. i-ii systolic ejection murmur best heard in and ll sb. chest: resp were unlabored, no accessory muscle use. bil crackles >1/2 up posterior lung fields. no wheezes, or rhonchi. abd: abdomen rounded, soft, bs+, diffuse abodominla tenderness to deep palpation, soft masses in llq and luq consistent with stool. no hsm or tenderness. ext: no c/c/e. no femoral bruits. skin: no stasis dermatitis, ulcers, scars, or xanthomas. pulses: right: carotid 2+ without bruit; femoral 2+ with bruit (not as loud as on l), 1+ dp/pt : carotid 2+ without bruit; femoral 2+ with loud bruit; 1+ dp/pt pertinent results: cath (): 2vd with subtotally occluded rca-difficult target for pci and in setting of rapid afib, gi bleed prefer medical therpapy for now lmca: short vessel lad: diffuse mild lcx: 60% irregular om1; distal diffuse 60% before lpl rca: serial 90% proximal. mid and distal with compewtitive flow to r pda from l-->r collaterals. very difficult to engage rca due to turtuosity and root anatomy . ck peak: 1316 . echo (): left atrium is normal in size mild symmetric left ventricular hypertrophy with normal cavity size moderate global left ventricular hypokinesis, with the basal segments contracting best (lvef = 35 %) no masses or thrombi are seen in the left ventricle right ventricular chamber size is normal with mild global free wall hypokinesis aortic valve leaflets are moderately thickened the mitral valve leaflets are mildly thickened with mild to moderate (+) mitral . echo (): no evidence of endocarditis. moderate mixed global and regional left ventricular systolic dysfunction. mild right ventricular systolic dysfunction. moderate mitral regurgitation. otherwise no change. . cta, chest (): 1. pulmonary emboli involving the left lower, right middle, and right lower lobes. 2. multiple patchy opacities in the lungs, including a more discrete nodular opacity in the right upper lobe measuring 8 mm. differential includes infectious and inflammatory etiologies. particularly given the more discrete right upper lobe nodule, followup within three months is recommended to demonstrate resolution. 3. suggestion of right subclavian vein thrombus in this non-tailored studies with chest wall and paraspinal collaterals. 4. prominent mediastinal lymph nodes. 5. extensive atherosclerosis with aortic valve calcifications as well. . us abd (): there are layering gallstones without cholecystitis. the liver shows no focal or textural abnormalities. the right kidney measures 10.4 cm. the left kidney measures 9.4 cm. there are no stones or hydronephrosis. the spleen and visualized portions of the pancreas are unremarkable. impression: 1. limited views of the kidneys. no stones or hydronephrosis. 2. cholelithiasis without cholecystitis. . abd portable (): mildly dilated air-filled small and large bowel loops. air is seen within the rectum; findings may represent an evolving ileus. . ct head (): there is loss of -white matter differentiation and mild focal effacement of the left mca territory with preservation of -white matter and sulci within the aca and pca territory. also noted is a asymmetrically dense left mca. together these findings are consistent with left mca occlusion and infarction. there is a small amount of mass effect exerted on the left of the lateral ventricles, however, no shift of the midline. no additional areas of infarction are identified. there is no hydrocephalus. there is no intracranial hemorrhage. impression: large left mca territory stroke likely secondary to left mca thrombus. mild mass effect exerted on the left frontal of the lateral ventricle, with no evidence of herniation. . brief hospital course: pt was admitted to the ccu at for further work-up and treatment of her medical condition. she appeared to be in acute heart failure when arriving to the ccu thought transfusion of red blood cell products at the osh and given the history of sob, fatigue and crescendo angina over 2-3 weeks she was thought to have acs in addition to the demand ischemia the hct of 16. pt was monitored on telemtery overnight with diuresis for chf. in the am pt was taken to cath lab for coronary catheterization. cath demonstrated 2vd with subtotally occluded rca which was considered a difficult target for pci due to turtuosity and root anatomy and given rapid afib, and hx of major gib bleed x2 it was decided to treat with medical management (asa, plavix, bb). the lcx did have a 60% irregular om1 that later was thought to likely be the culprit vessel and the plan was to return to the cath lab once the pt was stabilized. given the hx of melena and report from the osh that also had hematemesis (which likely was not the case in retrospect) the decision was made to not immediately dicontinue the subclavian central line plced at the hospital as there was a concern over not having any access in case of a sudden hemtocrit drop or hypotension. over the next 2 days the pt was diuresed successfully with pt being weaned from the non-rebreather to 2-3l of oxygen. at this time she was transferred to the floor. at the same time pt was found to have a urinary tract infection (later grew out to be pan-sensitive e.coli) for which she was initially placed on ciprofloxacin. when the skin appeared slightly red around the area surrounding the subclavian line on the morning after transfer to the floor, the subclavian line was discontinued and pt was switched to bactrim in order to cover both a possible skin infection and the uti. the following day (), a trigger was called on the floor due to tachycardia. when examined pt was febrile to 103.3 and was tachypnic. abg 7.48/46/230 on the non-rebreather with a lactate of 3.1. sepsis was suspected and therefore broad spectrum coverage was started with vancomycin and zosyn. pe from the subclavian line was also suspected and therefore heparin iv was initiated. pt was transferred to the ccu for further care at this time. a ct scan of the chest was done which confirmed bilateral pe's as well as subclavian thrombosis at the site of the previous subclavian line. in the unit pt stabilized and did not need to be intubated acutely. over the next 3 days pt continued to be in some respiratory distres with consinued oxygen requirement and with pleuritic chest pain consistent with bilateral pes. she intermittently had increased respiratory difficulties thought related to additional clot burden from the subclavian thrombosis. the team considered taking her to the vascular lab to reduce the clot burden, the plan on was to proceed with this should she again desaturate. the blood cultures drawn at the time of the trigger grew out staph aureus sensitive methicillin therefore pt was transitioned from vancomycin to nafcillin. a tte in the ccu on did not demonstrate any valvular abnormalities. daily serial blood cultures were checked and returned negative to date. the e.coli sensitivities came back pan-sensitive and therefore she was stiched to ciprofloxacin. from a gi standpoint pt was seen and evalutated by gi on the day of arrival; they planned to do an egd/colonoscopy on pt after the coronary cath. pt was therefore given the golytely on the evening of but was not able to tolerated the per; the procedure was therefore post-poned and planned for the following day. she was started on a mag citrate prep for this on but was aborted after the trigger event. regarding the melena with hct of 16 on presentation to the osh: had egd/ 3 weeks prior to presentation with gastritis and sigmoid diverticulosis. she was thoguht to have an upper source given melena such as an avm or aspirin induced gastritis. pt did have melena when she was receiving the bowel preps but aside from those 2 days did not have any furhter melena and her hct remined stable at post-transfusion level. pt did complain of abdominal pain but stated this was only slightly increased from her baseline. abdominal films were intially unrevealing but then showed ileus likely opiates pt was given, therefore stool softeners were increased. for her paroxysmal atrial fibrillation the coumadin was held acute massive gib with hct of 16. her inr was 1.3 on arrival to the ccu at . heparin drip was started on for pe. pt was rate controlled wih metoprolol. when pt was found ot be bacteremic the metoprolol was held --> subsequently went into afib with rvr that broke with boluses of lopressor and diltiazem. diltiazem drip was started at this time with good effect. in order to decrease the work of the heart, esmolol was started instead of diltiazem but unfortunately caused hypotension, and therefore diltiazem had to be restarted which was done with good effect. pt did have acute renal failure after cath with a creatinine trending 1.7 --> 2.2 --> 2.4 thought to be contrast nephropathy, and feurea was consistent with atn. pt had no hydronephrosis on u/s. as mentioned above pt was stabilized when back in the ccu, and did not need to be intubated acutely. over the next 3 days pt continued to be in some respiratory distres with consinued oxygen requirement and with pleuritic chest pain consistent with bilateral pes. on the morning of during team rounds it was explained to the pt that she may have to be intubated since she was tiring out with use of accessory muscles to breathe. she stated that she did not believe in prolonging a persons life when it is their time to go, but after dr. explained that he beleived it would be temporary she agreed to possible intubation should it become necessary. approx 2 hrs later when the team was still in rounds, the team was notified by the nurse that she looked worse and was difficult to arouse. when the team saw her she was unresponsive, and she was therefore ventilated with mask while anaesthesia was called for intubation. abg at this time was 7.36/56/119. pt was intubated for what was thought to be respiratory failure caused by multiple pes in addition to fluid overload. at approx 7pm on the same day the team was again approached by teh same nurse who now had noted a change in her exam; she was rigid in the lue and flaccid on the lue, and with bilateral babinskis. a stat ct scan was ordered demonstrating large left mca territory stroke likely secondary to left mca thrombus with mild mass effect exerted on the left frontal of the lateral ventricle, with no evidence of herniation. at this time the heparin was decreased to a ptt goal of 50-60 per neuro recs. neuro found it contraindicated to give tpa given any of large area of the stroke, gib and time lapsed from likely event. husband was who wanted to sleep on what to do further given the sudden change in her status. when seen in the the husband decided to make pt cmo as he felt it was her wishes, in addition the team agreed given she had stated she did not want to be intubated unless it was a likely reversible event. pt was therefore made cmo (including extubation) and expired shortly thereafter. medications on admission: aspirin 162 mg po daily cilostazol 100 mg metoprolol tartrate 75 mg pantoprazole 40 mg daily warfarin 1 mg daily nitroglycerin 0.4 mg sl prn discharge medications: n/a discharge disposition: expired discharge diagnosis: non st elevation myocardial infarction gastrointestinal bleed acute congestive heart failure multiple transfusions bilateral pulmonary embolisms mssa bacteremia e.coli uti l mca stroke discharge condition: expired discharge instructions: n/a followup instructions: n/a procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours venous catheterization, not elsewhere classified combined right and left heart cardiac catheterization coronary arteriography using two catheters insertion of endotracheal tube enteral infusion of concentrated nutritional substances diagnoses: subendocardial infarction, initial episode of care coronary atherosclerosis of native coronary artery esophageal reflux urinary tract infection, site not specified congestive heart failure, unspecified unspecified essential hypertension acute kidney failure, unspecified atrial fibrillation acute respiratory failure bacteremia methicillin susceptible staphylococcus aureus in conditions classified elsewhere and of unspecified site hemorrhage of gastrointestinal tract, unspecified urinary complications, not elsewhere classified cerebral artery occlusion, unspecified with cerebral infarction other pulmonary embolism and infarction 

Answer: The patient is high likely exposed to