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: milk / dilantin attending: chief complaint: seizure major surgical or invasive procedure: egd peg placement intubation history of present illness: 58 yo f w/ h/o dm1, htn, hyperlipidemia, who was found down at home by her son at approximately 3am. the patient was noted to be convulsing at that time. it is unclear how long the patient had been seizing for but was last seen 1d pta at approximately 1pm. by report the patient had previously been well, but was feeling somewhat lethargic yesterday. patients son reports that she has otherwise been well. also states that he believes that she has been stretching her insulin doses since she lost her mass health. reports that she developed dka on multiple occasions in this setting. . in the ed, the patient was found to be in sustained convulsion w/ r eye deviation, broke w/ ativan 2mg x2. noted to be febrile to 102.6 and hypertensive to 226/12. given labetolol x1. further assessment revealed bs to 700s and anion gap of 29. started on an insulin drip with improvement in ag. . lp was performed, positive for leukocytosis and patient was given ceftriaxone, vancomycin, dexamethasone, and acyclovir to cover empirically for meningitis. gram stain neg. . upon arrival in the micu, the patient is intubated and sedated with propofol, with eeg leads attached past medical history: type 1 diabetes mellitus w/ h/o multiple episodes of dka and poor compliance htn asthma hyperlipidemia fibroids cataracts adenomatous polyps social history: she is not married. she lives in an apartment in with her son. she used to work taking care of children. denies any tobacco or ivda. she drinks approximately a 6 pack of beer week. family history: aunt with type 2 diabetes. her mom had a fatal mi at the age of 54. her dad had ?copd. physical exam: t 101.1, bp 148/91, p 106, r 20, 100% ac 400 x 20, 50% fio2, peep 5 intubated, sedated. atraumatic, normocephalic, eeg leads in place. but sluggish op clear, around ett. 6 cm jvp regular s1,s2. no m/r/g lca b/l +bs. soft. nt. nd. no le edema/c/c. no rashes/skin breakdown. pertinent results: admission labs: 05:43am blood urean-34* creat-2.1* na-139 k-4.2 cl-97 hco3-13* angap-33* 05:43am blood pt-12.6 ptt-30.1 inr(pt)-1.1 05:43am blood plt ct-131* 05:43am blood wbc-20.1*# rbc-4.54# hgb-13.9# hct-40.9# mcv-90 mch-30.6 mchc-33.9 rdw-13.8 plt ct-131* 05:43am blood neuts-89.7* bands-0 lymphs-6.9* monos-2.6 eos-0.2 baso-0.6 05:43am blood calcium-10.1 phos-4.1 mg-1.7 05:43am blood asa-neg ethanol-neg acetmnp-neg bnzodzp-neg barbitr-neg tricycl-neg 03:37pm blood type-art temp-38.3 rates-20/ tidal v-400 peep-5 fio2-100 o2 flow-8.0 po2-515* pco2-29* ph-7.37 caltco2-17* base xs--6 aado2-190 req o2-40 -assist/con intubat-intubated . cxr: endotracheal tube terminating in the right main bronchus 2 cm below the carina. no consolidation or effusion in the lung. . head ct: head ct without contrast: comparison was made with a prior head ct dated . there is no acute intracranial hemorrhage. there is no mass effect. no shift of normally midline structure is noted. the appearance of the brain is unchanged since the prior study, and there are multiple hypodensities in the basal ganglia representing chronic lacunar infarct. there is mucosal thickening in ethmoid sinus and right maxillary sinus, with densely calcified cystic lesion as noted previously, now filled with secretions, not significantly changed from . this likely relates to chronic sinusitis. the osseous structures are otherwise unremarkable. unchanged appearance of the brain without acute intracranial hemorrhage. densely calcified cystic lesion in the right maxillary sinus, now opacified with mucus. . carotid us: bilateral less than 40% carotid stenosis . eeg : routine time sampling: showed a very low voltage background with occasional bursts of generalized slowing and some faster frequencies, also generalized. much of the background was very supressed and slow. there were no prominent focal features, and there were no epileptiform abnormalities. sleep: no normal waking or sleeping morphologies were seen. cardiac monitor: showed a generally regular rhythm. spike detection programs: showed some artifact and occasional sharp features but no definite epileptiform abnormality. seizure detection programs: there are 2 entries in these files. they showed some minimally rhythmic slowing but no epileptiform activity. pushbutton activations: there were none. impression: this telemetry captured no pushbutton activations. the background rhythm remained supressed throughout, often correlated with use of substantially sedating medications. there were still some cortical rhythms. there were no prominent focal features although encephalopathies and medication effect can obscure focal findings. there were no epileptiform features or electrographic features. . mri head : impression: 1. several areas of slow diffusion could be due to small subacute infarcts in the left cerebral hemisphere. 2. increased signal along the sulci predominantly in the parieto- occipital region indicates increased protein content of the csf and could be related to meningitis. clinical correlation recommended. . mrv of the head: head mrv demonstrates normal flow signal in the superior sagittal and transverse sinuses as well as in the deep venous system. impression: normal mrv of the head. . mri/mra head : findings: there is much more extensive restricted diffusion involving the cortex of the left cerebral hemisphere than on the study of three days previously. there is extensive involvement of the frontal and parietal cortex with some involvement of the insula as well. the abnormalities extend to involve the posterior surface of the occipital lobe, which can be occasionally supplied by the mca. there is probably some medial occipital involvement as well suggesting pca territory involvement. there is also involvement of the deep left frontal white matter near the caudate nucleus, as seen previously. . there are several small areas of relatively increased signal in the right cerebral hemisphere, on the diffusion-weighted images, which might be artifactual. currently the flair images show flair hyperintensity in the involved cortex and white matter but no increased signal and subarachnoid hemorrhage to suggest increased protein. . as seen previously, there is an old left putaminal hemorrhage with associated hemosiderin. there is old infarct in the left corona radiata. there is no mass effect on the ventricular system or midline structures. . impression: there is extensive primarily cortical infarct within the left mca territory. as discussed above, there is involvement of least portions of the occipital lobe, perhaps also supplied by the mca in this patient as opposed to representing a pca territory infarct. there are questionable right cerebral abnormalities. . mra of the head. the distal left internal carotid artery is widely patent. the proximal left mca remains normal and unchanged from . currently there is more extensive visualization of distal left mca branches than right, suggesting luxury perfusion. the left pca originates from the basilar artery and is symmetric with the right and normal in appearance. the acas remain normal. there is some irregularity of the right mca proximally and distally, which could be artifactual or perhaps related to mild atherosclerosis. this questionable finding was not present previously. the opacification of the paranasal sinuses has improved slightly compared to the prior study. . impression: there is no evidence of intracranial left internal carotid artery or left mca stenosis. the left mca is unusually well seen distally, and quite asymmetric with the right mca suggesting luxury perfusion. . tte : the left atrium is normal in size. no atrial septal defect or patent foramen ovale is seen by 2d, color doppler or saline contrast with maneuvers. there is mild symmetric left ventricular hypertrophy. the left ventricular cavity size is normal. overall left ventricular systolic function is low normal (lvef 50%) secondary to extensive, severe apical hypokinesis with focal dyskinesis. an apical thrombus was not seen but cannot be excluded with certainty on the basis of this study. there is no ventricular septal defect. right ventricular chamber size is normal. there is focal hypokinesis of the apical free wall of the right ventricle. the ascending aorta is mildly dilated. the number of aortic valve leaflets cannot be determined. the aortic valve leaflets are mildly thickened. the mitral valve appears structurally normal with trivial mitral regurgitation. there is no mitral valve prolapse. the left ventricular inflow pattern suggests impaired relaxation. there is mild pulmonary artery systolic hypertension. there is no pericardial effusion. . compared with the findings of the prior study (images reviewed) of , extensive apical akinesis is now present. . focused study using definity contrast . no masses or thrombi are seen in the left ventricle. there is no pericardial effusion. the left ventricular apex is severely hypokinetic with focal dyskinesis. no apical thrombus seen . tte : 1. the left atrium is mildly dilated. the left atrium is markedly dilated. 2. left ventricular wall thicknesses are normal. the left ventricular cavity size is normal. overall left ventricular systolic function is mild to moderately depressed. 3. right ventricular chamber size is normal. right ventricular systolic function is normal. 4.the aortic valve leaflets are moderately thickened. mild (1+) aortic regurgitation is seen. 5.the mitral valve leaflets are mildly thickened. moderate (2+) mitral regurgitation is seen. 6.there is moderate pulmonary artery systolic hypertension. 7. there is a small pericardial effusion. there are no echocardiographic signs of tamponade. . compared to the images of , the anterior and anteroseptal wall motion abnormalities were present ( though not mentioned in the last report)). the ef was decreased previously but it is probably slightly worse now. . ct abdomen: impression: 1. no evidence of intra-abdominal abscess or colitis. 2. small amount of perihepatic ascites, without enhancing rim or other suspicious features. 3. small bilateral pleural effusions with associated atelectasis, not significantly changed in appearance from prior study. no evidence of pneumonia. 4. mild mediastinal, axillary and inguinal lymphadenopathy again noted. clinical correlation recommended. 5. pancreatic calcifications, consistent with chronic pancreatitis. brief hospital course: ed and micu course: in the ed lp was performed and showed csf - protein 84, glucose 327, tube 4: 10 wbc 7 rbc, tube 1: 14 wbc 256 rbc poly 87 lymph 8. she was admitted to the micu and started on propofol gtt for seizures and acyclovir 500 mg iv q12h, ceftriaxone 2 gm iv q12h, vancomycin hcl 1000 mg iv q48h, and ampicillin 2 gm iv q6h to cover for meningitis. csf gram stain and cultures returned negative and hsv pcr was negative, so antibiotics were d/ced. no source was found for fevers, blood and urine cultures were negative. pt. was loaded on dilantin iv initially, but had 15 seconds of asystole and hypotension with this, and so was loaded instead on depakote. she was continued on this and was seizure free in the micu. she was monitored on bedside eeg x 2 days (see results above) which showed a suppressed rhythm with no assymetries or epileptiform discharges. . mr was performed on and showed some question of subtle areas of slow diffusion in the left cerebral hemisphere. it was initially unclear if this was changes from status or stroke, but when it was repeated on the lesions had evolved (see results below) and were felt to be most c/w infarct. it was felt that this could have been her seizure focus and could have been the seminal event. carotid us showed no stenosis and pt. has been in nsr on telemetry, but tte showed new apical hypokinesis (no clot seen on tte) . in terms of her dka she was initially covered with an insulin drip, which was transitioned to sliding scale insulin and nph (8u -> titrated up to 12 u ). her fs were well controlled prior to transfer to the floor. she was extubated on without incident and has had some upper airway secretions initially but has been stable from a respiratory standpoint recently. . floor course: 1. neuro (seizure/cva): as above, the patient was noted to have a l-sided cerebral infarction on mri. the patient was transitioned from depakote to trileptal given concern for possible coumadin/depakote reaction, and was therapeutic on 600 . given that the mechanism of her stroke was felt to most likely be cardioembolic from new apical hypokinesis it was felt that she would benefit from coumadin in the short term. she will likely need coumadin for 2-3 months, while the risk for apical thrombus is highest, and then her neurologist should consider stopping it given her co-morbidites with longterm coumadin. this was initially held given concerns for anemia, for procedures (peg placement), and later guaiac + stools (see below), but as hct stabilized and procedures were performed she was started on coumadin. however, during her course she developed an increased inr largely related to profound vitamin k deficiency, she was discharged on daily lovenox as described below. she remained on asa and a statin for the stroke, and trileptal for the seizures. she had no further seizures during her course. in collaboration with the hematology and neurology services, she will receive full-dose aspirin (325mg) for secondary stroke prophylaxis with regard to the lv apical akinesis. . 2. gi (gastritis): pt. failed a speech and swallow eval x 2 and peg was recommended. this was placed by ir on . after the procedure her hct dropped and she was noted to have guiac + stools. gi was consulted and felt that this was peg placement. hct stabilized after transfusion, and egd showed gastritis around the peg site but no other pathology. she should be continued on ppi while on anticoagulation. . 3. endocrine (dka/dm/hypoglycemia): as above, the patient's dka was treated and once resolved she was followed by on the floor, and transitioned to lantus and humalog sliding scale. she initially did well, but during her course developed hypoglycemia. consult decreased her insulin substantially, and an am cortisol level was sent to rule out adrenal insufficiency. this was normal, and the patient's hypoglycemia improved and her insulin was adjusted accordingly by . she was discharged with stable blood sugars. an receiving glargine insulin and every 6 hour fingersticks and humulin insulin sliding scale. . 4. id (fever of unknown origin): on the floor the patient spiked a low grade fever, which was felt to be aspiration pneumonia given right ll infiltrate on cxr and high risk for aspiration. she was started on levaquin on and changed to ceftriaxone and flagyl on given concern for prolonged qt on ekg on levaquin. she continued to spike fevers and ctx was changed to flagyl. all cultures were negative (blood, urine and stool), and her cxr was unchanged. ct chest/abd perfomed to r/o abcess or other source of infection and was negative. chest ct did not show evidence of pna. repeat cultures were negative. id consult was obtained. they felt that her continued fevers and increasing eosinophil count pointed to drug fever. all antibiotics were discontinued on . she continued to be febrile (to 101) and cultures were repeated. all cultures remained negative, though her sputum grew mrsa. id felt with a normal cxr and no hypoxia, treatment should be deferred. eventally her fever resolved with the holding of abx and lasix, and her fever was attributed to drug fever as she had high peripheral eosinophilia. she spiked again during her course, and at that time cultures were resent, and a ct abdomen and pelvis was obtained (which was non-revealing). she developed diarrhea, and while her cdiff remained negative she was empirically treated with flagyl. she continued to spike and per id aztreonam and vanco were added while all cultures continued to pend. as ultimately no source for an infection was found (including negative c. dif toxins a and b), all antibiotics were stopped and the patient remained afebrile until time of discharge. . 5. pulm (tachypnea): the patient has had periods of hyperventilation and apnea which are most likely central in origin, eeg obtained to r/o subclinical seizure activity and this showed encephalopathy, but no seizures. this resolved and then appeared again, an abg showed mild respiratory alkalosis. she was closely followed and her breathing gradually normalized. . 6. cv (elevated troponin/chf): during the patient's course she developed elevated troponins on the floor. cards was consulted and felt that the elevated troponins were likely due to demand ischemia from her illness and anemia. they recommended optimal medical management with aspirin, bb, ace, and statin. her cardiovascular status remained stable, though later in her course she had periods of increased wob and respiratory distress which were attributed to mild chf. her respiratory status improved with diuresis, and when she was euvolemic her diuresis was stopped. ultimately her blood pressure was controlled with the medicines listed in the discharge medication list. . 7. heme(anemia/coagulapathy). the patient has a baseline hct of ~ 27, and after her g-tube was placed her hct dropped. an egd showed gastritis, and with a ppi and 2 units of blood her hematocrit remained stable. given her stroke, as above she had been receiving coumadin, and during her course developed elevated pt/ptt/inr. dic was ruled out and coumadin and sc heparin was held. her mixing study was negative and heme was consulted. they felt her coagulapathy was due to vitamin k deficiency. her vitamin k was repleted, and her coags eventually normalized. however, she continued to have hematuria. after consulting neurology, it was decided to anticoagulate with 325mg aspirin daily for secondary stroke prevention. she will likely need continued tranfusion support while her hematuria persists. if it stops, the possibility of adding clopidogrel can be readdressed. . 8. renal (arf on cri): the patient appears to have a baseline creatinine ~ 1.3-1.5. post diuresis this rose slightly, but once diuresis stopped this remained at baseline for a while. later in her course the patient developed severe diarrhea and her creatinine increased and her uop decreased. her urine lytes revealed a pre-renal etiology and she was given fluids aggressively (while closely watching her exam and oxygen sats given her chf). her course was further complicated by and episode of contrast induce nephropathy with resulting transient decrease in renal function. upon discharge, her cr had normalized and she was stabilized on her acei regimen to decrease progression of her proteinuria. . 9. code status: full code medications on admission: atorvastatin 20 mg qd calcium carbonate 500mg tid asa 81mg qd mvi vitamin d 400u qd nifedipine sr 90 mg qd famotidine 20 mg qd metoprolol 100mg fluticasone albuterol furosemide 20mg qd riss discharge medications: 1. oxcarbazepine 600 mg tablet : one (1) tablet po bid (2 times a day). 2. acetaminophen 325 mg tablet : 1-2 tablets po q4-6h (every 4 to 6 hours) as needed. 3. albuterol sulfate 0.083 % solution : one (1) inhalation q6h (every 6 hours) as needed. 4. atorvastatin 80 mg tablet : one (1) tablet po daily (daily). 5. ipratropium bromide 0.02 % solution : one (1) inhalation q6h (every 6 hours) as needed. 6. miconazole nitrate 2 % powder : one (1) appl topical tid (3 times a day) as needed. 7. oxycodone-acetaminophen 5-325 mg/5 ml solution : 5-10 mls po q4-6h (every 4 to 6 hours) as needed for pain: ml po. 8. lansoprazole 30 mg tablet,rapid dissolve, dr : one (1) tablet,rapid dissolve, dr po bid (2 times a day). 9. hydrochlorothiazide 25 mg tablet : one (1) tablet po daily (daily). 10. epoetin alfa 40,000 unit/ml solution : one (1) ml injection once a week. 11. loperamide 2 mg capsule : one (1) capsule po qid (4 times a day) as needed for diarrhea: maintain <2 bm per day. 12. insulin glargine 100 unit/ml solution : eight (8) units subcutaneous at bedtime. 13. amlodipine 5 mg tablet : two (2) tablet po daily (daily). 14. lisinopril 20 mg tablet : two (2) tablet po daily (daily). 15. aspirin 325 mg tablet : one (1) tablet po daily (daily). 16. carvedilol 12.5 mg tablet : two (2) tablet po bid (2 times a day). 17. valsartan 80 mg tablet : one (1) tablet po daily (daily). discharge disposition: extended care facility: & rehab center - discharge diagnosis: primary: 1. diabetic ketoacidosis. 2. left mca stroke - presumed cardioembolic. 3. status epilipticus. 4. aspiration pneumonia. 5. ischemic cardiomyopathy. 6. acute renal failure - contrast nephropathy. 7. coagulopathy/vitamin k deficiency. 8. nephrotic range proteinuria ~ 10g/day. 9. diabetic nephropathy. 10. systolic heart failure. 11. non-st elevation mi. 12. fever nos. 13. diarrhea nos. 14. eosinophilia nos. 15. hypoproliferative anemia - ckd/inflammation. 16. mrsa colonized. secondary: 1. diabetes mellitus type i. 2. chronic kidney disease stage ii. 3. hypertension. 4. osteoporosis. 5. asthma. 6. coronary artery disease s/p anteroapical mi. discharge condition: improved with residual aphasia and r sided hemiparesis. tolerating g tube feeds at goal. discharge instructions: 1. you presented with seizures and dka. you were noted to have a stroke. you had a complicated course including difficulty controlling your sugars, mild heart failure, acute on chronic renal failure, anemia, and fevers. . make all follow-up appointments . please return to the er if you experience increasing weakness, fever to greater than 101f or new weakness. followup instructions: primary care: please call dr. office at to set up a follow up for 2-4 weeks. . neurology: dr. , , 8, , at 1:00. please call prior to the to update your insurance information. procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours venous catheterization, not elsewhere classified venous catheterization, not elsewhere classified venous catheterization, not elsewhere classified spinal tap incision of lung other endoscopy of small intestine insertion of endotracheal tube enteral infusion of concentrated nutritional substances transfusion of packed cells percutaneous (endoscopic) jejunostomy [pej] diagnoses: thrombocytopenia, unspecified anemia in chronic kidney disease subendocardial infarction, initial episode of care acute kidney failure with lesion of tubular necrosis acquired coagulation factor deficiency hypertensive chronic kidney disease, unspecified, with chronic kidney disease stage i through stage iv, or unspecified asthma, unspecified type, unspecified systolic heart failure, unspecified other specified forms of chronic ischemic heart disease acute respiratory failure pneumonitis due to inhalation of food or vomitus cardiac arrest osteoporosis, unspecified diabetes with ketoacidosis, type i [juvenile type], not stated as uncontrolled grand mal status long-term (current) use of anticoagulants late effects of cerebrovascular disease, hemiplegia affecting unspecified side cerebral embolism with cerebral infarction late effects of cerebrovascular disease, aphasia unspecified gastritis and gastroduodenitis, without mention of hemorrhage diabetes with renal manifestations, type i [juvenile type], not stated as uncontrolled chronic kidney disease, stage ii (mild) other late effects of cerebrovascular disease, dysphagia unspecified drug or medicinal substance causing adverse effects in therapeutic use nephrotic syndrome in diseases classified elsewhere central sleep apnea in conditions classified elsewhere 

Answer: The patient is high likely exposed to