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: service: history of present illness: mr. is a 41 year-old man with a past medical history significant for juvenile onset diabetes who presents in transfer from an outside hospital in diabetic ketoacidosis and with a question of a stroke or seizure presenting here for further workup. as the girlfriend and from outside records. according to the patient's girlfriend had been having shortness of breath recently, which was unexplained. he had a stress test done at an outside facility two days prior to his presentation, which according to her was read as normal. the day prior to admission on was complaining of an upset stomach. on we note that his brother spoke to him at about 5:00 appointments, therefore a friend from work went to his house and heard him on the floor. the friend broke down the door and found the patient awake, alert and lying in feces and urine. emergency medical services were called. he told somebody that he thought he had a stroke. he was taken to hospital. a note from the emergency department states that he complained to them of vomiting and diarrhea for two days. while in the emergency department blood pressure was quite labile ranging from 230/113 to 160/100. an electrocardiogram was done, which showed sinus tachycardia, nonspecific st changes. his blood glucose was 535 and this improved with hydration. he then seemed to become more confused and febrile, therefore a head ct was done, which was read as normal. he was given 2 mg of intravenous rocephin and acyclovir, which was followed by an lp. the lp results showed 1 white blood cell. he was then taken to the intensive care unit where the physician felt that he had an aphasia and a right arm weakness. he appeared to be moving his left legs and left side more readily. by the girlfriend's history he had been having difficulty moving when he was in the home, which was why he was found on the floor. however, he was able to move somewhat when she met him at the hospital. however, while she was with him in the hospital later she noticed a sudden weakening of his right side. notes from the hospital mentioned that he had an episode of loss of consciousness for two minutes and again an aphasia. it was thought that he perhaps had a seizure and that his right arm weakness was due to paralysis. he was therefore loaded on dilantin. over the night in the intensive care unit at hospital he had two major issues. the first was that he was the diabetic ketoacidosis and increased ketones and an anion gap and he was placed on intravenous insulin and fluids. the following morning his gap was resolving, the bicarb level was 16. additionally, he was thought to have seizure activity overnight. from the descriptions in the note it sounds like this was left arm posturing, left gaze and tapping of his left foot. he was given a total of 40 mg of valium over the course of that night. in the morning his language seemed to worsen to the point of this being nearly mute. he had a repeat head ct, which was read as showing a left frontal hypodensity. he was apparently sluggish, but awake. he was then intubated and transferred to the for further evaluation. past medical history: 1. insulin dependent diabetes mellitus since the age of 6, he presented in diabetic ketoacidosis. he has had very labile sugars and had a seizure at the age of 12 in the setting of a low glucose. he has triopathy and retinopathy with multiple laser surgeries. he has a peripheral neuropathy with very little sensation in his feet and hands. he has kidney problems as well and his doctor has talked to him about the possibility of dialysis at some point in the future. he has autonomic problems. cannot have a spontaneous erection. 2. recent history of dyspnea on exertion and reportedly had a recent stress test and workup of this. results are not available to us here, but they were reported as normal by the patient's girlfriend. 3. hypertension. 4. hypercholesterolemia. 5. sleeping problems. has been on ambien and now takes nightly xanax. medications: lantus 20 units in the a.m. 18 units in the p.m., lipitor 40 mg po q.h.s., zestril 7.5 mg po q day, humalog premeal on a sliding scale 4 units for blood sugars of 80 to 100, 6 units for blood sugar of 101 to 156, 8 units for blood sugars of 151 to 200. tiazac 240 mg, , and elavil 25 mg po q.h.s. allergies: no known drug allergies. social history: the patient has a girlfriend and owns his own business in metal welding. he has no smoking history and does not drink. no history of intravenous drug use. physical examination: on initial examination the patient's temperature was 101. blood pressure 130 to 150/103. heart rate 113. in general, the patient was intubated, sedated. he had no grimace to voice. he did grimace to sternal rub. cardiovascular examination revealed a normal s1 and s2 with no murmurs, rubs or gallops. lungs were clear to auscultation bilaterally. his neck had no bruits. there is no evidence of trauma. on cranial nerve examination pupils were 2 mm and reactive bilaterally, procedure to dull to the left and to the right. he had a very sluggish corneal on the left and then on the right. he had a positive gag and some right facial droop. on motor examination his right arm seemed flaccid, however, he did not respond to pinch in any extremity. he did withdraw to babinski bilaterally. on reflex examination his biceps are trace, the other reflexes were difficult to elicit and he had up going toes bilaterally. initial laboratories at the outside hospital: sodium of 138, potassium 4.9, chloride 107, bicarb 19, glucose 535, with an anion gap of 12. ck 298, mb negative, ast 19, alt 41, albumin 4.1. on at 8:00 a.m. his sodium was 153, potassium 4.4, with a chloride of 122, bicarb of 18, creatinine of 38, bun 1.9, glucose 239, gap of 13, blood culture was negative and pending. gram stain was negative from the cerebral spinal fluid. dilantin was 13 and his urine tox screen was negative. on presentation to on at 2:00 p.m. his white count was 14, hematocrit 38, platelets 387. his chemistries showed a sodium of 151, potassium of 4.4, chloride 119, bicarb 19, creatinine 1.8, bun of 37, glucose 241. his gap was 13. his free water deficit was 3.54 liters. arterial blood gas showed a ph of 7.4, pco2 35, po2 430. on pressure support 20/6/100%. ct of his head showed an area of hypodensity seemed to evolve from to in a watershed distribution in the left frontal area. possible area of hypodensity on the right, also in a watershed location. initial impression: the patient is a 41 year-old man with insulin dependent diabetes mellitus presenting in diabetic ketoacidosis with a stroke. unfortunately, his examination is compromised by the fact that he is intubated and sedated. by the reports from his girlfriend his are suggestive of a left mca. his imaging is suggestive of a watershed infarct, possibly on both hemispheres. he has a known autonomic neuropathy and reportedly had labile blood pressures in the hospital. it is unclear whether he had actually a prolonged drop in his blood pressure. the ct pattern of hypodensity would be consistent with watershed strokes due to hypoperfusion. furthermore, the mra that was obtained at suggested bilateral carotid occlusions, both mcas were open and the circle of was fed from the basilar artery and pcoms. in the setting of diabetic ketoacidosis he likely had worsening of his symptoms and it is possible that this was complicated by seizures either from diabetic ketoacidosis or from ischemia. usually the latter is associated with hemorrhages or emboli. hospital course: mr. was admitted to the neurological intensive care unit. he had an mri/mra performed on admission. the mri showed multiple areas of restricted diffusion in both cerebral hemispheres predominantly in the deep watershed distribution with bilateral parietal occipital watershed distribution. small areas of restricted diffusion are also identified in the left basal ganglia and right parietal occipital subcortical region. no evidence of midline shift, mass effect or hydrocephalus is seen. no evidence of hemorrhages identified. no definite flow signal is identified in the cavernous carotid, however. on the right side supraclinoid internal carotid is identified with normal flow signal in both anterior cerebral and right middle cerebral artery and a prominent right posterior communicating artery. on the left side diminished flow signal is identified in the middle cerebral distribution. no definite posterior cerebral arteries identified on the left. the posterior circulation demonstrates normal flow signal. impression bilateral marked diminished flow signal within the carotids, which could be due to dissection or high grade stenosis in the neck. neck mra and fat suppressed images would be helpful for further evaluation and if clinical indicated." the overall impression was that the patient had watershed infarcts worse on the left then on the right with little to no flow in his internal carotid arteries bilaterally. over the course of his first night at mr. blood pressure was allowed to auto regulate with the goal systolic blood pressure in the 140s to 160s to allow adequate perfusion given his stenosis. he was started on aspirin as there was no sign of bleeding. attention was paid to his blood sugars titrating with d5 normal saline and low dose insulin. the following morning on examination mr. was noted to have a slight anisocoria. his left pupil was 3 mm and minimally reactive. his right pupil was 2.5 mm and reactive. he has positive ocular cephalic reflexes. he had a weak, but present gag. corneal reflexes were present bilaterally. his motor examination was significant for an extension movement in the right upper extremity with less response on the left side to pain. in the lower extremities he had a triple flexion on the right side and less response on the left to painful stimuli. his toes were up going bilaterally. his laboratories were significant for a sodium of 153, white blood cell count 16.7, bun 35, creatinine 1.8, chloride 123, glucoses ranging from 117 to 310. cpk 1250 with an mb of 7. his dilantin level was 7.5 and so his dose is supplemented with an extra 750 mg in addition to his 100 mg t.i.d. mr. had an electroencephalogram performed. the impression of the electroencephalogram was "abnormal electrocardiogram due to epileptiform appearing activity from the midline and due to generalized background slowing, the latter suggest a diffuse disturbance during the encephalopathic process." in the evening mr. was noted to have increased extensor movements now happening spontaneously not only to painful stimuli, but occasionally even sitting upright in his bed. he was still averbal and unresponsive to verbal stimuli. his right pupil was now slightly more dilated then the left. the reversal from the morning and was no longer reactive to light. the left pupil was minimal reactive to light and .5 mm smaller then the right. a stat head ct was performed, which showed an extension of the previous infarcts with much greater involvement of the left mca territory including deep left mca territory. additionally, there is bilateral involvement of the anterior circulation as well as the other areas previously seen on his mri in a watershed distribution. there was effacement of the sulci in this distribution and with mild narrowing of the lateral ventricle. the basilar cistern patent without any obvious mass effects on the mid brain pons or medulla. at this time the family was informed of the patient's grim prognosis and asked to begin considering what his wishes would have been regarding continued life support in the face of little hope for a meaningful recovery. the following morning mr. examination was with little change. he was still having periodic extensive posturing. his gaze was dysconjugate, however, now. his pupils were much the same as last night with the right nonresponsive and .5 mm larger then the left, which was minimally unresponsive. he had no dolls eyes movements. he still had positive corneals bilaterally. on suctioning his endotracheal tube he had extensive posturing bilaterally. he had extension responses to pain in the right leg, minimal responses in the upper extremities bilaterally and none in the left leg. his white blood cell count had increased to 19.8 and his sodium was now 149. his arterial blood gas showed a ph of 7.45, pco2 29, po2 250. further discussions were held with the family regarding the patient's grim prognosis. it was decided to change the patient's code status to comfort measures, however, the patient did remain on the ventilator to prevent sudden pulmonary edema and resulting respiratory distress. the patient was given doses of morphine to ease his breathing as his oxygen supplementation was discontinued and he was placed on pressure support on the ventilator with room air. the patient was pronounced dead at 4:20 a.m. he had no electrocardiogram trace. his heart rate was 0. blood pressure not recorded. no heart sounds. pupils were fixed and dilated. , m.d.13.279 dictated by: medquist36 d: 15:14 t: 09:04 job#: procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours insertion of endotracheal tube diagnoses: pure hypercholesterolemia unspecified essential hypertension other convulsions polyneuropathy in diabetes diabetes with ketoacidosis, type i [juvenile type], not stated as uncontrolled cerebral artery occlusion, unspecified with cerebral infarction background diabetic retinopathy diabetes with neurological manifestations, type i [juvenile type], not stated as uncontrolled diabetes with ophthalmic manifestations, type i [juvenile type], not stated as uncontrolled 

Answer: The patient is high likely exposed to