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: patient recorded as having no known allergies to drugs attending: chief complaint: productive cough, fever, shortness of breath, tranferred from an outside hospital with a visual field deficit. major surgical or invasive procedure: transesophageal echocardiography. (otherwise, medical management: heparin gtt, then warfarin anticoagulation for cardioembolic stroke; started ccb for rate-control (afib); started acei and thiazide for htn; s/p iv antibiotics for multifocal pna) history of present illness: mr. is a 50-year-old right-handed who presented to an outside hospital with fever, productive cough, shortness of breath, transferred to after developing a visual field deficit. *** mr. was last well on saturday night. he works in a bar and was serving on for a large party. he had some beer and later snorted some cocaine. he stayed out, getting home at about 6 a.m. and sleeping through until 2 p.m. when he was due to return to work. he worked for about four hours before drinking two beers and returning home. by the end of that shift he was feeling unwell, with some chest congestion. he also felt fatigued. nonetheless, he slept well, waking at about 8:30 a.m. on morning (the timing of events varying slightly while taking the history). he stood, felt light-headed and fell, with brief loss of consciousness, but he recalls striking his head on a table and his neck flexing or extending (in which direction he cannot say). he did not suffer any superficial injury. he got back into bed. by this time he was feeling even sicker, now with some cough that became productive over the course of that day. he also gradually developed a pounding headache with severe pain that was in time with heart beats. he felt quite unwell, had become febrile with chills and was fatigued. he ate nothing and drank some water and coolaid, but noted that his urine was becoming darker. he slept very little that night. on tuesday he felt even less well, with continuing headache, fever, chills, and productive cough. again he slept poorly. on wednesday he and he and his girlfriend, who lives with him, decided that he should go to the hospital. she drove him there. in the osh, atrial fibrillation with a rapid rate was noted and diltiazem infusion started. neurologic examination was not performed in the osh ed. he was noted to be diaphoretic, unable to get out of bed, not eating, confused, but denied headache and chest pain. vital signs were 98.1 degrees, heart rate of 145, repiratory rate of 24, blood pressure of 179 systolic. right eye blurring was noted. oxygen saturation was 93%. laboratory data was significant for creatinine of 1.5, normal ck and ck-mb, slightly elevated troponin i at 0.07. bilirubin was also mildly elevated. ct head was performed. he was transferred to for further management. in ed, right field cut restricted to the right eye was recorded. cta chest was performed and the patient was given cetriaxone and levoquin, hydralazine given blood pressure of 175/123, aspirin and diltiazem. urinanalysis was significant for proteinuria, toxicology was positive for opiates and cocaine. *** he reports headache, tremulousness, sweats, fatigue, cough productive of sputum, shortness of breath. on neurologic review of systems, patient denies any history of seizures or unexplained loss of consciousness (other than syncope above), vertigo or dizziness, diplopia, difficulty hearing, tinnitus, difficulty with speech or swallowing, weakness, difficulty moving, abnormal movements, numbness, tingling, tremor, problems with gait, balance or coordination, difficulty with sphincter control or sexual function, difficulty with thinking or memory, problems sleeping (except as above) or excessive sleepiness, depressive symptoms. past medical history: - no significant - patient denied hypertension, hypercholesterolemia, prior arrhythmia social history: de facto relationship with girlfriend, have lived together for 18 years. works in bar, part-time for the last two years. worked as an appliance salesman prior to that time. completed eighth grade in school. rare cocaine use - once in 'long-time' on saturday. does not smoke. regular drinking - claims two or so most days. speaks english - this is his first language. family history: no family history of stroke. physical exam: t 98.1 f ; hr 95 bpm ; bp 164/117 (on arrival in icu), now 149/71 mmhg ; rr 19 bpm ; o2sat 94% (nc 3l) ; pain 0/10 general observations and appearance reasonable self care, looks stated age. diaphoretic. fine tremor. restless. general physical exam head - size appears within normal limits, symmetric, no exostoses nor tenderness. no injuries. eyes - no exophthalmos, normal , round pupils, normal sclera. ent/op - mm slightly dry and tongue surface normally papillated. tongue of normal size/muscle bulk. neck - no bruits, pulses normal, no lad, supple, normal appearance, thyroid normal. chest/thorax/breasts - cta, rr, good air entry, no dysmorphic features. no consolidation by vocal fremitus. cardiovascular - irregular, normal pmi, normal s1 s2, no m/r/g. peripheral pulses normal. abdomen - no scars, stigmata of liver disease, soft, non-tender, no masses nor organomegaly. spine - normal curvatures, non-tender, no dimpling or unusual hair growth. extremities - no deformities, nor contractures. no clubbing, cyanosis nor edema. no arthropathy. normal digits. no palmar erythema. skin - neither greasy nor dry, no spider angiomas, no tattoos, scars other markings. hair and nails - normal appearances. male pattern baldness with normal hairline. mental status alert and slightly hyper-aroused given setting. oriented to person and time, but not hospital. comprehension intact for simple and complex instruction, including across midline. naming was intact for colors and high frequency objects. anomia for low frequency objects. repetition intact. neglected right side of stroke scale pictures. writing with spelling errors and phrases, but not intact - could spell some words from stroke card, but with many errors and could not read (~ alexia without agraphia with preserved colors). forward, normal, could not perform in reverse. registered four words with one trial and recalled none, even with prompting. occasional paraphasic errors (phonemic) and perseveration on words. affect was not observed as full-range, mood euthymic. thought process logical, content appropriate. judgement not tested. insight retained. cranial nerves patient reports baseline olfaction. field deficit, right homonymous hemianopia on confrontation, then on careful inspection with hat pin: split in middle of macula and exact right visual fields. acuity not tested. pupillary reaction to light and accommodation intact (2 mm to 1.5 mm), including consensual reactions. eye movements were full without observed deviation of either eye nor report of diplopia. no neutral position nor end-gaze nystagmus. pursuit movements were smooth. jaw opening was symmetric and facial sensation intact to light touch. facial expressions were of reduced strength symmetrically at eyes and with decreased excursion on right side at mouth, with nasolabial fold flattening. hearing was grossly intact. soft palate symmetric at rest and with elevation. apparently normal salivation and swallowing. no dysphonia. shoulder shrug and head turning strong, full range and with symmetry within normal limits. tongue bulk and movements normal and symmetric. no dysarthria. tone slightly increase in right arm and both legs. normal axial/postural tone without negative myoclonus (asterixis). no spasticity. power and muscle bulk ( left ; right ) normal bulk throughout the upper and lower extremities deltoid ( 5 ; 5 ) triceps ( 5 ; 5 ) biceps ( 5 ; 5 ) wrist and finger extensors ( 5 ; 5 ) finger flexion ( 5 ; 5 ) finger (fifth) abduction ( 5 ; 5 ) hip flexors ( 5 ; 5 ) quadriceps femoris ( 5 ; 5 ) biceps femoris ( 5 ; 5 ) plantar flexors ( 5 ; 5 ) tibialis anterior ( 5 ; 5 ) toe extensors ( 5 ; 5 ) reflexes ( left ; right ) biceps ( ++ ; ++ ) triceps ( ++ ; ++ ) brachioradialis ( ++ ; ++ ) quadriceps ( ++ ; ++ ) plantar flexors ( ++ ; ++ ) plantar responses ( down ; down ) routing reflex, grasp, snout and palmar-mental reflexes not tested. clonus not present in plantar flexors. coordination, fine motor control and patterned movements hand roll and rapid sequential finger apposition normal. finger to nose normal with eyes closed. sensation light touch intact and symmetric on medial and lateral surface of upper and lower limbs. anterior surface of trunk intact. gait and station not tested given lines and drains, pneumoboots. other signs no pronator drift. no extinction on double simultaneous stimulation of the hands or legs. exam today significant for some spastic increase in tone on right, hyporeflexia on right. some improvement of macula vision loss. able to write, but still difficult. pertinent results: -------------- brain imaging: -------------- *osh* nchct (prior to xfer to ) there is a large area of and white matter hypodensity involving the left temporal, parietal, and occipital lobes with assiciated sulcal effacement. findings are compatible with cytotoxic edema in the setting of a left pca territory acute infarction. within this area of infarction are areas of intermediate density with a gyral pattern, could represent spared parenchyma. there is no definite evidence of hemorrhage. periventricular white matter hypodensity is noted compatible with chronic microvascular ischemic disease. there is slight prominence of the ventricles and the sulci, compatible with mild atrophy. there is minimal rightward shift of midline at the septum pellucidum of 2 mm. there is no evidence for herniation. bone windows: osseous structures are intact. there is mild mucosal thickening of the right and left maxillary sinuses and right and left sphenoid sinuses. the globes and orbits appear intact. impression: large left pca territory acute infarction. please correlate with mri. mri/mra extensive left pca territory infarction with internal areas of hemorrhage is redemonstrated, similar in distribution as compared to head ct. a thin peripheral rim of cytotoxic edema causes mild effacement of the occipital and exerts mass effect on the body of the left lateral ventricle. a 2-mm rightward midline shift is similar as compared to two days prior. suprasellar and basilar cisterns are patent. in addition, there are new foci of restricted diffusion within the left thalamus (24, 14) and right occipital lobe (24, 14 and 24, 16), concerning for new foci of microinfarct due to embolic disease. there are confluent and discrete flair and t2 signal hyperintensities within the periventricular and subcortical white matter, consistent with small vessel ischemic disease. there is mucosal thickening involving maxillary, ethmoid, sphenoid and frontal sinuses. fluid level is noted in the right maxillary sinus, suggestive of an element of acute disease. globes and soft tissues appear unremarkable. mra brain and neck: the intracranial internal carotid arteries, anterior cerebral arteries, middle cerebral arteries, posterior cerebral arteries, vertebral and basilar arteries appear patent without flow-limiting stenosis, aneurysm greater than 3 mm, or dissection. there is slight asymmetry of segmental left pca as compared to the contralateral site, which may be further assessed by cta if clinically indicated. cervical portions of carotid and vertebral arteries appear patent and normal in caliber. proximal vessel origins are poorly visualized due to motion and artifacts. impression: 1. large left pca territory infarct with hemorrhagic conversion and mild effacement of occipital of lateral ventricle as well as a stable 2-mm rightward midline shift. no evidence of transtentorial or tonsillar herniation. 2. additional foci of acute microinfarct of left thalamus and right occipital lobes are suggestive of central embolic disease. 3. moderate-to-severe small vessel ischemic disease. 4. patent anterior and posterior circulation vasculature. slight asymmetry of the left pca segmental branches as compared to the right. cta may be considered for further assessment if clinically relevant. 5. patent cervical vertebral and carotid arteries. poor visualization of vessel origins due to motion artifacts. 6. mild to moderate paranasal sinus disease, with right maxillary fluid level, suggesting an element of acute disease. nchct a large area of hypodensity in the left occipital, parietal and temporal lobes with sulcal effacement is again noted and consistent with known pca infarct. serpiginous areas of hyperdensity corresponding to hemorrhagic conversion are not significantly changed compared to the prior studies. there is persistent 2 mm rightward shift of the normally midline structures and effacement of the occipital of the left lateral ventricle. no evidence of uncal or transtentorial herniation. mild periventricular white matter hypodensity is compatible with chronic small vessel ischemic disease. ventricles and sulci are otherwise slightly prominent consistent with mild age-appropriate involutional change. globes and lenses are intact. there is mild mucosal thickening in the bilateral ethmoid air cells and right maxillary sinus. the remainder of visualized paranasal sinuses and mastoid air cells are well aerated. no osseous abnormality is identified. impression: 1. no significant change in known left pca infarct with hemorrhagic conversion. no evidence of new or worsening hemorrhage compared to prior mr , allowing for differences in technique. no new hemorrhage or infarct. 2. bilateral ethmoid and right maxillary sinus disease. -------------- chest imaging: -------------- ct-angiogram of the chest on there is no pulmonary embolism. the pulmonary artery is normal in caliber. there are coronary artery vascular calcifications. the aorta and great vessels appear normal. there is no pericardial fluid. there are diffuse multifocal bilateral air space opacities. there are moderate bilateral pleural effusions. there are several reactive hilar, mediastinal and pre-vascular lymph nodes. there is no axillary lymphadenopathy. lobes of the thyroid appear normal. the airways appear patent to the subsegmental levels bilaterally. there is pleural septal thickening. limited evaluation of the upper abdomen appears normal. bone windows: there are no suspicious-appearing sclerotic or lytic lesions. impression: 1. diffuse multifocal air space opacities with moderate bilateral pleural effusions concerning for pneumonia. 2. no pulmonary embolism. 3. pulmonary edema. ct-angiogram of chest on findings: comparison to cta of . there is no evidence of pulmonary embolism. bilateral pleural effusions and associated compressive atelectasis are moderately severe. the lungs are homogeneously ground-glass in appearance with concomitant left upper lobe consolidation in a bronchocentric distribution (4:9). comparison to the prior study indicates interval resolution of the majority of bronchocentric nodules with persistence of those in the left upper lobe, marked interval progression in size of the pleural effusion, there has been interval resolution of smooth septal thickening in the apices indicating resolution of interstitial pulmonary edema. the left atrium is moderately enlarged and the left atrial appendage thrombus is unchanged since . there is no pericardial effusion. reflux of contrast into the hepatic veins suggests triscuspid regurgitation. the airways are patent to the subsegmental level. anterior bowing of the posterior membrane of the upper trachea suggests image acquisition during the expiratory phase. right paratracheal, left peribronchial and subcarinal adenopathy is moderately severe, the largest node in the subcarinal station measures 15 mm (4:28), stable since . thoracolumbar osteophytosis is moderately severe. impression: worsening bilateral pleural effusions. overall improvement in the bronchocentric pulmonary nodules/opacities shown on the cta of with persistent diffuse ground-glass opacity and left upper lobe focal consolidation. the appearance suggests a resolving pneumonitis, possibly inhalational, resolving bronchopneumonia or pulmonary hemorrhage are also possible. this much less likely to represent cryptogenic organizing pneumonia as it has improved in such a short interval. ----------------- echocardiography: ----------------- tte mild spontaneous echo contrast is seen in the body of the left atrium. moderate to severe spontaneous echo contrast is present in the left atrial appendage. the left atrial appendage emptying velocity is depressed (<0.2m/s). a definite thrombus is seen in the left atrial appendage. no atrial septal defect is seen by 2d or color doppler. overall left ventricular systolic function is normal (lvef>55%). right ventricular chamber size and free wall motion are normal. the ascending, transverse and descending thoracic aorta are normal in diameter and free of atherosclerotic plaque to 32 cm from the incisors. the aortic valve leaflets (3) appear structurally normal with good leaflet excursion and no aortic regurgitation. the mitral valve appears structurally normal with trivial mitral regurgitation. there is no pericardial effusion. impression: thrombus identified in the left atrial appendage. there is dense spontaneous echo contrast in the body and appendage of the left atrium. the left atrial ejection velocity is very low (<10cm/s). tte the left atrium is markedly dilated. the right atrium is moderately dilated. the estimated right atrial pressure is 0-5 mmhg. there is mild symmetric left ventricular hypertrophy with normal cavity size. there is mild global left ventricular hypokinesis (lvef = 45-50 %). right ventricular chamber size is normal with mild global free wall hypokinesis. the aortic root is mildly dilated at the sinus level. the aortic root is moderately dilated at the sinus level. the ascending aorta is mildly dilated. the aortic valve leaflets (3) are mildly thickened but aortic stenosis is not present. trace aortic regurgitation is seen. the mitral valve leaflets are mildly thickened. there is no mitral valve prolapse. mild (1+) mitral regurgitation is seen. there is mild pulmonary artery systolic hypertension. there is a trivial/physiologic pericardial effusion. compared with the prior study (images reviewed) of , the biventricular systolic function is slightly worse. brief hospital course: is a 50 y/o rhm with no pmh who was transferred to our hospital in atrial fibrillation and hypertensive with a multifocal pneumonia and a large left pca-territory stroke following recent inhalation of cocaine. his workup revealed multiple interrelated problems, including a multifocal pneumonia with moderate bilateral effusions on cta-chest (no pe), atrial fibrillation with left atrial thrombus on tee, hypertension, and most importantly, a left-sided pca territory stroke involving a large extent of the left occipital lobe and inferior-posterior temporal lobe. his large left pca-territory stroke is certainly the cause of his visual deficits and his language and memory problems. this stroke was most likely cardioembolic in origin, given the atrial fibrillation with discovered in our icu. on heparin his hematologic system had significant difficulty maintaining a consistent therapeutic ptt (goal was 50-70 due to hemorrhagic conversion; note: abnormally low factor xa level was measured after doses ranging from 1600-2200 were needed with day-by-day large swings from 30s to 80s). likewise, his inr as well has been slow to come up on po warfarin (now 1.6 after up-titration to a dose of 12.5mg on ). there is likely an underlying coagulopathy. initially, he was monitored in our icu, where hemorrhagic conversion was seen on mri and a was discovered on bedside tee. heparin was started along with a low dose of po warfarin 2.5mg for several days with no response, then up-titrated with inr no higher than 1.6 after several days of uptitration through 5-7.5-10-12.5mg daily on the floor. heparin was stopped 3d prior to discharge on dr. advice, and the patient will be sent out with an inr below our initial goal range of 2.0-2.5, partly due to the patient's insistence on leaving the hospital. this was discussed at length with dr. , stroke attending on service as of . he was started on aspirin 81mg, which he will take until his inr is fully therapeutic. he will have his blood drawn every two days at - near his home, beginning friday (day after discharge), and dr. (neurology chief resident on the stroke service) will monitor the results and call him with recommendations. he will then be managed by dr. in / clinic beginning . regarding his pneumonia, his pulmonary symptoms improved initially in the icu on iv ceftriaxone monotherapy; he was never febrile and never developed a leukocytosis. culture data were unrevealing, but were sent after abx were initiated, so therapy was never tailored to a specific organism. however, on after two days on the floor (d4 of ctx), he began to decompensate with rr in the 30s and worsening hypoxia. given his low factor xa level (likely hypercoagulable state) and a d-dimer in the , anther cta-chest was ordered, but again did not reveal any significant pes. his mf-pna was still present and bilateral effusions were larger at that time. bedside tte showed decreased ef to 45-55%. we broadened his antibiotic coverage to iv vancomycin and cefepime, and diuresed him with 20mg furosemide two times over the next two days (he had jvd to the jaw at the time, no , and he improved rapidly over the next several days. vancomycin was peeled off after 4d and cefepime was stopped after 8d. also developed intermittent hyperphosphatemia to of unclear origin. this occurred despite relatively normal gfr (cr 1.0 with phos 5.8) and no hypocalcemia (ca 9.2 with low albumin) and should be followed up, likely insignificant. medications on admission: no home meds discharge medications: 1. lisinopril 10 mg tablet sig: three (3) tablet po daily (daily) as needed for hypertension. disp:*90 tablet(s)* refills:*2* 2. aspirin 81 mg tablet, chewable sig: one (1) tablet, chewable po daily (daily) as needed for stroke ppx: dr. will d/c this medication once your inr is therapeutic on warfarin/coumadin. disp:*30 tablet, chewable(s)* refills:*0* 3. warfarin 10 mg tablet sig: one (1) tablet po once daily at 4 pm: take a total daily dose of 12.5mg (one 10mg tablet plus one 2.5mg tablet);must have inr monitored by dr. . disp:*10 tablet(s)* refills:*0* 4. warfarin 2.5 mg tablet sig: one (1) tablet po once a day as needed for anti-coagulation (stroke prevention in a patient with atrial fibrillation and left atrial thrombus): take a total daily dose of 12.5mg (one 10mg tablet plus one 2.5mg tablet);must have inr monitored by dr. . disp:*10 tablet(s)* refills:*0* 5. diltiazem hcl 90 mg tablet sig: one (1) tablet po qid (4 times a day) as needed for atrial fibrillation / tachycardia. disp:*120 tablet(s)* refills:*2* discharge disposition: home discharge diagnosis: primary diagnoses: 1. left pca stroke, large, with hemorrhagic conversion. 2. right homonymous hemianopsia and anomia. secondary: 1. atrial fibrillation and left atrial thrombus. 2. hypertension. 3. multifocal pneumonia atop what is likely cocaine-induced pneumonitis. 4. labile personality, possibly difficulties with language and memory. discharge condition: right-homonymous hemianopsia. word-finding difficulties, mild anomia. discharge instructions: you came to our hospital with a large stroke in the back-left part of your brain. your blood pressure was very high, your heart was in an abnormal fast rhythm called atrial fibrillation which led to clot formation within your heart, which is likely the reason for your stroke, which caused your visual symptoms and headache. the area of brain damaged by the stroke (due to blood clots floating from your heart into your brain) also had some bleeding after the initial stroke. important: you need to take two critical medications to prevent another stroke from occurring. these two medications are warfarin (aka coumadin) and aspirin. for the warfarin (also called coumadin), you will take 12.5mg per day starting now -- this is one 10mg tablet plus one 2.5mg tablet once per afternoon for a total of 12.5mg. do not skip doses or take any extra. ***if blood tests are not performed regularly to monitor the effect of this medication, it can become dangerous instead of preventative, so it is extremely important that you follow up on the blood draws for inr monitoring (every two days for now) and always follow our instructions if there are any dose-changes. you can have your blood drawn either here or at our - location (1000 , laboratory). you must come here to visit dr. in clinic starting this friday in the building (see below). we will manage the warfarin/coumadin monitoring and dosing with him. for the aspirin, you will take one "baby aspirin" 81mg tablet per day until your inr is above 2.0. once your inr is 2.0, stop taking the aspirin. dr. will call to advise you about this. in addition to the blood thinner (warfarin/coumadin), you need to take three medications to control your heart rate and blood pressure so that you can function without further heart problems and to reduce your high risk of more strokes or heart attack in the future. these are called diltiazem (to control your fast heart rate because of atrial fibrillation), lisinopril (for blood pressure), and hydrochlorothiazide (for blood pressure); you will take each of these once every day in the morning. you also had a severe, multifocal pneumonia when you arrived. this may have been the result of a severe lung injury called pneumonitis from the cocaine you ingested, and then you had a subsequent superinfection with bacteria in your injured lungs. we never learned which bacterial species were causing the infection (mild antibiotics were given before cultures were taken), but you got substantially better after an eight-day treatment course with iv antibiotics (four days of iv vancomycin and eight days of iv cefepime). you do not need to take additional antibiotic medications for your infection, which appears to have resolved. dr. will re-evaluate your lungs when you visit him in clinic. followup instructions: 1. internal medicine (to monitor your blood-thinner levels, treat your high blood pressure, treat your atrial fibrillation, and monitor your heart and lung function): , at 3:00pm (please arrive 15-30min early) with dr. at the clinical center, , south suite ( clinical center is on the , on the northeast corner of the intersection of & .) 2. stroke neurology with dr. (the attending stroke physician stroke neurologist who saw you first in the icu and hospital floor when you came to ): tuesday, at 3:30pm at clinical center, , neurology suite. ( clinical center is at the northeast corner of .) md, procedure: diagnostic ultrasound of heart diagnoses: acute kidney failure, unspecified hypertensive chronic kidney disease, unspecified, with chronic kidney disease stage i through stage iv, or unspecified atrial fibrillation cocaine abuse, unspecified chronic kidney disease, unspecified disorders of phosphorus metabolism primary hypercoagulable state cerebral embolism with cerebral infarction dehydration other and unspecified alcohol dependence, unspecified alcohol withdrawal bacterial pneumonia, unspecified other ill-defined heart diseases homonymous bilateral field defects other symbolic dysfunction 

Answer: The patient is high likely exposed to