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: haldol attending: chief complaint: headache major surgical or invasive procedure: lp history of present illness: 40 yo rhm presents to ed for eval of ha, nausea and dizziness for 2 months. he started having ha 2 months ago. it was gradual in onset, initially mild and bifrontal. it was at the onset but later became over last few weeks. it is non throbbing, dull and not associated with photophobia or phonophobia. he thinks that it was worse after lying and may be after bending but is not very sure about this. he has woken up 3-4 times at night due to ha. over last 2 weeks he has continuous ha, now also occipital, and requires tramodol or tylenol for relief. he has nausea for 2 months. it was initially mild but severe over last 2 weeks. the nausea gets worse when he has severe ha. over last 2 weeks, he is not eating much, mainly due to nausea. he has vomited 2 times over last 2-3 weeks. he also feels dizzy esp over 2 weeks. he thinks it is combination of lightheadedness and spinning. the dizziness is severe when he changes positions suddenly esp from supine to sitting or if he suddnely stands up. he is feeling generalised weakness, malaise. he has not gone to work for last 2 weeks. he has lost some weight over this period. he is not sure about the amount lost, though. he has noted transient blurring of vision especially "the borders of objects" which is associated with severe ha and lasts few minutes. no diplopia or other neuro symptoms than described. because of increasingly severe ha, and dizziness , he went to osh ed this pm, where vitals - afeb, 105/43-140/52, 70, 18, 98 ra. exam- normal. cbc chem 7 ekg- nl. ct head showed " possible diffuse cerebral edema." was transfered to for evaluation. past medical history: positive ppd, unclear if and how much tx he received social history: married, has children, originially from . works in office job. smoking- half pack for 10 years non alcoholic no drugs family history: negative for cva, dm, htn physical exam: vs: 98.7 76 128/90 14 96 ra genl: awake, alert, nad, pleasant heent: sclerae anicteric, no conjunctival injection, oropharynx clear cv: regular rate, nl s1, s2, no murmurs, rubs, or gallops chest: cta bilaterally anteriorly and laterally, no wheezes, rhonchi, rales abd: +bs, soft, ntnd abdomen ext- normal. neurologic examination: mental status: awake and alert, cooperative with exam, normal affect. oriented to person, place, and date. attentive, says backwards. speech is fluent with normal repetition. naming intact. no paraphasic error. no dysarthria. intact. registers , recalls in 5 minutes and with clues. no right-left confusion. no evidence of apraxia or neglect. cranial nerves: fundoscopic examination - ? slight blurring of bl disc margins. pupils equally round and reactive to light, 4 to 3 mm bilaterally. visual fields are full to confrontation. extraocular movements intact. sensation intact v1-v3. facial movement symmetric. hearing intact to finger rub bilaterally. palate elevation symmetric. sternocleidomastoid and trapezius full strength bilaterally. tongue midline, movements intact. motor: normal bulk and tone bilaterally. no observed myoclonus, asterixis, or tremor. no pronator drift. tri we fe ff ip h q df pf te r 5 5 5 5 5 5 5 5 5 5 5 5 l 5 5 5 5 5 5 5 5 5 5 5 5 sensation: intact to temparature, vibration, position sense, and touch. no extinction to dss. reflexes: 2+ and symmetric in biceps, brachioradialis, triceps. knees and ankles. toes mute bl. coordination: finger-nose-finger, finger-to-nose, fine finger movements, and normal. gait: deferred. rhomberg- deferred pertinent results: 09:40pm blood wbc-10.3 rbc-5.33 hgb-15.6 hct-43.3 mcv-81* mch-29.3 mchc-36.1* rdw-13.1 plt ct-247 09:40pm blood neuts-59.7 lymphs-33.2 monos-5.0 eos-1.5 baso-0.6 09:40pm blood pt-12.4 ptt-23.3 inr(pt)-1.0 09:40pm blood glucose-96 urean-14 creat-0.9 na-140 k-3.9 cl-105 hco3-25 angap-14 09:40pm blood alt-27 ast-16 ld(ldh)-142 alkphos-43 amylase-38 totbili-0.5 09:40pm blood totprot-6.7 albumin-4.5 globuln-2.2 calcium-9.2 phos-3.9 mg-2.1 01:04am blood triglyc-113 hdl-43 chol/hd-5.4 ldlcalc-165* 09:40pm blood pep-no specifi igg-991 iga-287 igm-34* ife-no monoclo 01:04am blood hiv ab-negative 09:40pm blood asa-neg acetmnp-neg bnzodzp-neg barbitr-neg tricycl-neg csf: 07:10am cerebrospinal fluid (csf) wbc-9 rbc-4* polys-1 lymphs-75 monos-24 07:10am cerebrospinal fluid (csf) wbc-4 rbc-3* polys-0 lymphs-74 monos-26 07:10am cerebrospinal fluid (csf) totprot-124* glucose-73 ld(ldh)-48 micro: hiv ab neg rpr neg crypto ag neg csf bact, viral, fungal cx neg imaging: head ct no change. the small size of the ventricles and sulci may be within normal limits for age, but, given questionable diffuse hypodensity of the supratentorial white matter, a mild degree of cerebral edema is difficult to exclude. please correlate with the recent lumbar puncture findings. ct chest/ab/pelvis 1. 2-mm nodule in the right middle lobe of the lung. followup ct at 12 months is recommended if there are risk factors. 2. small area of soft tissue density in the anterior mediastinum likely represents thymic hyperplasia. scrotal u/s: no evidence of testicular mass. brain mri subacute-appearing moderate bilateral subdural collections, with associated sulcal effacement, cisternal effacement, and mass effect on the midbrain. evaluation for acute infarcts is limited in the absence of diffusion-weighted images. head ct impression: stable appearance of symmetric bilateral subacute subdural collections with stable central transtentorial herniation. no acute intracranial hemorrhage or ct findings to suggest a stroke. however, if suspicion of stroke persists, recommend further evaluation with mri. addendum at attehding review: there does appear to be slight caudal positioning of the left cerebellar tonsil- a finding which was also seen on the prior mr study of . head ct findings: the bilateral subdural fluid collections are stable in appearance since prior study. hounsfield unit sampling of fluid collections shows them to be consistent with blood, not csf collection and therefore these represent subdural hematomas as opposed to hygromas. there is stable mass effect with effacement of the sulci, bilateral lateral ventricles, third and fourth ventricles as well as suprasellar cisterns. there is continued preservation of the -white matter differentiation. there is no new intracranial hemorrhage or large area of mass or mass effect. impression: stable symmetric bilateral subdural fluid collections. stable effacement of sulci and ventricles. no acute intracranial hemorrhage. soft tissue ultrasound impression: right facial and left neck subcutaneous nodules with ultrasound appearance consistent with benign lipomas. if the nodules were to enlarge or there was clinical suspicion to pursue further workup, mri could be considered. mri brain pfi: bilateral subdural hematomas are again identified extending from frontal to occipital region with the maximum width and extent unchanged from prior study. given the hyperintensity on t1-weighted images, the collections appear to be subacute subdural hematomas than hygromas. no underlying brain edema is seen, but compression of the sulci and brainstem is identified, unchanged from previous study. subtle hyperintensities in the brainstem noted on flair and t2 images are unchanged from previous study. brief hospital course: the patient presented with headache associated with nausea and vomiting for 2 months. neurologic exam was concerning given patient's somnolence and fluctuating mental status. infectious meningoencephalitis was considered high on the differential, however there were also aspects of the history concerning for increased icp. patient underwent head ct, which showed diffuse cerebral edema. also concerning was that the patient had a history of a positive ppd that was reportedly only treated for 3 months; tuberculosis meningitis was considered. lp was then done, which was showed 9 wbcs and elevated total protein to 124. of note, patient's clinical status worsened after lp. this change in clinical status was initially concerning for elevated icp but further consideration led to the belief that he may have cerebral hypotension. an mri was subsequently obtained and showed bilateral subdural fluid collections, which are chronic residuals of acute sdh, but he denies any head trauma. it was later discovered that he may have fallen in the bathroom recently, but given these hygromas represent old bleeds; it is not likely related to this fall (note: ct on measured hounsfield and called these collections hematomas based on density). it is possible that given the cerebral hypotension, this may have resulted in disruption/tearing of the bridging veins, resulting in subdural hematomas. this was due to the history that on presentation, his headache was noted to be worse with standing and that his status worsened with lp. this could be from further removal of csf in a patient who already had csf hypotension. lp opening pressure was 12 to support a theory of intracranial hypotension. also supporting this diagnosis is low lying cerebellar tonsils that was seen on mri as well as the flattened pons noted on sagittal section. the reason for the cerebral hypotension being from a spontaneous leak or trauma is unknown. he was treated as if he had low pressure headaches; meaning he was told to lie flat when he got a headache and this did seem to help. to further evaluate for a source of csf leak (dural tear/ pachymeninges enhancement) an mri of the head and c-spine with and without contrast was ordered. an eeg was initially performed while the patient was in the icu, but this did not show any background activity and a repeat eeg was ordered to determine background activity as well as evaluate for epileptiform discharges. after the lp, he was started on broad spectrum empiric abx (vanco, ceftriaxone, ampicillin, acyclovir) and id was consulted. patient continued to wax and wane, but was overall somnolent. at id's recommendations, all antibiotics/antivirals were discontinued. a ppd was placed and was negative. for the cerebral edema noted on imaging, he was started on high dose dexamethasone to decrease intracranial swelling. rapid improvement was noted on the steroids. the steroids were initially tapered rapidly, but the day following taper, he was very somnolent/lethargic and was only minimally responsive to sternal rub. a repeat ct head was performed at that time and showed no change from prior studies. the steroids were restarted in the form of an oral taper following this somnolent episode; however the patient became extremely agitated and restless while on the steroids. he required 1:1 supervision and eventually a psych consult had to be obtained to help with his management. likely that the steroids were inducing this agitated/manic state, but it is unknown if his underlying brain edema was contributing. he was placed on haloperidol to control his agitation/psychosis induced by the steroids (after unsuccessful trials of seroquel and zyprexa). he had the unfortunate side effect of akathisia / dyskinesia. haldol was discontinued. movement disorders was consulted and was placed on cogentin and ativan for dyskinesia and anxiety, it was felt he had a significant psychiatric component to his dyskinesias, with arm and head shaking worsening as soon as medical personnel entered the room. within several days of cogentin he had improved significantly and mri brain was finally able to be performed, with results detailed as prior. it was deemed would be safe to return home and follow-up with dr. . medications on admission: cyclobenzaprine prn tramadol prn discharge medications: 1. benztropine 0.5 mg tablet sig: two (2) tablet po bid (2 times a day) as needed for dyskinesia. disp:*60 tablet(s)* refills:*2* 2. simvastatin 10 mg tablet sig: two (2) tablet po daily (daily). disp:*30 tablet(s)* refills:*2* discharge disposition: home with service facility: care group discharge diagnosis: bilateral subdural hematomas intracranial hypotension cerebral edema medication-induced dyskinesia discharge condition: level of consciousness: alert and interactive. activity status: ambulatory - independent. mental status: confused - sometimes. discharge instructions: you came to the hospital with symptoms of headache, nausea, vomiting. you were found to have subdural hematomas, which is the a collection of blood within your skull but outside your brain. these may have been caused by an otherwise unnoticed head injury, such as falling in the shower. you also have intracranial hypotension; it is currently unknown if this is from a leak or from old trauma. for this you were placed on a steroid taper. the steroids made you extremely agitated and restless; resulting in the necessity to start you on a medication called haldol to help calm you down. unfortunately, you had a common side effect of the haldol causing your head and arms to shake with uncontrollable blinking. the headaches you have been having are likely due to the intracranial hypotension and should you get a headache in the future, it would help to lie down flat and keep yourself hydrated. followup instructions: you need to call your insurance company to change your primary care doctor , who is a doctor here and will supervise , the doctor you are scheduled to see. you have an appointment to have a cat scan phone: date/time: 8:30 you have an appointment with neurosurgery , md phone: date/time: 9:45 you have an appointment with your pcp , md phone: date/time: 1:45 you have an appointment with neurology , m.d. phone: date/time: 5:00 you have an appointment with movement disorders drs. & phone: date/time: 11:30 procedure: spinal tap incision of lung diagnoses: adrenal cortical steroids causing adverse effects in therapeutic use unspecified fall cerebral edema other and unspecified special symptoms or syndromes, not elsewhere classified headache encephalopathy, unspecified other extrapyramidal diseases and abnormal movement disorders subdural hemorrhage following injury without mention of open intracranial wound, with no loss of consciousness other specified hypotension lack of coordination butyrophenone-based tranquilizers causing adverse effects in therapeutic use 

Answer: The patient is high likely exposed to