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: shortness of breath major surgical or invasive procedure: none history of present illness: 79 yo male with cad, diastolic chf, severe pvd, htn and dm admitted with rapid afib/a flutter in setting of hypoxia, hypotension, and possible underlying copd. he has had worsening sob over past two months. initially started as doe. he states that over the past few months, he has been feeling increasingly short of breath; he states he has to stop 3 times when walking up one flight of stairts. he denies any pnd/orthopnea (stable 1 pillow orthopnea), but he reports associated palpitations over the past few weeks. he denies any chest pain, jaw pain, diaphoresis, fever, chills, but does report intermittent nausea, vomiting and diarrhea over the past few days. he was started on combivent by pcp (had inhalers in the past but was not using. pt was recently hospitalized at nebh for left total hip arthroplasty (right hip done in ) where he had a postop course complicated by delirium, copd exacerbation, aflutter with 2:1 block (hemodynamically unstable, required neo; electrically cardioverted), ?pna (ceftaz) * in ed, hypoxic to 85%, tachycardic with afib/flutter to 150s with hypotension 80-100. he received 250cc bolusx2, combiventx3, and solumedrol 125. on exam, sitting upright with short, shallow breaths, poor air flow, wheezes and rhonchi, and trace edema. * past medical history: pmhx: cad; lad stent , cath - lmca patent, lad mild stenosis with 30% d2, lcx mild, 40% distal to om1, rca mild irregularities with mid 40-50% stenosis pvd-r sfa stent htn hyperlipidemia cardiomyopathy, depression osteoarthritis bilateral hip replacement social history: 50 pack-year tobacco history, quit 20 yrs ago history of 'heavy' alcohol use, quit 20 yrs ago lives with wife with assistance family history: non-contributory physical exam: vs: t = 96.5; hr = 98; bp = 108/36; rr = 25-27; o2 = 99% 3l gen: elderly man, sitting up, speaking in full sentences, shallow breathing, on nc o2, nad heent: perrl, eomi bilaterally, op clear, mmm neck: no jvd appreciated cv: rrr, very distant heart sounds, nl s1/s2, no m/r/g appreciated lungs: decreased bs throughout, expiratory wheezes diffusely, ?crackles at left base abd: obese, soft, nt/nd, no hsm appreciated extr: no c/c; 1+ pretibial pitting edema bilaterally, very weak peripheral pulses bilaterally in le neuro: grossly intact; sensation and motor intact bilaterally pertinent results: 08:30am blood wbc-18.3* rbc-3.90* hgb-10.3* hct-31.5* mcv-81* mch-26.4* mchc-32.8 rdw-13.0 plt ct-274 08:30am blood plt ct-274 08:30am blood pt-14.4* ptt-104.6* inr(pt)-1.3 04:36pm blood ptt-45.5* 08:30am blood glucose-164* urean-73* creat-2.8* na-137 k-4.5 cl-102 hco3-23 angap-17 08:30am blood calcium-9.0 phos-4.0 mg-1.6 03:45am blood tsh-0.37 * ekg- afib 120s-150s, nl axis, irregular cxr- unremarkable, ? cardiomegaly, mild failure p-mibi - ef38% * : tte: ef>40%, small pericardial effusion, not hemodynamically significant, mild dilation of left atrium, cannot exclude wall motion abnormality due to poor study * ekg : sinus rhythm; incomplete right bundle branch block; lateral st elevation since previous tracing of , no significant change * chest (portable ap) 9:48 am improving aeration at both lung bases. residual minor atelectatic changes and small pleural effusions. brief hospital course: 79 yo male with pmhx of cad, pvd, htn, dm2, diastolic dysfunction, cri, atrial fibrillation, admitted to the ccu in acute respiratory failure the setting of rapid afib in chf, intubated/extubated, called out to the floor, with persistent lower extremity edema refractory to multiple diuretic therapies. 1.respiratory failure: pt was transfered to the ccu from the floor after an acute episode of respiratory distress and hypoxia in the setting of recurrent rapid afib. sob did not resolve after attempted diuresis with iv lasix 120. pt's respiratory failure was most likely secondary to acute chf secondary to volume overload resulting from acute renal failure in a pt with underlying copd. pt initially was given bipap with progressive hypoxia. pt was intubated and started on ac. initially, pt was difficult to ventilate. pt started off with fio2 of 1 and peep of 15 on assist control. over the next several days, the ventilator settings were weaned down. the patient was difficult to extubate and therefore remained intubated for the next 2 weeks. the pt was maintained on assist control for a while, followed by multiple trials of pressure support, and 3 attempts at extubation. . since pt was significantly volume overloaded on admission, aggressive diuresis is what helped in weaning the ventilator and moving towards extubation. serial chest-xrays were consistent with congestive heart failure, without evidence of pneumonia. initially pt was not aggressively diuresed since it was thought that he was septic. after resolution of septic physiology, pt was aggressively diuresed with prn lasix. pt was able to tolerate ps for increasing periods of time. eventually, rsbi's decreased to 50-60s and pt was able to tolerate ps 5, peep 5. three attempts were made to extubate the patient. during the first attempt, pt had copious amounts of secretions, but lacked a good cough reflex and was re-intubated for inability to clear his secretions. the second time, the pt self-extubated himself. his appeared to be breathing decently, but the pt subjectively experienced respiratory distress and wished to be intubated; in addition, he continued to have lots of secretions. it was felt that tracheostomy was the most likely next step. at this point, the pulmonary service was consulted to help with extubation. pulmonary suggested continued aggressive diuresis. pt was started on lasix drip. they also suggested checking for a cuff leak; if <150cc consider short course of steroids for tracheal edema. pt did not have signs of tracheal edema. he was able to tolerate ps5, peep5 with low rsbi. third attempt at extubation was made. pt was able to stay extubated for 2 days ** since . at times, pt appears to be working hard to breath, but remained stable with rr 20-30, o2sats 95-100, and decent abgs. on , pt was noted to be wheezy and strigorous. re-intubation was considered. however, both pulmonary and anesthesiology felt that pt did not need re-intubation. pt was started on standing solumedrol and racemic epinephrine with improvement in his wheezing and strigor. pt became aggitated at times with increased in the work of breathing. pt was given prn sublingual zyprexa 5mg with little improvement in aggitation and breathing. haldol 2mg given with little improvement. morphine 2mg given with some improvement. on , pt was give zyprexa 10mg prn with improvement in agitation. eventually with aggressive diuresis the patient's respiratory status stabilized. he went through a short period of time ~ - where he would become increasingly agitatd and desaturate during the evening and require sedation with cpap. it was thought that the patient was sundowning and was sending himself into respiratory distress. the patient was placed on a standing haldol dose in the evening and the prophylactically given cpap during the night. the patient then no longer had desaturation episodes. he was transferred to the floor and no longer required sedation or ventilatory assistance. by discharge he required no oxygen supplementation. his steroids were tapered to off. . 2. hypotension: pt was hypotensive on transfer to ccu and started on dopamine drip. etiology of hypotension included new onset sepsis, afib, and chf. swan numbers were more consistent with sepsis with a relatively low cvp, high cardiac output/index, and low svr. pt was continued on dopamine and levophed drips. pt remained afebrile with an elevated wbc count. pt was started on empiric antibiotics of vanco, levo, flagyl. levofloxacin was switched to ceftazidime. blood and urine cultures were collected and remained negative. pt had positive urine culture on the floor 1 week prior to transfer to ccu which grew out e.coli, extended-spectrum beta-lactamase(esbl) producer considered resistant to all penicillins, cephalosporins, and aztreonam. given this information, ceftazidime and flagyl were discontinued and switched to meropenum; vanco was continued. over the next several days, pt's septic physiology resolved. however, pt still required small doses of levo and dopa. pt was very slowly weaned off of both pressors over a period of 2 weeks. pt maintained an adequate bp for the majority of his stay on the floor. ~ the patient has two episodes of hypotension and bradycardia. these episodes occurred in the setting of aggressive diuresis with dopamine and nesiritide and recent addition of patient's beta blocker to daily amiodarone. he also felt nauseated and had emesis during these two events. both times he was given atropine and had an appropriate response in bp and heart rate. the thought was that he had a vagal response in the setting of diuresis, beta blocker, and amiodarone. his beta blocker was held and nesiritide and dopamine stopped with no further episodes. . 3. rhythm: pt was in normal sinus rhythm on the floor (cardioverted by amio) before going to into rapid afib. diltiazem, which was previously used for rate-control had been held in order to keep map elevated for renal perfusion and diuresis. on , pt went into recurrent rapid afib with hr in 130s with associated shortness of breath and hypoxia. pt was given 5mg iv lopressor. after pt was intubated in the ccu, pt spontaneously converted back into sinus rhythm. pt was continued on po amio to maintain sinus rhythm. on , pt went into rapid aflutter. he was started on amio drip and was cardioverted into nsr. pt was continued on iv amio. later during hospitalization, pt was noted to be in first degree av block, which he continued to be in. pt has had no more episodes of afib or aflutter. since , pt has received 10gm of amio. this is an adequate loading dose. starting on the patient was started on amiodarone 200 mg po and had no major events on telemetry. . 4. pump: during pt's acute episode of afib, pt developed associated sob and hypoxia. a chest x-ray showed that pt was in heart failure. on the floor, pt was given total of 120 iv lasix and 5mg iv lopressor. heart rate decreased to 80s and bp improved from 90 to 100 systolic, but respiratory distress progressed despite attempted diuresis and rate-control. pt was transferred to ccu and intubated. on admission to the ccu, pt was had total body volume overload with signs of heart failure. pt has preserved systolic function of 55%, but likely has diastolic dysfunction. initially pt was not aggressively diuresed since it was thought that he was septic. after resolution of septic physiology, pt was aggressively diuresed with prn lasix, which was later switched to a lasix drip. pt lost 9kgs with a weight loss from 109 to 100kg. with increasing diuresis, pt was able to be better ventilated. the patient was extubated and evetually developed hypernatremia. he was corrected by a light continuous infusion of d5w because it was thought that he would not tolerate free water boluses in light of his diastolic dysfunction. his lasix was also held. eventually hypernatremia was corrected. the patient had persistent lower extremity edema on the floor and multiple interventions were attempted. the ultimate thinking was that his edema was from poor nutrition, immobility, and venous stasis disease. he did not appear to be in cardiac failure as his lungs remained clear and he had no jvd. he was given boost with meals to improve his nutritional status. he was started on dopamine and nesritide drips but felt nauseated and had occasionally became hypotensive. he was also tried on iv bumex and albumin. he responded maximally to lasix drip with zaroxyln po qd. prior to discharge he was switched to lasix 80 mg po bid and zaroxylyn 5 po bid which he showed strong reponse to. he was also treated with diamox prior to discharge for diuretic associated alkalosis. . 5. cad: pt had no active issues. on transfer to ccu, cardiac enzymes were cycled and found to be negative. pt was continued on asa and statin. beta-blocker and ace were held in the setting of hypotension and pressors. . 6. renal failure: pt presented with worsening acute on chronic renal failure. creatinine on transfer was 3.7. renal continued to follow the patient. ultrafiltration was considered as a means for removing volume. a dialysis line was place. however, ultrafiltration was not started because the pt began to diurese well on his own with a decrease in creatinine. aggressive diuresis with lasix helped decrease creatinine to 1.3, it did climb up to 1.7 with standing iv lasix and the other aggressive diuretic regimens. however, when the intervention were stopped, his creatinine always trended down towards his baseline. . 7. id: sepsis was considered as potential etiology of hypotension given swan numbers consistent with sepsis. pt was pan-cultured. pt was started on vancomycin, ceftazidime, and flagyl for broad spectrum coverage. pt had been on several antibiotics during this hospitalization including azithromycin, ceftriaxone, bactrim, zosyn for treatment of pna and uti. pt remained afebrile. blood and urine cultures remained negative. serial cxr had no evidence of pneumonia. pt was evaluated by id. on ccu day 3, ceftazidime and flagyl were discontinued and a switch was made to meropenem since a urine culture from the floor grew out e.coli resistant to ceftazidime. vancomycin was continued. renal ultrasound showed no perinephric abscess. a hypoechoic contour defect adjacent to the upper pole cysts brought up the question of a solid renal lesion. id requested mri of the abdomen to better evaluate this solid lesion, since there was no definitive source of sepsis. however, mri was not performed while pt remained intubated and on pressors as he was not stable enough to go to radiology. depite the fact that there was not definitive source of infection, it is most likely that sepsis was the source of the pt's initial hypotension. pt's overall clinical status significantly improved after starting on empiric antibiotics. pt's hypotension improved and serial swan numbers no longer appeared septic. most likely sources of infection include urosepsis from the pan-resistant e.coli and a question of lll pneumonia seen on a chest x-ray. pt completed a 14 day course of vanco and meropenum. on , patient began to have a productive cough with persistent upper airway secretions. he was pan cultured and started on levofloxacin and flagyl. pt grew coag - staph from blood cultures drawn from the picc line and wbc count became elevated to 23. pt never mounted a fever and was also on his steroid taper. on, his wbc count rose to 30.3 on vanco/levo. as a result he was started empirically on flagyl and his wbc began to trend down. he was treated with a 7 day course of vancomycin through his picc line and 14 day course of flagyl. surveillance blood cultures and urine cultures were all negative. sputum gram stain showed 2+ gram + cocci in pairs/clusters but cultures were oropharyngeal flora. after the full courses of abx therapy, the patient wbc normalized. . 8. gi: on presentation, pt had not had a bowel movement in around 10 days. a recent ct of the abdomen showed now signs of obstruction or perforation. several kubs was performed which all showed distended stool filled loops of bowel without obstruction or free air noted. pt has an ileus of multifactorial etiology. pt was continued on an extensive bowel regimen of po and pr medications. pt had difficulty absorbing the po meds, which were given through the og tube. pt put out greater than 1l of bilious fluid from his ogt daily. it was noted that pt had no stool in the rectal vault; disempaction was not an option. a rectal tube was placed and found very little stool at the tip of the tube. pt was started on around the clock enemas without success. gi agreed that pt had an ileus and recommended holding off on po med and enemas and continuing supportive care. pt had not had a bowel movement since . as his clinical exam became more stable he was placed on an aggressive bowel regimen and he began having normal bowel movements. . 9. dm: blood sugars were initially managed on an insulin drip. when tpn was started, insulin was given in the tpn mixture. pt was switched to insulin sliding scale. when pt was started on solumedrol, bs signficantly increased and pt was restarted on insulin drip. upon transfer to the floor, was reconsulted and pt resumed his humalog sliding scale w/ evening lantus. he continued to remain in reasonable glycemic control for the rest of his stay. . 10. ischemic foot: as the patient began having persistent lower extremity edema that was refractory to diuresis, his feet began to become erythematous. he has known pvd w/ a sfa graft on the right. he had skin breakdown with weeping on the dorsum of his left foot secondary to edema that required daily wound care. on the patient complained of right foot pain, had increased redness in his feet r>l, and had ischemic ulcers on his 2nd, 3rd, and 4th digits on the right. lower extremity non-invasivce studies were negative. pt had lower extremity doppler studies that showed and abi of 0 on the right and .44 on the left. consult was called to evaluate possible cellulitis. pt had plain films of his right foot that felt did not represent osteomyelitis. they felt his symptoms were from ischemia that were exacerabted by the patient's profound edema. he was placed in unna boots b/l. per attg dr. , angiographic studies were held off because of possible damage patinet's kidneys could endure from dye load. the decision was made to see how his feet would improve upon treatment of his lower extremity edema. patient reported improved symptoms when his feet were elevated and as he was effectively diuresed. he was given an appointment to follow up closely with both and dr. upon d/c. . 11. anemia - the patient had a persistently low hct in the 30's. hemolysis labs and anemia work up were all negative. it was deemed that his hct was likely low due to chronic phlebotomy. medications on admission: pletal 100 asa 81 lasix 80 zestril 10 lipitor 40 wellbutrin 150 flomax 0.4 glipizide er 10 lantus 50 u qhs insulin sliding scale nkda discharge disposition: extended care facility: life care center at discharge diagnosis: atrial fibrillation chf copd exacerbation pneumonia peripheral vascular disease discharge condition: good discharge instructions: please call dr. if you experience chest pain, shortness of breath greater than normal, heart palpitations, leg or foot pain or lack of feeling, cough with thick colored sputum, fever, shaking chills, blood in your stool. please follow up your appointments with dr. and after the new year regarding your leg swelling and poor blood flow to your feet. if your condition acutely worsens you can come back to the . followup instructions: you will have your blood drawn at the rehabilitation facility on to monitor needed changes in your coumadin and lasix medication. to rn at rehab facility - please check chem 7 and inr- re dose coumadin and potassium supplementation accordingly. provider: , clinic where: cc-2 unit phone: date/time: 2:40 provider: , , unit phone: date/time: 2:25 pm procedure: venous catheterization, not elsewhere classified continuous invasive mechanical ventilation for 96 consecutive hours or more parenteral infusion of concentrated nutritional substances transfusion of packed cells injection or infusion of nesiritide diagnoses: pneumonia, organism unspecified anemia, unspecified urinary tract infection, site not specified congestive heart failure, unspecified acute kidney failure, unspecified unspecified septicemia severe sepsis atrial fibrillation obstructive chronic bronchitis with (acute) exacerbation atrial flutter acute respiratory failure hyperosmolality and/or hypernatremia diastolic heart failure, unspecified 

Answer: The patient is high likely exposed to