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: history of present illness: ms. is a 42-year-old female with a history of depression and polysubstance abuse, who was transferred to from hospital for fulminant hepatic failure and renal failure. the patient was admitted to the outside hospital on . she was somnolent and hypotension. her vital signs at the outside hospital on admission were temperature 98.9, pulse 65, respiratory rate 16, blood pressure 74/39, o2 saturation 84% on room air, which increased to 93% on four liters by nasal cannula. laboratory data was significant for a white blood cell count of 34.5, ck 6,036, ast 23,580, alt 14,130, total bilirubin 0.6, alkaline phosphatase 126. serum toxicology screen was negative. hcg was negative. potassium was 6.8, bicarbonate 12. an arterial blood gas showed a ph of 7.27, pco2 31, and po2 77 on two liters nasal cannula. the patient was anuric and transiently placed on a lasix drip and renally dosed dopamine drip. renal consultation was obtained who recommended intravenous fluids and bicarbonate as well as transfer to the intensive care unit. a transfer to and medical intensive care unit was arranged. per the patient's husband, the patient has had worsening depression recently but adamantly denied a suicide attempt. she recently started a new diet pill called zantrex-3 the week prior to admission and has taken approximately 60 pills over the last five to seven days. the patient may have also taken methadone two days prior to admission. the family, however, is not very forthcoming with their previous history of substance abuse and exactly what the patient has been taking over the past several months. past medical history: 1. hypertension. 2. depression. 3. chronic pain status post motor vehicle accident. 4. history of oxycontin abuse. 5. history of alcohol abuse. 6. history of cocaine abuse which she snorted. 7. asthma/copd. medications at home: 1. neurontin. 2. toprol xl. 3. topamax. 4. zoloft. 5. trazodone. 6. prilosec. 7. albuterol inhaler. 8. flovent inhaler. 9. advil p.r.n. 10. tylenol p.r.n. 11. zantrex-3. allergies: the patient has no known drug allergies. social history: the patient is married with two children. she has a history of heavy alcohol abuse but last used alcohol four to five months prior to admission. she has a history of cocaine abuse which she last used two months ago. she denies any intravenous drug use history. there is a questionable history of smoking. physical examination: vital signs were temperature 99.8, blood pressure 123/71, pulse 85, oxygen saturation 97% on four liters by nasal cannula. in general she was somnolent but she opened her eyes to voice and answered questions with short responses before falling back asleep. heent: sclerae anicteric, pupils were equal, round, and reactive to light. dry mucous membranes and oropharynx was clear. neck: supple. cardiovascular: regular rate and rhythm with no murmurs, gallops, or rubs. lungs: chest was clear to auscultation bilaterally with decreased breath sounds at the bases bilaterally. abdomen: very tender with hepatomegaly, no splenomegaly, normal active bowel sounds. extremities: no lower extremity edema. her extremities were warm and she had 2+ pedal pulses bilaterally. neurologic: she was confused, somnolent, unable to assess for asterixis given the poor cooperation. she was moving all four extremities well. rectal: she was guaiac positive. laboratory data: on admission to the intensive care unit her white count was 25, hematocrit 34.3, platelet count 180, pt 20.7, ptt 34.1, inr 2.8. chem-7: sodium 137, potassium 3.6, chloride 100, bicarbonate 23, bun 46, creatinine 4.5, glucose 255. her alkaline phosphatase was 127, total bilirubin 0.8, lipase 70, amylase 101, albumin 3.2, alt 12,133, ast 20,570, ldh 21,890. hospital course: 1. hepatic failure: the patient was transferred from an outside hospital in hepatic failure. the liver team was consulted upon transfer. several etiologies were entertained as to the possible cause for her hepatic failure. the patient had been taking a large amount of a new diet pill called zantrex-3, the main component of which is niacin. niacin is known to cause liver failure in several cases. another possibility was hypotension leading to shocked liver. an infectious etiology for her fulminant hepatic failure was also considered, however the patient was found to be hepatitis c negative, hepatitis b negative. her cmv antibody titers were consistent with an old infection as there was no igm present. her - virus antibody titers were also consistent with an old infection with negative igm titers. toxoplasmosis was also negative. an rpr test for syphilis was also found to be nonreactive. a doppler ultrasound of the abdomen and pelvis was performed. the hepatic venous doppler interrogation was suggestive of a hyperdynamic state, however the hepatic vasculature was otherwise unremarkable, and there was no focal liver mass. the gallbladder wall showed thickening, possibly due to a low protein state or related cardiac disease. there was also increased echogenicity of the kidneys consistent with diffuse parenchymal renal disease. on admission the patient was believed to be encephalopathic from her liver failure and she was started on lactulose via a nasogastric tube. she was also started prophylactically on antibiotics with ceftriaxone and fluconazole until the results of her infectious work-up returned as negative. the patient was also given vitamin k to reverse her elevated inr. she was started on q. 2 hour fingersticks with regular insulin sliding scale due to the risk of hyperglycemia with liver failure. eventually the patient's liver enzymes started to improve and she was closely monitored throughout the remainder of her hospitalization. at the time of discharge the patient's liver enzymes had normalized. ultimately, it was believed the cause for her fulminant hepatic failure to be this niacin toxicity from the overingestion of diet pills, with a possible contribution from hypotension. 2. acute renal failure: the patient was transferred from an outside hospital with acute renal failure. at the time of admission her creatinine was elevated to 4.5. there were several possible etiologies for the acute renal failure including acute tubular necrosis from direct toxic effect, hypovolemia, questionable history of rhabdomyolysis, or liver failure. on admission the patient was anuric and she had an anion gap acidosis with increased phosphate, increased potassium and decreased calcium. a renal consultation was obtained to consider starting hemodialysis. in the meantime she was started on aggressive hydration and all of her medications were renally dosed. a renal ultrasound was performed which showed normal- sized kidneys. the kidneys also demonstrated increased echogenicity consistent with chronic parenchymal renal disease. there was no hydronephrosis but there was a small amount of fluid surrounding the kidneys. urine electrolytes were obtained which showed a picture consistent with acute tubular necrosis. the renal team initially attempted to manage the patient medically however the patient ultimately required hemodialysis. a temporary catheter was placed and the patient was started on hemodialysis initially every two to three days. the hemodialysis sessions were spaced further apart when the patient started producing more urine and she was started on diuretics to encourage urine output. at the time of discharge her renal function had improved since admission, and she making urinebut she was still requiring hemodialysis. a permanent line was placed prior to discharge for further outpatient hemodialysis. at the time of discharge it was believed that her acute renal failure was most likely due to acute tubular necrosis from medication and/or hypotension and/or rhabdomyolysis. it is unknown how much longer the patient will require hemodialysis, but the renal consultation team hopes that she will not require life-long dialysis. 3. hypertension: on admission the patient was hypotensive at the outside hospital, however soon after being transferred to the intensive care unit, the patient started to develop extremely elevated and labile blood pressures to a systolic blood pressure of 200. she was briefly on a labetalol drip in the intensive care unit and required multiple medications to control her blood pressure. the cause for her increased blood pressure was believed to be due partly to the acute renal failure and also partly due to agitation. it was noted that when the patient became extremely agitated, that her blood pressure would increase. at the time of discharge, however, the patient's blood pressure was well controlled with a systolic blood pressure from 120 to 160 on metoprolol, amlodipine, and clonidine. 4. seizure disorder: the patient has no previous history of seizures, however on she was found to have four seizures with 2 mg of ativan iv between each seizure. the first seizure was characterized as tonic and the following three seizures were generalized tonic-clonic seizures. since the ativan was not able to control her seizures, she was started on a dilantin load and was transferred from the floor to the intensive care unit for further management. a work-up was performed and her head ct showed bilateral frontal hypodensities as well as bilateral thalamic hypodensities. an mri was then performed which showed posterior leukoencephalopathy likely due to extremely elevated blood pressures combined with renal failure. despite the dilantin load the patient had another seizure on and had to be started on keppra. cerebrospinal fluid was obtained, which was found to be normal and there was no evidence of infection. the cause of the seizure was debated and the etiology is not entirely known. one possibility is that the patient was taking 5-6 mg of neurontin prior to admission, which was abruptly stopped, as the medical team was not aware of her neurontin use. acute neurontin withdrawal has been associated with seizures. another possibility raised was that flagyl, which the patient had been taking for a pneumonia, was a possible cause for seizures, however this is less likely as the patient was taken off flagyl following the first set of seizures and she had recurrent seizures even off the flagyl. a third possibility is that the combination of severely elevated blood pressures as well as acute renal failure could have led to malignant hypertension manifesting itself in seizures. the patient has a long history of substance abuse, which she has not been very forthcoming about. so it is quite possible that the patient was abusing another substance that is unknown to the team. she was continued on dilantin with daily dilantin and free dilantin level checks, as well as keppra throughout the remainder of her hospital course and she had no further seizures. neurology was consulted and assisted with the thorough work-up of her seizures as well as with medication dosing. the plan is currently to maintain her on dilantin and to change the dosing once she is off hemodialysis. she is on keppra 500 mg p.o. q. day with an extra 250 mg dose on dialysis days. the plan is to change the dosing of keppra also when the patient is no longer on hemodialysis. the remainder of the hospital course will be dictated at a later time. , m.d. dictated by: medquist36 procedure: continuous invasive mechanical ventilation for less than 96 consecutive hours spinal tap incision of lung insertion of endotracheal tube enteral infusion of concentrated nutritional substances hemodialysis venous catheterization for renal dialysis diagnoses: urinary tract infection, site not specified acute and subacute necrosis of liver acute kidney failure, unspecified hyposmolality and/or hyponatremia other convulsions pneumonitis due to inhalation of food or vomitus intestinal infection due to clostridium difficile candidiasis of vulva and vagina unspecified causes of encephalitis, myelitis, and encephalomyelitis 

Answer: The patient is high likely exposed to