A Groundhog, a Novel Bartonella Sequence, and My Father’s Death

D uring the summer of 2007, migratory joint pain developed in my (E.B.B.) 86-year-old father, previously an ironworker, farmer, and World War II veteran. Because of occasional tick attachments, a Borrelia burgdorferi ELISA was performed; antibodies were not detected, and no treatment was instituted. In the fall, subtle memory loss developed, and he fell twice a few weeks apart. Dad jok-ingly blamed the falls and the memory loss on " old timer's disease. " Subsequently, episodes of subtle confusion and more frequent memory loss generated family concern as to what the future might hold. On December 15, he broke his left femur during a fall while climbing 2 stairs to enter our home. Despite having successfully climbed those stairs thousands of times in the past, he would never climb those or any other stairs again. Retrospectively obvious, a pattern of insidious illness characterized by joint pain, memory loss, and inco-ordination, not recognizable by my father or other family members, had begun before that summer. Medically stable historical problems included coronary artery disease, ath-erosclerosis, carotid artery occlusion, hypertension, and atrial fi brillation. During the previous year, a normocytic, normochromic, nonregenerative anemia persisted. Despite normal serum iron, total iron binding capacity, ferritin, and vitamin B12 values, anemia was attributed to intestinal blood loss. When examined in May 2007, before anesthesia for endoscopy, mood and affect were appropriate, recent and remote memory were intact, insight and judgment were good. A hiatal hernia, mild antral gastritis, and duodenitis were visualized. Initial Hospitalization When my father was hospitalized December 15, 2007, with a broken femur, a resting pill roll tremor and cogwheel rigidity were suggestive of Parkinson disease. Preoperative neurologic consultation identifi ed severe confusion, inattention , and an inability to answer questions. Short-term memory and problem-solving abilities were decreased. There was mild ptosis of the right eye, normal cranial nerves, mild asterixis, and hand weakness. Laboratory abnormalities included anemia, hypercreatinemia, an elevated aspar-tate aminotransferase level, and hyperglobulinemia. Due to the severity of the femoral fracture, the femoral head was excised and replaced with a bipolar femoral prosthesis. Postoperatively, poor mentation was considered a se-quela of general anesthesia and peri-operative analgesics. For more than a week, dementia persisted. He did not recognize family members and had near constant hallucino-genic activities, including agitation, tying knots, sawing motions, and constantly pulling covers, bed clothes, and fl uid lines. Severe hematuria developed after he pulled an infl ated …