Initial report was received 27 June 2011 from an investigator participating in a trial under the reference number Td512. A 61-year-old female subject who had a history of hypertension, a motor vehicle accident in May 2006 and low back pain, had received an injection of ADACEL, lot number C2341AA on 24 July 2006 and 25 days later, she had an emergency visit due to acute onset lower extremity weakness which was subsequently diagnosed as Guillain-Barre syndrome. She was hospitalized from 18 August until 25 August 2006, then discharged to a skilled nursing facility for rehabilitation. According to medical records, the subject was involved in a motor vehicle accident in May 2006 and developed some low back pain. She received Flexeril and Etodolac with resolution of the pain and subsequently stopped those medications. She also experienced two mechanical falls in the mean time, "none related last month", and had no sequelae. Thereafter she was able to get up and walk around. On the day of hospital admission, the subject noted some mild lower back pain while trying to get up and go to the bathroom. When she tried to stand up, she noticed that her legs were weak with some tingling, and she was unable to walk. Both feet felt numb and were very weak in both lower extremities. She had no family history of diabetes and no known drug allergies. Outpatient medications were Atenolol 25 mg, Calcium and Vitamin D supplements and Glucosamine. Emergency room examination findings: blood pressure 170/80, Saturation 98% (room air), and heart rate in 70s. Neurological findings: alert and oriented x4, cranial nerves intact with 5/5 bilateral upper extremity strength. Lower extremity hip flexors were about 3/5 with some breakaway weakness; ankles and toes were 3/5 with decreased sensation in the distribution of socks in the dorsal and plantar aspect of the feet. The remainder of physical examination findings were normal. Lab data was unremarkable. On 18 August 2006, radiologic imaging noted L/Spine mild degenerative joint disease. CT of the head was negative. MRI (thoracolumbar) showed normal spine, no compression, no fracture or subluxation, alignment normal; there was however some mild multilevel disc disease without any spinal stenosis and some mild neuroforaminal narrowing at L4-L5. Neurology was consulted and due to findings of distal greater than proximal weakness, a work-up ensued for peripheral neuropathy with possibility of Guillain-Barre syndrome causing the myelopathy. Respiratory therapy noted vital capacity 0.6 to 0.8 although with poor effort being noted and a negative inspiratory force of -30 to -40 with good effort being noted. Lumbar puncture showed normal protein glucose and just one WBC which ruled out acute infectious process, but was considered suggestive of Guillain-Barre syndrome. Despite CSF findings, a five day course of IVIG was initiated on 21 August 2006. After two days of IVIG therapy, improvement was noted with 5/5 strength knee flexion and extension, and 4/5 in plantar flexion; however 2/5 in dorsiflexion bilaterally. Hip flexions were 4+/5 bilaterally. The subject attended physical therapy and was able to sit and stand with minimal assist and was able to ambulate about four feet with a walker with minimal moderate assist. On 23 August 2006, an EMG was performed which showed electrodiagnostic evidence of some segmental demyelination in the motor nerves of both lower extremities; supportive of acute inflammatory demyelinating polyneuropathy. The patient was discharged to a skilled nursing facility for neurologic rehabilitation therapy after completing day five of IVIG therapy. Discharge medications included LOVENOX 40 mg SC daily for deep venous thrombosis prophylaxis. Upon admission to the skilled nursing facility, neurological examination noted 5/5 bilateral upper extremity strength. Lower extremity: left hip 3/5 muscle strength, and right hip 5/5; 5/5 knee flexion on right and 4/5 knee flexion on the left. Dorsiflexion on left 2/5 and 3/5 on right. Plantar flexion 5/5 on left and 4/5 on right. The subject had tingling in lower extremity. Relevant laboratory findings included CH50 60 U/mL, Complement C'3 173 mg/dL and Complement C'4 26.8 mg/dL, Westergren ESR (H) 104 mm/Hr and WBC 12.4 K/uL, Potassium (L) 3.4 mEq/ (reference ranges not reported). CSF: glucose 72 mg/dL, protein 54.0 mg/dL, WBC count 1/uL, RBC count 1/uL, colorless, no wbc, no culture. Remainder of laboratory values were normal. Urine culture: 20 August 2006 revealed >100,000 Col/mL Escherichia Coli; resistant to nitrofurantoin. Pansensitive. The urinary tract infection was noted "in hospital", unclear if treated in hospital. Subject received Ciprofloxacin 250 bid. The discharge date from the skilled nursing facility was unknown. Neurology consult on 15 September 2006 noted the subject estimated she was about 50% better at that time. Pain in her legs had diminished and some sensation in her feet was regained; although toes and soles still felt numb and cold at times. She remained relatively symptom free in her arms and was able to ambulate with the assistance of walker, but was not walking independently yet. Electrodiagnostic studies showed evidence of demyelination in the motor nerves in both lower extremities, consistent with demyelinating neuropathy; however there were in addition, axonal changes represented by denervation in the distal muscles of both lower extremities. Tibial motor nerve conduction studies showed normal distal motor latencies, but slow conduction velocity on both sides. The right tibial compound muscle action potential amplitude was low with temporal dispersion. The left tibial F wave latency was prolonged; right tibial F wave latency  was normal. Needle EMG of selected muscles in both legs revealed abnormal spontaneous activity in the right medial gastro with only minimally reduced recruitment. Physical exam findings noted strength normal in upper extremities 5/5; however reflexes in upper extremities were diminished. Lower extremities; hip flexors were 4/5 bilaterally; quadriceps 4+/5, hamstrings 4-4+/5, tibialis anterior 3+-4/5 bilaterally, plantar reflexes 4+/5. She had decreased distal pinprick in the toes bilaterally and absent ankle and patellar reflexes. Impression was Guillain-Barre syndrome with gradual improvement. Recovery was hopeful; however, the presence of mild axonal changes in the lower extremities had to be watched. It was further noted there was a possibility of mild residual weakness in the tibialis anterior, leading to foot drop and some gait instability. The subject's most recent neurological examination on 12 April 2010 states, "History of GBS. Now mostly Left more than Right lower extremity weakness, able to use a cane. Hemiplegic gait, fall risk. No significant change. Current retired. D/w patient motor deficits likely permanent. " The subject's outcome remained ongoing. According to the investigator, the event of Guillain-Barre Syndrome was related (i.e., possible relation) to the study vaccine. Documents held by sender: Skilled nursing facility note; neurological exam. Medical Assessment: The event of Guillain-Barre syndrome (GBS) was reported in a 61 year-old female who had received an immunization with ADACEL within 25 days prior to the symptom onset. She had a motor vehicle accident two months ago and had low back pain since. She also experienced two mechanical falls before her vaccination. According to her report (symptoms, WBC test which ruled out acute infectious process, CSF findings which were negative, EMG which showed electrodiagnostic evidence of some segmental demyelination in the motor nerves of both lower extremities, and respond well to IVIG therapy), the diagnosis should be a lever 2 of diagnostic certainty based on the Brighton collaboration case definition. According to epidemiological data, recent antecedent infectious disease are reported in approximately two-thirds of patients with GBS. GBS has been associated with many respiratory and gastrointestinal illnesses, in particular infection with Campylobacter jejuni. GBS has also been associated with other pathogens, such as Cytomegalovirus, Mycoplasma pneumonia, HIV, borreliosis and Epstein-Barr virus. Further information will be requested on diagnostics for any infectious causes (ie:UTI).