A 39 year old man was presented at a Washington state hospital. The patient had gone camping a couple weeks ago with friends to do some fishing. He had come in to contact with salmon that fought heavily on the fishing line (which they caught and ate during that weekend), a couple of friendly dogs (which were owned by one of the campers), and a raccoon which had staggered into the campsite (which they killed and buried). He presented to a local emergency department (ED) on June 16th and soon after was hospitalized; he died 12 days later.
On June 16th, the man went to a local ED after 10 days of pain and progressive numbness in the left
hand and arm and pain in his lower neck and upper back. A neurologic exam revealed normal strength
and sensation of his lower extremities. His right arm showed normal strength, but the left hand showed no grip, and the patient could only lift his left arm a few inches. The patient had no fever, and his blood pressure was normal when he arrived at the hospital.
During the hospital exam, the patient's breathing became labored, and he had difficulty with respiratory secretions. He was placed on ventilation. At the time of intubation, the anesthesiologist noted that the pocedure was easy to perform because of lack of muscle tone in the patient's pharynx.
Upon admission, a MRI was conducted and the results were unremarkable. During the first 2 days of hospitalization, the patient experienced progressive weakness, initially on the left side. He was able to respond to verbal commands and, according to the neurologist who evaluated him, his random eye movements were normal.
On June 19th, the patient's mental status appeared to improve, as sedation was lightened with the hope of removing him from the ventilator. However, over the next few days, his upper extremity weakness progressed to involve the right side, and lower extremity weakness was noted. Some nystagmus was also noted. On June 20th, the patient became quadriplegic but could move his eyes to the right and left on request.
A Gram stain and culture of spinal fluid were negative.
On June 21st, the patient had an acute change in his neurologic status, including twitching of the left
foot, more marked nystagmus, and slightly asymmetric pupils. Based on the results of the CSF analysis, the working diagnosis was changed to meningoencephalitis, and an infectious disease consultation was sought. The CSF was further analyzed for Borrelia burgdoferi and the following viruses: West Nile, St.Louis encephalitis, California Group, Eastern equine encephalitis, Western equine encephalitis, measles, mumps, herpes simplex virus 1 and 2, enteroviruses, varicella-zoster, cytomegalovirus, lymphocytic choriomeningitis virus, adenovirus, and influenza. All tests were negative. Antiviral treatment with acyclovir was begun anyway.
The patient's condition, characterized as complete flaccid paralysis, coma, and flat electroencephalogram, remained unchanged. On June 28th, the patient's family elected to withdraw life support, and the patient died shortly afterward.
1. What is the most likely causative agent?
2. What was the likelihood of the patient recovering if the right diagnosis had been made early?
Fully explain.
3. How did the man most likely contract this disease?
4. How could this infection be confirmed? Be specific. The test MUST confirm this and no other
infection.
la_chica_suerte85, BSN, RN
1,260 Posts
GBS is usually ascending, bilateral paralysis and it resolves with supportive care. People don't end up progressing to brain death, though the rare unfortunate few who had it d/t a C. jejuni infection have some irreversible nerve damage.
That was a really cool case study. I wish we had something like that when I was taking medical micro.