Published Oct 6, 2016
hhaide1123
22 Posts
I'm taking microbiology and I've been doing really well so far, but we have our first case study and I'm completely stumped. It's a long one, but I've included it below:
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.
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.
I've been researching meningitis and trying to find which bacteria or virus the patient could have caught, and how. I'm just confused because it says a CSF culture came back negative. What would cause meningitis but have a negative CSF culture?
I'd like to find the answer on my own (obviously it's my hw) but could anyone point me in the right direction? What am I supposed to be looking for? Thanks in advance to anyone who can help!
jennmv
143 Posts
Rabies? From the raccoon who staggered into the campsite?
FutureNurseInfo
1,093 Posts
Wow, a very complicated and complex case study! To be honest, I have no idea. I am yet to take micro. But, really? I would expect this kind of homework for medical students! Good luck!
P.S. I am guessing the way he may contracted the disease was when he struggled to take the salmon off the hook. He might have punctured his thumb/finger?
Thanks, that was my thought too. I'll ask about that. I was also thinking a brain eating amoeba from the water he was fishing in. Does that sound more or less likely than rabies?
Banana nut, BSN, RN, EMT-B
316 Posts
Meningitis can be viral as well.
BrendanO, MSN, RN
155 Posts
Wow, interesting case! Key points to me: acute, descending flaccid paralysis; negative CSF culture; negative MRI; afebrile; meningoencephalitis diagnosis based on clinical symptoms, not imaging study.
Could be GBS caused by previously resolved campylobacter jejuni infection? The negative CSF and MRI together with the afebrile presentation, to me, could point to an infection local to another part of the body, where the neurological symptoms would be caused by toxins, not primary infection of the meninges. Seems like too long of an incubation to be botulism (and the symptoms are wrong - it usually shows first in cranial nerves), but it's possible. Can't be acute polio, as enterovirus assay was negative. Unlikely to be rabies, completely different set of symptoms. Also unlikely to be N. fowleri (brain eating amoeba), also completely different symptoms (and it would also show up in CSF Gram stain).
What a hard case! Please post the answer when you find out. :)
BAY AREA RN, BSN
184 Posts
yea i think its rabies. IF U HAVE YOUR MICRO BOOK LOOK FOR RABIES, IF NOT GOOGLE UR CASE STUDY CAUSE MOST OF THEM ARE ONLINE AND WILL POP UP
Kuriin, BSN, RN
967 Posts
edit: Nevermind. The dang Gram Stain came back negative, so, it can't be botulism. I guess it's rabies even though the case study shows that the patient had never been bitten. Ugh.
Thanks everyone! Turns out it is rabies!
I haven't gotten the assignment back so I don't know for sure but I think he must have had a cut or something and fluids from the raccoon that he killed got in it when he was burying it.
This thread cause me to learn about the "dumb rabies" clinical presentation. Cool! I guess the "staggering" raccoon is the biggest clue in the case. Thanks for posting the answer, @hhaide1123!
This one is tricky because there's a lot of extra information in it. Rabies can be transmitted even through contact and the patient had contact with the raccoon when he buried it!
jnava5
1 Post
OMG this is my case study too!! I totally had Rabies as my first causative agent!!