Case 28

Published on 18/02/2015 by admin

Filed under Allergy and Immunology

Last modified 18/02/2015

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CASE 28

Fred, a 40-year-old man, is well known to the local shelters, including the one you supervise, because he has lived on the streets for several years. He is a known alcoholic and has had tuberculosis in the past, for which he was successfully treated under careful supervision. You have noticed that he has been moving more slowly over the past few days and inquire whether he is feeling like himself. He admits to some general fatigue, particularly in the legs, which just “don’t seem to want to carry him around anymore like they used to.” The following morning, the fellow who sleeps in the cot next to Fred indicates to you that Fred cannot seem to get out of bed. You confirm this problem, and you call the emergency medical service (EMS) to transport him to the hospital. To your surprise, when you get to the hospital to visit him, the receptionist tells you that he is seriously ill, is in the intensive care unit, and has been intubated because he was no longer able to breathe for himself.

You arrive at the intensive care unit to find Fred in the condition reported. The attending physician describes Fred’s condition as one of ascending paralysis, typical of Guillain-Barré syndrome. He asks if Fred has recently suffered from a diarrheal illness (which he did, you recall, about 4 weeks ago), as well as about Fred’s alcohol history and other medical disorders. A stool culture was ordered to test for enteric bacteria.

The physician ordered a blood test for creatinine kinase (an enzyme released from destroyed muscle), a stool sample, and assays to detect antibodies that target the gangliosides GM₁ and GQ_1b. These are distributed throughout peripheral nervous system myelin.

QUESTIONS FOR GROUP DISCUSSION

1. This patient is an alcoholic. Despite this, alcoholic myopathy is low on your list of considerations. Explain. How would you rule out myopathy as a cause of Fred’s problem?

2. What factors, other than alcoholic myopathy, have been shown to cause altered neurotransmission with resulting paralysis?

3. Why would botulism toxin not be a consideration as the cause of Fred’s clinical presentation?

4. Fred’s condition is one of ascending paralysis, typical of Guillain-Barré syndrome. In this syndrome the myelin sheath of nerves is destroyed such that the nerve conduction is altered. Explain how this would lead to loss of muscle mass with time.

5. Antecedent infection with Campylobacter jejuni or cytomegalovirus may lead to Guillain-Barré syndrome and production of autoantibodies to gangliosides present in myelin, GM₁ and GM₂, respectively. Explain how an infection can lead to the production of autoantibodies.

6. What is the most common source of C. jejuni infection? What are the symptoms?

7. Describe possible mechanisms for destruction of myelin sheath after production of anti-GM₁ or anti-GM₂ autoantibodies.

8. Explain why Fred’s cerebrospinal fluid (CSF) analysis would show an elevated level of protein.

9. Explain why muscle paralysis is life threatening.

10. Describe the two recommended therapies for Guillain-Barré syndrome.

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