March 3, 2015 Grand Rounds

Case # 1. An 80 year old immunocompetent man, hospitalized for small bowel obstruction, who developed sudden onset hoarseness and shortness of breath; endoscopy demonstrated bilateral vocal cord paralysis, subglottic edema, and tracheal ulcer; tracheal aspirate was positive for HSV-1; case of Gerhardt's syndrome secondary to HSV-1 reactivation.

Taken from: https://www.google.com/search?biw=1920&bih=918&tbm=isch&q=bilateral+vocal+cord+paralysis&revid=405396170&sa=X&ei=H_L1VMHEOsOjyASYioKYCA&ved=0CCgQ1QIoAg#imgdii=_&imgrc=wkVSoy9XlEsq-M%253A%3B6g6M_JBd1l0h8M%3Bhttps%253A%252F%252Flifecaremedi.files.wordpress.com%252F2012%252F03%252Fparalysis_bi_inspiration.jpg%3Bhttps%253A%252F%252Flifecaremedi.wordpress.com%252F2012%252F03%252F17%252Fbl-vocal-cord-palsy%252F%3B581%3B436

1. Gerhardt's syndrome is the term given to bilateral vocal cord paralysis. Note that only 1% of vocal paralysis is attributed to infection. The most common causes are surgical complication, malignancy, and endotracheal intubation.

2. During the pre-antibiotic era, syphilis was reported as a common cause of Gerhardt's syndrome. Other infectious causes include: VZV (in the setting of Ramsay-Hunt syndrome), CMV, HSV, polio, tuberculosis, and Lyme disease.

3. There are only 5 reported cases of Gerhardt's syndrome secondary to HSV. All cases showed full recovery of vocal cord function after a course of acyclovir.

Case # 2. A 7 year old girl who presented with bilateral lower extremity weakness and numbness secondary to acute flaccid myelitis; her CSF NMO (neuromyelitis optica) antibody was also positive; case was presented to review acute flaccid myelitis/paralysis

Taken from: medscape.com

1. Infectious causes of acute flaccid paralysis: Guillain-Barre syndrome, poliomyelitis, transverse myelitis, enterovirus 71, and West Nile virus.

2. From August 2, 2014 to February 26, 2015, the CDC has confirmed reports of 112 children in 34 states who developed acute flaccid myelitis (AFM). The case definition for AFM is as follows: a) patient ≤21 years of age; b) acute onset of focal limb weakness; c) on or after August 1, 2014, and d) an MRI showing a spinal cord lesion largely restricted to the gray matter.

3. No specific cause has yet been identified but the CDC is investigating a link between Enterovirus D68, which caused an outbreak of severe respiratory illness in 2014. There is no established treatment. Some case reports have used glucocorticoid, intravenous immunoglobulin, plasmapheresis, interferon, or immunomodulating drugs.

4. For more of enterovirus D68, refer to Case # 3, September 9, 2014.

Case #3. A 49 year old woman who experienced fever, chills, and headache 10 days after returning from Nigeria secondary to Plasmodium ovale infection. 

Taken from: https://www.google.com/search?q=plasmodium+ovale&source=lnms&tbm=isch&sa=X&ei=o_P1VOvXA82WyASCrIK4CQ&ved=0CAcQ_AUoAQ&biw=1920&bih=918#imgdii=_&imgrc=ZjxrfKjasDIUqM%253A%3BPMLjshM8hSJIbM%3Bhttp%253A%252F%252Fwww.med-chem.com%252Fimages%252Fpara%252Forgan%252Fimage002_0007.jpg%3Bhttp%253A%252F%252Fwww.med-chem.com%252Fpara-site.php%253Furl%253Dorg%252Fplasoval%3B193%3B192

1. Plasmodium ovale is distinguished by the following on blood smear: involvement of reticulocytes, basophilic stippling, round gametocyte, and fimbriation of infected red blood cell.

2. Like Plasmodium vivax, Plasmodium ovale is characterized by delayed schizogony. Because of this, primaquine for 14 days should always be used during treatment (primaquine clears hypnozoites).

3. The drug of choice for Plasmodium ovale and Plasmodium vivax infection is chloroquine. If the infection is acquired in Papua New Guinea or Indonesia, where rates of chloroquine resistance for these infections are high, use atovaquone-proguanil (Malarone), mefloquine, or quinine sulfate plus doxycycline/tetracyline. Whichever drug is chosen, administer 14 days of primaquine.