Tuesday, March 3, 2015

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.

Tuesday, February 10, 2015

February 10, 2015 Grand Rounds

Case # 1: 22/F, intravenous drug user (IDU), who p/w acute right-sided hemiparesis secondary to cerebral zygomycosis.

 From: http://www.neurology.org/content/76/1/e1/F1.expansion.html

1. Among IDU's, cerebral involvement represents the most common form of disease zygomycosis. 

2. Suspect cerebral zygomycosis in the setting of IDU, unilateral basal ganglia involvement, rapid progression of a unilateral lesion to involve the contralateral side, and unexplained large infarcts in the brain.

3. Carries a very high mortality rate of almost 70%. Brain biopsy is always almost essential to establish the diagnosis. Of those who died from it, only 1/3 had a diagnosis of zygomycosis before death.

Case # 2. Update and review of measles.

1. Spread by aerosol, droplet, or contact. It is contagious 4 days prior and up to 4 days after the rash.

2. Usual course: 8-12 days of incubation period, followed by 2-4 days of fever, conjunctivitis, coryza, and cough, followed by 2-3 days of rash that begins from the hair line and spreads downward. Koplik's spots are bluish to whitish papules seen in the buccal mucosa 1 day before appearance of the rash and lasts for 2-3 days.

3. As of 2/6/2015, there have been 121 measles cases from 17 states. Illinois (mostly from Chicago) has 3 cases already.

Tuesday, February 3, 2015

February 3, 2015 Grand Rounds

Case # 1. 60/M with h/o refractory neutropenia secondary to large granular cell lymphoma, h/o kidney transplantation, who p/w acute mental status change, new-onset left axillary skin lesion, and progressive lung nodules and cavity formation secondary to disseminated mucormycosis.

1. Remember the most commonly encountered causes of mucormycosis: Rhizopus, Mucor, and Rhizomucor; Cunninghamella, Absidia, Saksenaea, and Apophysomyces.

2. The three most common disease presentations associated with mucormycosis are: rhinocerebral, pulmonary, and cutaneous mucormycosis.

3. Cutaneous mucromycosis can arise from direct inoculation. Reverse dissemination (from skin to other organ systems) rarely occurs (3%).

4. Treatment of choice is amphotericin. Posaconazole is an alternative agent. Not backed up by randomized controlled trials but combination therapy (amphotericin plus echinocandin, amphotericin plus posaconazole) has also been used for refractory cases. Use of adjunct deferasirox for refractory cases has also been reported.

5. This patient's treatment course was complicated by development of torsades de pointes while receiving a quinolone and posaconazole. QT prolongation persisted despite discontinuation of drugs. In this situation, intermittent amphotericin (once weekly) can be tried. This is supported by a small study where once weekly amphotericin was comparable to other prophylaxis for invasive fungal infection (see here).


Case # 2. A 10 year old girl with cystic fibrosis, s/p bilateral lung transplant, h/o post-transplant lymphoproliferative disorder who p/w persistent abdominal pain and fever; PET scan revealed diffuse uptake in the pancreas; multiple infectious disease work-up were negative; pancreas biopsy showed necrotizing granulomas and yeasts on Giemsa stain; beta glucan was elevated; believed to be secondary to Candida pancreatitis

1. Remember that Cryptococcus and the agents responsible for mucormycosis will test negative for beta glucan. Maybe helpful to distinguish cryptococcal versus candidal infection especially if cultures are negative and yeasts are evident on tissue biopsy.

Tuesday, January 13, 2015

Grand Rounds: January 13, 2015

Case # 1. A 45 year old immunocompetent woman with h/o recent AVR 2/2 RHD, recent h/o subarachnoid hemorrhage, p/w acute onset headache and fever 2/2 Mycobacterium mageritense

1. Mycobacterium mageritense is a rapid growing mycobacterial species that was first isolated in Spain in 1987 and assigned its own species in 1997. It has been reported to cause CLABSI in immunocompromised patients, post-surgical wound infection, disaster-associated soft tissue infection, and granulomatous disease. It is universally resistant to clarithromycin but susceptible to a variety of agents.

2. Prosthetic valve endocarditis secondary to mycobacterial species is mostly caused by rapid growers (M. chelonae > M. fotuitum > M. abscessus). Surgery and appropriate antimicrobial therapy are necessary. It is unclear as to the duration of antibiotic therapy but based on case reports, the duration of therapy is the same as other bacterial causes of endocarditis.

3. Differential diagnoses for AFB in the blood: rapid growing mycobaterial species, Nocardia, Rhodococcus, Tsukamurella, and Gordonia.

4. For this case, the infection may have been a result of her recent AVR done at an OSH. Infection control should always be alerted in such cases. Patient was treated with imipenem, moxifloxacin, and doxycyline.


Case # 2. A 9 year old girl s/p 2nd lung transplant and recent diagnosis of PTLD, p/w R eye pain and swelling associated with an invasive nasal mass on imaging 2 months after receiving chemotherapy; sinus culture grew MDR Pseudomonas plus other bacterial flora; endoscopy did not show evidence of invasive fungal infection; biopsy showed PTLD

1. Discussion focused on positive and negative predictors of survival in patients with acute invasive fungal sinusitis. Age and intracranial extension are negative predictors while diabetes and surgery are positive predictors.

2. Majority of pediatric PTLD are EBV negative while majority of adult PTLD are EBV positive.


Case # 3. A 65 year old immunocompetent veteran who originally p/w acute low back pain secondary to MSSA bacteremia and thoracic epidural abscess for which he was receiving nafcillin, presented with recurrence of fever and new-onset hematochezia secondary to CMV colitis

1. CMV reactivation can occur in immunocompetent patients who are critically ill. Most of these patients are admitted in the ICU, were older, and had h/o shock or organ failure. In once case series, 71% of these patients died during hospital admission.