Case #1. A 70 year old man with relapsed AML undergoing chemotherapy admitted with fever, fatigue, sore throat, and cough; CT scan showed tracheal enhancement and mediastinitis; bronchoscopy showed pseudomembranous lesions; a case of invasive trancheobronchial aspergillosis
Taken from: http://www.aspergillus.org.uk/secure/image_library/tracheobronch/fig7.jpg
1. Remember the different manifestations of aspergillosis in immunocompromised patients: pulmonary (from acute nodular lung disease to the more indolent necrotizing/cavitary form), tracheobronchitis, disseminated form, and rhinosinusitis. Less common manifestations that are well described in the literature include central nervous system involvement (brain abscess), endophthalmitis, endocarditis, gastrointestinal, or cutaneous lesions.
2. Invasive tracheobronchial aspergillosis (ITBA) is seen in <10% of patients with invasive aspergillosis. It is usually diagnosed late because it can have normal imaging early in its course. A predisposed patient who comes in with fever, significant cough, and shortness of breath without pneumonia on chest CT scan should alert you to this diagnosis. Bronchoscopy is the best way to look for it.
3. ITBA has 3 forms: ulcerative (seen in AIDS and heart-lung transplant patients), pseudomembranous (seen in patients with hematologic malignancies), and obstructive (mucus plugs are usually seen but no bronchial inflammation is evident). Mixed forms can also be observed in <10% of patients with ITBA.
4. ITBA is usually associated with a negative blood galactomannan.
Case # 2. A 15 year old girl presented with acute onset back pain and fever secondary to Group A Streptococcus epidural abscess
http://images.ddccdn.com/images/pills/mtm/Clindamycin%20300%20mg-RAN.jpg
1. Always keep epidural abscess in your differential diagnosis for fever and back pain especially if patients have neurologic deficits. Be aware of the different stages of epidural abscess symptomatology: stage I (back pain, fever, tenderness), stage II (spinal root signs such as radicular pain), stage III (sensory and motor deficits, bladder/bowel dysfunction), and stage IV (paralysis).
2. This patient was treated with both ceftriaxone and clindamycin initially. The basis of combining clindamycin with penicillin in the treatment of Streptococcus pyogenes infection (especially in cases of high burden infection) early in its course is not only to prevent toxin release (in cases of necrotizing fasciitis) but also to counteract the theoretical Eagle effect. The latter is the paradoxical reduction of the bactericidal activity of high dose penicillin in infections with heavy Streptococcus pyogenes burden. The proposed mechanism is the reduced expression of penicillin-binding proteins by bacteria induced to a stationary phase of growth by the heavy bacterial burden. Clindamycin kills these bacteria in the stationary phase as its ability to inhibit bacterial protein synthesis is not dependent on bacterial growth stage or bacterial load.
Case # 3. Update on enterovirus D68
1. Enterovirus D68 was first isolated in 1962 in California. Since then, sporadic outbreaks have been seen. From 2008-2010, outbreaks have been documented in the Netherlands, Japan, China, and the Philippines. It has rarely been reported in the US until last month (read here).
2. Enterovirus D68 manifests almost exclusively as a respiratory illness of varying severity (from mild illness to frank respiratory failure requiring ventilatory support or extacorporeal membrane oxygenation). Rare cases have been associated with neurologic manifestations (e.g. flaccid paralysis and meningoencephalitis).
3. The clinician should be alerted of this entity when a multiplex PCR give out a result "enterovirus/rhinovirus". The virology lab can be called for genotypic identification as this is the only way to diagnose enterovirus D68.
4. There are no specific treatments available for enterovirus D68 infection.
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