Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
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PMID:Cerebellar nocardiosis and myopathy from long-term corticosteroids for idiopathic thrombocytopenia. 2004 27

A 30-year-old woman with a past medical history of autoimmune hemolytic anemia presented with fever. Blood cultures grew Campylobacter. Her medical history was significant for four prior episodes of Campylobacter gastroenteritis and bacteremia. She received ciprofloxacin for the index presentation, then Meropenem de-escalated to doxycycline 6 months later following recurrence of Campylobacter. This prompted investigation for an immunodeficiency disorder. She was found to have hypogammaglobulinemia. Her Campylobacter infections resolved following the administration of intravenous immunoglobulins every 3 weeks. She did not have recurrence of Campylobacter during 5 years of follow-up. A literature search revealed additional four case reports of six hypogammaglobulinemic adult individuals presenting with recurrent Campylobacter infections. Three patients were already on intravenous immunoglobulin (IVIG) when Campylobacter infection occurred, and two patients achieved clinical cure following therapy with imipenem and IVIG. This case report highlights the importance of suspecting hypogammaglobulinemia in patients with recurrent Campylobacter infections, as this is sometimes the first manifestation of the condition.
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PMID:Recurrent Campylobacter Bacteremia as the First Manifestation of Hypogammaglobulinemia: a Case Report and Literature Review. 3178 75