We recently successful managed two patients with S. aureus sepsis and severe autoimmune hemolytic anemia without withholding immunosuppressive treatment. We are looking for any previously reported experience.
Hi Marco you can also see this
Bloodstream infections in hospitalized adults with sickle cell disease: a retrospective analysis. Am J Hematol. 2006 Oct;81(10):723-8
It's interesting that all hemolytic process in particular intravascular hemolysis can induce gram positive infections
But SA is not capsulated. Moreover hemolysis could influence SA infection
(The Influence of Hemolysis or Blood Loss on Susceptibility to Infection)
The hypothesis is offered that phagocytosis of heterologous or altered homologous erythrocytes by reticuloendothelial cells impairs the capacity of these cells to kill ingested bacteria.
And this
Prolonged neutrophil dysfunction after Plasmodium falciparum malaria is related to hemolysis and heme oxygenase-1 induction
Confirrmed hypothesis in humans!!! ;)
Hi Marco,
I hope these references be useful you:
1- [Park DC, Yang CH, Kim KY. Autoimmune hemolytic anemia in children. Yonsei Med J. 1987;28(4):313-21. PubMed PMID: 3439201.] Case #4 had S. aureus endocarditis and sepsis but there is limited data about this case in the article.
Unfortunately, at this time I do not have access to the fulltext of the next two:
2- [Silva VA, Seder RH, Weintraub LR. Synchronization of plasma exchange and cyclophosphamide in severe and refractory autoimmune hemolytic anemia. J Clin Apher. 1994;9(2):120-3. PubMed PMID: 7798158.]: I only know that one of the patients had pneumonia and sepsis caused by Proteus mirabilis and coagulase-negative(!) S. aureus which responded to doxycycline and cefuroxime.
3- [Singh L, Malhotra S, Kaur G, Basu S, Kaur R. Autoimmune hemolytic anemia due to auto anti-N in a patient with sepsis. Transfus Apher Sci. 2012 Dec;47(3):269-70. doi: 10.1016/j.transci.2012.07.022. Epub 2012 Sep 15. PubMed PMID: 22985536.]: I only know that patient had a positive blood culture for S. aureus and E. coli.
Hi Josè,
Pathogenic S. aureus strains are usually capsulated. Check this:
"Most S aureus strains of clinical importance have polysaccharide capsules, ..." Jawetz medical microbiology 2013, Chapter 13, Page 201.
Approximately 90% of Staphylococcus aureus isolates produce one of 11 serotypes of capsular polysaccharides. Serotypes CP5 and CP8 account for ∼25% and 50%, respectively, of isolates recovered from humans, offering support for their pathogenic significance.1 The importance and relevance of these capsule types is confirmed by the development of a conjugate vaccine, StaphVAX that includes type 5 and 8 capsule polysaccharides.2 CP5 and CP8 serotypes are considered as microcapsules because they are much smaller than those produced by the mucoid serotypes 1 and 2. The microcapsules of CP5 and CP8 are extracellular, uronic acid-containing polysaccharides that are too small to be visualized by negative stains such as India ink
Dear collegues,
I recently moved to another hospital in Tuscany, Italy. Few days ago I managed a case of cold agglutinin syndrome. The patient had a brief bout of fever during treatment with methylpredinosolone, and blood cultures yielded MSSA, again. She had no factors predisposing to endocarditis (including no central venous lines) and a transthoracic echocardiogram was unremarkable. I think that these three cases from two hospitals should be regarded as not casual. While I'm trying to understand if they are worth reporting, in my opinion we should consider the following statements: i) blood cultures should be promptly obtained during every fever bouts in patients with AHIA; ii) when choosing antibiotics we should cover for both MSSA and MRSA; iii) in the absence of endocarditis vancomicin should probably be the preferred agent, because beta-lactamic antibiotics are related to AHIA.
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