Splenic infarction complicated with immune reconstitution inflammatory syndrome due to disseminated Mycobacterium genavense infection in a patient infected with human immunodeficiency virus.

Mycobacterium genavense (M. genavense) is one of the most fastidious, difficult to culture Mycobacterium species. Patients infected with human immunodeficiency virus (HIV) may develop immune reconstitution inflammatory syndrome (IRIS) due to disseminated M. genavense infection as well as disseminated M. avium and intracellulare complex infection. Consensus regarding treatment of IRIS due to disseminated mycobacterium infection has not yet been obtained, although systemic steroid therapy has been recommended in recent guidelines. Here we report the case of a 48-year-old Japanese man diagnosed with HIV and disseminated M. genavense infection. His initial CD4-positive T cell count was 3/µL, and his HIV1-RNA viral load was 13,000 copies/mL. He developed IRIS due to disseminated M. genavense infection after two weeks of receiving antiretroviral agents. The patient's serum alkaline phosphatase level, as a barometer of disseminated M. genavense infection in this case, was difficult to control with several anti-mycobacterial agents, although his fever was improved by non-steroidal anti-inflammatory drugs. About five weeks after the onset of IRIS, the patient developed acute left upper quadrant pain and was diagnosed with splenic infarction by contrast-enhanced computed tomography. After the splenic infarction, the patient's serum alkaline phosphatase level decreased without systemic steroid therapy or anticoagulant agents, and his left upper quadrant pain improved naturally within a few days. This case suggests that IRIS due to disseminated M. genavense infection can complicate splenic infarction in patients with HIV, and splenic infarction could improve the IRIS due to disseminated M. genavense infection.

[Acute illness following chicken pox: spleen infarction as a complication of varicella zoster infection]. / Acuut ziek na waterpokken: miltinfarcten als complicatie van varicella-zosterinfectie.

BACKGROUND: Varicella zoster virus (VZV) infection can cause temporary acquired protein S or C deficiency via cross reacting antibodies and consequently inducing a hypercoagulable state. CASE DESCRIPTION: A 6-year-old girl with a history of congenital cardiac disease was seen at an Emergency Department with acute chest pain, dyspnoea and fever, seven days after developing chicken pox. Diagnostic tests revealed massive infarction of the spleen, and a protein S and C deficiency. In addition, blood cultures revealed a Lancefield group A ß-haemolytic streptococcus (GABHS). The patient recovered fully after treatment with low molecular weight heparin and antibiotics. CONCLUSION: In this patient, septic emboli caused splenic infarction. Thromboembolic complications should be suspected in children with VZV who present with acute symptoms, in particular if bacterial superinfection is found.

Mycoplasma pneumoniae, splenic infarct, and transient antiphospholipid antibodies: a new association?

We report 2 children with Mycoplasma pneumoniae pulmonary infection with splenic infarcts and transient antiphospholipid antibodies. This association has not been reported previously.

Splenic infarction due to transient antiphospholipid antibodies induced by acute Epstein-Barr virus infection.

Splenic infarction is a rare feature of infectious mononucleosis (IM) due to Epstein-Barr virus (EBV), limited to three case reports. We report the first case of splenic infarction during acute EBV infection associated with the transient induction of antiphospholipid antibodies. We discuss the role of antiphospholipid antibodies in thrombosis in acute viral infections and postulate other mechanisms of thrombosis. Once other more common causes of splenic infarction, such as endocarditis and lymphoma, have been excluded, the possibility of viral-induced antiphospholipid antibodies should be considered.

Splenic infarction associated with anti-cardiolipin antibody: a report of two cases.

There are few cases of splenic infarction associated with antiphospholipid antibody reported in the literature. We present two cases of splenic infarction associated with anticardiolipin antibody, one complicated by the development of a splenic pseudocyst. Clinical diagnostic features of splenic infarction are described. In addition, a review of the literature on thrombotic manifestations of antiphospholipid syndrome is presented.

[Functional asplenia after severe varicella zoster-infection diagnosis by colour Doppler ultrasound]. / Autosplenektomie nach Varizellensepsis bei einem Patienten mit M. Crohn unter immunsuppressiver Therapie.

Infiltrative, inflammatory or thromboembolic processes in the parenchyma of the spleen can cause a functional loss of the organ. This phenomenon is called functional asplenia and occurs as a complication especially in sickle cell disease, lupus erythematosus and after bone marrow transplantation. We present the case of a patient with Crohn's disease under immunosuppressive therapy who developed a spontaneous covered spleen rupture in the course of a septic shock with DIG due to a Varizella zoster infection. Later on, sonography showed a diminution of the spleen size. No flow signals could be derived by colour doppler measurements from the spleen. Because of the colour doppler findings we suspected a functional asplenia which was then verified by spleen scintigraphy and Howell-Jolly-Bodies in the blood count. Remarkably, the Crohn's disease remains in complete remission since the development of the functional asplenia (for 4 years now). The underlying pathomechanism remains unclear.

Acquired and transient RBC CD55 deficiency (Inab phenotype) and anti-IFC.

BACKGROUND: Antigens of the Cromer blood group system reside on the glycoprotein CD55 (decay-accelerating factor). The Inab phenotype is the null phenotype of this system. So far, only five propositi have been described who exhibit this phenotype, and single-nucleotide substitutions in the CD55 gene have been found in three of them. This report describes the first example of a patient with an acquired and transient form of the Inab phenotype. CASE REPORT: A 54-year-old black patient was admitted to the hospital because of abdominal pain. Multiple splenic infarctions were visualized in the abdominal computerized tomography scan, and a prophylactic splenectomy was performed. The patient's serum reacted by an IAT with all donor RBCs tested. RESULTS: Serologic analysis showed that the patient had the rare Inab phenotype and that his serum contained anti-IFC. Flow cytometry demonstrated the absence of CD55 on his RBCs, whereas lymphocytes, monocytes, granulocytes, and platelets expressed CD55, albeit at a weaker level than cells of common phenotypes. cDNA revealed no differences from the published sequences. Flow cytometry performed 12 months after splenectomy showed reappearance of the CD55 antigen; serologic tests performed after 17 months revealed that the anti-IFC had almost disappeared and that the RBCs were again agglutinated by various Cromer antibodies. CONCLUSION: A patient with an acquired and transient form of the Inab phenotype is described, in whom the CD55 deficiency is limited to the RBCs and is associated with splenic infarctions.

Isolated splenic infarction owing to group B Salmonella: case report.

The clinical spectrum of extra-intestinal salmonellosis, comprising enteric fever and invasive infections owing to non-typhoidal Salmonellae, is well known. We report an otherwise healthy patient with isolated splenic infarction caused by group B Salmonella. She was seropositive for the O antigen of Salmonella group B and stool cultures were positive for group B Salmonellae. After appropriate antimicrobial therapy, her complaints disappeared and microbiological tests for Salmonellae became negative.

Splenic and renal infarction in systemic lupus erythematosus: association with anti-cardiolipin antibodies.

A 37-year-old female, known to have systemic lupus erythematosus (SLE) and markedly raised anti-cardiolipin antibody levels in association with the lupus anticoagulant, presented with a symptomatic segmental splenic infarction. There was a past history of cerebral infarction. Abdominal computed tomography (CT) demonstrated the area of splenic infarction, and an asymptomatic right renal infarct. This patient illustrates the unusual occurrence of multiple visceral infarcts, in association with anti-cardiolipin antibodies, complicating SLE.