Seven cases of surgical native valve endocarditis caused by coagulase-negative staphylococci: An underappreciated disease.

BACKGROUND: Native valve endocarditis caused by coagulase-negative staphylococci is uncommon and the diagnosis is infrequently considered. The disease, however, appears to be increasing in frequency and can pursue an aggressive clinical course. We report the clinical features of 7 cases of coagulase-negative staphylococcal native valve endocarditis (CNS-NVE) seen at 1 institution with a large cardiovascular referral base over a 10-month period. All cases required valve replacement surgery. METHODS: Clinical history, echocardiograms, and microbiologic and histopathologic data were reviewed for 7 patients with surgical CNS-NVE. RESULTS: Four patients had intravenous central catheters, and 1 had recent surgery, whereas the remaining 2 had no identifiable risk factors. Presentations ranged from subacute (4 cases) to acute with complications (3 cases). Complications included congestive heart failure, stroke, and heart block. Echocardiography demonstrated valvular lesions in all 7 cases. Valve pathologic study demonstrated gram-positive cocci in all 7 cases; blood cultures grew coagulase-negative staphylococci in 6 cases and valve cultures grew Staphylococcus epidermidis in 5 cases. CONCLUSIONS: Coagulase-negative staphylococci, including S epidermidis, can cause severe native valve endocarditis requiring valve replacement. The increasing use of intravascular access devices in the community may herald an increase in the incidence of CNS-NVE. A high index of diagnostic suspicion in the appropriate clinical setting is critical for optimal management.

Concurrent Pneumocystis carinii and cytomegalovirus pneumonia after autologous peripheral blood stem cell transplantation.

A 46-year-old woman developed concurrent CMV and Pneumocystis carinii pneumonia (PCP) 140 days after autologous peripheral blood stem cell transplantation (APBSCT) for AML. She was seropositive for CMV before undergoing APBSCT and had required prednisone for immune thrombocytopenia and allergic dermatitis for 9 weeks prior to the onset of pneumonia. She had also been receiving PCP prophylaxis with pentamidine aerosol every month for 3 months before developing symptoms. The pneumonia was complicated by severe hypoxia, requiring ventilator support and pneumothorax requiring chest tube thoracostomy. She recovered following treatment with trimethoprim-sulfamethoxazole (TMP-SMX), prednisone, gancyclovir and intravenous immunoglobulin. Although the overall incidence of severe CMV disease is low after APBSCT, preventive measures such as surveillance culture and secondary prophylaxis with gancyclovir may be warranted in patients whose cellular immune response is further compromised by corticosteroid use or other factors.

Leukaemia inhibitory factor induces mitogenesis in Swiss 3T3 cells and selective enhancement via a variety of signalling events.

Leukaemia inhibitory factor (LIF) stimulates cellular DNA synthesis in confluent quiescent Swiss 3T3 cells. Insulin and prostaglandin E1 (PGE1), which fail to stimulate DNA synthesis alone, potentiate this effect. Prostaglandin F2alpha (PGF2alpha), which is mitogenic in these cells, enhances the effect of LIF on DNA synthesis. TGFbeta1 increases the effect of PGF2alpha but not that of LIF. R-59022, a diacylglycerol kinase inhibitor which increases protein kinase C (PKC) activity, enhances only the PGF2alpha response. 13-Tetradecanoyl-12-phorbolacetate-mediated PKC depletion prevents the action of PGF2alpha but not that of LIF, nor the PGF2alpha potentiation of LIF-stimulated DNA synthesis. 1-Oleoyl-2acetylglycerol, a PKC and tyrosine kinase (TK) activator which mimics some of the PGF2alpha effects, enhances only LIF-induced DNA synthesis in cells possessing intact PKC activity. These results suggest that stimulation of DNA synthesis by LIF, as well as its enhancement by PGF2alpha, may occur via a signalling pathway independent of PKC activation.

Unilateral optic neuritis caused by Histoplasma capsulatum in a patient with the acquired immunodeficiency syndrome.

PURPOSE: To evaluate the potential of Histoplasma capsulatum to cause optic neuritis in the setting of the acquired immunodeficiency syndrome (AIDS). METHODS: We examined a 35-year-old man with a history of AIDS and disseminated histoplasmosis who developed a unilateral progressive optic neuritis of enigmatic origin. An optic nerve sheath biopsy was performed to provide a tissue diagnosis. RESULTS: Histoplasma capsulatum was identified in both the optic nerve sheath and fungal culture. CONCLUSION: Histoplasma capsulatum should be considered in the differential diagnosis of optic neuritis in patients with AIDS, even in the absence of chorioretinal findings.

Cholecystectomy in patients with AIDS: clinicopathologic correlations in 107 cases.

The etiologic and clinical features of cholecystisis in infection due to human immunodeficiency virus (HIV) were studies retrospectively. The charts and histopathologic specimens of 136 HIV-infected patients who underwent cholecystectomy between February 1987 and May 1993 at a large tertiary care center were reviewed. Opportunistic pathogens infecting the 107 patients with AIDS included microsporidia (eight cases-- Enterocytozoon bieneusi in six and Septata intestinalis in two); cytomegalovirus alone (six cases); Cryptosporidium alone (eight cases); cytomegalovirus plus Cryptosporidum (15 cases); and Pneumocystis carinii and Isospora belli (one case each). In addition, histopathologic changes characteristic of Kaposi's sarcoma were seen in one case. Thirty-eight patients with AIDS had acalculous cholecystitis for which no etiologic agent was found. Twenty-eight AIDS patients had cholelithiasis, six with coexistent opportunistic gallbladder infection. In the 107 AIDS patients, no specific symptom was found to be predictive of opportunistic infection of the gallbladder, but such infection was significantly associated with an abnormal abdominal ultrasound (P = .017) and with nonvisualization of the gallbladder by radionucleotide biliary scan (P < .001).

Toxoplasmic myelitis mimicking intramedullary spinal cord tumor.

Toxoplasma gondii causes cerebral infection in individuals with impaired immunologic defense mechanisms. We report a case of toxoplasmic myelitis. Spinal cord toxoplasmosis has not been previously documented except in congenital infection.