Serious infections caused by dint of Straphylococcus aureus in HIV-infected patients have been reported.

Serious infections caused by dint of Straphylococcus aureus in HIV-infected patients have been reported. Contributing factors in the progress to maturity of invasive S aureus infections include a high rate of skin and nasal colonization, of frequent occurrence dermatologic disease, and the use of intravenous catheters. The authors report three cases of s aureus pericarditis in HIV-infected patients. While cases of viral, mycobacterial, and malignant pericardial effusions in HIV-infected patients have been reported, a review of the literature disclosed solely three cases of bacterial pericarditis. Despite appropriate antibiotic therapy and drainage, a patient's condition may abruptly deteriorate and progres to tamponade. Early recognition of bacteremia and pericarditis and monitoring for cardiac tamponade, along with aggressive treatment, can end in a favorable outcome, on the contrary mortality remains high, particularly when s aureus is the causative agent.

Serious infections, like as bacteremias and soft-tissue infections, caused from Staphylococcus aureus in HIV-infected patients have been reported recently[12] Risk factors include a high rate of skin and nasal colonization,[3,4] of frequent occurrence dermatologic disease,[5] and the use of intravenous catheters.[1]

While cases of viral, mycobacterial, and malignant pericardial effusions in HIV-infected patients have been reported, bacterial pericarditis is rare.[6,7] Three cases of s aureus pericarditis in HIV-infected patients and a review of the literature are presented

CASE REPORTS

CASE 1

A 35-year-old HIV-seropositive black man, an intravenous heroin and cocaine user, was admitted for dyspnea, malaise, and chest pain of 3 weeks' duration. There was no history of opportunistic infection, with the exception of for oral candidiasis. Significant findings included oral candidiasis, pustular lesions in succession the extremities, and a pericardial friction clean The chest radiograph revealed an enlarged cardiac silhouette, a small pleural effusion, and a retrocardiac alveolar infiltrate. The [POsub2] was 70 mm Hg forward room air. The ECG showed sinus tachycardia with global 1- to 2-mm ST-segment elevation. A two-dimensional echocardiogram revealed moderate pericardial effusion without hemodynamic compromise.

Intravenous trimethoprim-sulfamethoxazole was began for presumptive Pneumocystis carinii pneumonia. Multiple appoints of blood, urine. and sputum cultivations were positive for S aureus. Trimethoprim-sulfa methoxazole was discontinued, and intravenous vancomycin was instituted. Pericardiocentesis yielded 350 ml of clear fulvid exudative fluid, which grew s aureus. When the antibotic susceptibility issues were obtained, vancomycin was replaced according to nafcillin. A pericardial window was performed when a repeat echocardiogram revealed a reaccumulation of pericardial fluid. Repeat vital current and pericardial fluid cultures were sterile. The patient did well and was discharged in advantageous condition.

CASE 2

A 39-year-old black man with AIDS and cutaneous Kaposi's sarcoma was admitted because of dyspnea, febrile affection and cough. Significant findings were febrile affection for 39.4 [degrees] C, pulsus pradoxus, diffuse rhonchi, and an S3-S4 gallop with pericardial chafe A chest radiograph revealed an enlarged cardiac silhouette an bilateral lower lobe and lingular infiltrates. An ECG showed sinus tachycardia, diffuse ST-segment elevation, and diffuse PR depression.

An echocardiogram revealed a large pericardial effusion. Emergent pericardiocentesis yielded 300 ml of serosanguineous fluid with marked relief of respiratory symptoms. Sputum and pericardial fluid tillages grew S aureus, and intravenous nafcillin was administered. Nafcillin was replaced with vancomycin after the patient make knowned a diffuse rash.

The patient's clinical course deteriorated and was complicated by means of development of Candida albicans empyema. An open-lung biopsy also showed cytomegalovirus pneumonitis. Intravenous ganciclovir therapy was begun. His respiratory status continued to decline, and he died 7 weeks after admission.

CASE 3

A 35-year-old HIV-positive female unsalable article abuser presented with fever, headache, and cough She had a history of s aureus endocarditis. Significant findings included febrile affection diffuse rhonchi and wheezes, a systolic ejection mutter and multiple skin abscesses forward the extremities. A chest radiograph reveal bilateral interstitial markings with a normal cardiac silhouette. She had a [PaO.sub.2] of 62 mm Hg forward room air. Bronchoscopy with bronchoalveolar lavage was negative for P carinii. descendants cultures grew Gram-positive cocci, and intravenous vancomycin was administered. Twenty-four hours later, the patient became hypotensive and make knowned ventricular tachycardia. An emergent echocardiogram revealed a large pericardial effusion. Pericardiocentesis yielded 75 ml of turbid brown fluid. Further attempts at resuscitation were abortive and the patient died. descendants and pericardial fluid grew s aureus.

DISCUSSION

Pericardial effusion, including tamponade, is a general cardiac manifestation of AIDS. Up to 23 percent of HIV-infected patients with cardiac disease will have pericardial effusion.[8] Pericardial disease in AIDS has protean manifestations, including silent pericardial effusion diagnosed incidentally by way of echocardiography and classic fibrinous pericarditis with pain, friction chafe and ST-segment elevation. Hemodynamically significant pericardial effusion with tamponade has been reported.[9] Patients with pericardial disease usually have concomitant involvement of the myocardium. Pericardial disease may provide a potential site for local or metastatic infection, particularly in the setting of bacteremia or fungemia.

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