Toxoplasma peritonitis in a patient with acquired immunodeficiency syndrome.

Toxoplasma gondii was identified in a stained slide preparation of, and isolated from, peritoneal fluid specimens obtained from a patient with the acquired immunodeficiency syndrome (AIDS). At the time of admission to the hospital, the patient's serologic tests were positive for Toxoplasma. Toxoplasma was isolated from samples of the patient's blood by mouse inoculation. Findings of newly developed methods for diagnosis of the presence of T gondii in body fluids by assay for Toxoplasma-specific antigen and by use of a DNA probe were positive.

Chronic obstructive pneumonia caused by a vertebral body osteophyte.

Osteophytes associated with spondylosis have been implicated as a cause of multiple extraspinal manifestations. Symptoms are more likely to occur with the large osteophytes associated with diffuse idiopathic skeletal hyperostosis. In the thoracic region, osteophytes have been reported infrequently as a cause of extraspinal complications. We report a case in which an anterior thoracic vertebral osteophyte was responsible for chronic obstructive pneumonia due to obstruction of the right main stem bronchus. The patient's condition improved considerably after surgical resection of the compressing thoracic osteophyte.

Right-to-left shunt across a patent foramen ovale caused by cardiac tamponade: diagnosis by transesophageal echocardiography.

Cardiac tamponade can manifest as profound hypoxemia from intracardiac shunting across a patent foramen ovale. As a consequence, pulmonary embolus can be erroneously diagnosed. As demonstrated in the case described herein, transesophageal echocardiography can be useful in determining the correct diagnosis, especially if transthoracic echocardiography is technically limited. In our patient, the findings on transesophageal echocardiography also helped determine the appropriate treatment. The relative inaccessibility of the pericardial effusion to needle drainage prompted open surgical drainage.

Effect of sodium nitroprusside on hypoxic pulmonary vasoconstriction in the dog.

The objective of the study was to determine the direct actions of sodium nitroprusside (SNP) on the pulmonary vasculature actively constricted by hypoxic ventilation in the closed-chest dog. In 21 supine anesthetized (pentobarbital sodium, 25 mg/kg) dogs the left lower lobe was catheterized with a 20 F wedged-flow catheter. With constant flow to this lung lobe, lobar pulmonary artery pressure (PAP), left ventricular end-diastolic pressure (LVEDP), and lobar pulmonary vascular resistance (PVR) were studied during room air and 10% O2 mechanical ventilation. With lobar flow and LVEDP constant, observed changes of lobar PAP and PVR represent direct effects on vascular tone unaffected by passive factors. Ventilation with 10% O2 resulted in a significant increase in lobar PAP [12.2 +/- 1.6 to 17.2 +/- 1.2 (SE) Torr] and PVR [42.2 +/- 13.3 to 61.2 +/- 15.0 (SE) Torr X 1(-1) X min]. Then during continued hypoxia in 12 animals, femoral vein infusion of SNP at doses of 1, 2, and 5 microgram X kg-1 X min-1 resulted in significant decreases in lobar PAP to 14.8 +/- 1.5, 14.8 +/- 1.5, and 13.4 +/- 1.6 Torr, respectively, and in PVR to 56.7 +/- 14.1, 54.0 +/- 13.9, and 47.8 %/- 13.2 Torr X 1(-1) X min, respectively. In six animals the sequence of drug infusion was then reversed with similar results. It is concluded that the actively constricted pulmonary vascular bed is directly dilated by SNP infusion.

Nonoxidative microbicidal activity in normal human alveolar and peritoneal macrophages.

Although Toxoplasma gondii multiplies within normal murine alveolar and peritoneal macrophages, it is killed by normal rat alveolar and peritoneal macrophages. The killing by rat macrophages is by a nonoxidative mechanism. Studies on normal human alveolar macrophages have reported disparate results in regard to their ability to inhibit or kill T. gondii. We considered it of interest to explore further the effect of normal human alveolar and peritoneal macrophages on T. gondii. Unstimulated alveolar macrophages from each of seven individuals demonstrated a marked ability to kill or inhibit multiplication of T. gondii in vitro (e.g., the number of parasites per 100 alveolar macrophages was 31 at time zero and 2 at 18 h, whereas this value increased from 37 at time zero to 183 at 18 h in murine macrophages assayed in parallel). In quantitative assays of superoxide, alveolar macrophages released a substantial amount of superoxide when exposed to phorbol myristate acetate or to candidae. In contrast, alveolar macrophages incubated with T. gondii released no more superoxide than when in medium alone. Scavengers of superoxide anions, hydrogen peroxide, singlet oxygen, and hydroxyl radicals failed to inhibit killing of T. gondii by alveolar macrophages. Peritoneal macrophages from each of six normal women undergoing laparoscopy killed T. gondii in vitro; results of quantitative superoxide assays and scavenger experiments demonstrated that no oxidative burst was triggered in these macrophages by exposure to T. gondii. These data indicate that normal human alveolar and peritoneal macrophages can kill an intracellular parasite by nonoxidative mechanisms and suggest that these mechanisms are important in inhibition or killing of other opportunistic intracellular pathogens.