Guanidination and nitroguanidination of staphylococcal enterotoxin B.

Guanidination of the free amino groups of staphylococcal enterotoxin B with 3,5-dimethyl-1-guanylpyrazole converted 31-32 of 33 epsilon-amino groups and 30% of the N-terminal residue. This product, although markedly reduced in solubility, suffered no gross change in conformation and retained full biological activity. A derivative prepared by reaction with O-methylisourea with only one lysyl residue unaltered lost most of its emetic activity. Nitroguanidination with 3,5-dimethyl-1-nitroguanylpyrazole converted up to 28 of the epsilon-amino groups and essentially all of the N-terminus. This material was greatly reduced in ability to produce emesis and like the O-methylisourea prepared guanidinated enterotoxin, gave only a line of partial identity in double diffusion. The loss of activity is attributed to unfolding and it is concluded that the free amino groups of enterotoxin B do not critically participate in either its antigenic determinants or its active center for emesis.

Acute gonococcal sepsis in an HIV-infected woman.

This is a case report of a 35-year-old woman infected with the human immunodeficiency virus who presented with acute bacterial sepsis that proved to be secondary to Neisseria gonorrhoeae. Typical skin and joint findings developed only after the acute sepsis had resolved. Patients with disseminated gonococcal infection rarely have signs of acute bacterial sepsis. This case raises the question of whether HIV-infected patients are at an increased risk of contracting severe gonococcal disease.

Mycobacterium xenopi infection masquerading as pulmonary tuberculosis in two patients infected with the human immunodeficiency virus.

Mycobacterium xenopi infections have rarely been reported among patients infected with the human immunodeficiency virus (HIV). We recently treated two HIV-infected men, neither of whom had a history of pulmonary disease or AIDS-defining conditions, and who had M. xenopi lung infections. Both patients presented with night sweats, cough, and pleuritic chest pain. Chest radiographs showed an upper-lobe nodule in the first patient and a perihilar cavitary infiltrate in the second patient. Both patients were initially believed to have pulmonary tuberculosis and were treated accordingly; however, only M. xenopi grew on cultures of multiple respiratory specimens. This diagnosis was confirmed by cultures of biopsied lung tissue from the first patient and of fluid from a peritracheal abscess in the second patient. Both patients' clinical conditions improved after multidrug therapy (isoniazid, rifampin, pyrazinamide, ethambutol, and ciprofloxacin in the first case; isoniazid, rifampin, and pyrazinamide in the second case). The second patient's condition improved despite in vitro resistance of his isolate to isoniazid and rifampin.

Mycobacterium xenopi: innocent bystander or emerging pathogen?

Mycobacterium xenopi is a recognized cause of smoldering pulmonary disease in patients with chronic lung disease. This organism is frequently isolated from respiratory specimens from individuals infected with human immunodeficiency virus (HIV) and is often considered nonpathogenic. Cases of pulmonary and disseminated M. xenopi disease have been described in patients with HIV infection and other immunodeficiencies. Many physicians are unaware of the clinical significance of M. xenopi isolation. Whether this organism represents a commensal or a pathogen capable of causing considerable morbidity and mortality is not fully understood. In this study, we investigated the clinical significance of M. xenopi isolation and explored the clinical spectrum of M. xenopi disease. Clinical illness occurred both in elderly people with chronic lung disease and in young individuals with HIV infection. The repeated isolation of M. xenopi in association with pulmonary lesions suggests significant infection and mandates further workup and therapy.