Fatal streptococcal toxic shock syndrome in a child with varicella and necrotizing fasciitis of the face.

The report described here presents a fatal streptococcal toxic shock syndrome secondary to a necrotizing fasciitis of the face in a 3-year-old girl with varicella. Pathogenesis and treatment of streptococcal toxic shock syndrome are discussed below.

Diagnosis of Q fever using indirect microimmunofluorescence.

A microimmunofluorescence technique for the diagnosis of Q fever is described. Although this method is useful for serological diagnosis of Q fever, some technical difficulties are associated with it. First, the test antigens must be produced by a cell culture method in a level-3 biohazard facility and, second, the antigen Coxiella burnetii, which is the causative agent of Q, is characterized by the presence of two phases.

Imported Brucellosis associated with Plasmodium falciparum malaria in a traveler returning from the tropics.

We report a microbiologically confirmed case of Brucella melitensis and Plasmodium falciparum malaria coinfection in a febrile traveler returning from Chad, Africa. The patient had been doing veterinary research in rural Chad; during that time she took no antimalarial chemoprophylaxis. Our report highlights the importance of blood cultures as well as malaria smears in febrile travelers returning from the tropics.

Interleukin-4 induces Coxiella burnetii replication in human monocytes but not in macrophages.

Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic disease is characterized by impaired cell-mediated immune response and microbicidal activity of monocytes. We hypothesized that interleukin(IL)-4, a Th2 cytokine, interferes with the fate of C.

Dysregulation of cytokines in acute Q fever: role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever.

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines.