RESUMEN
Although Q fever is endemic in the northern coastal part of Croatia, it usually occurs sporadically. Analysis of 58 patients hospitalized for Q fever during the last 10-year period (1989-1998) revealed some differences in the clinical manifestation compared to a previous study (1954-1977). Most cases of Q fever (N = 55; 91%), presented with pneumonia, but no rash was noticed, compared to 46% of patients with Q fever developing exanthema in the previous study. The previously observed high seropositivity to Coxiella burnetii among domestic animals was confirmed in this study. A two-peak seasonal distribution of Q fever observed in 1991 was connected with the imported Russian sort of sheep with special biology of delivery. The clinical outcome was favorable for all patients, since no complications or chronic forms of the disease were recorded. Disproportion between the number of registered and hospitalized patients, including a number of asymptomatic and several undiagnosed or misdiagnosed infections, leads to a conclusion that the real number of persons infected with Coxiella burnetii in the area is several times higher.
Asunto(s)
Fiebre Q/epidemiología , Adolescente , Adulto , Anciano , Niño , Croacia/epidemiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Fiebre Q/diagnóstico , ZoonosisRESUMEN
The murine cytomegalovirus (MCMV) fcr-1 gene codes for a glycoprotein located at the surface of infected cells which strongly binds the Fc fragment of murine immunoglobulin G. To determine the biological significance of the fcr-1 gene during viral infection, we constructed MCMV fcr-1 deletion mutants and revertants. The fcr-1 gene was disrupted by insertion of the Escherichia coli lacZ gene. In another mutant, the marker gene was also deleted, by recombinase cre. As expected for its hypothetical role in immunoevasion, the infection of mice with fcr-1 deletion mutants resulted in significantly restricted replication in comparison with wild-type MCMV and revertant virus. In mutant mice lacking antibodies, however, the fcr-1 deletion mutants also replicated poorly. This demonstrated that the cell surface-expressed viral glycoprotein with FcR activity strongly modulates the virus-host interaction but that this biological function is not caused by the immunoglobulin binding property.