Dose titration study of enrofloxacin (Baytril) against respiratory colibacillosis in Muscovy ducks.

Four-week-old specific-pathogen-free Muscovy ducks were inoculated with reovirus. One week later, they were inoculated intratracheally with a O78:K80 strain of Escherichia coli. The next day, they were given enrofloxacin at different doses in the drinking water. Comparison of mortality rates, weight gain, macroscopic lesions, and E. coli re-isolations among treated and untreated birds showed that a 5-day treatment course with 12.5 or 25 ppm enrofloxacin in water for 4 hours in the morning provided good therapeutic efficacy against respiratory colibacillosis.

[Cerebrovascular complications of sickle-cell anemia]. / Complications cérébro-vasculaires de la drépanocytose.

Cerebrovascular disorders are frequent in sickle-cell anemia. They occur mainly in homozygous children. Traditionally, they were believed to result from an arteriolar sickle-cell thrombosis, the "sludge" phenomenon, which is generally responsible for sickle cell anemia disorders. It is now well known that several other kinds of cerebral damages are involved such as moya-moya syndrome, cerebral hemorrhage, subdural hematoma, extra-dural hematoma and cerebral thrombophlebitis. In this disease, the identification of these different processes cannot be always made by a simple clinical examination. However, specific therapies are sometimes necessary, such as neurosurgical intervention in the case of aneurysm or hematoma, and, according to some authors, the necessity of repeated appropriate transfusions, in the case of moya-moya. So it is imperative to carry out without delay a complete neuroradiological assessment of the lesions. At present, the most widely accepted theory to explain the arteriolar lesions, is that they result from a sickle-cell thrombosis of the vasa-vasorum, but, we think it is not the only valid hypothesis and we think that other phenomena may be involved with a genetic factor (patients with connective tissue disorders may have a particular genotype), and with infectious or autoimmune or coagulation disorders, the latter being frequently observed in this disease.

Endemic tropical spastic paraparesis associated with human T-lymphotropic virus type I: a clinical and seroepidemiological study of 25 cases.

Tropical spastic paraparesis (TSP) is a common myeloneuropathy with primary and predominant involvement of the pyramidal tract and minimal sensory loss. The epidemic form of TSP is related to toxic nutritional factors, but the endemic form occurs in clusters in tropical areas, especially in India, Africa, the Seychelles, Colombia, and areas of the Caribbean. We describe the clinical and epidemiological features of 25 TSP patients from Martinique (French West Indies) with serum antibodies to human T-lymphotropic virus type I (HTLV-I). Furthermore, all 11 patients who were seropositive for HTLV-I had specific HTLV-I antibodies in their CSF. All were women. The age of onset varied from 25 to 60 years (mean, 45 years). The main clinical features are spastic paraparesis or paraplegia with spasticity of the upper limbs, minimal sensory loss, and bladder dysfunction. Minimal estimated incidence and prevalence are 1 per 100,000 inhabitants per year and 8 per 100,000, respectively. Seventeen percent of the relatives of patients with HTLV-I-associated TSP have HTLV-I antibodies (1 husband and 7 children). In Martinique, the prevalence of HTLV-I antibodies in the general population is about 2% and reaches 10% for neurological disorders other than TSP. Since our initial report, the association between spastic paraparesis and HTLV-I has been confirmed in Jamaica, Colombia, and Japan, suggesting the neurotropism of this lymphotropic human retrovirus.

Polyclonal IgE increase after HgCl2 injections in BN and LEW rats: a genetic analysis.

An autoimmune disease and a dramatic increase in total serum IgE concentration are observed in BN rats that are chronically injected with HgCl2. In contrast, LEW rats do not develop the characteristic glomerulonephritis and are very "low IgE responders". In this study, we examined the genetic control of total serum IgE increase after HgCl2 injection in F1 and F2 hybrids, in both backcrosses between LEW and BN rats, and in LEW.1N congenic rats. Genetic analysis was performed using peak IgE concentrations expressed as log microgram/ml. A high IgE phenotype was found to be dominant. Eighty-five percent of F2 variance was due to genetic factors (VG) while only 15% of this variance was caused by environmental factors (VE). From observations in F2 hybrids and backcrosses, estimations of additive variance (VA) and dominance variance (VD) were made following three different methods. Genetic control by about four loci is demonstrated. One of these genes is RT1-linked. This gene contributes to 25% of the phenotypic difference observed between BN and LEW rats. No correlation was found between the peak total IgE level and autoimmune disease based on IgG deposition in spleen and/or kidney.