Importance of Q fever in community acquired pneumonia.

Coxiella burnetii appears to be endemic in animals in the Mauricie region of Quebec, and causes some human cases of Q fever annually. Unlike in other rural areas, patients in this study experienced few respiratory symptoms. To determine whether C burnetii pneumonia is underdiagnosed, adults admitted to hospital for community acquired pneumonia were included in a one-year serological study. Significant immunofluorescent antibody (IFA) titres in four of 118 patients with pneumonia (fewer than 4%) were studied. Clinical presentation, standard laboratory tests and epidemiological data did not allow identification of these cases; however, Q fever increased during the warm months. There were no detectable complement fixing (CF) antibodies in these four cases. C burnetii causes few cases of pneumonia in Mauricie. IFA seems to be a more sensitive test than CF.

Q fever in Quebec (1989-93): Report of 14 cases.

Q fever, a zoonosis acquired by inhalation of the rickettsia Coxiella burnetii, is rarely diagnosed in Canada. The world incidence has been increasing since 1960, because of progressive dissemination of this microorganism in animal populations, particularly domestic ruminants. Some recent outbreaks were caused by cats. Of 14 cases reported in Quebec between 1989 and the beginning of 1993, nine occurred successively in an 18-month period in the rural region surrounding Trois-Rivières, after contact with livestock or cats. These cases are reported here, with the results of serological screening of the workers of an abattoir where one of the cases worked. Five additional cases reported in Quebec during the same period are briefly reviewed.

Atrial natriuretic peptide stimulates submandibular gland synthesis and secretion of cGMP.

Binding of atrial natriuretic peptide (ANP) to rat submandibular gland and its effect on guanosine 3',5'-cyclic monophosphate (cGMP) formation and salivary secretion were investigated. Membranes rapidly and specifically bound 125I-ANP. Binding was inhibited by unlabeled ANP (IC50 approximately 1.6 nM), but not by atriopeptin I, other COOH- and NH2-terminal deleted ANP fragments, or agents such as pilocarpine or substance P. Scatchard analysis revealed a single class of high-affinity sites (dissociation constant 0.74 +/- 0.25 nM; maximal binding capacity 20.5 +/- 6.3 pmol/mg protein). Intravenous infusion of ANP with pilocarpine caused a significant dose-dependent increase in the levels of cGMP detected in plasma and saliva. Because salivary cGMP may have originated in plasma, the effect of ANP on cGMP formation was evaluated in dispersed cells. ANP evoked a concentration-dependent increase in both cGMP synthesis and secretion (EC50 approximately 1.7 x 10(-8) M). The atrial peptide did affect basal or l-isoproterenol-stimulated adenosine 3',5'-cyclic monophosphate synthesis in dispersed cells. When infused by itself and/or with pilocarpine, ANP did not alter the rate of spontaneous or pilocarpine-induced salivary flow, secretion of chloride, or protein release. The data demonstrate the presence of guanylate cyclase-coupled ANP receptors in submandibular gland; the atrial peptide, however, does not exert an effect of the secretory function of the gland.

Bovine adrenal medullary cells contain functional atrial natriuretic peptide receptors.

The recent report that bovine adrenal chromaffin cells synthesized and secreted atrial natriuretic peptide, ANP, suggested that the peptide may have binding sites in the gland itself. Studies in bovine adrenal medulla membranes did reveal a single class of high affinity [125I]-ANP binding sites with a KD of 94 pM and a density of 1.7 pmol/mg protein. Binding was very rapid (association half-time: 2.5 min), and specific in that only unlabelled ANP displaced bound [125I]-ANP. Application of ANP to bovine chromaffin cells in culture, resulted in a concentration-dependent increase in cGMP synthesis. The data suggest the presence of biologically functional ANP receptors in adrenal chromaffin cells.