Rabies diagnosis and serology in bats from the State of São Paulo, Brazil

INTRODUCTION: Bats are one of the most important reservoirs and vectors of the rabies virus in the world. METHODS: From 1988 to 2003, the Zoonosis Control Center in São Paulo City performed rabies diagnosis on 5,670 bats by direct immunofluorescent test and mouse inoculation test. Blood samples were collected from 1,618 bats and the sera were analyzed using the rapid fluorescent focus inhibition test to confirm rabies antibodies. RESULTS: Forty-four (0.8%) bats were positive for rabies. The prevalence of rabies antibodies was 5.9% using 0.5IU/ml as a cutoff. Insectivorous bats (69.8%) and bats of the species Molossus molossus (51.8%) constituted the majority of the sample; however, the highest prevalence of antibodies were observed in Glossophaga soricina (14/133), Histiotus velatus (16/60), Desmodus rotundus (8/66), Artibeus lituratus (5/54), Nyctinomops macrotis (3/23), Tadarida brasiliensis (3/48), Carollia perspicillata (3/9), Eumops auripendulus (2/30), Nyctinomops laticaudatus (2/16), Sturnira lilium (2/17) and Eumops perotis (1/13). The prevalence of rabies antibodies was analyzed by species, food preference and sex. CONCLUSIONS: The expressive levels of antibodies associated with the low virus positivity verified in these bats indicate that rabies virus circulates actively among them

Renal Effects and Underlying Molecular Mechanisms of Long-Term Salt Content Diets in Spontaneously Hypertensive Rats.

Several evidences have shown that salt excess is an important determinant of cardiovascular and renal derangement in hypertension. The present study aimed to investigate the renal effects of chronic high or low salt intake in the context of hypertension and to elucidate the molecular mechanisms underlying such effects. To this end, newly weaned male SHR were fed with diets only differing in NaCl content: normal salt (NS: 0.3%), low salt (LS: 0.03%), and high salt diet (HS: 3%) until 7 months of age. Analysis of renal function, morphology, and evaluation of the expression of the main molecular components involved in the renal handling of albumin, including podocyte slit-diaphragm proteins and proximal tubule endocytic receptors were performed. The relationship between diets and the balance of the renal angiotensin-converting enzyme (ACE) and ACE2 enzymes was also examined. HS produced glomerular hypertrophy and decreased ACE2 and nephrin expressions, loss of morphological integrity of the podocyte processes, and increased proteinuria, characterized by loss of albumin and high molecular weight proteins. Conversely, severe hypertension was attenuated and renal dysfunction was prevented by LS since proteinuria was much lower than in the NS SHRs. This was associated with a decrease in kidney ACE/ACE2 protein and activity ratio and increased cubilin renal expression. Taken together, these results suggest that LS attenuates hypertension progression in SHRs and preserves renal function. The mechanisms partially explaining these findings include modulation of the intrarenal ACE/ACE2 balance and the increased cubilin expression. Importantly, HS worsens hypertensive kidney injury and decreases the expression nephrin, a key component of the slit diaphragm

Histological analysis.

<p>(A) Photomicrographs of kidney sections stained with Periodic Acid Schiff (PAS) to determine glomerulosclerosis score (percentage of the PAS-positive in glomerular tuft area) and morphometric changes in the groups. (B) Photomicrographs of kidney sections stained with Picrosirius Red to determine interstitial collagen deposition. Data are represented as mean ± SEM. NS: normal salt diet. LS: low salt diet. HS: high salt diet. Scale bar: 20 μm.</p

Renal enzymatic activity of ACE, ACE2 and the ACE/ACE2 ratio.

<p>(A) ACE enzymatic activity. (B) ACE2 enzymatic activity. (C) ACE/ACE2 ratio. Data are means ± SEM. NS: normal salt diet. LS: low salt diet. HS: high salt diet. *P<0.05 vs. NS; + P < 0.05 vs. HS. (NS n = 12, LS n = 10, HS n = 9).</p

Evaluation of the urinary protein loss.

<p>24-h urine samples from SHRs were subjected to 12% SDS-PAGE and silver stained. NS: normal salt diet. LS: low salt diet. HS: high salt diet.</p

Glomeruli ultrastructural examination.

<p>Transmission electron microscopy images show the ultrastructural pedicels (fp) and slit diaphragms (SD, arrows) from the podocytes. Images A and B show the normal podocyte structure from Normal and Low salt group respectively, with SD integrity. Image C shows that the high salt group has lost the morphological integrity of its podocyte processes (fusion/effacement*) along with the slit diaphragms (black arrow head). BM, basement membrane; EC, endothelial cell.</p

Analysis of megalin and cubilin renal protein expression.

<p>(A) Megalin. (B) Cubilin. Data are means ± SEM. (NS) normal salt diet. LS: low salt diet. HS: high salt diet. *P<0.05 vs. NS; + P < 0.05 vs. HS. (n = 6 / group).</p

Analysis of nephrin and podocin renal protein expression.

<p>(A) Nephrin. (B) Podocin. Data are means ± SEM. NS: normal salt diet. LS: low salt diet. HS: high salt diet. *P<0.05 vs. NS; # P < 0.05 vs LS. (N = 6 / group).</p

Analysis of ACE, ACE2 expression and ACE/ACE2 protein ratio.

<p>(A) ACE kidney expression. (B) ACE2 kidney expression. C: ACE/ACE2 protein ratio. Data are means ± SEM. NS: normal salt diet. LS: low salt diet. HS: high salt diet. *P<0.05 vs. NS; + P < 0.05 vs. HS; # P < 0.05 vs LS.</p