Natural infection of cortelezzii complex (Diptera: Psychodidae: Phlebotominae) with Leishmania braziliensis in Chaco, Argentina

In Argentina, American Cutaneous Leishmaniasis (ACL) extends up to 29°S in the phytogeographic regions of the Yungas (west), Chaco (center) and Paranaense (east). Since the Phlebotominae vectors of this disease in the western Chaco (dry Chaco) are unknown, in the present work, we studied the natural infection in Phlebotominae by PCR-ERFLP and Dot blot in order to incriminate these organisms as potential vectors. Captures with CDC-type traps were performed monthly in the domicile, the peridomicile and the forest in the Municipio Misión Nueva Pompeya, Chaco, Argentina, in two sites with human cases of ACL: Los Pozos (24°54'S, 61°22'W) and Fortín Arenales (24°58'S, 61°21'W), from November 2006 to December 2007. A total of 1702 Phlebotominae were captured: Mygonemyia migonei (83.8%), cortelezzii complex (11.1%), Mycropigomyia peresi (3.3%), Mycropygomy quinquefer (1.2%), Pintomyia torresi (0.2%) and Nyssomyia neivai (0.2%). Although no significant differences were found in species diversity, there were significant differences in abundance between both sites studied. A total of 80 phlebotomine females were analyzed: 50 of the cortelezzii complex and 30 My. migonei. No intestinal flagellates were observed by light microscopy. Two pools of 10 individuals of the cortelezzii complex of the peridomicile and forest of Fortín Arenales were reactive by PCR and Dot blot for Leishmania (Viannia) braziliensis. In Argentina, Evandromyia cortelezzii has been incriminated as a likely vector of ACL because of its abundance in areas of sporadic outbreaks. In the present work, Ev. cortelezzii females were found naturally infected, thus reinforcing the hypothesis that the members of the cortelezzii complex act as vectors of the disease.     

Reversible posterior leukoencephalopathy in a venomous snake (Bothrops asper) bite victim

An 18-year-old man developed posterior reversible leukoencephalopaty after being bitten by a venomous snake (Bothrops asper). It is possible that this previously unrecognized neurological complication of snake bite envenoming occurred as the result of endothelial dysfunction induced by the venom of the offending snake. This pathogenetic mechanism has also been implicated as the cause of cerebral infarctions in snake bite victims. Alternatively, the leukoencephalopathy might have been a complication of antivenom therapy.     

Role of novel DSP_p.Q986X genetic variation in arrhythmogenic right ventricular cardiomyopathy

Introduction

Arrhythmogenic right ventricular cardiomyopathy is an inherited disease characterized by a progressive myocardium fibrofatty replacement. This abnormality disrupts electrical transmission causing ventricular arrhythmias and sudden cardiac death. This genetic disease is transmitted mainly with an autosomal dominant pattern. Our aim was to identify the genetic defect responsible for the pathology in a Spanish family, and to perform its phenotype connotations.

Material and methods

A total of 15 individuals in a three-generation Spanish family were screened after the sudden cardiac death of one family member. All they underwent a complete physical examination, 12-lead electrocardiogram, 2-dimensional echocardiography, magnetic resonance imaging, exercise stress test, 24-h Holter and genetic testing.

Results

Autopsy revealed the presence of biventricular arrhythmogenic dysplasia in deceased member. Six family members showed clinical symptoms but only three of them fulfilled definite diagnostic criteria of the disease. Genetic analysis showed a novel nonsense genetic variation in nine family members. All family members with clinical symptoms carried the genetic variation.

Conclusions

Genetic testing in families affected by arrhythmogenic right ventricular cardiomyopathy helps to identify the genetic cause responsible for the disease. The incomplete penetrance and variable phenotypic expression highlights the need of comprehensive genetic analysis and further phenotype implications of genetics to clarify the pathophysiology of the disease.     

Displacement of Dental Implants in Trabecular Bone under a Static Lateral Load in Fresh Bovine Bone

Aim: The study aims to provide objective data for the displacement of titanium screw implants in trabecular bone specimens. One hundred Semados implants (Bego, Bremen, Germany) were inserted in bovine type IV bone specimens. All implants had a diameter of 3.75 mm; 50 implants had a length of 8.5 mm and 50 implants had a length of 15 mm. Insertion torque was determined at intervals of 10, 20, and 30 Ncm. Implants were loaded horizontally with 10, 20, and 30 N for 2 seconds. An indicator strip was attached to the implant abutment to allow direct observation of implant movement relative to the bone surface. Horizontal displacement was assessed with an accuracy of measurement of 10 µm. Seven implants got lost by visible loosening. Degree of displacement was subject to evaluation with all others. Those implants showed a mean displacement of 59 µm for 10 N (n = 100), 173 µm for 20 N (n = 99), and 211 µm for 30 N (n = 93). The mean displacement of 15‐mm implants (16, 37, 51 µm) was significantly lower compared with 8.5‐mm implants (103, 311, 396 µm) corresponding to 10, 20, and 30 N as lateral loads. Conclusions: Displacement of screw implants in trabecular bone can be detected and visualized using commercially available endoscopes with a high magnification. A lateral load of 20 N indicates a mean displacement of over 100 µm and therefore results in a critical displacement.