Two unusual occurrences of pleural trichomonosis due to a new Tetratrichomonas species previously reported but not named were confirmed. In one patient, Trichomonas tenax and a Tetratrichomonas species were also detected in the oral cavity by molecular methods. We suggest that this new Tetratrichomonas species be named Tetratrichomonas empyemagena. CASE REPORTSC ase 1 is that of a 54-year-old male from Mexico City with uncontrolled type 2 diabetes who was admitted to the hospital with a history of 1 week of malaise, poor food intake, chills, and fever after developing right thoracic pain, dyspnea, and fatigue; he denied any history of choking or trauma in recent days. Dullness on percussion and decreased breathing sounds were noted over his right chest. His blood pressure was 120/50 mmHg, his heart rate was 120 beats/min, his respiratory rate was 30 breaths/min, his white blood cell count was 45,000/mm 3 , his platelet count was 565,000/mm 3 , his glucose level was 503 mg/dl, his albumin level was 1.6 g/dl, and his arterial HCO 3 level was 5.6 meq/liter. An initial chest X-ray and computed tomography (CT) scan showed a right pleural effusion that was drained (700 ml), and the pleural fluid was sent for microbiological analysis. Its macroscopic appearance was that of a brownish purulent fluid. Microscopic examination revealed Gram-positive cocci and Gram-negative bacilli, as well as numerous motile and flagellated protozoa that were initially identified as trichomonads because of their morphological characteristics (form, size, and motility). These flagellates were not cultured, and their identification was confirmed by microscopic examination of an empyema fluid smear. Samples were mixed with whole blood at 1:3, spread onto glass slides, air dried, methanol fixed, and stained with Giemsa stain (Fig. 1A and B). Some aliquots of empyema fluid were stored at Ϫ20°C for molecular analysis. Bacteriological cultures of the fluid were performed for aerobic and anaerobic microorganisms, yielding Staphylococcus auricularis, but no bacilli were identified until after PCR sequencing of an empyema fluid sample. A Prevotella species was demonstrated by using universal primers for the 16S rRNA gene (1). Antibiotic therapy with metronidazole and piperacillin-tazobactam was administered.Case 2 is that of a 33-year-old man from Mexico City with a history of smoking and alcohol consumption who was admitted to the hospital with a 2-week nonproductive cough and chills, dyspnea, and left pleural chest pain. His blood pressure was 70/40 mmHg, his heart rate was 150 beats/min, and his respiratory rate was 40 breaths/min. During subsequent days, fever and diaphoresis were added to the clinical course, as well as worsening of dyspnea until he developed acute respiratory failure and septic shock. Thorax auscultation revealed bilateral crackles and diminished breath sounds on the left side; he was placed on mechanical ventilation. A chest X-ray and a thorax CT scan showed a right pneumothorax and left pleural effusion. He underwent bilater...

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Human Adenovirus 36 (HAdV-36) has been related to diverse effects on metabolism and may attenuate the lipid accumulation in kidneys with increased adiposity. Some of these effects would be related to viral persistence. However, until now, a model of persistent in vitro infection by HAdV-36 is unknown. In this study, we examined the cells of the Vero lineage to explore their permissiveness to long-term HAdV-36 infection. HAdV-36 was productively replicated in Vero cells and maintained long-term infection for up to 35 cell passages. A subculture was obtained from the cells that survived the primary infection at a low MOI (0.5). The production of the extracellular infectious virus with titers ranging from 10 4 to 10 6 TCID 50 /mL and DNA-bearing cells was detected. In long-term infected cells, the intracellular distribution of viral antigen was demonstrated by performing immunolocalization (IFI) and expression of cell-viral antigen in 50% of cells by flow cytometry, using anti-HAdV-36 hyperimmune rabbit serum. Furthermore, E1a and E4orf1 genes in long-term infected passages showed a decreasing trend. Our preliminary results reveal that renal epithelial monkey cells are permissive for the productive infection of HAdV-36. Vero cell culture long-term infection might be a promising model for addressing the fundamental aspects of the HAdV-36 biology that cannot reveal broadly-used cultures, which do not maintain longterm infection in primary or transformed cells.

There have been few reports on extra-enteric infections by <i>Blastocystis</i> STs and none have been molecularly identified in samples from human reproductive organs. We report for the first time the identification of 3 different subtypes of <i>Blastocystis</i> (ST1-3) in vaginal and sperm samples, from patients infected with <i>Trichomonas vaginalis</i>. <i>Blastocystis</i> STs were identified by PCR-sequencing and by phylogenetic inferences using 28 vaginal swab samples and 7 sperm samples from patients trichomoniasis. <i>Blastocystis</i> STs were identified in 6 of 28 vaginal swabs (21.4%) and in 3 of 7 sperm samples (42.8%). In both biological samples, STs 1-3 were found; one vaginal sample showed subtype co-infection with ST1 and ST3. High genetic variation was observed in the sequences obtained and no specific clustering in the phylogenetic trees was detected. Most of the haplotypes identified were placed far from the main dispersal centers. Our finding suggested that incorrect cleaning of the genital area or a contamination by combination of anal and vaginal intercourse.

It has been proposed that infection by adipogenic viruses constitutes a “low risk” factor for obesity. Here, we report the presence of adenovirus 36 (Ad36) and its viral load copy number in fat tissue of participants with obesity and normal weight; phylogenetic analysis was performed to describe their relationship and genetic variability among viral haplotypes. Adipose tissue obtained from 105 adult patients with obesity (cases) and 26 normal‐weight adult participants as controls were analyzed by quantitative polymerase chain reaction (qPCR) amplifying the partial Ad36 E1a gene. The amplicons were examined by melting curves and submitted to sequencing. Then, genetic diversity and phylogenetic inferences were performed. Ad36 was identified at rates of 82% and 46% in the case and control groups, respectively (p = 1.1 × 10−4, odds ratio = 5.28); viral load copies were also significantly different between both groups, being 25% higher in the case group. Melting curve analysis showed clear amplification among positive samples. Phylogenetic inferences and genetic diversity analyses showed that the Ad36 E1a gene exhibits low genetic variability and differentiation with strong gene flow due to an expanding process. Our results suggest that the phenomenon of infectobesity by Ad36 might not be a low‐risk factor, as has been previously argued by other authors.