Anemia infecciosa equina en una yegua pony (Equss caballus). Estudio clinico patologico

La anemia infecciosa equina (AIE), es una enfermedad infecto contagiosa que afecta a équidos: caballos y ponis (Equss caballus), mulas y burros (E. asinus), ocasionada por el Lentivirus de la familia Retroviridae, subfamilia Orthoretrovirinae. La infección produce cuadros febriles recurrentes, anemia autoinmune, ictericia y edema; el curso clínico de la enfermedad puede ser agudo o crónico, y alta letalidad de los animales afectados. En el presente trabajo se expone el caso clínico patológico de una yegua pony (Equss caballus), enviada para diagnóstico; en la historia clínica se refirió: un cuadro de diarrea aguda persistente, palidez de mucosas, cuadro febril recurrente ypostración. Se obtuvieron muestras de sangre para estudio hematológico y la prueba de inmunodifusión en gel de agar; el animal fue sometido a un protocolo de eutanasia mediante un método físico de insensibilización, se realizó el estudio anatomopatología e histopatología. El estudio hematológico mostró una disminución del paquete celular sanguíneo, anemia no regenerativa, neutropenia y linfocitosis.El único cambio significativo del urianalisis fue la presencia de hemoglobina (+) y bilirrubinuria (++).Al realizar el estudio posmortem los hallazgos principales fueron: linfadenopatía de ganglios submandibulares y retroescapulares. Coloración amarillo oro de la grasa del tejido subcutáneo relacionada con la ictericia, presencia de hemorragias petequiales en tejido subcutáneo. En cavidad torácica se observó, enfisema pulmonar moderado, zonas de demarcación costal en pulmón y hemorragias multifocales en la pleura parietal. En cavidad abdominal se identificaron múltiples petequias en la serosa de las vísceras abdominales, hidroperitoneo moderado (presencia de líquido de color amarillento). Vesícula biliar pletórica con aumento de volumen del hígado de coloración amarillenta y rosada, con una consistencia friable y grasosa.Enriñón: seobservaron hemorragias subcapsulares corticales y palidez del parénquima renal; esplenomegalia; hemorragias en la serosa intestinal y contenido sanguinolento en intestino delgado. El diagnóstico emitido, fue: un cuadro agudo de anemia infecciosa equina, con base a la prueba de inmunodifusión en gel de agar, por lo cual deben considerarse las medidas necesarias de este tipo de afección y reforzar la prevención y/o control de la enfermedad

Manipulation of epithelial cell death pathways by Shigella

Shigella,a major cause of bacterial dysentery, knows when it is not wanted. To generate and maintain its niche within host cells, this unwelcome guest injects several dozen virulence factors via a type 3 secretion system (T3SS). In this issue, Ashidaet al(2020) have elucidated the role of two such factors fromShigella flexneri-OspC1 and OspD3-that together counteract apoptotic and necroptotic death pathways in colonised epithelial cells. As a result,Shigellacan replicate to high levels within the colonic epithelium, leading to the substantial epithelial damage in shigellosis and efficient bacterial release for faecal transmission

Tea tree oil extract causes mitochondrial superoxide production and apoptosis as an anticancer agent, promoting tumor infiltrating neutrophils cytotoxic for breast cancer to induce tumor regression

The antitumor activity of the tea tree oil (TTO) derived product, Melaleuca Alternifolia Concentrate (MAC) was characterized mechanistically at the molecular and cellular level. MAC was analyzed for its anticancer activity against human prostate (LNCaP) and breast (MCF-7) cancer cell lines growing in vitro. MAC (0.02–0.06% v/v) dose-dependently induced the intrinsic (mitochondrial) apoptotic pathway in both the LNCaP and MCF-7 cell lines, involving increased mitochondrial superoxide production, loss of mitochondrial membrane potential (MMP), caspase 3/7 activation, as well as the presence of TUNEL+ and cleaved-PARP+ cell populations. At concentrations of 0.01–0.04% v/v, MAC caused cell cycle arrest in the G0/1–phase, as well as autophagy. The in vivo anticancer actions of MAC were examined as a treatment in the FVB/N c-Neu murine model for spontaneously arising breast cancers. Intratumoral MAC injections (1–4% v/v) significantly suppressed tumor progression in a dose-dependent manner and was associated with greater levels of tumor infiltrating neutrophils exhibiting anticancer cytotoxic activity. Induction of breast cancer cell death by MAC via the mitochondrial apoptotic pathway was also replicated occurring in tumors treated in vivo. In conclusion, our data highlights the potential for the Melaleuca-derived MAC product inducing anticancer neutrophil influx, supporting its application as a novel therapeutic agent

The NUP98-HOXD13 fusion oncogene induces thymocyte self-renewal via Lmo2/Lyl1

T cell acute lymphoblastic leukaemia (T-ALL) cases include subfamilies that overexpress the TAL1/LMO, TLX1/3 and HOXA transcription factor oncogenes. While it has been shown that TAL1/LMO transcription factors induce self-renewal of thymocytes, whether this is true for other transcription factor oncogenes is unknown. To address this, we have studied NUP98-HOXD13-transgenic (NHD13-Tg) mice, which overexpress HOXA transcription factors throughout haematopoiesis and develop both myelodysplastic syndrome (MDS) progressing to acute myeloid leukaemia (AML) as well as T-ALL. We find that thymocytes from preleukaemic NHD13-Tg mice can serially transplant, demonstrating that they have self-renewal capacity. Transcriptome analysis shows that NHD13-Tg thymocytes exhibit a stem cell-like transcriptional programme closely resembling that induced by Lmo2, including Lmo2 itself and its critical cofactor Lyl1. To determine whether Lmo2/Lyl1 are required for NHD13-induced thymocyte self-renewal, NHD13-Tg mice were crossed with Lyl1 knockout mice. This showed that Lyl1 is essential for expression of the stem cell-like gene expression programme in thymocytes and self-renewal. Surprisingly however, NHD13 transgenic mice lacking Lyl1 showed accelerated T-ALL and absence of transformation to AML, associated with a loss of multipotent progenitors in the bone marrow. Thus multiple T cell oncogenes induce thymocyte self-renewal via Lmo2/Lyl1; however, NHD13 can also promote T-ALL via an alternative pathway