RESUMEN
Tectona grandis L.f. es una especie forestal de madera dura que, a pesar de no ser nativa de América, su plasticidad de adaptación ha permitido que en Ecuador se establezcan plantaciones intensivas con fines de exportación. Una compleja enfermedad con características de marchitez vascular está matando miles de árboles de diferentes edades en el país. Se planteó conocer el agente fitopatógeno causante de la patogénesis y muerte de los árboles. Se aislaron los hongos Fusarium sp. y Ceratocystis fimbriata Ellis & Halst. desde árboles enfermos. A nivel de invernadero se plantearon los postulados de Koch, para el efecto 30 plantas de T. grandis de cuatro meses de edad por cada tratamiento, se inocularon con los microrganismos como se describe a continuación: T1= C. fimbriata, T2 = Fusarium sp., T3 = C. fimbriata + Fusarium sp., T4 = agar-agar (control). Se empleó un diseño completo al azar (DCA) y las plantas se evaluaron a los 45 días después de inoculadas. Los tratamientos C. fimbriata, y C. fimbriata + Fusarium sp., mostraron mayores volúmenes aparentes de necrosis, con 1.52 cm3 y 1.93 cm3, y plantas muertas por la infección durante el tiempo de evaluación, mientras que Fusarium sp. mostró baja o nula patogenicidad y comportamiento similar al control, con 0.27 cm3 y 0.16 cm3 respectivamente. Estos resultados sugieren que el agente causal de la enfermedad de marchitez vascular en T. grandis es C. fimbriata y sería el primer reporte del fitopatógeno atacando teca en Ecuador. (AU)
Tectona grandisL.f. it is a hardwood forest species, which despite not being native to America, its adaptive plasticity has allowed intensive plantations to be established for export purposes in Ecuador. A complex disease with characteristics of vascular wilt is killing thousands of trees of different ages in the country. It was proposed to know the phytopathogenic agent causing the pathogenesis and death of the trees. Fusarium sp. andCeratocystis fimbriata Ellis & Halst. were isolated from diseased trees. At the greenhouselevel, Koch's postulates were proposed, for the effect 30 four month old T. grandisplants for each treatment were inoculated with the microorganisms as described below: T1 = C. fimbriata, T2 = Fusariumsp ., T3 = C. fimbriata+ Fusariumsp., T4 = agar-agar (control). A complete randomized design (DCA) was used and the plants were evaluated 45 days after inoculation. The treatments C. fimbriata, and C. fimbriata+ Fusariumsp. showed higher apparent volumes of necrosis, with 1.52 cm3and 1.93 cm3, and plants killed by the infection during the evaluation time, while Fusariumsp. showed low or no pathogenicity and behavior similar to the control, with 0.27 cm3and 0.16 cm3respectively. These results suggest that the causative agent of vascular wilt disease in T. grandisis C. fimbriataand it would be the first report of phytopathogen attacking teak in Ecuador. (AU)
Asunto(s)
Árboles/microbiología , Ceratocystis/patogenicidad , Bosques , Ecuador , Fusarium/patogenicidadRESUMEN
Aims: The outbreak of papaya dieback disease in Malaysia has been reported since 2003. Several reports previously confirmed Erwinia papayae and E. mallotivora to be the causal pathogen of the disease. The present study aimed to identify the causal pathogen of papaya dieback disease in Sabah. Methodology and results: Infected tissues of papaya dieback disease were collected from Kota Belud, Sabah and the bacterium responsible for the infection was isolated on Luria Bertani (LB) agar and nutrient agar (NA). Seven isolates with similar characteristics to Erwinia were isolated, subjected to the Koch’s Postulates test and then identified using 16S rRNA sequencing technique. The bacterium was identified to be E. psidii, a common pathogen to guava but not to papaya. Conclusion, significance and Impact of study: This report serves as the first confirmation of the E. psidii in causing papaya dieback disease, suggesting the possibility of this bacterium undergoing host shifting to papaya plants and the possibility of becoming another major threat to the papaya industry in the future.
RESUMEN
The proportion of the reported cases of Zika virus (ZIKV) infection reached the status of a pandemic. Numerous studies are being conducted on the isolation of ZIKV strains from various epidemics, diagnosis of the infections, various animal models and cell culture designs to study the pathogenesis of ZIKV in the attempts to find an effective ZIKV vaccine. This review focuses upon the 'Off-Spectrum' body of studies which analyses the epidemiology, pathogenesis and other attributes of ZIKV in the light of various dissident hypotheses.
RESUMEN
The proportion of the reported cases of Zika virus (ZIKV) infection reached the status of a pandemic. Numerous studies are being conducted on the isolation of ZIKV strains from various epidemics, diagnosis of the infections, various animal models and cell culture designs to study the pathogenesis of ZIKV in the attempts to find an effective ZIKV vaccine. This review focuses upon the ‘Off-Spectrum’ body of studies which analyses the epidemiology, pathogenesis and other attributes of ZIKV in the light of various dissident hypotheses.
RESUMEN
Despite important human and financial resources and considerable accumulation of scientific publications, patents, and clinical trials, cancer research has been slow in achieving a therapeutic revolution similar to the one that occurred in the last century for infectious diseases. It has been proposed that science proceeds not only by accumulating data but also through paradigm shifts. Here, we propose to use the concept of ‘paradigm shift’ as a method of investigation when dominant paradigms fail to achieve their promises. The first step in using the ‘paradigm shift’ method in cancer research requires identifying its founding paradigms. In this review, two of these founding paradigms will be discussed: (i) the reification of cancer as a tumour mass and (ii) the translation of the concepts issued from infectious disease in cancer research. We show how these founding paradigms can generate biases that lead to over-diagnosis and over-treatment and also hamper the development of curative cancer therapies. We apply the ‘paradigm shift’ method to produce perspective reversals consistent with current experimental evidence. The ‘paradigm shift’ method enlightens the existence of a tumour physiologic–prophylactic–pathologic continuum. It integrates the target/antitarget concept and that cancer is also an extracellular disease. The ‘paradigm shift’ method has immediate implications for cancer prevention and therapy. It could be a general method of investigation for other diseases awaiting therapy.