Región endémica y regímenes de infección con el virus del síndrome de la mancha blanca (wssv) en las granjas camaronícolas del noroeste de México

El cultivo de camarón, con un valor aproximado de 711 millones de dólares anuales, es una de las actividades primarias más importantes en México. Sin embargo, ha tenido que enfrentar diversos problemas que han limitado su desarrollo, dentro de los cuales la mortalidad causada por el virus del síndrome de la mancha blanca (WSSV) es el más importante. Para contar con elementos científicos enfocados a acciones de manejo sanitario preventivo, es preciso conocer, entre otros elementos, aspectos de la epidemiología de la enfermedad de la mancha blanca (WSD). Por esta razón el presente trabajo se enfocó a delimitar la región endémica de la WSD, sus regímenes temporales de infección y la discusión sobre los posibles factores de riesgo que pueden estar relacionados con sus brotes en las granjas camaronícolas del noroeste de México. Se utilizó información de las bases de datos de los Comités Estatales de Sanidad Acuícola de Baja California Sur, Sonora, Sinaloa y Nayarit; así como del Programa Integral de Sanidad Acuícola en Camarón (PISA 2007-2008) y de la Alianza Estratégica y Red de Innovación de la Industria Acuícola (AERI-2008). El análisis de la información mostró, para los ciclos de producción de camarón 2007-2008, una región endémica con presencia del virus WSSV, ubicada entre la región de Tuxpan, Nayarit al sur y de Agiabampo, Sonora, al norte. Los brotes de primavera de la WSD en las granjas acuícolas tuvieron un desplazamiento espacio-temporal, indicando tres regímenes de infección: (1) marzo-abril en la región sur del área de cultivo (Juntas Locales de Sanidad Acuícola [JLSA] de Mazatlán, El Rosario, Escuinapa, Tecuala y Tuxpan); (2) abril-mayo al centro (JLSA de Navolato Norte y Sur y El dorado); (3) mayo-junio en la parte norte (JLSA de Agiabampo-Sonora, Ahome, Guasave Norte y Sur). Los registros de la WSD fueron consistentes entre el 2007 y el 2008, con ligeras variaciones en algunas JLSA respecto al inicio o presencia de los brotes en primavera. Se muestra la asociación de los regímenes de infección a lo largo de la región endémica con la ubicación de las cuencas oceanográficas de Mazatlán, Pescadero y Farallón, en función del incremento diferencial de la temperatura dentro de ellas, la cual puede ser un factor condicionante para la presencia de brotes de la WSD

Detection of white spot syndrome virus in filtered shrimp-farm water fractions and experimental evaluation of its infectivity in Penaeus (Litopenaeus) vannamei

White spot syndrome virus (WSSV) may spread through water to neighbor ponds or farms. Routine water exchange and wastewater released during white spot disease (WSD)-emergency harvests may preserve WSSV in shrimp farming areas. To test this hypothesis, on-site experiments were performed in a WSSV-affected farm in Guasave, Sinaloa, Mexico. Plankton and shrimp hemolymph were collected from 12 ponds during a WSD outbreak. PCR analyses showed that 72% of the hemolymph pools (26 out of 36) were WSSV-positive. In contrast, only 14% (4 of 28) plankton samples (filtered through 10 and 0.45 µm) from three ponds (2, 7 and 10) were WSSV-positive. Plankton from pond 9 was WSSV-negative, but 14 days later, shrimp began to die. At this point, a differential filtration experiment was performed in pond 9. WSSV-positive samples were only found in three fractions [particulate fraction (PF) 1 µm and liquid fractions (LF) 0.65 µm) became WSSV-positive. Results indicate that water fractions between 100 and 0.65 µm induced WSSV infection to shrimp. Results showed that pond water and/or particulate fractions are vehicles for WSSV dispersion via virus suspended in water, attached to microalgae, or carried by zooplankton

Infection of WSSV-negative Shrimp, Litopenaeus vannamei, Cultivated under Fluctuating Temperature Conditions

To test whether effluents released from white spot syndrome virus (WSSV)-infected farm ponds are a pathway for spreading WSSV, WSSV-negative Pacific whiteleg shrimp, Litopenaeus vannamei, were exposed to WSSV-containing water under conditions of fluctuating water temperatures. White spot disease outbreaks occurred at the shrimp ponds before and during the experiment. Two cages were placed inside each test pond, and one was placed at the outlet canal. Each cage was stocked with 30 shrimp. Hemolymph from stocked shrimp was collected at intervals of 24, 48, 72, 120, 168, and 360 h after exposure and analyzed for presence of WSSV DNA by nested polymerase chain reaction. At diurnal variation of water temperature from 28.0 to 33.4 C, WSSV was detected as early as 120 h (ca. 11% of shrimp hemolymph pools) and 168 h (ca. 18% of shrimp hemolymph pools). WSSV was detected by 360 h (ca. 33% of shrimp hemolymph pools) in all cages, when water temperature varied from 24.9 to 28.5 C during a 48-h period. Cumulative mortality in cages inside ponds was ≤50.0 and 86.7% at the outlet canal. These data show that grow-out operations during the summer–autumn transition are at risk of WSSV outbreaks. The experiment demonstrated that WSSV can be spread by shrimp farm water drainage

Drug resistance phenotypes and genotypes in Mexico in representative gram-negative species: Results from the infivar network.

AimThis report presents phenotypic and genetic data on the prevalence and characteristics of extended-spectrum β-lactamases (ESBLs) and representative carbapenemases-producing Gram-negative species in Mexico.Material and methodsA total of 52 centers participated, 43 hospital-based laboratories and 9 external laboratories. The distribution of antimicrobial resistance data for Escherichia coli, Klebsiella pneumoniae, Enterobacter cloacae complex, Acinetobacter baumannii complex, and Pseudomonas aeruginosa in selected clinical specimens from January 1 to March 31, 2020 was analyzed using the WHONET 5.6 platform. The following clinical isolates recovered from selected specimens were included: carbapenem-resistant Enterobacteriaceae, ESBL or carbapenem-resistant E. coli, and K. pneumoniae, carbapenem-resistant A. baumannii complex, and P. aeruginosa. Strains were genotyped to detect ESBL and/or carbapenemase-encoding genes.ResultsAmong blood isolates, A. baumannii complex showed more than 68% resistance for all antibiotics tested, and among Enterobacteria, E. cloacae complex showed higher resistance to carbapenems. A. baumannii complex showed a higher resistance pattern for respiratory specimens, with only amikacin having a resistance lower than 70%. Among K. pneumoniae isolates, blaTEM, blaSHV, and blaCTX were detected in 68.79%, 72.3%, and 91.9% of isolates, respectively. Among E. coli isolates, blaTEM, blaSHV, and blaCTX were detected in 20.8%, 4.53%, and 85.7% isolates, respectively. For both species, the most frequent genotype was blaCTX-M-15. Among Enterobacteriaceae, the most frequently detected carbapenemase-encoding gene was blaNDM-1 (81.5%), followed by blaOXA-232 (14.8%) and blaoxa-181(7.4%), in A. baumannii was blaOXA-24 (76%) and in P. aeruginosa, was blaIMP (25.3%), followed by blaGES and blaVIM (13.1% each).ConclusionOur study reports that NDM-1 is the most frequent carbapenemase-encoding gene in Mexico in Enterobacteriaceae with the circulation of the oxacillinase genes 181 and 232. KPC, in contrast to other countries in Latin America and the USA, is a rare occurrence. Additionally, a high circulation of ESBL blaCTX-M-15 exists in both E. coli and K. pneumoniae