Activity of two novel insecticides against permethrin-resistant Pseudoplusia includens

Two experimental insecticides, AC 303,630 and MK 244, were tested against a laboratory colony and three field strains of Pseudoplusia includens (Walker). Topical application bioassays indicated that permethrin resistance in the field strains ranged from 3.9 to 489.0-fold. In leaf dip bioassays, LC₅₀ and LC₉₀ values for AC 303,630 ranged from 6.7 to 15.1 mg litre ?1 and 8.7 to 28.2 mg litre ?1, respectively, for third-instar larvae. The Louisiana 1991 field strain was significantly more susceptible to AC 303,630 than the laboratory and other field strains. The LC₅₀ (but not LC₉₀) for the Louisiana 1992 field strain was significantly higher than that of the laboratory strain. However, there was no difference in toxicity of AC 303,630 between the field strain with the highest level of permethrin resistance and the laboratory strain. LC₅₀ and LC₉₀ values for MK 244 in leaf dip bioassays ranged from 0.014 to 0.023 mg litre ?1 and 0.079 to 0.174 mg litre ?1, respectively. There were no significant differences in LC 50 or LC 90 among any of the strains for MK 244. Field trials in soybean were also conducted in 1991 and 1992 in an area of Louisiana where permethrin efficacy against P. includens has declined. In both years, AC 303,630 at 0.11–0.22 kg ha ?1, and MK 244 at 0.0042–0.0084 kg ha ?1, provided significantly better control than permethrin at 0.11 kg ha ?1, and control equal to the recommended standard, thiodicarb. These studies indicate no cross-resistance exists between the experimental insecticides and permethrin.     

A PCR diagnostic for cyclodiene insecticide resistance in the red flour beetle Tribolium castaneum

A molecular diagnostic was used to examine the conservation of cyclodiene resistance associated mutations between different strains of Tribolium castaneum (Herbst.). An improved insecticide bioassay for discrimination between resistant genotypes was developed and seven resistant strains were established from five different continents. In order to develop a molecular diagnostic a partial cDNA of the cyclodiene insecticide resistance gene Rdl, a γ-aminobutyric-acid-gated chloride-ion channel, was cloned and sequenced. This cDNA spans exon 7, the region containing the resistance-associated mutation, and part of exon 8. An ‘allele-specific’ oligonucleotide primer, carrying the resistance-associated mutation at its 3′ end, was used in combination with a flanking ‘allele-independent’ primer in the polymerase chain reaction to selectively amplify a single resistance-associated mutation from all seven strains collected worldwide. The implications of these findings for the population genetics of insecticide resistance and its management in pest insects via quarantine are discussed.     

Blood chemistry values of juvenile red pacu (Piaractus brachypomus)

Abstract: Blood samples were collected from 29 juvenile red pacu ( Piaractus brachypomus ), ornamental freshwater fish, to establish baseline blood chemistry values. Mean (minimum-maximum) values, obtained by automated bichromatic analysis and ion selective electrode analysis, were as follows: sodium, 150.4 (146–159) mmol/L; potassium, 3.93 (2.7–5.0) mmol/L; chloride, 138.7 (128–150) mmol/L; total CO₂, 7.5 (6–10) mmol/L; albumin, 0.86 (0.5–1.0) g/dL; lactate dehydrogenase, 237.8 (65–692) IU/L; aspartate aminotransferase, 49.1 (0–125) IU/L; creatinine, 0.31 (0.2–0.4) mg/dL; calcium, 10.80 (9.5–12.5) mg/dL; anion gap, 6.89 (1.2–12.5) mmol/L; and phosphorus, 7.29 (4.1–8.9) mg/dL.     

Dual Sarcocystis neurona and Toxoplasma gondii infection in a Northern sea otter from Washington state, USA

Dual Sarcocystis neurona and Toxoplasma gondii infection was observed in a Northern sea otter from Washington, USA. The animal was found stranded, convulsed, and died shortly thereafter. Encephalitis caused by both S. neurona and T. gondii was demonstrated in histological sections of brain. Immunohistochemical examination of sections with S. neurona specific antisera demonstrated developmental stages that divided by endopolygeny and produced numerous merozoites. PCR of brain tissue from the sea otter using primer pairs JNB33/JNB54 resulted in amplification of a 1100 bp product. This PCR product was cut in to 884 and 216 bp products by Dra I but was not cut by Hinf I indicating that it was S. neurona [J. Parasitol. 85 (1999) 221]. No PCR product was detected in the brain of a sea otter which had no lesions of encephalitis. Examination of brain sections using T. gondii specific antisera demonstrated tachyzoites and tissue cysts of T. gondii. The lesions induced by T. gondii suggested that the sea otter was suffering from reactivated toxoplasmosis. T. gondii was isolated in mice inoculated with brain tissue. A cat that was fed infected mouse brain tissue excreted T. gondii oocysts which were infective for mice. This is apparently the first report of dual S. neurona and T. gondii in a marine mammal.     

Muscular dystrophy in female dogs

The most common form of muscular dystrophy in dogs and humans is caused by mutations in the dystrophin gene. The dystrophin gene is located on the X chromosome, and, therefore, disease-causing mutations in dystrophin occur most often in males. Therefore, females with dystrophin deficiency or other forms of muscular dystrophy may be undiagnosed or misdiagnosed. Immunohistochemistry was used to analyze dystrophin and a number of other muscle proteins associated with muscular dystrophy in humans, including sarcoglycans and laminin alpha2, in muscle biopsy specimens from 5 female dogs with pathologic changes consistent with muscular dystrophy. The female dogs were presented with a variety of clinical signs including generalized weakness, muscle wasting, tremors, exercise intolerance, gait abnormalities, and limb deformity. Serum creatine kinase activity was variably high. One dog had no detectable dystrophin in the muscle; another was mosaic, with some fibers normal and others partly dystrophin-deficient. A 3rd dog had normal dystrophin but no detectable laminin alpha2. Two dogs could not be classified. This study demonstrates the occurrence of dystrophin- and laminin alpha2-associated muscular dystrophy and the difficulty in clinical diagnosis of these disorders in female dogs.     

Occurrence of Piscirickettsiosis-like syndrome in tilapia in the continental United States.

From 2001 to 2003, tilapia (Oreochromis sp.) farms in Florida, California, and South Carolina experienced epizootics of a systemic disease causing mortality. The fish exhibited lethargy, occasional exophthalmia, and skin petechia. The gills were often necrotic, with a patchy white and red appearance. Grossly, the spleen and kidneys were granular with whitish irregular nodules throughout. Granulomatous infiltrates were observed in kidney, spleen, testes, and ovary tissues, but not in the liver. The granulomas contained pleomorphic coccoid bacteria, measuring 0.57 +/- 0.1 x 0.8 +/- 0.2 microm, that were Giemsa-positive, acid-fast-negative, and Gram-negative. The bacteria had a double cell wall, variable electron-dense and -lucent areas, and were present in the cytoplasm and within phagolysosomes. The syndrome was associated with cold stress and poor water conditions. These findings are consistent with an infectious process caused by a Piscirickettsia-like bacterium described previously in tilapia in Taiwan and Hawaii. This report involves the first identified cases of a piscirickettsiosis-like syndrome affecting tilapia in the continental United States.     

Assessment of biological and molecular variability between and within field isolates of Plasmodiophora brassicae

Plasmodiophora brassicae is an obligate biotroph that causes clubroot, one of the most damaging diseases of crucifers. Differential cultivars and random amplified polymorphic DNA markers were used to assess the extent of genetic diversity among nine single-gall populations of P. brassicae and 37 single-spore isolates (SSI) derived from four of those field samples. Isolates were classified into eight pathotypes, and each isolate was associated with a unique molecular genotype. Virulence and DNA polymorphisms were detected within and between field isolates, and among SSIs from different pathotypes, hosts and geographical origins. The relatively high level of genetic diversity among field isolates was similar to that among SSIs derived from a single-club field isolate. Molecular and pathogenicity-based classifications were not clearly correlated, but isolates belonging to pathotype P1 were clustered. Two RAPD markers were specific to pathotype P1. The finding that genetic differences can occur in P. brassicae field isolates will be an important consideration in resistance genetic studies and in choosing breeding strategies to develop durable clubroot resistance.