Abstract. Understanding pathogenesis during progressive stages of infection by Mycobacterium avium subsp. paratuberculosis (MAP) and finding suitable methods for its diagnosis are key to the control of Johne's disease in animals. Paratuberculosis was experimentally produced in 20 crossbred lambs by oral administration of MAP to study the sequential development of lesions between 10 and 330 days postinfection and to assess commonly used diagnostic methods such as bacterial culture, lymphocyte stimulation test (LST), and enzymelinked immunosorbent assay (ELISA) during progressive stages of infection. Histologic lesions were classified into four grades from grade 1 (least severe) to grade 4 (most severe) on the basis of location of granulomatous lesions in different regions and layers of intestines, their association with intestinal lymphoid tissues, pattern and distribution of lesions, types of cellular infiltration, and presence of acid-fast bacilli. It is evident that infection first establishes in lymphoid tissues of the small intestine, possibly at multiple sites, producing segmental lesions and from there spreads to lamina propria and local lymph nodes. Wide variability in the histologic lesions in relation to postinfection periods and initial tropism of MAP to the intestinal lymphoid tissues (Peyer's patches) suggests a differential susceptibility of young animals, possibly because of compositional phenotypic variation of Peyer's patches influencing subsequent course of infection. Histopathology was found to be a better indicator of paratuberculous infection than bacteriology in sheep. The LST (reflecting the cellular immune response) and ELISA (reflecting the humoral immune response) had overall sensitivities of 65% (11 of 17) and 42% (8 of 19), respectively, in sheep with different types of pathology but when employed together could detect about 88% of infected animals.

In a field study carried out at three different locations, the dissipation of spiromesifen on cotton and chili was studied and its DT50, and DT99 were estimated at each location. Spiromesifen was sprayed on chili at 96 and 192 g a.i. ha(-1) and cotton at 120 and 240 g a.i. ha(-1). Samples of chili fruits were drawn at 0, 1, 3, 5, 7, 10, 15, 21, 30 days after treatment and that of cotton seed and lint at first picking and harvest. Soil samples were drawn 30 days after treatment from 0 to 15 and 15 to 30 cm layer. Quantification of residues was done on GC-MS in Selected Ion Monitoring (SIM) mode in mass range 271-274 m/z. The LOQ of this method was found 0.033 microg g(-1), LOD being 0.01 microg g(-1). The DT50 of spiromesifen when applied at recommended doses in chili fruits was found to be 2.18-2.40 days. Ninety-nine percent degradation was found to occur within 14.5-16.3 days after application. Residues of spiromesifen were not detected in cotton seed and lint samples at the first picking. In soil, no residues of spiromesifen were detectable 15 days after treatment.

Flubendiamide, a phthalic acid diamide protects the plants against a broad range of economically important lepidopterus pests and thiacloprid a second generation neonicotinoid is effective against the sucking insects, white flies and jassids. To estimate the residues of flubendiamide and thiacloprid on tomato, analytical methods were validated by conducting recovery studies, residues were quantified by using HPLC on C(18) column and PDA at 260 λ. Residues of flubendiamide declined below detectable level of 0.01 mg kg(-1) after 5 and 7 days of application at lower and higher dose with RL(50) of 0.72 and 1.32 days, respectively. Thiacloprid residues reached below its detectable level of 0.01 mg kg(-1) after 5 and 7 days of its lower and higher dose with RL(50) of 0.83 and 1.79 days, respectively.

The outer membrane proteins (OMPs) of Pasteurella multocida are potential immunogens. The 16 kDa OMP of P. multocida P52, serotype B:2, was identified as one of the major immunodominant antigens. The gene omp16, encoding a 16 kDa outer membrane protein, was amplified, cloned into a pBluescript SK(-) vector and sequenced. Complete sequence homology was observed between the 16 kDa OMP gene of P. multocida P52 (serotypes B:2) and P. multocida T16 (somatic serotype 3,4). This gene was distributed among different serotypes of P. multocida and found to localize in a 6.0 kb HindII fragment of the P. multocida genome.

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