Efficacy of parenteral administration of ivermectin in the control of strongylidosis in donkeys

Investigations into the efficacy of parenteral ivermectin (Pandex) administration for strongylidosis control in donkeys were carried out. The preparation was applied subcutaneously at a dose of 0.2 mg / kg (1mℓ / 50 kg body weight). One day prior to the treatment and 14 days post-treatment, individual coprological samples were obtained for faecal nematode egg counts and larval culture. The study was performed on 263 donkeys originating from different regions of Bulgaria. Prior to the treatment and 20 days after that, blood samples were obtained from 64 previously infected animals for monitoring of changes in eosinophil leukocyte counts. The subcutaneous application of ivermectin had an efficacy of 96 % in terms of reduction of faecal egg counts. In 92.2%of infected donkeys, a complete reduction of faecal eggs count occurred (0 eggs per gram of faeces epg), whereas in the remaining 7.8%of the infected donkeys, the egg counts were reduced by 72 %. The reduction in faecal egg counts did not result in changes in eosinophil counts. The results obtained as well as the lack of local changes after the subcutaneous application of ivermectin in donkeys allow us to recommend its use for control of strongyles in donkeys.

Mouse strain difference in bile duct lesions induced by swine serum injections

The mouse strain difference in bile duct lesions was studied on male A/J, BALB/c, C57BL/6, C3H/He, DBA/2 and DDY mice 4 weeks old given intraperitoneal injections of swine serum (0·05 or 0·2 ml per mouse) twice a week for 4 weeks. The hepatic lesions were restricted to the portal tract. Biliary epithelial cells showed hypertrophy and hyperplasia, and eosinophilic and homogeneous or needle-shaped material appeared in the cytoplasm of such hypertrophied epithelial cells and in the ductular lumen. Around these damaged biliary epithelia, eosinophil leukocyte and plasma cell infiltration with proliferation of collagen fibres was commonly detected. These changes became more apparent with increasing size of bile duct. Such histopathological characteristics of hepatic lesions were essentially the same in all strains, but the severity showed a clear strain difference: the lesion was marked in the DDY, A/J and BALB/c strains, moderate in C3H/He and slight in C57BL/6 and DBA/2. A high production of anti-swine-serum antibodies associated with a marked increase in the number of mouse IgG-producing lymphocytes in the spleen was detected in the strains showing the marked hepatic lesions.

MECHANISMS OF IRON II AND IRON III SEQUENCE HEMATOXYLIN STAINS

Undifferentiated Fe II and Fe III hematoxylins yield blue to black nuclei, keratin, keratohyalin, enterochromaffin, Paneth and eosinophil leukocyte granules, erythrocytes, myelin and bile casts, gray to blue smooth and striated muscle, variable collagen and elastin staining and lighter gray cytoplasms. Staining is more intense with formol-free fixations. Staining is not prevented by acid hydrolysis which abolishes the Feulgen reaction and cationic dye staining. Acetylation and sulfation have little effect. Methylation and nitrous acid deamination sufficient to prevent cationic and anionic dye staining, respectively, prevent staining of erythrocytes, muscle, cytoplasm and zymogen granules but not that of nuclei, keratin, keratohyalin, trichohyalin, Paneth and eosinophil granules. These blockade effects are more complete with Fe II than Fe III. Saponification after methylation restores staining. With sublimate, Carnoy, alcohol and methanol-chloroform fixations, 2 N NaNO2/HAc deaminates in 1 hr; with formol 18-24 hr or more may be required. The sites which stain with Fe II hematoxylin after adequate deamination have all given positive Sakaguchi reactions by α-naphthol, 8-hydroxyquinoline and 2,4-dichloro-l-naphthol technics . The new β-naphthoquinone-4-SO3Na method also shows the same sites. The combined deamination, Fe II, hematoxylin technic merits further investigation as a possibly specific method not entailing hypochlorite or strong alkali and yielding stable blue to black stains of protein-bound arginine. Without deamination it appears that lysine, hydroxylysine and histidine and histamine should also react. Mast cells are often readily identified in blue or violet-black but are not found after deamination. Alkaline benzil, 9,10-phenanthrenequinone, 1,2-cyclohexanedione and glyoxal treatments irregularly weaken the deamination-resistant Fe II hematoxylin staining, though they do not prevent it. Low reactivity of hair cortex and coarse collagen bundles (requiring higher iron concentrations) is assigned to lower penetrability. Goblet cell, salivary gland, gastric and other mucins, pepsinogen granules, lipofuscins and cutaneous melanins do not stain with either Fe II or III sequence hematoxylins, either directly, after periodic acid oxidation, or after aminoisophthalic acid condensation at periodic acid-oxidized gastric mucin. Thus carboxylic, sulfuric and sulfonic acid and aldehyde sites are excluded. With the acylation effects, hydroxyl, tyrosyl and histidyl sites also appear to be excluded, and iron binding appears to be largely restricted to lysyl and arginyl sites. Impairment of the β-naphthoquinone-4-SO3Na-arginine reaction by prior iron binding supports the arginyl participation.

AN EOSINOPHIL LEUKOCYTE CHEMOTACTIC FACTOR OF ANAPHYLAXIS

The capacity of actively or passively sensitized guinea pig lung to react with antigen to release a factor specifically chemotactic for eosinophil leukocytes (ECF-A) has been demonstrated. The release of ECF-A was also accompanied by the elaboration of both histamine and SRS-A and the appearance of all these mediators exhibited a similar response in terms of the time course of passve sensitization, the effect of antigen dose, the time course of release, divalent cation dependence and enhancement by the presence of succinate or maleate. Decomplementation by the administration of purified cobra venom factor had no effect on the antigen-induced release of ECF-A from actively or passively sensitized lung fragments. When fragments of guinea pig lung were passively sensitized with fractions of guinea pig 7S IgG, only the IgG1-containing fractions prepared tissue for the antigen-induced release of ECF-A. Histamine, SRS-A, bradykinin, serotonin, and the prostaglandins PGE1, PGE2, and PGF2α were not eosinophilotactic per se; neither was ECF-A detected following the incubation of these agents with sensitized lung in the absence of antigen. Both eosinophilotactic activity and SRS-A survived extraction in 80% ethanol and evaporation to dryness. SRS-A, however, withstood boiling in alkaline solution for 20 min, whereas ECF-A activity was abolished by this procedure. SRS-A and ECF-A could also be separated by gel filtration. ECF-A activity was completely recovered following its passage through a column of Sephadex G-25 and had an estimated molecular weight of between 500 and 1000. On the basis of size and a formation mechanism independent of the complement system, ECF-A is distinguishable from a previously described complement-dependent eosinophilotactic factor (ECF-C). Thus, ECF-A represents a hitherto undescribed agent which selectively attracts eosinophil leukocytes.