Environmental source of mycobacteriosis in a California swine herd.

Between July 1985 and April 1986, mycobacterial lymphadenitis was recorded in six of 2407 slaughter pigs from a commercial swine herd in which the majority of pigs were raised in confinement. Records showed that all six affected pigs had access to dirt-floored pens at least 81 days prior to slaughter. The mycobacteriosis lesion rate for pigs exposed to dirt pens was 9.4% while in nonexposed pigs the lesion rate was zero. The risk associated with movement of pigs from concrete floored pens to dirt pens was evaluated by a field trial. In the field trial, two litters (5 of 15 pigs) exposed to dirt pens at 12-24 days of age but none of nine nonexposed litters (39 pigs) developed lesions. Mycobacterium avium-complex bacteria were recovered from both exposed litters (9 of 15 pigs) but from none of nine nonexposed litters. Serovars of M. avium-complex isolated from trial pigs included 1, 4, 8, 9, the dual serovar 4/8, and an untypable serovar. Incense-cedar bark (Calocedrus decurrens) used as a flooring material in the pens was demonstrated to be a potential source of M. avium-complex serovar 9. The dual serovar 4/8 and an untypable M. avium-complex were isolated from the dirt-floored pens. No evidence of cross-transmission of M. avium-complex infection was detected. The sporadic pattern of mycobacteriosis observed in the herd probably resulted from infrequent exposure to a common environmental source.     

Cellular injury and lipid peroxidation induced by hexavalent chromium in isolated rat hepatocytes

In order to elucidate the relationship between cellular injury and lipid peroxidation induced by hexavalent chromium (CrVI), isolated rat hepatocytes treated with any one of scavengers of active oxygen species, antioxidants or antichromium agent were incubated with K2Cr2O7 as CrVI (1 mM Cr). After the incubation, the development of lipid peroxidation was determined as thiobarbituric acid (TBA)-reacting materials in total lipid extracts from the incubated hepatocytes. Cellular injury was observed as a leakage of lactate dehydrogenase (LDH) from hepatocytes into incubation medium. The contents of reduced glutathione (GSH) in hepatocytes were also assessed. Results obtained were as follows: (1) CrVI facilitated lipid peroxidation in isolated hepatocytes after 20 min of incubation. On the other hand, the cellular injury induced by CrVI was barely observed even after 60 min of incubation. (2) The CrVI-induced lipid peroxidation was inhibited by catalase and mannitol as scavengers of active oxygen species, or N,N'-diphenyl-p-phenylenediamine and alpha-tocopherol as antioxidants. However the cytotoxicity of CrVI could not be prevented by these chemicals. (3) CrVI depleted the contents of intracellular GSH and diminished the activities of glutathione reductase (GR) and glutathione-S-transferase (GST) except glutathione peroxidase. (4) The scavengers of active oxygen species and the antioxidants could not prevent the depletion of intracellular GSH induced by CrVI. (6) Ascorbic acid, antichromium agent, prevented all of the lipid peroxidation, the cellular injury and intracellular GSH depletion induced by CrVI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of nemadectin, a new broad-spectrum endectocide, against natural infections of canine gastrointestinal helminths

Nemadectin, a new broad-spectrum endectocide, was highly efficacious against natural infections of all the major canine gastrointestinal helminths. At single oral dosages of 0.2-0.4 mg kg-1 body weight (BW), a liquid formulation administered in gelatin capsules was 100% effective in eliminating natural infections of Toxocara canis, Toxascaris leonina, Ancylostoma caninum and Uncinaria stenocephala. Tablets (267 mg) containing 4.6% nemadectin given at a rate of 1/3 tablet per 20 kg BW (0.2 mg nemadectin kg-1) were 100% active against T. canis, A. caninum and U. stenocephala. With both formulations, an increase in the dose rate to 0.6-0.8 mg kg-1 BW resulted in 99-100% elimination of Trichuris vulpis infections. No adverse reactions were observed in any of the treated dogs.     

Situation of glasshouse pests in Hungary1

The area of protected crops in Hungary is about 5300 ha. Most of it is under plastic, the area under glass being only about 250 ha. Vegetable growing makes up 80%, mostly on private farms. The main crops are capsicum, tomato and cucumber. On relatively small areas, ornamentals, principally cut flowers, are produced: carnation, gerbera, rose and chrysanthemum. The three most important, commonly occurring pests are Trialeurodes vaporariorum, Tetranychus urticae and aphids (Aphis gossypii, Myzus persicae, A. nasturtii). Polyphagotarsonemus latus, Liriomyza trifolii and Aculops lycopersici caused considerable economic damage during the eighties. However, in the last few years these pests have not been observed in any crops. Two new glasshouse pests have been described from ornamentals during the last 2 years in Hungary: Frankliniella occidentalis and Bemisia tabaci. Their accidental appearance in vegetable crops could lead to direct economic loss, besides endangering biological control systems.     

Intra‐uterine Infection with Babesia bovis in a 2‐day‐old Calf

Infection with Babesia bovis was diagnosed in a 2‐day‐old female calf apparently transmitted in utero. The calf was born as the second calving to a cross‐bred beef cow permanently on pasture. Diagnosis was based upon identification of B. bovis in peripheral blood smears and clinical signs which included fever, jaundice, pale mucous membranes and convulsions. Anaemia, leucocytosis, thrombocytopenia and lymphocytosis were noted at the febrile acute stage of the disease. The blood smears revealed evidence of regeneration of toxic neutrophils with a left shift, severe spherocytosis and high degree of basophilic stippling. Elevated concentration of aspartate aminotransferase, lactate dehydrogenase, and creatine kinase were also noted, and were probably the result of haemolysis, dehydration and muscle damage because of recumbancy. Elevated total bilirubin concentration following haemolysis resulted in jaundice. The neurological symptoms observed were probably caused by sludging of parasitized erythrocytes in the brain capillaries. The calf recovered following treatment with diminazene aceturate and the recovery was followed up clinically, haematologically and biochemically.     

Light and electron microscopic studies of calf kidneys after exposure to subtoxic lead levels]

Eight calves were fed from the fourth to the twentieth week of age a milk powder diet containing 40 mg lead acetate per kg dry substance. This is twice the lead concentration legally permitted. In average, each animal has daily taken up 0.834 mg lead per kg body weight. Eight calves were used as controls. The animals gained the usual fattening weights and did not show clinical symptoms. Beginning with week 14, increased levels of blood urea were encountered in the animals which received lead in their diet. Morphologically, severe renal lesions were found in these calves. The kidneys were increased in weight, pale and of firm consistency. Histologically, fibrosis and periglomerular interstitial non-purulent nephritis were found. Light- and electronmicroscopically, numerous intranuclear inclusion-bodies typical for lead poisoning were demonstrated in epithelial cells of proximal tubules. The results show, that daily uptake of less than 1 mg lead per kg body weight must be considered as a toxic dose for calves, and not 5-7 mg as stated in literature.