Effect of porcine reproductive and respiratory syndrome virus (PRRSV) on alveolar lung macrophage survival and function

Porcine reproductive and respiratory syndrome virus (PRRSV) recently emerged as an important cause of reproductive disorders and pneumonia in domestic pigs throughout the world. Acute cytocidal replication of PRRSV in alveolar lung macrophages causes the acute pneumonia; however, it remains largely unresolved whether there may also be a predisposition to longer-term local immunodeficiency in the PRRSV-convalescent lung. We applied various flow cytometric techniques to study the interplay between PRRSV replication and macrophage viability/function in pure cultures of porcine alveolar lung macrophages. Monitored by flow cytometric detection of intracellular PRRSV nucleocapsid protein, acute (24 h post infection) PRRSV replication did not impede the ability of alveolar macrophages to ingest fluorescently labelled Escherichia coli. At 48 h post infection, PRRSV-induced cytotoxicity (quantitated by flow analysis of cell size and membrane integrity) led to 40% reduction in the total number of phagocytozing cells. However, viable/uninfected macrophages in PRRSV-infected cultures exhibited normal phagocytic ability at 48 h, indicating that no soluble phagocytosis-suppressive mediators were induced by PRRSV infection in this system. In short, in our minimal system containing only a single cell type, phagocytosis-suppressive effects of PRRSV infection were detected, that acted at the culture level by reducing the total number of alveolar lung macrophages.     

Progression of Mycoplasma hyosynoviae infection in three pig herds. Development of tonsillar carrier state, arthritis and antibodies in serum and synovial fluid in pigs from birth to slaughter

In this investigation, natural infection with Mycoplasma hyosynoviae was followed in groups of individual pigs in three different herds with regard to occurrence of tonsillar carrier state, clinical arthritis and development of antibodies in serum and in synovial fluid. Antibodies were detected by a polyclonal enzyme-linked immunosorbent assay (ELISA) developed for experimental use. The infection with M. hyosynoviae progressed very differently in the three herds investigated. In one herd, the infection was apparently limited to adult pigs. In a second herd, all pigs became tonsillar carriers of M. hyosynoviae, but no mycoplasma-related arthritis nor any serological response was demonstrated within the growing-finishing period. In the third herd investigated, tonsillar infection was detected in all pigs, clinical cases of M. hyosynoviae arthritis followed and a moderate serological response was observed in some, but not all, pigs. In all three herds, M. hyosynoviae infection was carried in the tonsils of the adult pigs, but it was only occasionally transmitted from sows to piglets. Maternal antibodies were transferred to the piglets and persisted for approximately 8-12 weeks. After weaning, some pigs became infected before 20 weeks of age, while others did not. In the majority of cases, the tonsillar infection was established from 11 weeks of age or older. A latent tonsillar infection was present for a period of several weeks within the group of investigated pigs before cases of generalized infection and arthritis were seen. In some cases, generalization of M. hyosynoviae infection in the blood and in joints was observed in spite of the detection of an active serological response a few weeks earlier. The present work suggests that generalization of the infection and development of arthritis may depend on age, immunity, virulence factors and/or infection pressure; in some herds maybe combined with certain triggering mechanisms such as stress and lowered general resistance.     

Depressed immunoconglutinin responses in calves experimentally infected with Trypanosoma congolense

Contrary to expectation, immunoconglutinin levels failed to rise significantly in calves infected with Trypanosoma congolense. In addition, it was shown that trypanosome infection appeared to inhibit the immunoconglutinin response to Brucella abortus strain 19. The possible reasons for these findings are discussed.     

Concentrations of trimethoprim and sulphadoxine in tissues from goats and a cow.

The concentration of trimethoprim and sulphadoxine in plasma and tissue from goats and a cow have been determined after a single intravenous injection. Furthermore, the concentration of the two drugs and their metabolites in plasma and tissues have been determined after continuous intravenous infusion for 2½–3 hrs. Trimethoprim was present in all tissues but brain at higher concentrations than in plasma while the concentration of sulphadoxine in the different tissues were lower than in plasma. The highest concentration of the 2 drugs and their metabolites was found in the kidney. The distribution pattern of trimethoprim and sulphadoxine was similar in cow and goats.     

Mercury and mink. I. The use of mercury contaminated fish as a food for ranch mink.

Adult female and juvenile ranch mink were fed rations containing 50 and 75% of fish containing 0.44 ppm total mercury over a 145 day period. There was no clinical or pathological evidence of intoxication in these animals and mercury concentrations in tissue appeared to be at a level below that associated with toxicity.     

Dietary calcium-phosphorus ratios for growing pigs in relation to serum levels and bone development

Two experiments comprising a total of 80 Danish Landrace pigs in the period 20–90 kg live-weight were carried out to study the effect of dietary levels and ratios of Ca and P on serum values of Ca, inorg. P, and alkaline phosphatase and on the development of degenerative arthritis and atrophic rhinitis.In both experiments each kg feed (Table 1) was supplemented with 600 i. u. vitamin D₃ and 80 p. p. m. Zn.In the first experiment the Ca:P ratio was 1.2 and the amount of Ca increased from 0.48 % to 1.20 % without influencing daily gain, feed conversion, carcass performance (Table 2) or frequency of atrophic rhinitis (Table 3). The Ca:P ratio in scapula was 2.15. Only when the diet was supplemented with 1.20 % Ga and 1.00 % P the bone quality was histomorphologically adequate (Figs. 1–4).In the second experiment various Ca:P ratios (ranging from 0.1 to 3.0) were compared with the recommended level and ratio of 0.72 % Ga and 0.60 % P. Performance of pigs on the normal level was better than for the other pigs (Table 4). Clinically, various degrees of leg-weakness and -deformation occurred, most pronounced in the high Ca — low P group. Very little lameness and no convulsions were observed. Marked hypocalcemia was not found. Unilateral high Ca intake increased serum Ca significantly, and serum alkaline phosphatase slightly, and decreased serum P (Figs. 5–7). Advanced pericytic osteolysis, poor mineralization and generalized osteodystrophia fibrosa were found in the low Ca groups (Figs. 8–13). The groups showed no differences in frequency of atrophic rhinitis (Table 5), and rickets was not observed.The incidence of degenerative joint lesions was not increased in pigs on the unfavourable Ca:P ratios, and depended apparently more on litters than on diets.     

Intoxication in cattle caused by a batch of sugar beet pulp (author's transl)]

During the period from Dec. 7th 1972 to Jan. 8th 1973 76 cattle deaths were reported in 20 herds on the island of M?on and the adjacent south-eastern area of Sealand. The disease was characterized by a sudden onset and a rapid and invariably fatal course. Initially, there was a loss of appetite, depression, excessive salivation and incoordination. These symptoms progressed to paralysis and, in some animals, trmor and convulsions. Death usually ensued less than 2 hours after the first observation of symptoms. Losses in the herds varied from 1 to 12 animals. In herds with multiple incidents the majority of deaths occurred in the 24-hour-period following observation of the first case. Pathology: Gross lesions were few and inconclusive. Histology revealed marked dilatation of cerebral and maningeal blood vessels (arterioles, venoles and capillaries), with perivascular edema and haemorrhage. Adjacent neurons and glia cells showed various degrees of degeneration, apparently secondary to the vascular lesion. In all affected herds sugar beet pulp from one particular sugar mill had been used during the period preceding the outbreak. The syndrome was reproduced by feeding sugar beet pulp from this batch to two heifers. The heifers showed symptoms after 19 and 32 days' feeding, resp. and died after a few hours. Clinical and pathological features were identical with those observed in the spontaneous disease. Thus, it was proved that the particular batch of pulp was responsible for the disease. The investigation did not, however, reveal a toxic factor in this batch. Analyses for lead, arsenic, mercury, nitrite, alkyl phosphates, chlorinated insecticides and Cl. botulinum toxin were negative. Batches of the sugar beet pulp showed pronounced microbial deterioration, the flora being dominated by yeasts and filamentous fungi (moulds). Several species of fungi have been isolated but so fat their possible role in the etiology of the syndrome remains unsettled. The syndrome bears some resemblance to cerebrocortical necrosis (C.C.N.) but differs in several clinical and pathological details. It is tentatively suggested that the beet pulp may have contained one or more toxic substances that interfere with microbial activity in the rumen, resulting in a disturbance of synthesis or absorption of essential metabolites. The clinical, epidemiological and pathological findings are compatible with the hypothesis that the syndrome might be due to fungal toxins. Accordingly, the isolated fungi are now being studied in more detail.