Anti-canine distemper virus antibodies in common and grey seals.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to S D Carter.
Explore the source record for details and available documents.
Serological surveys of common and grey seals were performed to monitor the spread of the phocid distemper outbreak in 1988 and its effects on the host immune response. The disease affected mainly common seals; grey seals were largely unaffected but did have anti-CDV antibodies which developed during 1988. Canadian seals, both common and grey, showed evidence of a morbillivirus infection but without the apparent mortality observed in British common seals. Common seal circulating immunoglobulin levels were not greatly affected during the outbreak, although there was some reduction in the most severely affected pups. Vaccination of common seals with CDV antigens elicited high titres of antibodies and produced clinical protection. Vertical transmission of host immunity was shown in grey seals although the longevity of protection has not been determined. The large population of common seals which are not immune emphasises that such an epizootic could have serious consequences again in the future.
A factor in Taenia multiceps coenurus fluid (TMCF) has previously been shown to modify the accessory activity of murine macrophages in vivo and in vitro. The factor (TMCF-F24) has been purified by ion exchange in a fast protein liquid chromatography (FPLC) system. This study was conducted to determine whether TMCF-F24 is an antigen in naturally occurring cerebral coenuriasis, and whether it can also modify normal sheep blood monocytes. Specific IgG antibodies to TMCF-F24 were detected, using ELISA, in serum and cerebrospinal fluid of sheep with clinical coenuriasis. Alterations in monocyte accessory activity were detected by an assay which measured the rate of increase in mitogen-induced lymphocyte transformation caused by addition of increasing numbers of the monocytes. Normal monocytes caused a positive increase in lymphocyte transformation. Monocytes incubated with TMCF-F24 caused progressive inhibition of transformation. This factor may therefore modify monocyte-T cell interaction in natural infection.
This study examined whether increased intestinal permeability in Irish setters with gluten-sensitive enteropathy was associated with altered immune responses to ingested antigens, and whether a humoral immune response to gluten is involved in the pathogenesis of the condition. Affected setters reared on a wheat-containing diet were compared with littermates reared on a cereal-free diet and age-matched control setters. Measurement of serum immunoglobulins revealed increased serum IgA concentrations in affected dogs. Antibody responses to a variety of dietary antigens were measured by ELISA. Antibody levels to ovalbumin, collagen I and II and soya were not significantly different from normal dogs. Anti-gliadin antibody concentrations were lower in affected dogs than controls, and correlated with immune complex formation as assessed by C1q binding. The study suggested a modified immune response in dogs with increased intestinal permeability, although there was no major systemic antibody response to dietary antigens.
Lymphocyte populations in the synovial membranes of dogs with canine rheumatoid arthritis (CRA) were investigated by immunohistochemical staining techniques. T-lymphocytes were the predominant cell type distributed throughout the supporting layer of the synovial membranes. B-lymphocytes expressing IgG were seen far more commonly than those expressing either IgA or IgM. Synovial membrane biopsies from normal and osteoarthritic joints did not have the marked cellular infiltrates seen in joints with CRA. The synovial immunohistopathological features in dogs with CRA are similar to those seen in human rheumatoid arthritis.
Two experiments were performed to investigate the effects of cessation of feeding milk substitute (weaning) on antibody responses to Keyhole Limpet haemocyanin (KLH) in young calves. In the first experiment, 47 calves were weaned at 42 days of age, while a further 47 calves remained unweaned until 84 days of age. All calves were immunized with KLH at 43 and 85 days of age. Serum IgG1, IgG2 and IgA responses to KLH were increased in the early weaned calves compared with the late weaned calves following both primary and secondary immunizations. In the second experiment, 24 calves were immunized with KLH at 21 days of age. Subsequently, at 35 days of age, eight calves were weaned, eight calves were sham-weaned and eight calves remained unweaned. Sham-weaning involved continuing to feed milk substitute of greatly decreased nutritional value in an attempt to isolate nutritional from behavioural effects of weaning. No effects of treatments on antibody responses were detected. It was concluded that weaning affects antibody responses to antigens given near weaning but not to antigens given 2 weeks before weaning.
The effects of Ostertagia ostertagi infection and diet on antibody responses to O. ostertagi third stage larval (L3) antigen and to an unrelated antigen, Keyhole Limpet Haemocyanin (KLH) were determined in calves experimentally infected with 3000 L3 on alternate days for 6 weeks. Calves were given one of two diets, and were either infected or not infected with O. ostertagi L3. The diets were either high (H) or low (L) in protein/energy and were within the range of normal husbandry practice in the UK. Both IgG1 and IgG2, but not IgA, responses to L3 antigen were increased in the L-diet compared with the H-diet. IgA responses to L3 antigen were not affected by dietary treatment. The effects of diet and infection on anti-KLH IgG1 were independent of each other; IgG1 anti-KLH responses were decreased by infection and by the L-diet compared with the H-diet. The data suggest that there is a strong interrelationship between diet and immunity during nematode infections.
Specific IgG and IgA antibodies against adult Taenia pisiformis excretory/secretory antigen were detected in sera and saliva by enzyme-linked immunosorbent assay (ELISA) in experimentally infected dogs. IgG titres in serum and IgA in saliva corresponded with infection status, while serum IgA levels closely reflected faecal egg counts. The salivary IgA response was particularly raised and could have significant immunodiagnostic use for taeniasis in dogs.
The regulatory role of tumour necrosis factor (TNF) was investigated in murine infection with tetrathyridia of Mesocestoides corti. Recombinant TNF alpha reduced macrophage larvicidal activity in vitro. M. corti primed mice for TNF release in response to bacterial lipopolysaccharide (LPS) in vivo. TNF activity was amplified 100-fold at 14 days post-infection (p.i.), with a further rise at day 28 p.i. Maximal inflammatory reaction was observed histologically in the liver at the height of TNF activity. Hepatic necrosis was located within inflammatory foci, but not within the vicinity of the parasite itself, suggesting that TNF may contribute to the pathogenesis of infection. Peritoneal cells from infected mice, when stimulated with tetrathyridia in vitro, showed a 4-fold increase in TNF alpha activity at day 14 p.i. However, when peritoneal cells were stimulated with LPS in vitro, a marked increase in TNF alpha secretion was observed at 2 months post-infection followed by a slow decline. It is suggested that impaired macrophage effector function, previously attributed to endogenous endotoxin, which gains access to peritoneal macrophages through an inability of the liver to detoxify endotoxin, may be mediated through TNF alpha.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The pathogenesis of canine coronavirus (CCV) infection in 10-week-old puppies was studied up to 14 days after oronasal inoculation. Mild diarrhoea was seen from three to 11 days after inoculation, approximately coincident with faecal virus shedding. Virus was initially isolated from the tonsils on day 3, and then from both small and large intestinal tissues up to 14 days after inoculation. Virus was also isolated from liver and lung. Histological changes were not seen in any tissues, but CCV antigen was detected, using a peroxidase antiperoxidase staining technique, mainly in epithelium overlying gut-associated lymphoid tissue. Virus neutralising antibody was first detected on day 10. Specific anti-CCV IgM was first detected in plasma three days after inoculation and IgG on days 4 to 7. Small amounts of anti-CCV IgG, IgM and IgA were detected in duodenal secretion, but none in bile.
Synovial fluid samples of horses with osteoarthritis were investigated to detect interleukin-1 (IL-1) activity which could contribute to the disease pathogenesis. Of the 32 samples tested, 12 (37.5 per cent) showed an augmented phytohaemagglutinin induced proliferation of C3H/HeJ mouse thymocytes. Positive results were also seen in horses with infected arthritis, osteochondritis, traumatic arthritis and undefined synovial effusions. Normal synovial fluid and sera from all groups failed to show any detectable IL-1 activity. Fractionation of synovial fluid showed that the IL-1 activity was in the 15 to 20 Kd fractions. In the absence of mitogen, synovial fluid failed to stimulate thymocytes and did not stimulate the growth of an interleukin-2 (IL-2) dependent CTLL cell line, but synovial fluid stimulated IL-2 release by mouse spleen cells incubated with suboptimal doses of lectin. Evidence of an IL-1 inhibitor in synovial fluid from osteoarthritic horses was provided by ultrafiltration experiments and by the inhibitory activity of synovial fluid at particular dilutions in the thymocyte assay. The presence of IL-1-like activity could be relevant in the pathogenesis of arthritis in horses.
Dogs with canine rheumatoid arthritis had significantly elevated levels of antibodies to canine distemper virus. This increase was particularly seen in the synovial fluids, compared with paired sera, and was not found in dogs with infective arthropathies, osteoarthritis or in osteoarthritis secondary to rupture of the cranial cruciate ligament. Analysis of the immune complexes precipitated from synovial fluids showed immunoglobulins in all types of arthropathy. Western blotting analyses showed reactivity with anti-distemper antisera in immune complexes from dogs with rheumatoid arthritis, but not in immune complexes from dogs with other joint diseases. These results suggest that there are increased immune responses to distemper in canine arthritis and that these may be due to the presence of this paramyxovirus in affected joints. The implications for the role of a possible infectious agent in rheumatoid arthritis in the dog are considerable.
Serum immunoglobulin concentrations and densities of IgA-producing immunocytes in intestinal mucosa were compared in a group of clinically healthy dogs of various breeds, a group of clinically healthy German shepherd dogs, and a group of German shepherds with bacterial overgrowth in the proximal small intestine. Serum concentrations of IgA, but not IgM or IgG, were significantly lower in the clinically healthy German shepherd dogs than in other purebreed and mixbreed dogs, indicating that production of IgA by gut-associated lymphoid tissue might be relatively low in this breed. However, densities of IgA-producing cells were not significantly different comparing these two groups, suggesting that any impairment of mucosal IgA production is more likely to be related to defective synthesis or secretion of IgA than to reduced numbers of IgA-producing immunocytes. Comparable findings in German shepherd dogs with small intestinal bacterial overgrowth provided further indirect evidence that local immunity might be defective in this breed, since these luminal bacteria would be expected to stimulate mucosal IgA production. However, it is not clear whether such a defect is directly responsible for the overgrowth, or whether there is an indirect relationship between defective local immunity and bacterial overgrowth in German shepherd dogs.
The efficacy of keyhole limpet haemocyanin (KLH) as a test antigen was determined in calves. Humoral and cellular (in vivo and in vitro) responses were compared. Calves were immunized with KLH at either 3 weeks or up to 5 months of age and immune responses were subsequently tested. Class and subclass antibody responses were detected by ELISA, lymphocyte blastogenesis was measured using a whole blood culture technique (LTT) and skin sensitivity responses were measured as an increase in skin thickness following intradermal injection. In young calves, skin test responses were maximal at 24 h and were found to correlate with IgG1 and IgG2 responses (P less than 0.01), with IgA (P less than 0.05) but not with IgM or LTT. Histological examination of skin swellings found a sequence of cellular events, with polymorphonuclear cells dominating until 48 h after intradermal injection, when mononuclear cells became involved. However, in older calves, skin test responses correlated not only with IgG1 and IgA responses but also with lymphocyte transformation (P less than 0.05). These findings suggest that, while immune responses to KLH may be a useful indicator of immune competence in calves, interpretation should be made with caution particularly in young calves.