Effects of Ostertagia ostertagi and omeprazole treatment on feed intake and gastrin-related responses in the calf.

Infection with the bovine abomasal nematode, Ostertagia ostertagi, results in a loss of acid-secreting parietal cells and an increase in gastric pH. The effects of an experimental infection with Ostertagia and/or daily treatment with omeprazole (OMP) at 2mgkg(-1) bodyweight for four consecutive days (experiment days 24-27, inclusive) on voluntary feed intake, blood and tissue gastrin concentrations, abomasal G-cell numbers, gastric pH, and blood cholecystokinin (CCK) and pepsinogen concentrations were investigated in the calf. Ostertagia-infected calves demonstrated a significant drop in feed intake between days 24 and 27 post-infection (38%; P<0.001) and in G-cell numbers (42%; P<0.05) and significant increases in abomasal pH (P<0.001), fundic mucosal weight (99%; P<0.01), and blood gastrin (P<0.05) and pepsinogen (P<0.0001). OMP treatment of worm-free animals resulted in a significant drop in intake between days 24 and 27 (30%; P<0.001) and in G-cell numbers (17%; P<0.05) and significant increases in abomasal pH (P<0.01) and blood gastrin (P<0.001). OMP treatment of Ostertagia-infected animals with an existing hypergastrinaemia had no effect on feed intake, abomasal pH, blood gastrin or pepsinogen or abomasal G-cell numbers. Blood CCK concentrations were also unaffected by either Ostertagia infection or OMP treatment. These data suggest that: (a) the depression in feed intake associated with OMP in worm-free calves was not due to a side effect of drug treatment; (b) inappetance in Ostertagia-infected animals is closely associated with the parasite-induced hypergastrinaemia; and (c) the elevation in abomasal pH was a major factor responsible for the elevated blood gastrin concentrations seen in parasitised and OMP-treated animals.

Effects of Ostertagia ostertagi on gastrin gene expression and gastrin-related responses in the calf.

1. Infection with the bovine abomasal nematode Ostertagia ostertagi results in a loss of acid-secreting parietal cells and an increase in gastric pH. The effects of an experimental infection on gastrin mRNA expression, blood and tissue gastrin concentrations, the different molecular forms of gastrin in each, and pyloric mucosal chromogranin A-derived peptides were investigated in the calf. 2. An increase in blood gastrin concentrations in the infected group reached a peak by day 28 postinfection (635 pg ml-1; P < 0.01). Gel chromatography analysis of blood samples revealed that the hypergastrinaemia comprised largely gastrin-34 (G-34) in parasitized calves while gastrin-17 (G-17) predominated in control animals. 3. An 11-fold increase in gastrin mRNA expression was recorded in the parasitized animals which was accompanied by a 23.8% reduction in pyloric mucosal gastrin content and an apparent drop of 24.7% in the number of gastrin-producing G cells detected. There was no major change in the relative abundance of G-17 and G-34 in the pyloric mucosa of infected calves. No significant differences in the concentration of pyloric mucosal chromogranin A-derived peptides were recorded between infected and control groups. 4. These data suggest that the hypergastrinaemia seen in parasitized calves results largely from an increase in gastrin synthesis and that depletion of previously stored peptide makes virtually no contribution to elevated blood gastrin concentrations.

Protection conferred by Trypanosoma evansi infection against homologous and heterologous trypanosome challenge in rabbits.

The response of rabbits, infected with Trypanosoma evansi, to challenge with homologous and heterologous trypanosome species was investigated. Protection against homologous challenge was complete with partial protection observed against heterologous T. evansi and Trypanosoma brucei challenge. No protection was seen against challenges with Trypanosoma vivax or Trypanosoma congolense. The recognition of the surface components of the parasite by the host antibodies was closely linked with complete protection. However, the degree of antigenic relatedness between infection and challenge parasite populations and the magnitude of antibody response to several non-surface components of the parasites appeared to influence the outcome of the challenge infections. Non-antibody dependent factors also appeared to influence the host response to challenge.

Early events following challenge of rabbits with Trypanosoma evansi and T. evansi components.

The intradermal injection of Trypanosoma evansi or T. evansi components into rabbits evoked trypanosome-specific responses in the skin. The strongest responses, which were those against the parasite surface-associated components, had the characteristics of an immediate type hypersensitivity reaction, followed by a delayed type. The responses were greater in rabbits from which infections had been cleared by chemotherapy than in animals with patient infections. These findings suggest that variant surface glycoprotein (VSG)-specific antibody activity and immunosuppression are effective in the skin and influence the outcome of infection with T. evansi in previously infected animals.

Gastrin and gastrin-related responses to infection with Ostertagia ostertagi in the calf.

The effects of a single challenge with 60,000 infective Ostertagia ostertagi larvae on blood and gastrointestinal mucosal gastrin concentrations, gastrin-producing G-cell numbers in the pyloric mucosa and growth of different parts of the gut were investigated in 16, two-and-a-half-month-old calves. Infected calves exhibited a rise in abomasal pH which was accompanied by a 145 per cent increase in wet weight of the fundic mucosa (P < 0.05) and a significant rise in blood total gastrin concentrations (P < 0.01). Circulating little gastrin (G-17) was unaffected. Pyloric mucosal total gastrin concentrations remained unaltered in the infected calves until day 28 when levels fell to 36.9 per cent of control group values (P < 0.01). Pyloric mucosal G-cell numbers declined during the experiment in the infected group. It is suggested that release of previously stored tissue gastrin and not a change in G-cell numbers contributes to the hypergastrinaemia associated with ostertagia infection in the calf.

Pathways of complement (C3) activation in rabbits infected with Trypanosoma evansi.

Immunoelectrophoresis was used to evaluate the pathways of complement (C3) activation with sera from rabbits infected with Trypanosoma evansi. C3 activation via the classical pathway was of a higher magnitude than via the alternative pathway using both the intact parasite and soluble parasite antigens. This observation indicates that although the two pathways may be activated during infection, the activation of the classical pathway may be dominant in a host's response to a T. evansi infection during both the early and late stages of the disease.

Effect of complement (C3) depletion on the generation of memory in rabbits primed with antigens of Trypanosoma evansi.

Using the antibody response during secondary exposure of rabbits primed with antigens of Trypanosoma evansi as an indirect measure of immunological memory, it was shown that C3 decomplementaemia resulted in a reduced antibody response, with IgM being predominant in the sera samples followed by IgG and then IgA [corrected]. While significant differences were observed in the levels of IgG produced by the C3-depleted and C3-intact rabbits no differences were recorded in the levels of IgM and IgA produced by the two groups after C3 decomplementaemia. These results demonstrate that C3 depletion did not abolish memory of the T. evansi antigen in these rabbits but only modified the magnitude and pattern of their response. The host response to reinfection may be affected by such changes as those observed in this study.

Class-specific antibody response in rabbits experimentally infected with Trypanosoma evansi.

The antibody response to Trypanosoma evansi antigens in rabbits experimentally infected with T. evansi was monitored by SDS-PAGE and "Western" blotting. As defined by the number of antigenic components recognised and the intensity with which they were labelled, responses were predominantly IgG, followed by IgM and IgA. During infection and subsequent drug treatment seven major antigenic components (94, 85, 75.5, 67, 60.5, 43, and 28.6 kDa) were identified by IgG. Antibodies to a 32.4 kDa and three other components (30, 28.6 and 12.5 kDa) appeared during infection and after chemotherapy respectively. Three components (94, 67 and 60.5 kDa) recognised by IgG were also detected by IgM and IgA. Furthermore, two bands (30 and 12.5 kDa) were identified by IgM and one (12.5 kDa) by IgA only after drug treatment, while a 28.6 kDa component was recognised by IgM and IgA during the same period. These findings constitute a basis for the exploration of class-specific antibody responses to T. evansi antigens with relevance to diagnosis, protection and pathology.

Antibody patterns in rabbits showing different levels of susceptibility to an experimental Trypanosoma evansi infection.

Using SDS-PAGE and Western blotting, the antibody spectrum of rabbits infected with Trypanosoma evansi to homologous T. evansi antigens was monitored. Animals that developed parasitaemia later or had lower levels of parasitaemia as the infection progressed were considered to have a degree of resistance to the infection. Sera of these resistant animals recognised the T. evansi antigens earlier and subsequently identified more antigens than their susceptible counterparts. The susceptible animals developed patent parasitaemia earlier and had higher parasite counts as the infection progressed, and their sera recognised T. evansi antigens later with fewer parasite components labelled during the course of the infection. These observations demonstrate clear differences between animals in response to T. evansi infections. Selection of T. evansi-tolerant animals on an individual basis may be possible as has been suggested for other trypanosome species.

Complement (C3) levels and activation in rabbits experimentally infected with Trypanosoma evansi.

Rocket immunoelectrophoresis was used to monitor the levels of the third complement component (C3) in the blood of rabbits experimentally infected with Trypanosoma evansi. Although a reduction in the circulating levels of C3 was associated with C3 activation in rabbits with high levels of parasitaemia, there was no evidence for C3 activation in uninfected rabbits, rabbits with early-stage, light infections or rabbits cleared of infection by drug treatment. Host-tolerance to current infection and to re-exposure to the parasite are probably affected by such changes in C3.

Identification of the surface components of Trypanosoma evansi.

125I-labelling was used to characterise the surface components of five stocks of Trypanosoma evansi. Two components of 67 and 60.5 kD were labelled in two of the stocks, a single 60.5 kD component in two other stocks and no components in the remaining stock. These differences are probably related to the labelling method and biochemical differences between the stocks.

Pathology of experimental Trypanosoma evansi infection in rabbits.

Histopathological examination of tissue sections from the organs of rabbits experimentally infected with Trypanosoma evansi revealed evidence of a vigorous immunological response. Changes in the spleen, lymph nodes, vulva, eyelids and ears indicated a protective immune response, but changes in the kidneys, lungs and heart were destructive in nature and capable of causing sudden death of the host. Hepatic damage capable of interfering with the host's immune response was also observed. The presence of many parasites in the vulval tissue calls for further investigation into the possibility of sexual transmission of T. evansi.

Bacterial isolates from Nsukka meat market: a zoonotic appraisal.

Swabs collected from butchers hands, knives, tables and meat displayed for sale at Nsukka meat market showed that every item screened was contaminated. Bacteria isolated include Streptococcus faecalis, coagulase positive Staphylococcus, Clostridium perfringens, Brucella species, Corynebacterium haemolyticum, Proteus mirabilis, P. vulgaris, Escherichia coli, Salmonella enteritidis, Enterobacter aerogenes, Pseudomonas multophilia, P. rubescens and beta-haemolytic Streptococci. The zoonotic or public health implications of such contaminations, their probable sources and possible ways of minimizing them are discussed.