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Rift Valley fever (RVF) in Zambia was first reported in 1974 during an epizootic of cattle and sheep that occurred in parts of Central, Southern and Copperbelt Provinces. In 1990, the disease was documented in nine districts of the provinces of Zambia. In the last two decades, there have been no reports of RVF. This long period without reported clinical disease raises questions as to whether RVF is a current or just a perceived threat. To address this question, World Organisation for Animal Health (OIE) disease occurrence data on RVF for the period 2005-2010 in the Southern Africa Development Community (SADC) was analysed. From the analysis, it was evident that most countries that share a common border with Zambia had reported at least one occurrence of the disease during the period under review. Due to the absence of natural physical barriers between Zambia and most of her neighbours, informal livestock trade and movements is a ubiquitous reality. Analysis of the rainfall patterns also showed that Zambia received rains sufficient to support a mosquito population large enough for high risk of RVF transmission. The evidence of disease occurrence in nearby countries coupled with animal movement, and environmental risk suggests that RVF is a serious threat to Zambia. In conclusion, the current occurrence of RVF in Zambia is unclear, but there are sufficient indications that the magnitude of the circulating infection is such that capacity building in disease surveillance and courses on recognition of the disease for field staff is recommended. Given the zoonotic potential of RVF, these measures are also a prerequisite for accurate assessment of the disease burden in humans. [ABSTRACT FROM AUTHOR]

The course of Trypanosoma brucei infection in the wildebeest (Connochaetes taurinus) was studied. A low but persistent parasitaemia developed in all five wildebeest following intravenous inoculation with 1 × 108 organisms of clone ILTat 2.1. Unlike cattle controls, however, the wildebeest did not develop anaemia. In both cattle and wildebeest, radioimmunoassay studies revealed a classical sequence of production of IgM, IgG1 and IgG2 antibodies which had the capacity to bind to the corresponding purified variable surface glycoprotein and to neutralize the infectivity of ILTat 2.1. Investigations into the interaction between post-infection sera, trypanosomes and freshly isolated peripheral blood leucocytes (PBL) of wildebeest and cattle showed that sera from the wildebeest had a higher capacity to induce adherence of trypanosomes to homologous PBL. The adherence and phagocytosis-inducing activity resided in the IgM fraction. Cross-testing of the antibodies and PBL revealed that wildebeest IgM antibodies induced high adherence indices when tested on cattle PBL. High adherence indices were also observed when cattle IgM antibodies were tested on PBL of wildebeest. It was concluded (i) that the phagocytic system of the wildebeest was superior to that of cattle, (ii) that freshly prepared wildebeest PBL bear receptors for wildebeest as well as cattle IgM, and (iii) that cattle PBL bear a receptor for wildebeest IgM that would appear to be different from that for cattle IgM. [ABSTRACT FROM AUTHOR]

The antigenic relationship amongst sporozoites of several Theileria parva strains isolated from different parts of East Africa was investigated. It was found that antibodies to T. parva (Muguga) sporozoites neutralized the infectivity of homologous sporozoites as well as those of T. parva (Uganda), T. parvo lawrencei, T. parva (Kiambu 5), T. parva (Kabete 1) and T. parva (Marikebuni). The results correlated with those obtained from an in vivo challenge, in that cattle immunized against T. parva (Muguga) were either solidly resistant or developed only a transient parasitosis when challenged with T. parva lawrencei or T. parva (Uganda). The immunity exhibited by these animals paralleled the level of anti-sporozoite anti- bodies, such that animals with high titres were completely protected whereas those with low levels developed transient parasitosis. Furthermore, monoclonal antibodies made against sporozoites of T. parva (Muguga) were also capable of neutralizing the infectivity of sporozoites of other strains. These results indicate that the outcome of cross-challenge may depend on the level and avidity of the anti-sporozoite antibodies at the time of challenge. In addition, these findings show that then is a common protective antigenic determinant on sporozoites of all the T. parva strains investigated in this study. [ABSTRACT FROM AUTHOR]

The role of antibodies in the neutralization of sporozoites of Theileria parva was investigated. It was found that serum obtained from cattle recovered from East Coast fever (ECF) and rabbits immunized with sporozoites was capable of neutralizing the parasites. The serum was then fractionated by gel filtration and anion exchange chromatography to identify which antibody class or subclass was responsible for the neutralization. In bovine hyperimmune serum the neutralizing capacity was in the fraction containing IgG2 immunoglobulins. In rabbit anti-sporozoite serum the neutralizing capacity also resided in the IgG2 containing fraction. These results suggest that humoral antibodies may play a role in resistance to reinfection with T. parva. A mechanism for this acquired resistance is proposed based upon the recently established biological properties of bovine IgG2 immunoglobulins. [ABSTRACT FROM AUTHOR]

Mouse spleen cells from animals immunized with bovine peripheral blood lymphocytes were fused to X63.Ag8 myeloma cells and the activity of one of the resulting myeloma hybrids was characterized. The product of this clone (B5/4.1.4) binds to pentameric bovine IgM isolated from serum but not to serum IgG1 or IgG2. This reagent also binds to cell surface (monomeric) IgM and can be used in immunofluorescence assays to enumerate IgM-bearing cells in lymphoid cell suspensions and to examine B lymphocytes or B lymphocyte derived cells in tissue sections. [ABSTRACT FROM AUTHOR]

Bovine immunoglobulin G subclass (IgGI and IgG2) antibodies were found to fix bovine complement while only IgGI fixed guinea-pig complement in vitro. Similar results were noted when IgGI and IgG2 antibodies were tested by passive cutaneous anaphylaxis (PCA) in that Both IgGI and IgG2 caused PCA in Bovine skin while only IgGI mediated the reaction in rat skin. In precipitation reactions IgGI antibodies to DNP failed to cause precipitation of DNP19-ovalbumin while IgG2 antibodies to DNP precipitated DNP19-ovalbumin. Both IgGI and IgG2 antibodies to ovalbumin precipitated ovalbumin. Surprisingly, IgG2 antibodies to equine erythrocytes caused phagocytosis by bovine neutrophils and peripheral blood monocytes while IgGI antibodies failed to cause either phagocytosis or adherence. Results with peripheral blood monocytes cultured for 7 days demonstrated that both IgGI and IgG2 could mediate phagocytosis. [ABSTRACT FROM AUTHOR]

Chemical inhibitors of immediate hypersensitivity were used to treat rats passively immunized against Taenia taeniaeformis with serum containing 7Sγ2a, and reaginic antibodies. There was no significant reduction in protection against oral challenge with eggs in these animals, indicating that reagin-mediated hypersensitivity reactions were not an essential component of the protective mechanism. However, systemic reagin sensitization was shown to result in an acceleration of the rate at which challenge organisms were destroyed in immune rats. By 12 h after infection most of the parasites had been killed in the livers of rats which had been both passively immunized and reagin-sensitized, whereas a large proportion survived in rats passively immunized, but not reagin-sensitized. This effect of reagin appeared to be limited to the early stages of resistance since parallel groups left for 21 days after challenge were shown to have been equally well protected. In an effort to determine if vasoactive amines liberated by reagin-mediated reactions could act directly on invading parasites, early larval stages of T. taeniaeformis were exposed to histamine or serotonin (5HT) in vitro or in vivo. Consistent results were not obtained, but significant inhibition (P<0.05) of viability of parasites exposed to histamine occurred on two occasions. Significant (P<0.01) inhibition of infectivity of T. taeniaeformis also resulted when peritoneal anaphylactic diffusate was introduced into isolated gut loops containing hatched embryos of the parasite. The results are discussed in terms of the possible means whereby reagins may participate in protective immunity to infectious organisms. [ABSTRACT FROM AUTHOR]

Chemical inhibitors of immediate hypersensitivity were used to treat rats passively immunized against Taenia taeniaeformis with serum containing 7Sγ2a, and reaginic antibodies. There was no significant reduction in protection against oral challenge with eggs in these animals, indicating that reagin-mediated hypersensitivity reactions were not an essential component of the protective mechanism. However, systemic reagin sensitization was shown to result in an acceleration of the rate at which challenge organisms were destroyed in immune rats. By 12 h after infection most of the parasites had been killed in the livers of rats which had been both passively immunized and reagin-sensitized, whereas a large proportion survived in rats passively immunized, but not reagin-sensitized. This effect of reagin appeared to be limited to the early stages of resistance since parallel groups left for 21 days after challenge were shown to have been equally well protected. In an effort to determine if vasoactive amines liberated by reagin-mediated reactions could act directly on invading parasites, early larval stages of T. taeniaeformis were exposed to histamine or serotonin (5HT) in vitro or in vivo. Consistent results were not obtained, but significant inhibition (P<0.05) of viability of parasites exposed to histamine occurred on two occasions. Significant (P<0.01) inhibition of infectivity of T. taeniaeformis also resulted when peritoneal anaphylactic diffusate was introduced into isolated gut loops containing hatched embryos of the parasite. The results are discussed in terms of the possible means whereby reagins may participate in protective immunity to infectious organisms. [ABSTRACT FROM AUTHOR]

Weanling rats born of mothers infected with Taenia taeniaeformis were found to be passively protected against homologous challenge. Cross-fostering of normal suckling rats onto immune mothers established that passive transfer occurred via the colostrum and milk. Immunoglobulin fractions containing γA from immune colostrum were fed to 12-14-day-old rats for 4 days via stomach tube. Significant passive protection against challenge with T. taeniaeformis was achieved with γA from one of three colostrum pools. The effect of colostral γA preparations on the infectivity of freshly hatched oncospheres of T. taeniaeformis was measured by the intra-intestinal inoculation of immunoglobulin solutions into isolated gut loops containing hatched eggs of the parasite. γA from one of three pools of immune colostrum caused a significant reduction in the number of parasites which reached the liver. This appears to be the first time that protective activity against a hel- minth infection has been achieved with γA. A fraction of immune colostrum containing both 7Sγ1 and 7Sγ2 immunoglobulins was found to confer passive protection when inoculated parenterally. In view of the prolonged period of absorption (ca 18 days) of 7S immunoglobulins from the gut by the suckling rat, it seems likely that these antibodies are primarily responsible for the natural passive transfer of protection from mother to young. [ABSTRACT FROM AUTHOR]

The interaction between bovine peripheral blood monocytes and Trypanosoma brucei organisms in the presence of immune whole serum or specific purified IgM or IgG1 antibodies from infected cattle was investigated. Adherence of antibody-sensitized trypanosomes to freshly isolated monocytes from non-infected animals was not observed, confirming the absence of receptors for IgM and IgG1 on fresh monocytes. After in-vitro cultivation of the monocytes for at least 3 hr, adherence of IgM-sensitized trypanosomes was consistently demonstrable, while the adherence of lgG1-sensitized trypanosomes was not observed until the monocytes had been cultured for 7 days. The adherence of IgM-sensitized trypanosomes occurred in the absence of bovine complement and was Ca++-dependent, indicating that the interaction between sensitized trypanosomes and bovine monocytes was mediated through a specific combining site for monocytes in the Fc region of the IgM molecule rather than through a C3b receptor. In contrast to the monocytes from uninfected animals, freshly isolated peripheral blood monocytes from T. brucei- or T. congolense-infected cattle were capable of binding IgM- or IgG1-sensitized trypanosomes after only 30 min and 24 hr of in-vitro cultivation, respectively, suggesting that peripheral blood monocytes from infected animals were already in an `activated' state. Electronmicroscopic examination revealed that IgM- or IgG1-sensitized trypanosomes were rapidly engulfed and digested by the monoctycs. [ABSTRACT FROM AUTHOR]

We have identified cloned populations of trypanosomes, derived from different original field isolates and species, which appeared to possess similar variable surface-antigen types when assayed by immune lysis and immunofluorescence tests. Variable surface glycoproteins (VSGs) were isolated from these ‘isotypic’ trypanosomes. Isolated VSGs had identical apparent mol. wt of 60,000 but different isoelectric points. Radioimmunoassay, using 125I-labelled VSGs and rabbit anti-VSG sera, showed that isotypic VSGs contained not only the cross-reacting determinants found in all other VSGs (Barber & McGuire, 1978) but also other cross-reacting determinants shared between isotypes. Peptide mapping revealed extensive amino-acid sequence homology between isotype VSGs. [ABSTRACT FROM AUTHOR]