<span style="font-family: arial,helvetica;"><em>Ehrlichia canis</em> is an intracellular pathogen that causes canine monocytic ehrlichiosis. Although the role of antibody responses cannot be discounted, control of this intracellular pathogen is expected to be by cell mediated immune responses. The immune responses in dogs immunized with inactivated <em>E. canis</em> organisms in combination with Quil A were evaluated. Immunization provoked strong humoral and cellular immune responses, which were demonstrable by Western blotting and lymphocyte proliferation assays. By Western blotting antibodies to several immunodominant <em>E. canis</em> proteins were detected in serum from immunized dogs and antibody titres increased after each immunization. The complement of immunogenic proteins recognized by the antisera were similar to those recognized in serum from infected dogs. Upon challenge with live <em>E. canis</em>, rapid anamnestic humoral responses were detected in the serum of immunized dogs and primary antibody responses were detected in the serum from control dogs. Following immunization, a lymphocyte proliferative response (cellular immunity) was detected in peripheral blood mononuclear cells (PBMNs) of immunized dogs upon stimulation with <em>E. canis</em> antigens. These responses were absent from non-immunized control dogs until after infection with live <em>E. canis</em>, when antigen specific-lymphocyte proliferation responses were also detected in the PBMNs of the control dogs. It can be thus concluded that immunization against canine monocytic ehrlichiosis may be feasible. However, the immunization regimen needs to be optimized and a detailed investigation needs to be done to determine if this regimen can prevent development of acute and chronic disease.</span>

<span style="font-family: arial,helvetica;">The objective was to develop a non-terminal, acute normovolaemic anaemia model in dogs that has minimal effects on patient well-being. Eleven normal Beagle dogs were used. About 20 % of the circulating blood volume was removed from the jugular vein 1-3 times per day over a 3-4 day period until a haematocrit (Ht) of 13-17 % was obtained. Normovolaemia was maintained by replacing the volume deficit of the red blood cells with Ringer's lactate and re-infusing the plasma. Full blood count and Ht were monitored twice daily. The 13-17 % Ht was reached within 3-4 days with the number of phlebotomies ranging from four to seven. The model was primarily developed to determine echocardiographic values as well as Doppler abdominal splanchnic blood flow parameters in anaemic dogs as part of a study that will compare these results to similar studies in babesiosis-induced anaemia. The model may also be useful in the evaluation of the pathophysiology of anaemia in dogs or as a model for anaemia in humans.</span>

<table border="0" width="100%"><tbody><tr><td width="85%" align="left" valign="top"><span style="font-family: arial,helvetica;">Lumpy skin disease (LSD) is a disease of cattle, primarily in Africa and Madagascar and rarely in the Middle East. It is caused by a capripoxvirus that belongs to the family Poxviridae. The disease is of economic importance in endemic areas. Effective control of LSD requires accurate and rapid laboratory techniques to confirm a tentative clinical diagnosis. Comparative studies on different diagnostic tests used at different stages of the disease have not been done. The aim of this study was to compare several of these tests. <br />Six seronegative bulls, between 11 and 20 months of age, were infected intravenously and kept in an insect-free facility. The course of the infection was monitored. During a 3-month period blood samples and skin biopsies were collected for virus isolation and polymerase chain reaction (PCR). Skin biopsies were also examined using transmission electron microscopy (TEM). <br />The incubation period in infected animals varied from 4-5 days. The length of the viraemic period did not correlate with the severity of clinical disease. Viraemia was detected from 1-12 days using virus isolation and from 4-11 days using the PCR, which is longer than has previously been reported. Virus was isolated from skin biopsies until Day 39 post infection (p.i.) and PCR could demonstrate viral DNA until Day 92 p.i. Transmission electron microscopy of negatively stained skin biopsies detected LSD virus only in one of the four bulls that developed skin lesions until Day 33 p.i. <br />The PCR was a fast and sensitive method to demonstrate viral DNA in blood and skin samples. It could detect viral nucleic acid in skin lesions 53 days longer than virus isolation. Virus isolation from blood and skin samples was sensitive and reliable, but as a single test it may be too time-consuming to use although this depends on how rapidly the diagnosis must be confirmed. <br />In conclusion, this study showed the PCR to be superior in detecting LSD virus from blood and skin samples. However, virus isolation is still required when the infectivity of the LSD virus is to be determined.</span></td></tr> <tr><td align="right" valign="top"><span style="font-family: arial,helvetica;"><strong>Indexed by</strong></span></td> <td width="85%" align="left" valign="top"><span style="font-family: arial,helvetica;">Sabinet Online</span></td></tr></tbody></table>

<span style="font-family: arial,helvetica;">The lectin-binding characteristics of the epithelial lining of the thoracic air sacs of the chicken were determined. Con A, LCA and PSA bound to the apical membrane as well as to the cytoplasm distal to the nucleus of the surface epithelium, indicated the presence of <span style="font-family: Symbol;" lang="AF"><span>a</span></span>-linked mannose as well as Nacetylchitobiose- linked <span style="font-family: Symbol;" lang="AF"><span>a</span></span>-fucose residues in the glycoproteins. GSL I bound to the apical membrane and cytoplasm distal to the nucleus, but not to the cilia of the epithelium, where-as MPL, DBA and RCA120 bound to the apical membrane, cilia and cytoplasm, indicated the presence of <span style="font-family: Symbol;" lang="AF"><span>a</span></span>-linked Nacetylgalactosamine residues. However, neither SJA or SBA showed any binding, indicating the absence of <span style="font-family: Symbol;" lang="AF"><span>b</span></span> anomers of galactosyl (<span style="font-family: Symbol;" lang="AF"><span>b</span></span>1.3)N-acetylgalactosamine and <span style="font-family: Symbol;" lang="AF"><span>b</span></span>-linked N-acetylgalactosamine residues. UEA I bound to the apical membrane and cilia, as well as to the cytoplasm of a few cells, indicated the presence of <span style="font-family: Symbol;" lang="AF"><span>a</span></span>-linked fucose residues. PNA bound to the apical membrane of some, but not all, surface epithelium cells, indicated the presence of galactosyl (<span style="font-family: Symbol;" lang="AF"><span>b</span></span>1.3)N-acetylgalactosamine residues. WGA bound to the apical membrane and cilia, as well as to the cytoplasm of a few cells, indicated the presence of neuraminic acid residues.</span>

<span style="font-family: arial,helvetica;">Three hundred and eighty-four samples of leaf litter, soil, faeces from domestic and game animals, compost and aqueous cultures of infective nematode larvae contaminated with unidentified fungi were plated out on water agar, baited with pure infective larvae of <em>Haemonchus contortus</em>, incubated and examined for the presence of nematophagous fungi. <br /><em>Duddingtonia flagrans</em> was isolated from five samples, and 73 samples were positive for other nematophagous fungi.</span>