Prevalence of gastrointestinal helminth infections of dog in Enugu State, South Eastern Nigeria.

The prevalence of gastrointestinal helminth infections of dog in Enugu State, South Eastern Nigeria was studied retrospectively and prospectively. In the retrospective study, records of all diagnosed helminth infections of dogs brought to the University of Nigeria Veterinary Teaching Hospital, Nsukka from January, 2006 to September 2013 were collated and analyzed. The prospective study was carried out between October 2013 and July 2014 by examination of 263 faecal samples collected per rectum from dogs presented to a purposively selected Veterinary Clinics in Enugu metropolis and the Veterinary Teaching Hospital of the University of Nigeria, Nsukka. The results of the 8 year retrospective prevalence study gave an overall prevalence of 56.1% and Ancylostoma species as the most prevalent helminth in the study area (33.2%). Mixed infections with more than one helminth parasite species were recorded in 8.6% of the cases. Annual breakdown of the prevalence data showed that the highest prevalence was recorded in 2009. Breed and age of the dogs were found to significantly influence the prevalence. In the prospective study, an overall prevalence of 51.7% was obtained. Ancylostoma spp. was also found most often in the study area, with a prevalence rate of 33.6%. Mixed infections with more than one helminth parasite species were found in 16.3% of the cases. A strong association was obtained between prevalence and breed of the dogs and also between prevalence and season. Due to the zoonotic nature of most of the encountered parasites and the close association between children and dogs, routine deworming, proper management of dogs and adequate personal hygiene is therefore recommended.

Efficacy of repeated doses of diminazene aceturate (Dinazene®) in the treatment of experimental Trypanosoma brucei infection of Albino rats.

The efficacy of repeated doses of Dinazene® in Albino rats experimentally infected with Trypanosoma brucei (Gboko strain) was investigated. A total of 30 adult female Albino rats weighing 130-190 g were used for the study. They were assigned to six groups (groups A-F) of five rats each. Groups A-D were infected intraperitoneally with 1.0 × 106 trypanosomes in 400 µL of PBS diluted blood while groups E (uninfected treated) and F (uninfected untreated) served as controls. The rats in the groups A-D as well as those in group E were treated with 7.0 mg/kg body weight at day 11 post infection. Groups B, C and D however received two, three and four repeated doses of the drug at weekly intervals following initial treatment. There was complete clearance of the parasite within 120 h post treatment. Parasitaemia, packed cell volume (PCV), total red blood cell (RBC) and white blood cell (WBC) counts, haemoglobin concentration (Hb), rectal temperature, and body weight were used to assay the efficacy of treatment. Following treatment and parasite clearance from the blood, there was improvement (P<0.05) in the values of parameters measured when compared to the uninfected controls. However, relapse infection was observed in the rats of group A, B and C, with a resultant decline in clinical condition and values of parameters used to assess efficacy. We concluded that four consecutive treatments using same dose at weekly intervals proved efficacious in the experimental management of T. brucei infection in rats.

Efficacy of levamisole and ivermectin in the control of bovine parasitic gastroenteritis in the sub-humid savanna zone of southeastern Nigeria.

Faecal egg count reduction test was used to evaluate the efficacy of levamisole and ivermectin in the control of bovine parasitic gastroenteritis in a part of Nigeria not previously surveyed. Ninety (90) randomly selected N'dama cattle from two herds in Nsukka, Enugu State of Nigeria, were studied. The animals were divided into two groups, namely, levamisole and ivermectin treatment groups. Faecal samples were collected prior to the administration of the respective anthelmintic and faecal egg count/gram of faeces determined. Post-treatment faecal samples were collected after 10 and 14 days of levamisole and ivermectin administration, respectively, and faecal egg count (FEC) determined. Thereafter, the faecal egg count reduction was calculated based on the formula [Formula: see text]. Pooled faecal samples for the respective treatment groups were cultured for larval identification and count. Pre-treatment FEC showed that the animals were readily infected with gastrointestinal nematodes with mean FEC of 233.0 ± 35.13 and 302.0 ± 19.94, respectively, for the levamisole- and ivermectin-treated groups. Post-treatment FEC of 0 was recorded for both groups, showing a 100% reduction of the pre-treatment faecal egg count. We concluded that the anthelmintics used in this work were very effective in the control of bovine parasitic gastroenteritis in the study areas, and no resistance was detected.

The effect of dietary protein on the productivity of West African Dwarf (WAD) goats infected with Haemonchus contortus.

The effects of increased dietary protein on the performance of West African Dwarf (WAD) goats infected with Haemonchus contortus were investigated. 28 pubertal 9-12-month-old female goats were divided into two equal groups A and B and fed on high and low protein diets, respectively, from day 1 of pregnancy (day of mating) to 6 weeks post-partum. Each animal was trickle infected with a total of 2400 infective larvae of H. contortus over 4 weeks starting from day 1 of pregnancy and the prepatent period recorded. Live weights and body condition scores were measured weekly and the changes determined by subtracting the initial value from each of the subsequent values. Birth and weaning weights of kids as well as stillbirths and foetal loses were also determined. High protein diet improved the ability of goats to resist worm establishment and patency, which was manifested as significant increase in the prepatent period in group A than in the low protein diet group B (p<0.001). Also high protein diet resulted in significantly higher increase in body weight during pregnancy (p<0.01). During lactation both groups rapidly lost weight although body weight increase relative to preinfection value remained significantly higher in group A than B (p=0.05). Between weeks 3 and 13 post infection, the body condition scores increased but were significantly higher in group A than in group B (p<0.001). From weeks 16 to 27, the body condition scores remained significantly higher in group B than group A although both experienced severe losses during lactation. Group A delivered significantly heavier kids than group B (p<0.001) and had no foetal losses as occurred in the latter. However, the level of supplementation had no influence on weaning weights as there was no significant difference in the weaning weights of kids of both group (p>0.05). It is concluded that lactation demand for dietary protein is higher than that for gestation since both body weights and body condition scores deteriorated in both group during lactation, and that improved dietary protein enhances resistance to parasite establishment (increased prepatent period) and resilience in terms of kidding performance, birth weight and survival of neonates.

Enhanced survival of rats concurrently infected with Trypanosoma brucei and Strongyloides ratti.

The interaction between the blood protozoan parasite, Trypanosoma brucei and the gastrointestinal nematode parasite, Strongyloides ratti was studied in outbred white albino rats. Rats were grouped and given either single infection with T. brucei or S. ratti or concurrently infected with both parasites. Blood parasitaemia and packed cell volume, faecal egg/larva output, adult worm burden and survivability were monitored in order to assess the interactive effects of the infections. All trypanosome-infected rats became parasitaemic within 1 week of infection but surprisingly parasitaemia was higher in the single than concurrently infected group of rats. In addition all animals with single T. brucei infection had died by 14 days after the infection, whereas animals with concurrent infection were still alive by day 28 after the infection when the experiment was terminated. Concurrent infection resulted in significant increase in daily S. ratti egg/larval output in faeces (P < 0.01), but lesser number of adult worms were recovered from the intestine of sacrificed rats on day 8 post-infection. Taken together these results suggest that T. brucei and S. ratti interact in a manner that ameliorates their pathogenic effects resulting in a decrease in the level of parasitaemia and intestinal worm burden and in increased life span of the infected rats. These results differ from the classical immunosuppressive attributes of T. brucei and the results are discussed in the context of the possible immune responses that might have contributed to this outcome and the potential significance of the findings in alternative control method of trypanosomosis.

Clinical features of paragonimiasis cases recently found in japan: parasite-specific immunoglobulin M and G antibody classes.

We retrospectively analyzed clinical features in 30 patients who were referred to our laboratory and given a diagnosis of Paragonimus westermani infection in 1999. Our results indicate that pleurisy with eosinophilia and dominant immunoglobulin (Ig) M antibody are characteristic features of the early stage of paragonimiasis, whereas IgG antibody is dominant in the late stage. Thus, in addition to tests for parasite-specific IgG antibody, tests for IgM-class antibody should always be considered for patients with pleurisy in whom paragonimiasis is suspected.

Drug resistance in pathogenic African trypanosomes: what hopes for the future?

Trypanosomosis is a serious threat to both man and animals mostly in Africa. Although the first pathogenic trypanosome was discovered over a hundred years ago, there is still no prospect for effective control or eradication of the disease through the development and use of vaccines because of the phenomenon of antigenic variation. Control continues to rely heavily on chemotherapy and vector control strategies. This therapy and prophylaxis depends on the use of drugs which, apart from having been developed over 5 decades ago, suffer from such limitations as toxicity and with their continued use, drug resistance. Resistance to currently used drugs is a serious problem in most fields of anti-microbial chemotherapy, particularly in the case of trypanosomosis where resistance and cross-resistance in animals and man have been developing rapidly. The frequently and widely reported decreasing efficiency of available trypanocides, difficulties of sustaining tsetse control and little hope that a conventional, anti-trypanosome vaccine will be produced in the near future, increase the imperative need for new drugs and alternative effective ways for the control of trypanosomosis. This review examines aspects of drug resistance in pathogenic trypanosomes, measures to minimise it, areas of future research in new drug targets and alternative control strategies. Based on these, it is our opinion that for now the management and control of trypanosomosis will continue to depend on proper usage of the few available trypanocides, especially strategic deployment of the sanative drugs in order to reduce the development of drug resistance, in addition to the continued use of environmentally friendly vector control programmes such tsetse trapping.

Clinical features and parasite-specific IgM/IgG antibodies of paragonimiasis patients recently found in Japan.

Clinical features of a total of 30 paragonimiasis westermani patients referred to and diagnosed in our laboratory in 1999 were analyzed retrospectively. Most patients were middle-aged (average: 48 years, range: 13-72 years) with the male/female ratio of 19/11. Over 70% of the patients had respiratory symptom and over 80% had peripheral blood eosinophilia and high serum IgE level. All but two cases had radiologic abnormalities on the chest X-ray. Only in 3 cases were Paragonimus eggs detected in the sputum smear. We classified the patients into two groups depending on the chest X-ray findings: patients having pleurisy alone and those having nodular/cavitating lesions in the lung parenchyma. We measured parasite specific IgM/IgG antibodies in all patients sera by microplate ELISA. The mean parasite-specific IgM/IgG antibody ratio was significantly higher in the parenchymatous lesion group than in the pleurisy group. While IgM antibody titer had a strong positive correlation with the degree of eosinophilia in peripheral blood, IgG antibody titer had an inverse correlation. Although the degree of eosinophilia in peripheral blood was higher in the pleurisy group than in the parenchymatous lesion group, total IgE level in serum was comparable between the two groups. The present results indicate that pleurisy with eosinophilia and dominant IgM antibody are the characteristic features of the early stage of paragonimiasis, whereas parenchymatous lesions in lungs with low grade eosinophilia and dominant IgG antibody are of the late stage. These results suggest that detection of IgM antibody should always be considered for the immunodiagnosis for paragonimiasis-suspected patients with pleurisy.

Mucosal defense against gastrointestinal nematodes: responses of mucosal mast cells and mouse mast cell protease 1 during primary strongyloides venezuelensis infection in FcRgamma-knockout mice.

A possible role for the gamma subunit of immunoglobulin Fc receptors (FcR) in mucosal defenses against intestinal nematode parasites was studied using age-matched FcRgamma-knockout (FcRgamma(-/-)) and wild-type (FcRgamma(+/+)) C57BL/6 mice. Mice were infected subcutaneously with 3,000 infective larvae of Strongyloides venezuelensis, and the degree of infection was monitored by daily fecal egg counts and adult worm recovery on days 8 and 13 postinfection. Mucosal mast cell (MMC) responses were assayed by in situ intestinal mast cell counts in stained histological sections of the jejunum and by measuring mouse mast cell protease 1 (MMCP-1) release in serum using sandwich enzyme-linked immunosorbent assay. FcRgamma(-/-) mice had significantly higher egg counts (P<0.01) and numbers of adult worms (P<0.05) than FcRgamma(+/+) mice, but mastocytosis and serum MMCP-1 release were comparable. It was concluded that MMCP-1 release may be spontaneous, does not depend on mast cell degranulation via the FcRgamma signaling system, and appears to play no role in the expulsion of S. venezuelensis. The delay in worm expulsion in the FcRgamma(-/-) mice might be related to inability of the MMC to degranulate and release effector molecules other than MMCP-1, since FcRgamma deletion abrogates mast cell degranulative responses.

Effects of the depletion of CD8(+) T cells and monocytes on the proliferative responses of peripheral blood leucocytes from Trypanosoma evansi-infected sheep.

Sheep peripheral blood mononuclear cells and those depleted of CD8(+) T cells and/or monocytes were stimulated with polyclonal mitogens and specific antigens, and analysed by means of cell proliferation assay procedure to examine whether these cell populations are involved in Trypanosoma evansi-induced immunosuppression. The removal of CD8(+) T cells failed to normalize the proliferative responses of peripheral blood mononuclear cells from infected sheep to concanavalin A stimulation while the depletion of monocytes resulted in full and enhanced response, showing that macrophages are mainly responsible for the suppression. Although the depletion of CD8(+) T cells, monocytes or both restored the responses of the cells to lipopolysaccharide stimulation, the responsiveness of the undepleted cells to this mitogen was significantly higher from day 24 post infection (p<0.01). The results were discussed in relation to current known mechanisms of depressed lymphocyte proliferation in tsetse-transmitted African trypanosome infections.

Murine model study of the practical implication of trypanosome-induced immunosuppression in vaccine-based disease control programmes.

The relevance of trypanosome-induced immunosuppression in relation to the efficacy of vaccine-induced immunity was studied in mice. Mice were immunised with crude Trichinella spiralis muscle larvae homogenate vaccine and infected with T. spiralis and/or Trypanosoma brucei. Vaccination significantly decreased adult worm burden (p<0. 05) and accelerated worm expulsion in mice infected with T. spiralis only. T. brucei superinfection resulted in monocytosis, suppressed eosinophilia, significant decrease in PCV (p<0.001), higher numbers of adult worms (p<0.001) and failure to expel all adult worms by Day 12 post infection (p.i.). Regardless, they produced anti-Trichinella IgG(1) responses similar to those of the vaccinated non-T. brucei-infected group. T. brucei also suppressed the proliferative responses of spleen cells to stimulation with Con A and T. spiralis antigen, and induced strong production of interferon-gamma (IFN-gamma) in culture supernatants of antigen stimulated spleen and mesenteric lymph node cells. Interleukin-5 (IL-5) production was suppressed by T. brucei in supernatants of Con A- and antigen-stimulated spleen cells. It was concluded that trypanosome infections and the associated immunosuppression are of great practical significance in trypanosome endemic areas, especially with regards to disease control programmes involving vaccine-induced herd immunity.

Mucosal immunity against parasitic gastrointestinal nematodes.

The last two decades witnessed significant advances in the efforts of immunoparasitologists to elucidate the nature and role of the host mucosal defence mechanisms against intestinal nematode parasites. Aided by recent advances in basic immunology and biotechnology with the concomitant development of well defined laboratory models of infection, immunoparasitologists have more precisely analyzed and defined the different immune effector mechanisms during the infection; resulting in great improvement in our current knowledge and understanding of protective immunity against gastrointestinal (GI) nematode parasites. Much of this current understanding comes from experimental studies in laboratory rodents, which have been used as models of livestock and human GI nematode infections. These rodent studies, which have concentrated on Heligmosomoides polygyrus, Nippostrongylus brasiliensis, Strongyloides ratti/S. venezuelensis, Trichinella spiralis and Trichuris muris infections in mice and rats, have helped in defining the types of T cell responses that regulate effector mechanisms and the effector mechanisms responsible for worm expulsion. In addition, these studies bear indications that traditionally accepted mechanisms of resistance such as eosinophilia and IgE responses may not play as important roles in protection as were previously conceived. In this review, we shall, from these rodent studies, attempt an overview of the mucosal and other effector responses against intestinal nematode parasites beginning with the indices of immune protection as a model of the protective immune responses that may occur in animals and man.

Trypanosome-induced suppression of responses to Trichinella spiralis in vaccinated mice.

Mice vaccinated against the gastro-intestinal (GI) nematode Trichinella spiralis by injection of muscle larval homogenate antigen express a strong immunity to subsequent infection, reflected in earlier expulsion of adult worms from the intestine and reduced female worm fecundity. Infection with Trypanosoma brucei at the time of vaccination, or at the time of infection with T. spiralis, significantly reduced the level of immunity expressed, the effect being greatest when vaccination and T. brucei infection were given together. Trypanosome infection reduced T. spiralis-specific antibody responses in vaccinated mice, the effect being most apparent against IgM, IgG1 and IgG2b, and ablated the eosinophil response to T. spiralis. In vaccinated mice infected with both trypanosomes and T. spiralis, the proliferative responses of lymphocytes to the mitogen Con A or to T. spiralis antigen were much lower than in vaccinated mice infected only with the nematode. Whereas cells from mice infected only with T. spiralis produced the cytokine IL-4 and little or no IFNgamma when stimulated in vitro, cells from animals infected with T. spiralis and with trypanosomes released large amounts of IFNgamma but no IL-4. These observations are consistent with the known, IFNgamma-dependent, nitric-oxide-mediated suppressive effects of trypanosomes on lymphocyte function and the Th1 bias associated with these infections, both of which reduce the effectiveness of the Th2-mediated responses involved in immunity against GI nematode infections. The data are discussed in the context of the possible use of vaccines against GI nematodes in ruminants in countries where concurrent trypanosome-GI nematode infections are widespread.

Changes in peripheral blood lymphocyte subpopulations and parasite-specific antibody responses in Trypanosoma evansi infection of sheep.

This paper reports on changes in the lymphocyte composition of the peripheral blood in sheep infected with Trypanosoma evansi. In addition, parasite-specific IgG1 and IgM antibody responses were monitored using a double-sandwich enzyme-linked immunosorbent assay (ELISA) technique. Eight sheep were infected with 2 x 10(6) T. evansi TREU 2143. The infection was characterised by chronicity and ended in self-cure in two of the sheep. These two sheep were designated group A, whereas the other six sheep, which remained parasitaemic until treated, were designated group B. Analysis of the peripheral blood lymphocytes (PBLs) by indirect immunofluorescence staining and flow cytometry revealed significant alterations in the numbers of T- and B-cell subsets detected in all infected sheep. In group A, whereas the numbers of CD8+ cells decreased, CD4+ cells showed marginal decreases, remaining at or above pre-infection figures and resulting in increase in the CD4:CD8 ratio. In group B, CD8+ cells showed few marginal decreases, being at or above pre-infection figures most of the time, whereas CD4+ cells decreased significantly from day 26 post infection (p.i.) such that the CD4:CD8 ratio decreased. Infection also resulted in significant increases (P < 0.001) as of day 26 p.i. in circulating B-cells in group B as shown by the numbers of sIg+, CD45R+, CD1+ and major histocompatibility complex (MHC) II+ cells. The increases, however, were moderate and biphasic in group A. T. evansi-specific IgM and IgG1 antibody isotypes were detected in all infected sheep, but their levels were significantly higher in group A than in group B (IgM P < 0.05; IgGI P < 0.01). In addition, although an initially higher level of IgM response was subsequently replaced by a higher level of IgG1 response in group A, this was never the case in group B until after drug treatment.

Proliferative responses of peripheral blood leucocytes of sheep infected with Trypanosoma evansi.

The effects of Trypanosoma evansi on the proliferative responses of ovine peripheral blood leucocytes (PBL) were examined in in vitro cell culture systems. Sheep were vaccinated against pneumonic pasteurellosis with a monovalent Pasteurella haemolytica vaccine and then infected with T. evansi TREU 2143. From 1 week post-infection (p.i.), the PBL were separated and stimulated in cultures with either Concanavalin A (Con A), bacterial lipopolysaccharide (LPS), pasteurella antigen (P.ag), or homologous trypanosome antigen (T.ag). The proliferative responses of the cells to Con A and LPS were significantly (P < 0.001) suppressed by the infection. This suppression was associated with active infection, as treatment of the sheep with a trypanocide restored the proliferative ability of the cells to both mitogens. Similarly, active infection significantly (P < 0.001) suppressed specific responses to P.ag and T.ag but although treatment resulted in full specific proliferative responsiveness to the homologous trypanosome antigen, the same was not true of P.ag, in which the responsiveness of cells from uninfected vaccinated sheep to it were still significantly higher (P < 0.001) than those of cells from infected sheep.

Increase in CD5+ B cells and depression of immune responses in sheep infected with Trypanosoma evansi.

The effects of Trypanosoma evansi on the cellular and humoral immune responses of sheep to Pasteurella haemolytica vaccine were studied. Peripheral blood lymphocytes (PBLs) from the sheep were analysed using single and double-colour indirect immunofluorescence staining and flow cytometry to monitor changes in circulating B and T cell subsets. Serum antibody responses were assayed using the enzyme-linked immunosorbent assay technique (ELISA), in addition to measuring local skin reactions at the site of vaccine administration. Results showed significant increases in circulating B cells in all sheep after the primary (p < 0.01) and secondary (p < 0.001) vaccinations although the increases were much more dramatic in the T. evansi-infected sheep. In addition, infection induced significant increases (p < 0.004) both in proportions and numbers of CD5+ B cells with more than 70% of circulating B cells expressing the CD5 antigen and showed significant differences (p < 0.01) from those of control sheep in which vaccination alone failed to induce similar increases. Also, infection resulted in significant decreases in CD5+ (p < 0.003), CD4+ (p < 0.03) and CD8+ (p < 0.03) T cell subsets in contrast to their increases in all control animals after vaccination. Moreover, there were significant suppression of both local skin reaction (p < 0.005) and serum Ig and IgG1 (p < 0.001) antibody responses to the vaccine antigen.

Induction of CD4+CD8+ double positive T cells and increase in CD5+ B cells in efferent lymph in sheep infected with Trypanosoma evansi.

The effects of Trypanosoma evansi on efferent lymphocyte phenotypes draining from a lymph node primed with Pasteurella haemolytica vaccine were studied in sheep. The prefemoral efferent lymphatic ducts of the infected sheep along with those of two uninfected sheep were surgically cannulated. Lymph was collected and lymphocytes recovered from it analysed by two-colour indirect immunofluorescence staining and cytofluoremetry in a fluorescence activated cell analyser (FACSCAN). The study showed the appearance and persistence of T. evansi in the efferent lymph for a long period of time and the appearance of CD4+CD8+ (double positive, DP) T lymphocytes in the efferent lymph of infected animals. The infection also resulted in increases in CD5+ B cells in the prefemoral efferent lymph. In addition, there were decreases in the output of conventional B cells, CD5+ and CD4+ T cell subsets but large increases in CD8+ cells followed by terminal depletion of all cell subsets. In contrast, inoculation of sheep with pasteurella vaccine antigen alone produced little alterations in the proportions, but large increases in the numbers of all T cell subsets except that of CD8+ cells which also showed little variation; and there was a concurrent increase in the numbers and proportions of efferent B cells. In addition, the abnormal expression of DP and CD5+ B cells did not occur in the uninfected vaccinated sheep. It is concluded that these abnormal changes in the kinetics of efferent lymphocyte phenotypes are likely to play a role in the genesis of the generalized immunosuppression seen in trypanosome-infected hosts.

Effects of Trypanosoma evansi on the output of cells from a lymph node draining the site of Pasteurella haemolytica vaccine administration.

The prefemoral efferent lymphatics of sheep infected with Trypanosoma evansi and inoculated with P. haemolytica vaccine and of those given only the vaccine, were surgically cannulated to study the effects of the infection on the total cellular output and output of blast cells from the node in response to the vaccine. T. evansi delayed and depressed the increases in total cell and lymphoblast outputs. In uninfected sheep, the total cellular output increased and peaked at more than twice the prevaccination values on days 4 and 5 after primary vaccination, but the increases were smaller and peaked on days 6 and 8 after primary vaccination in the infected sheep. The output of lymphoblasts mirrored the total cell output, though it was suppressed to a greater degree by T. evansi. The output of blasts peaked at more than 8 and 14 times the prevaccination values in the uninfected animals after primary and secondary (booster) vaccinations, respectively; but in infected animals, it peaked at twice the prevaccination values after the primary vaccination and showed no increase after booster vaccination until 11 days later. It is concluded that the inhibition of total and blast cell outputs by T. evansi may limit the early systemic dissemination of antigen-specific cells, thus playing a role in the induction of immunosuppression by the parasite.

Haematological changes in sheep experimentally infected with Trypanosoma evansi.

Sheep were infected with 2 x 10(6) Trypanosoma evansi TREU 2143 through the external jugular vein. The parasite kinetics as well as the effects on body temperature, packed cell volume (PCV), erythrocyte counts and total and differential white blood cell counts were monitored twice weekly for 3 months. The results showed that T. evansi produced a chronic form of the disease in sheep characterised by low-level and often cryptic parasitaemia, with self-cure occurring in two cases; mild anaemia as evidenced by decreases in PCV and erythrocyte counts; and significant (P < 0.02) leucocytosis by day 22 post infection (p.i.). The leucocytosis was a result of marked lymphocytosis whose significant rises (P < 0.02) parallelled the rises in total white blood cell (TWBC) counts. These changes were less obvious in the animals that underwent self-cure. We conclude that T. evansi produces pathological changes in the peripheral blood of sheep similar to those produced by its tsetse-transmitted counterparts. It would thus appear that the sheep/T. evansi model is suitable for long-term study of the immunopathology of pathogenic trypanosomes since the sheep is easily available, easy to handle and a natural host to all pathogenic trypanosomes.

Taenia solium cysticercosis and human taeniasis in the Nsukka area of Enugu State, Nigeria.

The prevalence of Taenia solium cysticercosis in slaughter pigs and of taeniid ova in hospital patients were determined in the Nsukka area of Enugu State, Nigeria, in March 1986-September 1988 and May 1986-May 1988, respectively. Cysticercus cellulosae were detected in the pigs by ante-mortem examination of the pigs' tongues and detailed post-mortem examination of the dressed pig carcasses using standard meat-inspection procedures. Human infection was assessed by examining iodine-stained stool samples collected from patients from one selected hospital in the study area. Over 20% (483) of the 2358 trade pigs examined were found infected with C. cellulosae. Most of the cases were generalized, all the musculature being heavily infested with live cysticerci. The age and sex of the pig and the season of the year in which it was examined had no significant effect on the occurrence of cysticerci in the animals (P > 0.01) but there was a highly significant year-to-year decrease (P < 0.001) in the prevalence of cysticerci. The overall prevalence of taeniid ova in the 1525 human-stool samples analysed was 8.6%, most (78.6%) of the cases occurring in adults aged > 30 years. The epidemiological factors which might have influenced these results are identified and discussed, and suggestions are made for the control of this important zoonosis.