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Biomedical subjects

G Mohammed

Publications and source records attributed to G Mohammed.

6 recordsLinked to original sources

Studies of infectivity and pathogenicity of an isolate of Trypanosoma evansi in Yankasa sheep.

The course of experimental infection and pathogenicity of an isolate of Trypanosoma evansi were investigated using eight infected and six uninfected control Yankasa sheep. The sheep were each infected intravenously via the jugular vein with approximately 2.0 x 10(6) T. evansi parasites. The effects of the parasite on body temperature, packed cell volume (PCV), haemoglobin, erythrocytes, total protein, were monitored three times a week for approximately 9 weeks. Body weights were determined once every week for the duration of the experiment. The results showed that all the infected sheep were positive for the parasite. The prepatent period varied between 3 and 6 days. T. evansi produced parasitaemic waves at an average of 8.3 days interval. Two distinct forms of the disease were produced namely, acute (4-14 days postinfection), and chronic (43-59 days postinfection). Anaemia was a distinct feature of the disease. While the mean rectal temperatures were significantly elevated (P < 0.05), the mean values of the haematological parameters of the infected sheep dropped significantly (P < 0.05) compared to the preinfection levels. Observed clinical signs included pale mucous membrane, epiphora, loss of appetite, emaciation, dullness and rough hair coat together with fluctuating pyrexia which in most cases coincided with rise in parasitaemia. It is suggested that the isolate of T. evansi is pathogenic for Yankasa sheep.

Animals↗

Reduced ovulatory and oestrous activity in zebu heifers following Trypanosoma vivax infection.

This paper describes a study on the oestrous and ovarian activity and responses to prostaglandin F2 alpha (PGF2 alpha) administration and artificial insemination in zebu heifers. Four cycling heifers were artificially infected with 5 x 10(6) Trypanosoma vivax organisms. Two heifers served as controls. Two injections of PGF2 alpha were given 11 days apart, commencing at the peak of parasitaemia in the infected animals, followed by artificial insemination 72 and 96 h after the second administration of PGF2 alpha. Sera were analysed for progesterone by radioimmunoassay, while ovarian activity and oestrus were determined by rectal palpation and visual observation, respectively. All the infected heifers developed the clinical disease. All control and infected heifers had progesterone profiles consistent with luteolysis and the occurrence of oestrus following the second administration of PGF2 alpha. Progesterone levels did not return to normal luteal values in infected animals, however, whilst they did so in control animals. No control or infected heifers became pregnant. The findings suggest that PGF2 alpha will induce a non-fertile oestrus in zebu heifers acutely infected with T. vivax. Re-ovulation is also inhibited within 22 days in a majority of infected animals.

Animals↗

Trypanosoma (Nannomonas) godfreyi sp. nov. from tsetse flies in The Gambia: biological and biochemical characterization.

We provide evidence from isoenzyme analysis, hybridization with repetitive DNA probes, behavioural studies and morphometrics that 4 trypanosome isolates from Glossina morsitans submorsitans in The Gambia constitute a new species now named Trypanosoma (Nannomonas) godfreyi. The bloodstream trypomastigotes of T. (N.) godfreyi are relatively small with a mean length of 13.7 microns (range: 9.1-21.8 microns) and a mean width of 1.65 microns (range: 0.65-2.69 microns). There is no free flagellum and the marginal kinetoplast is subterminal to a rounded posterior end; the undulating membrane is usually conspicuous. As with other Nannomonas, T. godfreyi developed in the midgut and proboscis of Glossina and infections matured in 21-28 days in laboratory G.m. morsitans. In The Gambia the normal vertebrate host appears to be the warthog, Phacochoerus aethiopicus, although elsewhere other wild and domestic suids may also be implicated in the life-cycle. T. godfreyi was identified unequivocally using a 380 bp DNA probe specific for a major genomic repeat sequence; its isoenzyme profile distinguished it clearly from T. simiae and three strain groups of T. congolense: savannah, riverine-forest and kilifi.

Animals↗

T cell function in children with acute lymphoblastic leukaemia.

Modern intensive chemotherapy has dramatically improved the prognosis of acute lymphoblastic leukaemia (ALL) in children. However, once remission has been established, quality of life and even survival may be threatened by exacerbation of viral infections in the prolonged period of continuation therapy necessary to prevent relapse. Often the viruses involved in the most severe infections are from the herpesvirus and paramyxovirus groups, suggesting that patients suffer from a defect in the cellular immunity thought essential to control such cell-associated infections. This may result from a T cell defect and, in this study, T cell responsiveness of patients under therapy for leukaemia has been investigated. In vitro proliferative responses of peripheral blood leucocytes (PBL) to the T cell mitogen phytohaemagglutinin (PHA) were impaired in children with ALL before treatment and in the induction of remission. Impairment was attributable to reduced T cell numbers, the presence of inhibitors in the patient's serum and direct damage to lymphocytes. On achieving remission, proliferative responses to PHA of both CD4+ and CD8+ T cell subsets quickly returned to normal levels with the switch to continuation chemotherapy. Proliferative responses to Herpes simplex virus antigens were also apparently normal in the majority of patients tested in remission. Further investigations, however, have suggested a persisting defect in CD8+ lymphocyte function. Gamma interferon secretion by PHA-stimulated PBLs was severely reduced for children with ALL in remission when compared with control children of similar age. Further, cytotoxic T lymphocyte responses to allogeneic cells could only be induced in PBL isolated from two of 13 children in remission from ALL whilst all control children of similar age and adults produced anti-allogeneic responses.

Adolescent↗