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Biomedical subjects

M Tanner

Publications and source records attributed to M Tanner.

At least 271 records · Page 15Linked to original sources
PubMed1981

Risk factors for staphylococcal toxic-shock syndrome.

Fifty-two cases of toxic-shock syndrome that occurred in January 1, 1976 through August 31, 1980, were reported to the Utah State Health Department between February 1 and August 31, 1980. The annual attack rate for Utah based on a six-month surveillance period was 14.4 per 100,000 women ages 12-49 years. All cases were in women who had onset of illness within two days of menses. Potential risk factors were investigated with a case-control study utilizing 29 women hospitalized with toxic-shock syndrome and 91 neighborhood female controls. Nine of the 29 (31%) women reported recurrences of similar illness. Use of tampons (p = 0.012) and use of a single brand of tampon-Rely-during the month of illness (p less than 0.005, RR =6.11) were associated with a significantly increased risk of acquiring toxic-shock syndrome. More controls were sexually active than women who had toxic-shock syndrome (p less than 0.05, RR - 0.277). This epidemiologic investigation of toxic-shock syndrome in menstrual-age women has identified tampons generally and a single brand specifically as significant risk factors in acquiring toxic-shock syndrome.

Adolescent↗
PubMed1981

Dipetalonema viteae (Filarioidea): development of the infective larvae in vitro.

The development of Dipetalonema viteae third stage larvae was attempted in vitro. A monophasic culture system consisting of BHK-21 medium supplemented with 10% tryptose-phosphate broth and 15% fresh jird serum allowed the growth of previously in vivo triggered larvae, but not of those isolated from ticks. The larvae could complete their third moult and grew on a fourth stage larvae up to 5 mm. This development was comparable to that observed in vivo. The presence of an irradiated hamster kidney cell feeder layer could replace an in vivo trigger. The development of the infective larvae took place up to the third moult. Some larvae completed the moult to the fourth stage and reached a maximum length of 3 mm after 14 days. These culture systems offer the possibility to study in vitro the complete development of the infective larvae to fourth stage larvae.

Animals↗
PubMed1980

Characterization of Trypanosoma brucei isolated from lymph nodes of rats.

Forms of Trypanosoma brucei isolated from lymph nodes of cyclically or intravenously infected rats, at different stages of infection, were morphologically compared with the corresponding bloodstream forms. Unlike the pleomorphic bloodstream trypanosome population, the lymph node trypanosome population was essentially monomorphic and resembled the slender forms of the bloodstream. Values for the morphometric parameters indicated a position between the slender and the stumpy forms. The number of trypanosomes/ml of blood showed the well-known periodic fluctuations while the number of trypanosomes/g of lymph node remained fairly constant. Serology revealed that lymph node trypanosome populations differed antigenically from the trypanosome populations isolated simultaneously frrom the bloodstream.

Animals↗
PubMed1980

Studies on the mechanisms supporting the continuous growth of Trypanosoma (Trypanozoon) brucei as bloodstream-like form in vitro.

The conditions which enable growth of Trypanosoma (T.) brucei stock S 427 as bloodstream-like form over bovine fibroblast-like cells (BHF) were analyzed. The experiments with different BHF conditioned media indicated that there is no stable factor produced by the BHF which can trigger growth as bloodstreamlike form. Only living, actively metabolizing BHF could support continuous growth. The intercellular localization of trypanosomes in the BHF feeder-layer was a main feature of an intact culture. The number of trypanosomes per mm(2) BHF-layer was fairly constant. Light- and scanning electron microscopy revealed that there is no regular arrangement of the intercellular trypanosomes. No contact structures such as desmosomes or hemidesmosomes could be observed between trypanosomes and the BHF by transmission electron microscopy. Whenever trypanosomes were separated from the BHF by micropore membranes in different chamber systems the continuous growth as bloodstream-like form was no longer possible. An obligatory short-term trypanosome/BHF association is therefore assumed as growth trigger. Whether this inductive shortrange signal is transmitted by an exchange of unstsable, low concentrated factors or by cell contact interactions is not yet clear. The fibroblast surface antigen, fibronectin, did not seem to be involved in mediating the trypanosome/BHF association.

Animals↗
PubMed1980

Studies on Dipetalonema viteae (Filarioidea). 5. Ultrastructural aspects of the antibody-dependent cell-mediated destruction of microfilariae.

The antibody-dependent cell-mediated destruction of Dipetalonema viteae microfilariae was followed by electron microscopy both in vitro and within micropore chambers in vivo. There was a correlation between the degree of adherence (1% mf with adhered cells) and the degree of microfilarial damage. Polymorphonuclear leukocytes, predominantly neutrophils, seemed to be responsible for the destruction of microfilariae in vivo. An in vitro assay indicated that eosinophils also have a role as potent effectors against microfilariae. The first sign of microfilarial damage is the disintegration of cuticular layers. In a later stage of destruction, lysis of the hypodermis or even of the whole microfilarial tissues was observed.

Animals↗
PubMed1979

Development of Dipetalonema viteae third-stage larvae (Nematoda: Filarioidea) in micropore chambers implanted into jirds, hamsters, normal and immunized mice.

Development of third-stage larvae of Dipetalonema viteae within subcutaneously implanted micropore chambers proceeded in all hosts tested up to the fourth-stage larvae and occasionally to adolescent worms. In the jird the timing of development was comparable to a natural infection. Although the mouse is an insusceptible host, larval development could take place, but was very slow. Two intraperitoneal inoculations of living third-stage larvae into mice induced the production of antibodies against the larval cuticle and against common antigens. In such immune mice the development of third- and fourth-stage larvae within micropore chambers was significantly inhibited, larval mortality was increased, and the larval motility was impaired.

Animals↗
PubMed1979

Studies on Dipetalonema viteae (Filarioidea) 3. Antibody-dependent cell-mediated destruction of microfilariae in vivo.

Antibody-dependent cell-mediated destruction of Dipetalonema viteae microfilariae could be demonstrated in the golden hamster using a micropore chamber technique. Microfilariae were eliminated within 24 hours in chambers of 3.0 and 5.0 microm pore size when implanted into amicrofilaremic hamsters (week 30 post infection). At peak microfilaremia (week 12 post infection), only some hamsters could efficiently destroy microfilariae. In chambers with 0.3 microm pore size, microfilariae survived for more than 3 weeks in all hamsters. In uninfected hamsters, microfilariae could only be eliminated if they had been preincubated with serum or its 19S fraction containing antibodies to the cuticle of microfilariae. The opsonizing activity of the serum was abolished by 2-mercaptoethanol treatment. The composition of cells adhering to microfilariae was always significantly different from the composition of cells which migrated into a chamber. The adhesion patterns on individual microfilariae indicated that no single effector cell type was responsible for the destruction of microfilariae. The eosinophil was the predominant cell type but neutrophils, lymphocytes and monocytes also adhered to the microfilariae. Cellular adhesion led to the immobilization of microfilariae and subsequently to their disintegration within large cell clusters. During the final stages of destruction the contribution of the monocyte became more pronounced.

Animals↗
PubMed1979

Studies on Dipetalonema viteae (Filarioidea). 4. Passive transfer of immunity to circulating microfilariae by spleen cells.

Passive transfer experiments provided clear evidence for a role of spleen cells in the immunity of hamsters against Dipetalonema viteae microfilariae. 106 or more spleen cells from postpatent (amicrofilaraemic) hamsters suppressed incipient microfilaraemia in syngeneic recipients when transferred at either week 2 or week 6 of a primary infection. Spleen cells from microfilaraemic donors (week 15-16 post infection) were also capable of transferring immunity against microfilariae. The spleen cell transfer never affected the survival of adult worms. After transfer of spleen cells from either patent or postpatent hamsters, antibodies to the cuticle of microfilariae could be found in the sera of recipients as early as week 8 of a primary infection.

Animals↗
PubMed1978

Studies on Dipetalonema vitae (Filarioidea). II. Antibody dependent adhesion of peritoneal exudate cells to microfilariae in vitro.

Peritoneal exudate cells from normal uninfected hamsters adhered in vitro to microfilariae in the presence of 19S antibody fractions from hamsters which had suppressed or were going to suppress their microfilaremia. The adhering cells were predominantly mononuclear, although eosinophils were occasionally found. Experiments with sensitized microfilariae and peritoneal exudate cells indicated that the macrophage probably recognizes the microfilariae/antibody complex. Macrophage cytophilic antibodies did not seem to be involved. This adhesion reaction may initiate the trapping of microfilariae in vivo, thus contributing to the observed acquired immunity to circulating microfilariae in the hamster.

Animals↗
PubMedDate not supplied

In vitro resistance patterns of Plasmodium falciparum to chloroquine--a reflection of strain-specific immunity?

Studies in vitro among children on the response of Plasmodium falciparum to chloroquine were conducted as part of the national long-term monitoring of drug resistance in a holo- to hyperendemic malarious area of Tanzania between 1983 and 1989. Overall, no significant increase in chloroquine resistance was observed. However, in children under 5 years old resistance increased during this period, whereas in schoolchildren resistance decreased from 1986 to 1989. A hypothesis based on antigenic differences between resistant and sensitive strains is proposed to explain this age-specific pattern. If immunity develops principally against the most frequent parasite strains, then as it develops the numbers of the most frequent strains will be reduced, whilst, the rare strains may become predominant and thus be detected in the blood of immune patients. Thus, in an endemic area, the observed resistance pattern in non-immune infants will differ from that in immune schoolchildren, as was observed in the present study. These findings may have important implications for the control of malaria and the development of vaccines.

Adolescent↗
PubMedDate not supplied

Ultrasound scanning for detecting morbidity due to Schistosoma haematobium and its resolution following treatment with different doses of praziquantel.

A study to assess the resolution of urinary tract morbidity due to Schistosoma haematobium was conducted on 2 cohorts of schoolchildren attending neighbouring schools in Kilombero District, southern Tanzania. Schoolchildren were screened for S. haematobium infection using the standard World Health Organization filtration technique and subsequently examined for urinary tract pathology using a portable 3.0 MHz sector scanner (Siemens Sonoline 1300). Treatment with praziquantel was given to all infected children. Children with observed urinary tract pathology received either 20 (n = 52) or 40 (n = 79) mg/kg body weight and were sonographically re-examined one, 2, 3 and 6 months following treatment. Geometric mean outputs of 21 and 19 eggs/ml of urine were detected in the 2 cohorts before treatment. Urinary tract pathology correlated positively with egg output (chi 2, P = 0.02) and microhaematuria (P = 0.0001). Bladder (wall irregularities and polyps) and kidney (congestive changes) pathologies were found in 81% and 36%, respectively, of the group that received 20 mg/kg of praziquantel, and in 78% and 46% of the group that received 40 mg/kg. Six months after treatment, 90.4% and 88.0% parasitological cure rates were obtained using 20 or 40 mg praziquantel/kg body weight. The respective pathology clearances were 88% and 91%. 20 mg/kg of praziquantel was as effective with regard to cure rates and reversibility of morbidity as 40 mg/kg.

Adolescent↗