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Biomedical subjects

H M Seitz

Publications and source records attributed to H M Seitz.

At least 91 records · Page 5Linked to original sources

[Amebic keratitis: clinico-histopathologic case report].

The present paper describes a case of amebic keratitis in a 63-year-old female patient, who had been wearing hard contact lenses to correct myopia. The clinical course was characterized by early superficial corneal infiltrates accompanied by a marked iritis and excruciating pain. Later a ring abscess developed, combined with a disciform infiltration of the deep central stroma and a recalcitrant superficial corneal ulcer. The disease ran a very chronic course over more than 3 months. After various conservative treatments including topical steroids, antibiotics, antimycotic, and antiviral drugs, a penetrating keratoplasty had to be performed. The histopathologic examination of the corneal button revealed many encysted amebas and a few trophozoites which were classified by direct immunofluorescence as belonging to the genus Acanthamoeba (Hartmannella). Six months after keratoplasty the eye was quit without any signs of recurrence. As far as the authors know, this is the first reported case of an amebic keratitis associated with contact lenses.

Amebiasis↗

Observations on possible immunity to reinfection among Kenyan schoolchildren after treatment for Schistosoma mansoni.

In February 1977, 306 out of 409 six- to 16-year-old Kenyan schoolchildren were found to be infected with Schistosoma mansoni. Prevalence and intensity were directly related to age and indirectly to the distance between the child's home and the transmission site, but were not related to the child's sex. Most children were treated with hycanthone in July 1977. Pretreatment blood samples were taken from 100 study children for eosinophil counts and measurements of cytotoxic anti-schistosomular antibody levels. Blood and faecal samples were re-examined five times between November 1977 and July 1979. Whole school resurveys in July 1978 and 1979 confirmed the continuation of transmission after chemotherapy. 'Reinfection' rates in the study children, incorporating both failed treatment and true reinfections, were significantly reduced in children, with both detectable antibody and eosinophil counts above 400/mm3, compared with children with neither. Children with either detectable antibodies or high eosinophil counts (mainly the latter) had intermediate reinfection rates. Neither sex, age nor pretreatment intensities influenced reinfection rates, but location of dwelling did: children from distant homes had lower rates. However, the effects of residence and 'protection' were not directly linked. The implication of these results, namely that infection can confer immune protection to reinfection after treatment, is being explored in further studies.

Adolescent↗

[Experiments in vitro with Litomosoides carinii (Nematoda: Filarioidea). I. Maintenance of adult females and microfilariae as well as release of microfilariae in different culture media (author's transl)].

Embryos of L. carinii continue intrauterine development to microfilariae and are totally released into the medium within 5--6 days when the latter (Tc 199) is changed daily and air is used as the gas phase. Oogenesis or further fertilization of eggs, however, does not occur in vitro in any of the media examined by us. One female releases 140 X 10(3) microfilaria/day on an average in vitro within 5--6 days. Mean initial numbers of 300 X 10(3) Mf/female/day are observed. Addition of equine serum inhibits microfilarial release in vitro; normal cotton rat serum prolongs survival of females while total numbers of released microfilariae or retained embryonic stages are not increased. The serum of post-patent animals does not influence the numbers of released microfilariae or their viability or survival of females. Microfilariae released in vitro in Tc 199 + 33% normal cotton rat serum survive for more than 8 days, when air is used as the gas phase and the medium is changed daily. Microfilariae isolated from the blood of patent animals survive for at most 6 days, at a 48-hourly change of medium survival does not even exceed 4 days.

Animals↗

[Light microscopic and scanning electron microscopic observations on phagocytosis of Plasmodium berghei infected erythrocytes by mouse macrophages [author's transl)].

Peritoneal macrophages from mice were cultured in Leighton tubes for 2 hours. Thereafter suspensions of washed red blood corpuscles originating from Plasmodium berghei-infected mice were offered to the cultured cells for phagocytosis. After 15 minutes of incubation 13,5% of the macrophages showed phagocytized parasites if the peritoneal cells came from malariaimmune mice. Cells from normal mice or from infected mice had lower rates (4,8/9,1%). After an incubation of 3 hours about 50% of the cells showed phagocytosis in all three groups. The system used allowed to estimate the halftimes for intracellular elimination of the parasites. The values are 27 minutes for cells from immune animals, 57 minutes for cells from normal animals, and 66 minutes for cells from infected animals. Details of the process of phatocytosis were recorded by scanning electron microscopic pictures.

Animals↗

The plasmodium berghei-infection in isogenic F1(C57B1 x DBA)-mice. II. Antibodies and antigens in the serum.

Using the fluorescent antibody technique it was possible to demonstrate antibodies in the sera of F1(C57B1 x DBA)-mice already during the first week of infection with Plasmodium berghei, strain K 173. These antibodies reached high titers during the second and third week, but, nevertheless, the animals died from the infection. Coincidently with the FAT-antibodies plasmodial antigens could be found in the sera of infected mice. The numbers of these antigens increased in the course of the infection. Finally up to seven could be precipitated by using a double diffusion technique in cellulose acetate membranes. Since antibodies directed against these antigens were only found in immune animals they must be different from the antibodies measured in the FAT. Comparison of the antigens found in the sera of infected animals with antigens prepared by physical desintegration of parasite material showed that in the sera antigens appeared which could not be demonstrated in the plasmodial extracts. If parasite material was phagocytized by macrophages in cell cultures in the culture supernatant also antigens appeared which could not be found in the plasmodial extracts. Similar antigens were found if isolated parasites were allowed to degrade without the action of phagocytic cells.

Animals↗

The Plasmodium berghei-infection in isogenic F1 (C57B1 x DBA)- mice. III. neonatal thymectomy and cell transfer experiments.

In neonatally thymectomized F1(C57BL X DBA)-mice the course of an infection with Plasmodium berghei, strain K 173, was unaltered if compared with the course in normal animals. No shortening of the survival time was observed. Cell transfer experiments were carried out. In numerous trials it was not possible to convey the protective immunity of immune animals to non-immune animals by the transfer of lymphoid cells. If an acquired immunity was destroyed by heavy x-irradiation it could be restored by the injection of immune spleen and lymphnode cells.

Animals↗

The Plasmodium berghei-infection in isogenic F1 (C57Bl x DBA)-mice. I. The course of the infection and immunization experiments.

The malarial infection caused by Plasmodium berghei (strain K 173) was observed in the isogenic mouse strains C3H, C57Bl, DBA, and the F1 (C57Bl x DBA)-hybrids. In addition immunization experiments were carried out by intermittent suppression of the parasite multiplication through maintaining the infected animals on a milk diet for various length of time. The F1-hybrids were the most resistant mice and immunization was most effective in these animals, too. But if the course of the infection was not influenced experimentally all animals succumbed to the infection. If the mice were inoculated with very small parasite numbers a bimodal mortality pattern was usually observed with a pronounced peak of eary mortality. The changes in body weight, temperature, and hematocrit during the infection are shown.

Animals↗