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Biomedical subjects

A WOLF

Publications and source records attributed to A WOLF.

At least 91 records · Page 5Linked to original sources
PubMed1951

Studies on acute disseminated encephalomyelitis produced experimentally in rhesus monkeys.

The white cell count, total protein, gamma globulin, and percentage of gamma globulin in the cerebrospinal fluid of monkeys with acute disseminated encephalomyelitis produced by the injection of brain emulsions with adjuvants have been studied. The acute phase of the disease is characterized by a rise in the white cell count, total protein, and gamma globulin in the cerebrospinal fluid. In some instances the percentage of gamma globulin, to the total protein may be normal while in others it is elevated. As the acute process subsides, the total protein declines and animals frequently show an increase in the percentage of gamma globulin to total protein. The relation of the cerebrospinal fluid findings in acute disseminated encephalomyelitis in the rhesus monkey to those in human multiple sclerosis is discussed.

Adjuvants, Immunologic↗
PubMed1950

Experimental congenital toxoplasmosis. I. The vagina as a portal of entry of toxoplasma in the mouse.

Toxoplasmosis can be transmitted to mice by the introduction of Toxoplasma into the vagina. Pregnant mice were more susceptible to infection than non-pregnant animals in the ratio of 3 to 1. Obvious signs of vaginitis were not observed. Many of the infected mice remained entirely free of external signs, while a minority showed neurological or respiratory disturbances. Pregnant animals, especially those infected 6 to 10 days following conception, often died in the terminal stages of pregnancy or shortly after parturition. The possibility that the vagina may serve as one of the portals of entry of Toxoplasma in the human being and that infection may occur by sexual contact or by contamination by feces or other Toxoplasma-containing materials is discussed. The high susceptibility of the pregnant mouse to toxoplasmosis under the conditions of these experiments suggests a possible explanation for the higher incidence of congenital as compared to postnatal human toxoplasmosis and for the associated asymptomatic maternal infection. The infected but clinically normal human mothers may be compared to some vaginally infected pregnant mice which remained symptom-free.

Animals↗
PubMed1950

Experimental congenital toxoplasmosis. II. Transmission of toxoplasmosis to the placenta and fetus following vaginal infection in the pregnant mouse.

Pregnant mice infected with Toxoplasma by the vaginal route have been found to transmit toxoplasmosis to the placentas and fetuses in utero. The microorganism entered the blood stream of the mother from primary foci of infection in the vaginal wall and produced disseminated lesions in the labyrinth of the allantoic placenta at the same time as other peripheral maternal tissues were involved. Placental lesions were observed in mice infected with Toxoplasma by vagina between the 3rd and the 9th day of pregnancy. They consisted of microscopic foci of degeneration, without inflammation, in the syncytial trophoblast, and parasites undergoing multiplication were readily identified in them. Here Toxoplasma gained access to the fetal circulation. Following the vaginal instillation of Toxoplasma on the 8th day of pregnancy, subinoculation of test animals revealed the parasites in the maternal peripheral and placental blood on the 13th day and later, while the first histopathologic changes in the placenta were found on the 17th day. Toxoplasma could be demonstrated in suspensions of fetal tissues on and after the 17th day by the injection of normal test animals. However, no lesions of toxoplasmosis, or Toxoplasma, were found in histologic sections of fetuses 11 to 21 days old removed at autopsy from vaginally infected mothers. It is concluded that before birth the parasites were confined to the fetal blood. The experiments provide the first direct histological demonstration of placental toxoplasmosis. The possible bearing of the experimental disease on human placental and fetal toxoplasmosis is briefly considered. It is probable that a maternal parasitemia during the latter part of pregnancy, whatever the portal of entry may be, is an essential factor in the pathogenesis of human congenital toxoplasmosis and that this occurs shortly after exposure to Toxoplasma rather than in a later chronic stage of the infection. The suggestion is offered that some instances of spontaneous abortion or fetal death in man, as in the mouse, may be due to inapparent toxoplasmosis.

Animals↗
PubMed1950

Experimental congenital toxoplasmosis. III. Toxoplasmosis in the offspring of mice infected by the vaginal route. Incidence and manifestations of the disease.

A study has been made of congenital toxoplasmosis in the offspring of mice infected with Toxoplasma by the vaginal route during pregnancy. Some of the young mice were retarded in postnatal development, and some became ill or died in the 2nd to 4th weeks of life while the majority remained symptom-free in spite of the presence of toxoplasmic lesions of varying degrees of severity. Congenital toxoplasmosis developed only in offspring whose mothers had been infected on the 7th to 9th day of pregnancy. Infection of the offspring without active toxoplasmosis in the mother was not observed. The highest incidence of congenital infection (57.6 per cent) was obtained by giving 2 vaginal instillations of Toxoplasma-infected mouse brain on the 8th and 9th days of pregnancy. Mice infected before the 7th day developed placental toxoplasmosis but rarely delivered viable young. When the mother was infected after the 9th day, the offspring were normal. When congenital toxoplasmosis occurred in a litter, a majority or all of the individual offspring were usually infected. Although pathologic changes were not present in the suckling mice at birth, and did not appear before the 9th postnatal day, reasons are stated for excluding the possibility of postnatal contact or milk-borne infection. It cannot be assumed from the experimental disease that the vagina is a portal of entry of Toxoplasma in human congenital toxoplasmosis. Any route of infection leading to a maternal parasitemia during pregnancy might result in toxoplasmosis of the placenta and transmission of the disease to the offspring before birth. Unlike the restricted time interval effective in the mouse, there is a long period during the later months of pregnancy in the human being in which transplacental passage of the infection may occur. When transmission to the fetus takes place shortly before parturition, evidence of disease in the human infant, as in the mouse, may not become manifest until several weeks postpartum, and the prenatal origin of the infection may not be apparent. When the fetus becomes infected well before parturition, symptoms of congenital toxoplasmosis may be present at birth. The asymptomatic character of the infection in many of the young mice would appear to have a counterpart in certain instances of human congenital toxoplasmosis.

Animals↗
PubMed1950

Studies on acute disseminated encephalomyelitis produced experimentally in Rhesus monkeys; complement-fixing antibodies.

1. Animals injected with emulsions of monkey brain with adjuvants show a complex pattern of antibody response as determined by complement fixation tests. 2. Organ-specific complement-fixing antibodies to constituents of brain tissue may be formed which fix complement with brain tissues of various animal species but fail to react with other organs or with rabbit placenta. 3. Antibodies may be formed to some constituent of brain other than nervous tissue. It would seem that these can be detected by the strong complement fixation given with rabbit placenta. 4. Sera from individual animals may contain antibodies to the brain or placenta constituents, to both, or to neither. Occasional individual sera show unique patterns of antibody response as determined with various additional antigens such as fetal brain, posterior pituitary, or peripheral nerves. 5. No evidence of any etiological relationship between the development of encephalomyelitis and the complement-fixing antibodies to brain demonstrable in the sera could be found. The complement-fixing antibody to the placental constituent was unrelated to the encephalomyelitis.

Animals↗