Journal of The Japanese Society of Veterinary Science
Online ISSN : 1883-9193
ISSN-L : 1883-9193
Volume 8, Issue 1
Displaying 1-4 of 4 articles from this issue
  • KISAJIRO OGURA
    1929Volume 8Issue 1 Pages 1-38_3
    Published: 1929
    Released on J-STAGE: March 31, 2009
    JOURNAL FREE ACCESS
    1. Als Erreger der Rinderpiroplasmose in diesem Gebiete sind 2 Arten des Pirplasmas, nämlich eine grosse, Bigeminum ähnliche und eine kline, Mutans ähnliche, zu erkennen.
    2. Die Mischinfektion dieser beiden Arten kann etwa die eine Hälfte der infizierten Rinder mit charakteristischen Symptomen mindestens ohne besondere Bedingung befallen, während die Reininfektion der kleinen erst mit besonderer Bedingung (Abweidung, Gebären, Transportion usw.) befallen kann. Die durch diese Mischund Reininfektion verursachten Krankheiten machen fast keinen Unterschied.
    3. Unten dem Mikroskope zeigt sich die kleine Art immer im periphren Blute der infizierten Rinder, die grosse dagegen nur selten. Für die Bestimmung der Grosspiroplasmeninfektion ist somit der Uebertragungsversuch die sicherste Methode.
    4. Die Krankheit oder die Mischinfektion der beiden zu bestehen gibt den Rindern eine gewisse Immunität, die Reininfektion der kleinen selbst gibt aber keine.
    5. Dir künstliche Michinfektion mit besonderer Berücksichtigung ist als Schutzimpfung gegen diese Krankheit in diesem verseuchten Gebiete zu brauchen.
    6. Die charkteristischen Symptome dieser Krankheit sind folgende: Mattigkeit, Anämie, Gelbscucht, Hämoglobinurie und Abnormalerythrozyten in Peripherblute. Von allem spielt die letzte die Hauptrolle, diese Krankheit zu diagnosieren.
    7. Die wichtigste Sektionsbefunde sind: Milz: Vergrösserung infolge Ueberfüllung mit Blut, ausstrichbare Pulpa (häufig weich zerfliessend in subakuten Fällen). Leber: Stark Gallenstauung, parenchymatöse Degeneration. Niere: Parenchymatöse Degeneration und Hämosiderose (besonders in den gewundenen Harnkanälchen. Lunge: Oedem (mitunter). Ausserdem in fast allen Organen Oedem, Gelbsucht und Hämosiderose.
    8. Trypanblau (Cassella, Höchst) gibt keine besondere (chemotherapeutische) Wirkung gegen diese Piroplasmose.
    Der Autor hat viele Mitteilungen über Rinderpiroplasmose studiert und auch die Blut- und Organausstrichpräparate von Piroplasma bigemium, mutuns und parvum, die Sir A. Theiler, Herrn Prof. Dr. Ch. Kohanawa gegeben hatte, und die Blutausstrichpräparate von P. bovis, die P. Iwanoff (Kharkov) dem Autor freundlich geschenkt hatte, genau untersucht. Von diesen Präparaten zeigen einige Abnormalerythozyten aufweisende Präparate ziele Kleinpiroplasmen (P. mutans), aber die Grosspiroplasmen (P. bigeminum oder P. bovis) nur gering oder gar nicht. Morphologisch ist das Grosspiroplasma in dieser Gegend dem Piroplasma bigeminum oder Piroplasma bovis und das Kleine dem Piroplasma mutans sehr ähnlich. Durch diese vergleichenden Untersuchungen wurde folgende Annahme vom Autor gewonnen: Es kann möglich sein, dass die Kleinpiroplasmen und die Grosspiroplasmen (ausschliesslich des P. parvum) die gemeinschaftlichen Erreger einer über verschiedene Länder verbreiteten Piroplasmose sind, die in ihren Symptomen verschiedene Variationen zeigen, mit anderen Worten, es müssen die Rinderpiroplasmosen ausser dem Küstenfieber in verschiedenen Ländern für gleich gehalten werden.
    Zum Schlusse spreche ich meinem hochverehrten Lehrer, Herrn Prof. Dr. K. Kasai, für seine jederzeit freundliche Belehrung uud Unterstützung meinen besten Dank aus. Herrn Prof. Dr. K. Ichikawa danke ich herzlich fur seine wertvollen Ratschläge. Den Herren Prof. Dr. S. Takamatsu, R. Kurosawa, Ch. Kohanawa und P. Iwanoff, bin ich fur die freundlich Erlaubnis, das Material für diese Krankheiten benutzen zu dürfen, zu grossem Danke verpflichtet.
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  • HIKOJIRO FUTAMURA
    1929Volume 8Issue 1 Pages 39-50_2
    Published: 1929
    Released on J-STAGE: February 19, 2009
    JOURNAL FREE ACCESS
  • I Report Gymnopleurus Sinnatus as the Intermediate Host of Spirocerca Sanguinolenta and Inquiry into Grassi's Experiment with Blatta Orientalis
    S. ONO
    1929Volume 8Issue 1 Pages 51-58_3
    Published: 1929
    Released on J-STAGE: February 19, 2009
    JOURNAL FREE ACCESS
    1. It is proved by the infestation experiment with dogs that Gymnopleurus sinnatus is the intermediate host of Sp. sanguinotenta in the vicinity of Mukden, its larvae especially invading the wall of aorta.
    2. Rabbits, if fed with lanolin or lard, also can be infested with larvae of the present parasite forming aneurysma, but these larvae can not develop to their mature stage in this improper host, being entirely destroyed within 4 months after infestation. Rabbits fed with the normal diet can not contract infestation with Sp. sanguinolenta.
    3. The broken elastic lamellae are detected in the preparation from the invaded tissue of aorta stained with Weigert's fuchsin-resorcin solution.
    4. The larvae of Sp. sanguinolenta, as the adults do, also carry the blood-colored fluid in their body cavities even 1 day after infestation.
    5. It is deduced from various points of view that the parasite from Bl. orientalis pointed out as Sp. sanguinolenta by Grassi is in all probability one of allied species (Spirura sp.?).
    I tender my warm thanks to Dr. K. Kasai, Director of the Institute, and to Prof. S. Yoshida for their cordial guidance.
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  • SHIRO ITAGAKI
    1929Volume 8Issue 1 Pages 59-73_2
    Published: 1929
    Released on J-STAGE: February 19, 2009
    JOURNAL FREE ACCESS
    No study has been hitherto reported as regards the parasitic nodular typhlitis in chickens due to heterakid worms, though a considerable number of works has been made on the same lesion in pheasants by Lucet & Henry, Klee, Railliet, Letulle et Marotel, Schwartz and others.
    Having examined six-hundred and twenty specimens of the chicken intestines taken from various poultry yards for other experimental purposes during past five years, I have found many larger and smaller helminthic nodules in the coecal wall of eighty specimens of them. The larger nodules, varing in size from a linseed to a pea, were found in the subserous and muscular coats, and not in the submucosa of the coeca in few specimens. These nodules could be detected easily with the naked eye from the outside of the coeca. By closer examination a caseous or calcareous degenerated part was seen in the centre of the nodules.
    Each nodule was demonstrated to have contained single or several heterakid worms in various stages of the development.Many of the worms extracted from these nodules showed that they were appearently fully grown, but not yet sexually matured. In one of such nodules, seven specimens of fully developed mature worms were contained and determined to be Heterakis vesicularis.
    Judging from the discovery of various stages of the worms from the coecal nodules and from the enlarged cavities of the coecal glands, it may be concluded that some of early-stage larvae might have penetrated the mucosa from the coecal glands and encysted in the muscular layer where they continued to grow and attained their sexual maturity.
    The smaller nodules were found in the submucosa of the coeca of many specimens and were remarked to have the similar construction to those of the nodules due to the larvae of Ascaridia perspicillum which were discovered previously by the author in the muscular layer of the small intestine. About 12.1% of the chickens examined, were more or less affected with this nodular disease. The number of nodules found in a coecum counted one to twenty. Each nodule contained single specimen of a larval nema, measuring about 1mm. in length.
    No difference was remarked between the larval worms in the coecal nodules and those in the nodules of the small intestine, and in my feeding expriments with the embryonated eggs of Heterakis vesicularis to chickens, such parasitic nodules could not be produced.
    From the fact above mentioned it can be said that both larval worms may be identical. It is highly probable that a part of the larvae of Ascaridia perspicillum after hatching in the muscular stomach of the chickens undergo their further development in the lumen of the small intestine and some of the larvae especially in the winter season, penetrate the wall of the small intestine and are embedded there making the parasitic nodules and the remained part of them enter the coeca to produce the same nodular lesion in the submucosa.
    Development of Heterakis vesicularis. A series of young chickens were used in the study of the development of Heterakis vesicnlaris.
    These chickens were fed on the ripe infective eggs of this worm and after a period of from thirty-six hours to two months the chickens were examined postmortem to observe the state of the development of the worms. By carefully examining the contents of the coeca successive stages in the development of the larvae were obtained.
    Within thirty-six hours after feeding of the eggs most of them hatched in the muscular stomach and a few freed larvae were found in the coeca, and on the examination of the chickens killed on the fourth day and thereafter, the young worms were seen in a large number in the coeca. But in many instances a few larvae still remained in the deep part of the mucosa of the small intestine, without producing nodules there for a long time.
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