The present report concerns a new born patient with rapid fatal clinical course due to granulomatosis infantiseptica by the infection with Listeria monocytogenes. The case is of interest not only because of the rarity of this disease but also because of the difficulty in establishing a diagnosis.Recently, Listeriosis has been a wider spread disease among domestic animals in Japan as in western countries and the possibility of infection to man is increasing.
HISTORYThe patient was the first born delivered on November 12, 1958 at the Sapporo Medical College Hospital. Her mother had only a slight edema on the legs at the end of the ninth month of pregnancy and had an episode of fever up to 39°C 2 days before delivery. Otherwise, gestation was uneventful and delivery was normal and spontaneous.At birth the patient was well developed weighing 2520g. but was in a first grade of asphyxia. With oxygen therapy and subcutaneous robelin injection, the patient began to cry 3 minutes after birth, and cyanosis disappeared. Then the patient was put into the incubator.
PHYSICAL FINDINGS AND COURSEExaminations were negative except for severe meteorism, which was slightened by gas-aspiration. In the afternoon of the third hospital day the temperature rose to 38.4"C, and she appeared unusually listless. Although the temperature fell to 37.5"C at that night, next morning it rose again to 38°C with dyspnea and nose-bleeding. The temperature showed intermission at that day with dyspnea. Intramuscular chloromycetin was started, first 250 mg. and then 100mg. every 8 hours. On the fifth day the patient had attacks of clumps of whole body and showed tachypnea and cyanosis. Heart and respiration stimulating medicines were of no avail, and she expired at that afternoon. Clinical diagnosis was undetermined.
One of the most satisfactory procedures for investigating the metabolic reactions associated with virus multiplication may be said to be to compare the biochemical properties of normal tissues and of virus-infected ones, in which virus is actively multiplying in the host cells. This is of impcrtance, because, the metabolic pattern of the host cells following virus infection should turn to that for virus biosynthesis.Much(l)-(2*) has been studied on the metabolism of tissues infected in vivo or in vitro with many kinds of virus with respect to the energy relation in the host-virus system and to virus biosynthesis. ,It is believed that virus biosynthesis takes place at the expense of considerable metabolic energy produced in the course of aerobic cellular metabolism, especially of phosphorylative oxydation in the host cells. In fact, it has been reported by some authors( 4)-( 7),( 13)~( 14),( 16), ( 2 O ) > ( z 6 ) that virus multiplication in the host cells was inhibited by the use of the metabolic inhibitors which act on the Krebs citric acid cycle or on ATP-ase activity. Other authors(l7) reported, however, that virus could multiply well in such tissues in which glycolytic and oxydative activity has been impaired.The present experiment was undertaken in order to clarify the metabolic changes in the chorioallantoic membranes of embryonated eggs, which were produced by the multiplication of ectromelia virus inoculated therein in vivo or in vitro. This experiment is one phase of the series of studies dealing with metabo!ic reactions in the host-virus systems.
MATERIALS AND METHODSTwo kinds of experiments were made. The first experiment was to examine the metabolic changes in the chorioallantoic membranes inoculated in vivo with the virus. To this end, the virus material was dropped on the chorioallantoic membranes of 12 day-old embryonated eggs, and at regular intervals, the in-Directed by Prof. K. Shimpo and Prof. T. Onoe.
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