[100 years of Pfeiffer's glandular fever]. / Hundert Jahre Pfeiffersches Drüsenfieber.

Glandular fever was described by Emil Pfeiffer in 1889. He characterized the disease as an infectious process with fever, a swelling of the lymph nodes including an enlargement of the liver and the spleen and with a pharyngitis. It was the beginning of a very interesting chapter of medical investigations during the next 100 years. The reports of leucocytosis in reaction to this acute infection were the next important step. Sprunt and Evans recommended therefore the term "infectious mononucleosis" in 1920. Further Paul and Bunnell (1932) found the presence of heterophil antibodies in glandular fever. In 1968 Henle and Henle discovered the relations of Epstein-Barr-Virus (EBV) to infectious mononucleosis. In this connection the pathogenesis of glandular fever was investigated. Also the diagnosis of the disease found a certain base by the EBV-antibodies and it was possible to give a reliable interpretation of the clinical course, the symptoms and the complications of infectious mononucleosis. Furthermore the atypical manifestation of glandular fever could be identified. In recent years the problems of persistent and chronic infections were discussed. At last the antiviral chemotherapy was tested.

[Hyperpyrexia and shock (author's transl)]. / Hyperpyrexie und Schock

In childhood hyperpyrexia is the most important factor causing the irreversibility of shock. The combination of high fever and circulatory impairment is more frequent during the first years of life. This behaviour is due to the high resistance of the arterial system in infancy. Marked general vasoconstriction increases the risk of a reduction in circulation and of heat loss, and causes hypoxia and rise of fever. The further course of shock is largely determined by microcirculatory failures. Under hyperpyrexia the disturbance of homeostasis can be intensified by shivering, blocking of perspiratio sensibilis, hyperosmolarity, brain edema, and DIC. In most cases of meningococcal sepsis shock and DIC begin with vasoconstrictive centralisation of circulation. The high-output-shock is extremely rare in children with high fever. The control of all important functions of a febril child in shock is the best baseline for the treatment. It is necessary in all shock patients in hyperpyrexia to reduce the fever and to repair the peripheral circulation. The therapy consists of antipyretic drugs, physical cooling, infusions of buffer-bases, dopamine, antibiotics and so on. In DIC heparin or streptokinase are indicated. In severe circulatory impairment combined with high fever prednisone is useful, in brain edema dexamethasone. The fatality rate of our cases has been diminished by a systematic therapy of hyperpyrexia and shock from 10 to 3 percent.