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Biomedical subjects

W B WOOD

Publications and source records attributed to W B WOOD.

64 records · Page 4Linked to original sources
PubMed1950

Host-parasite relationships in experimental pneumonia due to pneumococcus type III.

Experimental pneumonia was produced with a highly virulent strain of type III pneumococcus which synthesizes, during rapid growth, large amounts of capsular polysaccharide. The type III pneumonia differed from that caused by pneumococcus I in that (a) death occurred more promptly in the type III infection, (b) the local pulmonary lesion became more heavily infected, and (c) frank suppuration was common even after otherwise effective chemotherapy. The greater pathogenicity of the type III organism was shown by special histologic techniques to be due primarily to its capsular slime layer which interferes with surface phagocytosis. Capsular polysaccharide shed from the organism during growth was also demonstrated in high concentration in certain parts of the pneumonic lesion. Removal of the excess polysaccharide from the alveoli resulted from (a) lymphatic drainage to regional lymph nodes and (b) phagocytosis, particularly by macrophages. The possible relationship of the free carbohydrate to the malignancy and the characteristically viscous exudate of type III pneumonia was discussed. The lung abscesses which resulted from type III infection were observed to occur in those areas in which the maximum number of organisms had accumulated. Evidence was obtained that suppuration was due, not to necrotoxic products peculiar to the type III pneumococcus, but rather to the survival of large numbers of bacteria in the tissues, brought about primarily by the antiphagocytic effect of the slime layer. When pneumonia was produced with an intermediate type III mutant lacking the protective slime layer, back mutation to the mucoid parent occurred during the course of the infection, and the mucoid form eventually predominated in the lung as a result of selective phagocytosis of the intermediate organisms. Similar mutation to the maximally virulent type III form was noted with a transformed intermediate type III strain grown from single cell preparations.

Host-Parasite Interactions↗
PubMed1949

Cellular mechanisms of antibacterial defense in lymph nodes; pathogenesis of acute bacterial lymphadenitis.

Acute pneumococcic lymphadenitis produced in rats by intradermal inoculation of the foot-pad is characterized by rapid infiltration of polymorphonuclear leucocytes into the intermediary sinuses of the node, and prompt phagocytosis of pneumococci by both the macrophages of the sinuses and the recently arrived leucocytes. After 5 to 7 hours the polymorphonuclear leucocytes are found densely congregated about the hilar region, and 9 hours after inoculation most of the phagocyted organisms have been digested. At the end of the 24 hour period the popliteal node presents the picture of a subsiding inflammation with a marked macrophage reaction and regenerating lymph follicles. Phagocytosis of encapsulated pneumococci in the foot-pad and popliteal node occurs in less than 30 minutes after inoculation. It is assumed that this prompt phagocytosis is effected by the non-antibody mechanism of "surface phagocytosis." The majority of polymorphonuclear leucocytes that enter the sinuses of the inflamed node appear to come from capillaries within the node itself rather than from the primary site of inflammation in the foot-pad. The prompt inflammatory response of the nodal tissues serves as an active defense against lymph-borne infection. Macrophages invade nodal sinuses only after most of the pneumococci have been destroyed by polymorphonuclear leucocytes. It is suggested that the macrophage reaction follows removal of the primary inflammatory stimulus by the granulocytes, and thus constitutes only a late phase of recovery. Fibrin formation in the sinuses of the lymph node is rare during acute lymphadenitis. This finding may be related to the observation that within 5 minutes after entrance of bacteria into the node, heparin-containing granules from mast cells are strewn throughout the sinuses.

Animals↗
PubMed1949

Cellular mechanisms of antibacterial defense in lymph nodes; the origin and filtration effect of granulocytes in the nodal sinuses during acute bacterial lymphadenitis.

The origin of the polymorphonuclear leucocytes found in the intermediary and subcapsular sinuses of the popliteal lymph node during acute bacterial lymphadenitis, and the effect of this leucocyte infiltration on the passage of bacteria through the lymph node have been investigated. It has been demonstrated that: 1. The polymorphonuclear leucocytes in the nodal sinuses originate both from blood vessels of the lymph node and from the primary inflammatory focus in the tissues. 2. Granulocytes invading the intermediary sinuses of the infected lymph node arise primarily from capillaries lining these sinuses. 3. Most of the polymorphonuclear leucocytes in the subcapsular sinus, on the other hand, originate from the inflammatory focus in the tissues and appear to traverse the node by way of this peripheral sinus. 4. The bacteremia following direct intralymphatic injection of pneumococci is suppressed by the presence of preformed inflammatory exudate in the nodal sinuses indicating that the filtering capacity of the node is thereby greatly increased.

Anti-Bacterial Agents↗