What Are Bacterial Diseases?


What Are Bacterial Diseases?

Enthusiastic reports about proteolytic enzymes in the treatment of pneumococcal meningitis, but these agents have not been evaluated in sufficient detail to recommend their general use. Other supportive therapy Bacterial Diseases (22c)z.2des ADM;2zistra-notion of adequate but not excessive parenteral fluids and anticonvulsants when indicated sedation should be employed with caution, even for delirious patients; of the many agents available, partial beauty, h. N., and Oppenheimer. S.: CSF lactic dehydrogenase and its enzymes in infections of the central nervous system new fa mai- vi:1197, 1968 be, j., and hosellemp. H, recurrent attacks of bacterial meningitis: a new clinical problem.

Report of five cases. A.; I. lolled— .N:465, 1960-‘- R. R… and Petersdorf, R. G.: The clinical spectrum cirisseitsaa621. June-t. , 23162,1%62. Company„ J. D., and Sheenan, C. P.: Bacteriologic relapse in licompopkilus influenza meningitis. New Eng. J. Med., 278: 1601, 1968. Harter, D. H., and Petersdorf, R. G.: A consideration of the pathogenesis of bacterial meningitis: Review of experimental and clinical studies. Yale•J. Biol. Med., 32:280,1960. Olafsson, M., Lee, Y. C., and Abernathy, T. J.: Mima polymorpha meningitis: Report of a case and review of the literature. New Eng… J. Med., 258:465, 1958. Oppenheimer, -S. J., ()Toole, R. D., and Petersdorf, R. Q.: Bacterial meningitis: In Shy, G. M., Goldensohn, E. S., and Appel, S. H. (eds.): The Cellular and Molecular Basis of Neurological Disease, Bacterial Diseases, Philadelphia, Lea, and Febiger, (in press). Snyder; S. N., and Brunjes, S.:H. influenza meningitis in adults. Amer. J. Med. Sci., 250:658. 1965. Swartz, M. N.,.and Dodge, P. R.: Bacterial meningitis—A review of selected aspects. New Eng. J. Med., 272:725, 779, 842, 898, 954, 1003, 1965. Welshimer, H. J., and Winglewish, N. G.: Listeriosis Summary of seven cases of listeria meningitis. J.A.M.A., 171:1319, 1959.

WHOOPING COUGH (Pertussis) Stephen I. Morse

Definition. Whooping cough is an acute respiratory Bacterial Diseases illness that primarily affects infants and young children. The etiologic agent is usually Bordetella pertussis; occasionally B. parapertussis, and rarely B. bronchiseptica produce a similar syndrome. The descriptive name derives from a distressing, prolonged inspiratory effort that follows, paroxysmal coughing. Although both morbidity and mortality have markedly declined, whooping cough is still responsible for a significant number of deaths in infants. History. The disease was first recorded in the middle of the sixteenth century by Moulton and by DeBaillou. Whether whoop-ing cough was indigenous to Europe or had been transported there in the preceding century is uncertain.

Sydenham applied the name “pertussis” to any illness accompanied by violent coughing, but the term became restricted to the epidemic dis-ease that was a well-recognized clinical entity by, the middle of the eighteenth century. In 1900 Bordet and Gengou observed coccobacilli in the sputum of a child with whooping cough, but it was not until 1906 that they were able to culture the organ-ism_ Many years passed before the Bordet-Gengou bacillus was universally accepted as the etiologic agent of whooping cough.

Leslie and Gardner (1931) recognized that B. pertussis underwent marked biologic and morphologic changes on prolonged cultivation, thereby accounting for the difficulties in establishing the etiologic role of the agent and the inconstant protective effect of immunizing preparations. Although the mortality rate of whooping cough in the United States began to decline in the early part of this century, the incidence in young children did not significantly decrease until after the use of prophylactic vaccines became widespread 25 years ago. Etiology.

When first isolated, Bordetella pertussis is a minute, nonmotile, poorly staining, gram-negative coccobacillus, 0.5 p, to 1.0 µ in length. Capsules can be demonstrated by special procedures, and bipolar metachromatic granules are present. The complex medium containing blood originally employed by Bordet and Gengou is still often used for cultivation. Primary isolates, phase pih‘SMS, nit, gym, and tone tonal laboratory media, but will do so after prolonged passage. At the same time colonial morphology changes, marked pleomorphism of individual cells is evident, and there is an alteration in anti-genic composition. The change from phase I to phase IV has been likened to the smooth to the rough transition of other microbes.

The only phase I won-isms is virulent, and the only phase I organisms provide effective immunizing material. Members of the Bordetella genus were formerly regarded as species of Hemophilus. However, the Bordetella group does not have a strict requirement for X and V growth factors, and they are antigenically distinct. Although the addition of blood to the Bordet-Gengou medium is required for the growth of phase I organisms, the blood acts to neutralize bactericidal substances, probably fatty acids, rather than to provide nutrients. Media containing charcoal, starch, or ion exchange re-sins will support the growth of phase I bacteria. B. pertussis produces a heat-stable toxin (endotoxin) and a heat-labile toxin. A role of toxins in the development of disease has not been demonstrated. A hemagglutinin has also been isolated. The capsular material does not swell in the presence of antiserum.

A species agglutinogen has been recognized as well as agglutinating factors that differ between strains. Serotyping is there-fore a useful epidemiologic tool. The role of the interaction between the organism and phagocytes has not been defined, although the presence of antisera appears to increase uptake of B. pertussis by leukocytes. Remarkable biologic effects are induced in laboratory animals by the injection of killed phase I organiSms. These include the development of heightened sensitivity to histamine and serotonin; in-creased susceptibility to anaphylaxis and experimental allergic encephalomyelitis; increased antibody production in response to heterologous antigens; and hyperleukocytosis and hyperlym-phocytosis.

The factors responsible for these reactions have not been characterized, and the relationship of any of these effects to the primary clinical expression of whooping cough is obscure. It should be emphasized that none of the cellular components or products of B. pertussis has

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