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Biomedical subjects

L W Wannamaker

Publications and source records attributed to L W Wannamaker.

120 records · Page 7Linked to original sources
PubMed1967

Bacterial interference in experimental burns.

A standardized, full thickness, dermal burn in rabbits was used to study interference between strains of Staph. aureus inoculated on the wound surface. Several strains appeared equally capable of colonizing lesions and of preventing superinfection by other staphylococci inoculated at a later time. In addition, cross-infection between rabbits colonized by different strains (502A and Q461) and placed together in cages was prevented, presumably by the same mechanism. Interference appeared to be a strictly local phenomenon, since it did not occur when an animal was colonized by strain 502A at one burn site and subsequently challenged with strain Q461 at a separate lesion. For interference to occur, a minimal time interval (9 hr) was required between inoculation of the interfering strain and inoculation of the challenge strain. In vivo growth rates indicated rapid growth in the first 24 hr by the interfering strain but no detectable multiplication by the challenge strain. Heat-killed staphylococci, even in large numbers, were incapable of producing interference. Penicillin treatment of animals colonized by strain 502A (penicillin-sensitive) abolished interference with strain Q461 (penicillin-resistant). These findings indicate that bacterial multiplication by the interfering strain is an essential feature of this phenomenon. The mechanism of interference between strains of Staph. aureus remains obscure. There was no evidence in these studies for direct bacterial antagonism in vitro or in vivo between most of the strains examined; yet, all were capable of producing interference. Attempts to identify antistaphylococcal activity in passively transferred tissue homogenates and serum collected from infected animals were also negative. The ability of large inocula of staphylococci grown in broth to superinfect colonized lesions indicates that the numerical superiority of the interfering strain over the challenge strain is an important aspect of interference. The observation that in vivo-grown organisms may superinfect in significantly smaller quantities is suggestive of a qualitative advantage as well.

Animals↗
PubMedDate not supplied

Changes and changing concepts in the biology of group A streptococci and in the epidemiology of streptococcal infections.

Concepts of the cellular structure of group A streptococci have been modified by the recognition of surface fimbriae and by problems with the older view of a layered arrangement of cell wall components. Evidence of genetic drift of serologic types and of some increase in the prevalence of erythromycin-resistant strains has appeared. A curiois bimodal age distribution for streptococcal pharyngitis and an increase in the prevalence of non-group A strains has been detected. Despite repeated challenges, the value of throat cultures for confirming the possibility of streptococcal pharyngitis remains firmly established; throat cultures are superior to saliva cultures, which more frequently detect non-group A streptococci. Difficulties in detecting subclinical steptococcal infections and in defining streptococcal infection in children in endemic situations (particularly in separating true streptococcal infection from carriage of streptococci in individuals whose illness is due to some other agent) continue to present problems to clinicians and epidemiologists. The value of school culture surveys and of treatment of asymptomatic family contacts of cases remains uncertain. A 20% bacteriologic failure rate has been reported after intramuscular treatment with benzathine penicillin, but no in vitro evidence of resistance to penicillin has appeared. No adequate explanations are available for the decline in the problem of rheumatic fever in industrialized countries, for its increased recognition in tropical countries, for the failure of rheumatic fever to occur after streptococcal pyoderma, or for the emergence of group B Streptococcus as a predominant bacterial pathogen in newborn infants.

Adolescent↗
PubMedDate not supplied

Streptococcal toxins.

Few of the cellular components of group A streptococci appear to be directly toxic for animals or humans. Some preparations of M protein produce an immunotoxic effect on human platelets and neutrophils. Cell wall fragments produce a chronic multinodular inflammatory lesion of dermal connective tissue. The peptidoglycan component of cell walls has many of the biologic features of endotoxins. The exotoxins of group A streptococci include the erythrogenic toxins (pyrogenic exotoxins) and the cytolytic toxins (streptolysins S and O). The high prevalence of erythrogenic, toxin-producing strains is difficult to reconcile with the epidemiologic behavior of scarlet fever; the variations may be due to quantitative differences in toxin production or to a shift from the early scarlet fever-associated strains that produce A toxin to the currently prevalent strains that produce B and C toxins. Experiments with animals suggest that a positive Dick test and the rash of scarlet fever result not from a direct toxic effect but rather from enhancement by pyrogenic exotoxin(s) of acquired hypersensitivity to diverse streptococcal products. The mechanism of toxigenic phage conversion is not clear. The pyrogenic exotoxins are associated with the enhancement of endotoxin shock and a wide variety of other biologic properties. Streptolysin S is a nonantigenic polypeptide associated with various stabilizing carrier molecules. It lyses a wide range of mammalian cells, influences T lymphocyte functions, and is probably responsible for the leukotoxic property of group A streptococci. Rheumatic fever has been associated with a streptococcal outbreak due to a nonhemolytic (streptolysin S-negative) strain. Streptolysin O is an oxygen-labile (thiol-activated) cytolysin. It is inhibited by nonesterified cholesterol and binds to cholesterol in the membranes of mammalian cells and organelles, an interaction producing ring-like and C-shaped structures demonstrable by electron microscopy. Streptolysin O affects a number of leukocyte functions. It produces profound electrocardiographic changes in experimental animals and toxic effects on pulsating heart cells in tissue culture. The observation that rheumatic fever is not associated with infection of the skin due to group A streptococci has suggested that nonesterified cholesterol in the epidermis may inhibit a toxic effect of streptolysin O, an effect necessary for the development of rheumatic fever.

Animals↗