scholarly journals HOST-PARASITE RELATIONSHIPS IN EXPERIMENTAL PNEUMONIA DUE TO PNEUMOCOCCUS TYPE III

1950 ◽  
Vol 92 (1) ◽  
pp. 85-100 ◽  
Author(s):  
W. Barry Wood ◽  
Mary Ruth Smith
Keyword(s):  
Capsular Polysaccharide ◽  
Virulent Strain ◽  
Lymphatic Drainage ◽  
Intermediate Type ◽  
High Concentration ◽  
Regional Lymph Nodes ◽  
Experimental Pneumonia ◽  
Type Iii ◽  
Slime Layer ◽  
Virulent Type

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.

scholarly journals THE INHIBITION OF SURFACE PHAGOCYTOSIS BY THE CAPSULAR "SLIME LAYER" OF PNEUMOCOCCUS TYPE III

1949 ◽  
Vol 90 (1) ◽  
pp. 85-96 ◽  
Author(s):  
W. Barry Wood ◽  
Mary Ruth Smith
Keyword(s):  
Methylene Blue ◽  
Electron Microscope ◽  
Large Volume ◽  
Logarithmic Phase ◽  
Type Iii ◽  
Slime Layer ◽  
Virulent Type ◽  
Specific Polysaccharide ◽  
Pneumococcus Type

Five strains of type III pneumococcus have been shown to possess wide capsular slime layers during the logarithmic phase of growth in serum broth. The slime layer stains metachromatically with methylene blue and can be visualized under the electron microscope as a fuzzy halo which extends well beyond the surace of the capsule proper and causes centrifugates of the organism to be of extremely large volume. This outer capsular structure is most readily demonstrated in vivo and in nutrient broth containing glucose and serum. It disappears from the surface of the cell with aging of the culture, and is easily removed by dilute alkali, alcohol, and heat. Exposure of slime-covered type III pneumococci to homologous antibody and to type III polysaccharidase reveals that the slime layer contains the same type-specific polysaccharide that is present in the rest of the capsule. From a type III strain producing a prominent slime layer an intermediate mutant has been isolated which forms small non-mucoid colonies on blood agar and possesses a relatively small capsule with a barely discernible slime layer. The wide slime layer protects virulent type III pneumococci from surface phagocytosis. Whenever the type III cells lose their broad slime layer, whether from aging of the culture, from mutation, from exposure to injurious chemicals, or from the action of type III polysaccharidase, they become susceptible to phagocytosis by the surface mechanism. Once phagocyted the type III pneumococci are promptly destroyed, even in the absence of antibodies.

scholarly journals THE PROTECTIVE ACTION OF A SPECIFIC ENZYME AGAINST TYPE III PNEUMOCOCCUS INFECTION IN MICE

1931 ◽  
Vol 54 (1) ◽  
pp. 73-89 ◽  
Author(s):  
Oswald T. Avery ◽  
René Dubos
Keyword(s):  
Capsular Polysaccharide ◽  
Protective Action ◽  
Specific Enzyme ◽  
Animal Body ◽  
Type Iii ◽  
Bacterial Enzyme ◽  
Virulent Type ◽  
Favorable Influence ◽  
Living Organisms

The bacterial enzyme which decomposes the purified capsular polysaccharide of Type III Pneumococcus in vitro also destroys the capsules of the living organisms growing in media and in the animal body. Potent preparations of this same enzyme protect mice against infection with virulent Type III Pneumococcus. The protective action is type-specific. The protective activity of the specific enzyme is destroyed by heat (70°C. for 10 minutes). The enzyme remains in an effective concentration 24 to 48 hours after its injection into normal mice. The enzyme has been found to exert a favorable influence on the outcome of an infection already established at the time of treatment. A definite relationship has been found to exist between the activity of the enzyme in vitro and its protective power in the animal body. The mechanism of the protective action is discussed with special reference to the relation between the decapsulation of the bacteria by the enzyme and the phagocytic response of the host.

scholarly journals CHEMO-IMMUNOLOGICAL STUDIES ON CONJUGATED CARBOHYDRATE-PROTEINS

1931 ◽  
Vol 54 (3) ◽  
pp. 437-447 ◽  
Author(s):  
Oswald T. Avery ◽  
Walther F. Goebel
Keyword(s):  
Experimental Data ◽  
Capsular Polysaccharide ◽  
Horse Serum ◽  
Single Component ◽  
Animal Protein ◽  
Specific Antibodies ◽  
Type Iii ◽  
Active Immunity ◽  
Virulent Type ◽  
Protective Antibodies

1. Type-specific antipneumococcus immunity has been induced in rabbits by immunization with antigen prepared by combining a specific derivative of the capsular polysaccharide of Type III Pneumococcus with globulin from horse serum. 2. Rabbits immunized with this antigen acquire active immunity against infection with virulent Type III pneumococci. 3. The sera of the immune rabbits contain type-specific antibodies which precipitate the Type III capsular polysaccharide, agglutinate Type III pneumococci, and specifically protect mice against Type III infection. 4. The experimental data are discussed with reference to: (1) the concurrence in the immune sera of type-specific antibodies for Pneumococcus and precipitins for horse globulin; (2) the determining influence of the capsular polysaccharide on the specificity of the antigen as a whole; (3) the unity of the type-specific precipitins, agglutinins, and protective antibodies induced by a single component of the pneumococcus in chemical union with an unrelated, animal protein.

scholarly journals SOME ULTRAVIOLET PHOTOMICROGRAPHS OF B. SUBTILIS

1931 ◽  
Vol 54 (3) ◽  
pp. 449-451 ◽  
Author(s):  
Ralph W. G. Wyckoff ◽  
Adrian L. Ter Louw
Keyword(s):  
Experimental Data ◽  
Capsular Polysaccharide ◽  
Horse Serum ◽  
Animal Protein ◽  
Specific Antibodies ◽  
Type Iii ◽  
Active Immunity ◽  
Virulent Type ◽  
Protective Antibodies

1. Type-specific antipneumococcus immunity has been induced in rabbits by immunization with antigen prepared by combining a specific derivative of the capsular polysaccharide of Type III Pneumococcus with globulin from horse serum. 2. Rabbits immunized with this antigen acquire active immunity against infection with virulent Type III pneumococci. 3. The sera of the immune rabbits contain type-specific antibodies which precipitate the Type III capsular polysaccharide, agglutinate Type III pneumococci, and specifically protect mice against Type III infection. 4. The experimental data are discussed with reference to: (1) the concurrence in the immune sera of type-specific antibodies for Pneumococcus and precipitins for horse globulin; (2) the determining influence of the capsular polysaccharide on the specificity of the antigen as a whole; (3) the unity of the type-specific precipitins, agglutinins, and protective antibodies induced by a single compo of the pneu mococcus in chemical union with an unrelated, animal protein.

scholarly journals THE DEMONSTRATION OF LESIONS AND VIRUS IN THE LUNGS OF MICE RECEIVING LARGE INTRA-PERITONEAL INOCULATIONS OF EPIDEMIC INFLUENZA VIRUS

1938 ◽  
Vol 67 (6) ◽  
pp. 953-972 ◽  
Author(s):  
E. R. Rickard ◽  
Thomas Francis
Keyword(s):  
Influenza Virus ◽  
Lymph Nodes ◽  
Intraperitoneal Injection ◽  
High Concentration ◽  
Regional Lymph Nodes ◽  
Intranasal Infection ◽  
Pulmonary Lesions ◽  
Resistance To Infection ◽  
Subcutaneous Inoculation ◽  
Intraperitoneal Inoculation

Following the intraperitoneal inoculation of mice with large doses of epidemic influenza virus (50,000 to 1 million intranasal M.L.D.) it can be recovered from the lungs in high concentration, and pulmonary lesions of moderate extent may be observed. The virus reaches its highest titer in the lungs 48 to 72 hours after intraperitoneal injection and may persist for 10 days. Virus may be recovered from the blood in the first 24 hours, but is readily detected in the omentum and peritoneum for 5 to 6 days. Mice which as a result of the intraperitoneal injection of virus show a high concentration of virus in the lungs do not die but become solidly immune to intranasal infection. Moreover, as early as 24 to 48 hours after intraperitoneal inoculation of large amounts of virus the animals may exhibit resistance to infection with fatal doses of virus given intranasally. Influenza virus given intravenously to mice is rapidly removed from the blood but persists in the lungs and induces pulmonary lesions. Virus can also be recovered from the liver for several days. With subcutaneous inoculation of influenza virus, however, the virus does not reach the blood or lungs in detectable amounts although the regional lymph nodes may yield considerable quantities of the agent. A brief consideration is presented of the mechanisms of infection and resistance which may be involved.

scholarly journals FACTORS AFFECTING THE YIELD OF SPECIFIC ENZYME IN CULTURES OF THE BACILLUS DECOMPOSING THE CAPSULAR POLYSACCHARIDE OF TYPE III PNEUMOCOCCUS

1932 ◽  
Vol 55 (3) ◽  
pp. 377-391 ◽  
Author(s):  
René Dubos
Keyword(s):  
Capsular Polysaccharide ◽  
Free Enzyme ◽  
Appreciable Amount ◽  
Specific Substrate ◽  
Specific Enzyme ◽  
Factors Affecting ◽  
Type Iii ◽  
Cultural Conditions ◽  
Bacterial Enzyme ◽  
Specific Substance

All improved method is described for the preparation, concentration, and purification of a bacterial enzyme capable of decomposing the capsular polysaccharide of Type III Pneumococcus. The cultural conditions for the growth of the specific microorganism must be such that the capsular polysaccharide is completely decomposed before any appreciable amount of free enzyme is released into the medium. This reduces to a minimum the decomposition of the specific substrate by the free enzyme. As a result, a larger part of the specific substance remains as a source of energy for the growing microorganism and less enzyme is lost through inactivation during the course of decomposition of the specific substrate. A marked stimulation of growth and of enzyme production occurs when small amounts of yeast extract are added to the medium and when the cultures are incubated under conditions of increased aeration. Special emphasis is placed upon the fact that, thus far, appreciable amounts of the specific enzyme have been obtained only when the capsular polysaccharide itself, or the aldobionic acid derived from it, was present in the culture medium.

scholarly journals The Serotype of Type Ia and III Group B Streptococci Is Determined by the Polymerase Gene within the Polycistronic Capsule Operon

2000 ◽  
Vol 182 (16) ◽  
pp. 4466-4477 ◽  
Author(s):  
Donald O. Chaffin ◽  
Stephen B. Beres ◽  
Harry H. Yim ◽  
Craig E. Rubens
Keyword(s):  
Capsular Polysaccharide ◽  
Single Gene ◽  
Functional Characterization ◽  
Neonatal Morbidity ◽  
Polymerase Gene ◽  
Chromosomal Dna ◽  
Group B Streptococci ◽  
Sequence Comparisons ◽  
Type Iii ◽  
Type Ia

ABSTRACT Streptococcus agalactiae is a primary cause of neonatal morbidity and mortality. Essential to the virulence of this pathogen is the production of a type-specific capsular polysaccharide (CPS) that enables the bacteria to evade host immune defenses. The identification, cloning, sequencing, and functional characterization of seven genes involved in type III capsule production have been previously reported. Here, we describe the cloning and sequencing of nine additional adjacent genes, cpsIIIFGHIJKL,neuIIIB, and neuIIIC. Sequence comparisons suggested that these genes are involved in sialic acid synthesis, pentasaccharide repeating unit formation, and oligosaccharide transport and polymerization. The type III CPS (cpsIII) locus was comprised of 16 genes within 15.5 kb of contiguous chromosomal DNA. Primer extension analysis and investigation of mRNA from mutants with polar insertions in their cpsIII loci supported the hypothesis that the operon is transcribed as a single polycistronic message. The translated cpsIII sequences were compared to those of the S. agalactiae cpsIa locus, and the primary difference between the operons was found to reside in cpsIIIH, the putative CPS polymerase gene. Expression of cpsIIIH in a type Ia strain resulted in suppression of CPS Ia synthesis and in production of a CPS which reacted with type III-specific polyclonal antibody. Likewise, expression of the putative type Ia polymerase gene in a type III strain reduced synthesis of type III CPS with production of a type Ia immunoreactive capsule. Based on the similar structures of the oligosaccharide repeating units of the type Ia and III capsules, our observations demonstrated that cpsIaH andcpsIIIH encoded the type Ia and III CPS polymerases, respectively. Additionally, these findings suggested that a single gene can confer serotype specificity in organisms that produce complex polysaccharides.

Initial Studies of the Molecular Basis of Peptide Mimicry of Group B Streptococcal Type III Capsular Polysaccharide

2001 ◽  
Vol 20 (2) ◽  
pp. 221-227 ◽  
Author(s):  
Seth H. Pincus ◽  
Stephen R. Lepage ◽  
Robert F. Jung ◽  
Jennifer G. Massey ◽  
Mahesh Jaseja
Keyword(s):  
Molecular Basis ◽  
Capsular Polysaccharide ◽  
Type Iii ◽  
Peptide Mimicry ◽  
Group B

scholarly journals Polysaccharides and virulence of Burkholderia pseudomallei

2007 ◽  
Vol 56 (8) ◽  
pp. 1005-1010 ◽  
Author(s):  
M. Sarkar-Tyson ◽  
J. E. Thwaite ◽  
S. V. Harding ◽  
S. J. Smither ◽  
P. C. F. Oyston ◽  
...  
Keyword(s):  
Burkholderia Pseudomallei ◽  
Capsular Polysaccharide ◽  
Gene Clusters ◽  
Type I ◽  
Wild Type ◽  
Time To Death ◽  
Type Iii ◽  
Type Iv ◽  
Mutant Strains ◽  
Delayed Time

Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease of humans and animals. Gene clusters which encode capsular polysaccharide (type I O-PS) and LPS (type II O-PS), both of which play roles in virulence, have previously been identified. Here, the identification of two further putative clusters, type III O-PS and type IV O-PS, is reported. Mice challenged with type III O-PS or type IV O-PS mutants showed increased mean times to death (7.8 and 11.6 days) compared to those challenged with wild-type B. pseudomallei (3 days). To investigate the possible roles of polysaccharides in protection, mice were immunized with killed cells of wild-type B. pseudomallei or killed cells of B. pseudomallei with mutations in the O antigen, capsular polysaccharide, type III O-PS or type IV O-PS gene clusters. Immunization with all polysaccharide mutant strains resulted in delayed time to death compared to the naïve controls, following challenge with wild-type B. pseudomallei strain K96243. However, immunization with killed polysaccharide mutant strains conferred different degrees of protection, demonstrating the immunological importance of the polysaccharide clusters on the surface of B. pseudomallei.

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