The 2018 rift eruption and summit collapse of Kilauea Volcano.

In 2018, Kilauea Volcano experienced its largest lower East Rift Zone (LERZ) eruption and caldera collapse in at least 200 years. After collapse of the Pu'u 'O'o vent on 30 April, magma propagated downrift. Eruptive fissures opened in the LERZ on 3 May, eventually extending ~6.8 kilometers. A 4 May earthquake [moment magnitude (M w) 6.9] produced ~5 meters of fault slip. Lava erupted at rates exceeding 100 cubic meters per second, eventually covering 35.5 square kilometers. The summit magma system partially drained, producing minor explosions and near-daily collapses releasing energy equivalent to M w 4.7 to 5.4 earthquakes. Activity declined rapidly on 4 August. Summit collapse and lava flow volume estimates are roughly equivalent-about 0.8 cubic kilometers. Careful historical observation and monitoring of Kilauea enabled successful forecasting of hazardous events.

Endotoxin inactivating activity of rat serum.

The ability of rat serum to inactivate endotoxin (LPS) was assessed with the aid of the limulus amebocyte lysate assay. Following the addition of various amounts of endotoxin to normal serum the mixture was incubated for 1 hr at 37 degrees C and the residual endotoxin activity determined. One milliliter of rat serum inactivated between 5 and 10 micrograms Escherichia coli LPS per hour. Heating serum for 45 min at 56 degrees C resulted in loss of 80-90% of the LPS inhibitor (LPSI) activity. Serum from cobra venom factor (CVF)-treated rats inactivated between 0.5 and 2.5 micrograms LPS/ml serum. Serum from tolerant rats, even after heating for 45 min at 56 degrees C, inactivates between 10 and 15 micrograms LPS/ml serum/hr; decomplemented tolerant rat serum neutralizes between 5 and 10 micrograms LPS/ml serum/hr. Clearly, the tolerant rat has large quantities of LPSI activity, which does not appear to be complement. The inhibitor found in tolerant rat serum is not species specific since it inactivates Salmonella minnesota and Salmonella typhimurium endotoxins to the same degree and in the same amount as E. coli endotoxin, the agent used to induce tolerance. Both heating serum (56 degrees C) and lead acetate reduce LPSI activity.

Enzyme immunoassay for the detection of group A streptococcal antigen.

A competitive inhibition enzyme immunoassay for the detection of Streptococcus pyogenes directly from throat specimens or from solid bacteriological medium is described. Group A-specific polysaccharide adsorbed onto treated polystyrene beads, in conjunction with rabbit antibody to S. pyogenes, was used to determine the presence of the polysaccharide antigen. Inhibition values in excess of 65% were observed with 10(4) or more CFU of S. pyogenes per test. An inhibition of 25% was demonstrated with as few as 10(3) CFU per test. Heterologous microorganisms tested at 10(6) CFU per test reacted at levels of inhibition less than 25%. Two types of bacterial transport medium and swabs of different fiber compositions did not alter the assay performance. Accurate identification of S. pyogenes was achieved by testing single colonies picked directly from blood agar plates which had been incubated for 18 to 24 h. In addition, the assay was performed on throat specimens from children and adults having pharyngitis. A single-swab, blind study was conducted in which enzyme immunoassay reactivity was compared with results of blood agar culture and bacitracin sensitivity. When there were discordant results, serological identification was used as the confirmatory test. At an optimal cutoff value of 40% inhibition, sensitivity and specificity by enzyme immunoassay were 97.0% and 97.9%, respectively, as compared with confirmed culture results. The assay has an incubation time of 3 h and is a sensitive and specific method for the detection of S. pyogenes antigen.

Acute hepatotoxin exposure effects lymphoid and accessory cell types in inbred mice.

The effect of acute hepatotoxin exposure on in vivo and in vitro immune responses were investigated in inbred mice. Splenic anti-SRBC PFC responses were slightly enhanced by carbon tetrachloride or galactosamine administration 5 hr prior to immunization. Whereas splenic anti-SRBC PFC responses were slightly enhanced in euthymic mice exposed to carbon tetrachloride 5 hr prior to immunization, immune responses to the TI antigens, Fl-LPS, Fl-Ficoll, and TNP-LPS, were significantly suppressed. Athymic mice receiving similar hepatotoxin exposure elicited enhanced immune responses to the TI immunogens, thereby suggesting that the activities of B cells and macrophages are enhanced in treated animals and in euthymic mice, T suppressor cells are also activated. By admixture of purified B- and T-cell and macrophage populations from either carbon tetrachloride-treated or control animals, it was demonstrated that hepatotoxin exposure also induces suppressor T cells regulating immune responses to the T-dependent antigen, SRBC, and that macrophages from treated animals are more functional. Further, B-cell responsiveness is enhanced. In addition to these observations, an active factor could be demonstrated in sera from hepatotoxin-treated animals which augments immune responses to SRBC in normal mice and promotes immune responses to this antigen in athymic mice. These findings indicate that the effects of acute hepatotoxin exposure are multifocal, influencing the activity of lymphoid and accessory cells.

In vivo quantitation of the rat liver's ability to eliminate endotoxin from portal vein blood.

The in vivo uptake of endotoxin by the liver from portal vein blood was assessed during a single passage through the liver. 51Cr labeled and unlabeled endotoxin were infused in different amounts into the femoral vein of three groups of lead-sensitized rats: a nonoperated, a sham-operated, and a surgically created reversed Eck fistula (REF) group. Whereas in the former two the infused endotoxin encounters the lung as the first filter organ, the liver performs this function in the latter experimental model. The mortality rates observed in control and sham-operated, lead-sensitized rats were found to correlate closely and reproducibly to the degree of endotoxemia. This assay was then applied to determine the amount of endotoxin eliminated by the liver by establishing, in the REF rat, the amounts of endotoxin that escaped hepatic clearance. Following infusion of 1 microgram of endotoxin/hr into REF rats, approximately 985 ng is found to be taken up by the liver; following 2 micrograms, 1965 ng is sequestered; following 3 micrograms, 2810 ng; and after 4 micrograms, 3175 ng is retained by the liver. Hence, the capacity of the liver to eliminate endotoxin from portal vein blood during a single passage increases as the portal vein endotoxin level rises; it approaches a maximum, suggesting that endotoxin's interaction with the Kupffer cells conforms to classical saturation kinetics. A Lineweaver-Burk plot prepared from these data indicates that the maximal in vivo capacity of the liver to remove endotoxin from portal vein blood approximates 1.5 micrograms/gm liver/hr. Data obtained with the use of radiolabeled endotoxin corroborate the information obtained with the bioassay technique. Endotoxin eliminated by the Kupffer cells in these quantities is slowly disintegrated; 4 hr after termination of the endotoxin infusion, less than 4% of the radiolabel is found in the urine and none in the bile. These observations indicate that the Kupffer cell's functional capacity to sequester and detoxify endotoxin is extensive and far exceeds the requirements imposed by physiological and most pathological conditions.

LPS regulation of the immune response: suppression of immune responses to orally administered T-independent antigen.

The regulation of immune responses to gastrically administered TI antigens has been investigated, and the characterization of a regulatory cell population has been performed. Intragastric administration of TNP-haptenated homologous erythrocytes (TNP-MRBC) induced splenic IgM anti-TNP PFC responses in LPS nonresponsive C3H/HeJ mice that were higher than those in LPS-responsive C3H/HeN mice and similar to those noted in athymic (nu/nu) C3H/HeN animals. The simultaneous intragastric administration of LPS with TNP-MRBC augmented immune responses in a manner similar to that previously reported for parenterally administered LPS and antigen. Further, LPS-induced augmentation of TNP-MRBC responses was greater in athymic mice. These findings were substantiated using in vitro spleen cultures. Intragastric challenge with a 2nd TI antigen, TNP-LPS, induced approximately 8-fold higher splenic anti-TNP PFC responses in athymic C3H/HeN mice compared with those in euthymic littermates. By admixture of B and T cell populations, it was demonstrated that the host responsiveness to TNP-LPS was negatively regulated by suppressor cells. Suppressive activity resided in a Thy 1.2-bearing, irradiation-resistant, nylon wool-nonadherent cell population. These cells could be demonstrated in spleen and Peyer's patches from young or old LPS-responsive C3H/HeN mice, but not in tissues from LPS nonresponsive C3H/HeJ mice. The specificity of the regulator cells was not limited to TNP-LPS responses, since immune responsiveness to another TI antigen, TNP-dextran, was also under the control of this cell population. These studies confirm the TI nature of TNP-MRBC and indicate that immune responses to gastrically administered antigens such as TNP-LPS, TNP-dextran, and possibly TNP-MRBC are negatively regulated by a suppressor T cell population. A role for endogenous LPS in the generation of regulator cells and the effect of these cells on host responses to gut-derived antigens is discussed.

Relationships between serological groups and deoxyribonucleic acid homology groups in Bacteroides fragilis and related species.

The serological properties of antigens extracted from strains of Bacteroides fragilis and related species belonging to several different deoxyribonucleic acid homology groups were investigated. Antisera prepared against Formalin-treated whole cell suspensions of representative strains were tested against cell suspensions, cell wall preparations, and extracts of homologous and heterologous strains by using agglutination, immunodiffusion, and hemagglutination techniques. Serological results indicated that the species were antigenically distinct, although minor cross-reactions were observed. Homology groups, including the two B. fragilis subgroups, were relatively homogeneous, although the presence of serotypes within each homology group was suggested. Immunodiffusion tests demonstrated, however, that each possessed a mosaic antigen composition; at least 6 antigenic determinants could be demonstrated in B. fragilis 2553, and up to 10 were found in B. fragilis 2393. Hemagglutination tests using antigen extracts also indicate a mosaic of antigens in each strain.

Mice refractory to lipopolysaccharide manifest high immunoglobulin A responses to orally administered antigen.

Lipid A-nonresponding C3H/HeJ mice manifested high immune responses to orally administered (either by feeding or by intragastric immunization) heterologous erythrocytes when compared with syngeneic lipid A-responding C3H/HeN mice. Prolonged consumption of horse erythrocytes resulted in a significant secretory immune response in both C3H mouse strains as evidenced by high salivary agglutinin titers. Although salivary agglutinin titers were only slightly greater in C3H/HeJ mice than those of C3H/HeN mice, serum agglutinin titers and immunoglobulin A (IgA) levels were consistently higher (two- to fourfold) in C3H/HeJ mice. The appearance of anti-horse erythrocyte plaque-forming cell responses in spleens of immunized animals was followed by an increase in salivary anti-horse erythrocyte agglutinin activity. Peak levels of both responses were attained after approximately 3 weeks of immunization. Differences in immune responsiveness between C3H mouse strains were also evident at the cellular level since splenic IgA anti-horse erythrocyte plaque-forming cell responses in fed C3H/HeJ mice were twofold higher than those in similarly treated C3H/HeN mice. This higher response pattern was also observed when C3H/HeJ mice manifested threefold higher splenic IgM and IgA plaque-forming cell responses to intragastrically administered sheep erythrocytes. Thus, higher responsiveness was observed in the C3H/HeJ mice given heterologous erythrocytes by the oral route. Furthermore, levels of serum IgA in 10- to 12-month-old nonimmunized C3H/HeJ mice were higher than those of C3H/HeN mice. These findings suggest that lack of host responsiveness to lipopolysaccharide affects the manifestation of subsequent immune responses to orally administered antigens. The possible mechanisms and implications of this high responsiveness are discussed.

Virulence of Streptococcus mutans: in vivo reversion of a low-virulence mutant results in partial displacement and pathogenesis.

A mutant of Streptococcus mutans 6715 wild type (WT), designated C4, has been shown previously to be defective in glucosyltransferase synthesis of insoluble glucan and to have low virulence in monoassociated gnotobiotic rats. The present investigation was concerned with the detection of WT-like variants of C4 in monoassociated rats, the supplantation of C4 by these WT-like organisms, and finally, the pathogenic potential of these WT-like organisms in gnotobiotic rats. In the first series of longitudinal studies with C4-monoassociated rats, WT-like organisms were detected at a low frequency (0.001%) in oral swab samples from only one of four cages of animals analyzed on day 7 after infection (age 27 days). The frequency of variants isolated from animals in the one cage increased, and by age 45 days these organisms represented approximately 1% of the mandibular plaque flora. After random redistribution of rats in the four cages (age 45 days), microbial analysis of oral swab samples (age 60 days) demonstrated the presence of variants in samples taken from rats in all four cages. The frequency of recoverable variants increased in older animals (age 90 days) and correlated with high caries activity. WT-like organisms were transmissible, since offspring (age 45 days) from these animals had high levels of variants as well as high caries activity. Similar results were obtained in a second longitudinal study; however, variants, although present in all four cages, were not detected until rats were 45 days old. All variant isolates exhibited morphological, biochemical, and in vivo virulence characteristics more similar to S. mutans 6715 WT than to C4. In vitro mixing experiments with C4 and either WT or a selected variant suggested that C4 was rapidly displaced by WT organisms. The results of this investigation demonstrate that the glucosyltransferase-defective, low-virulence C4 reverts to virulent WT-like organisms in vivo which compete more favorably for smooth surfaces than C4. Subsequently, these variants reached significant numbers in plaque which correlated with increased dental caries.

Encapsulation of Bacteroides species.

Capsules were detected by the India ink method in cultures of Bacteroides fragilis, B. vulgatus, B. thetaiotaomicron, and B. ovatus. No capsules were found in the five strains of B. distasonis examined.

Selective induction of an immune response in human external secretions by ingestion of bacterial antigen.

Ingestion of capsules which contained killed Streptococcus mutans by four healthy human subjects led to the appearance of specific antibodies in external secretions. Salivary and lacrymal antibodies were detected within 1 wk of ingestion and continued to increase throughout a 14-day immunization period, with a gradual decline during the 2 ensuing months. A second period of immunization resulted in a pronounced increase of specific antibody levels which occurred earlier than in the primary immunization period and reached peak levels by day 10. No change was detected in serum antibody levels throughout either immunization period. The antibody activity in all secretions was associated with the immunoglobulin A class, as determined by immunochemical analyses. These data indicate that ingestion of bacterial antigens selectively stimulates the immune response in secretions.

Induction of secretory antibodies in humans following ingestion of Streptococcus mutans.

1) Ingestion of Streptococcus mutans antigen by human volunteers induced the selective appearance of antibodies in saliva and tears but not in serum. 2) These antibodies were associated with the IgA class as determined by enhanced or blocked agglutination, immunofluorescence and gel filtration. 3) A second series of antigen ingestion resulted in a secondary response in these secretions characterized by an earlier appearance of antibodies which reached higher titers than in the primary response.

Concept of the local and common mucosal immune response.

The available information concerning the origin of IgA-producing plasma cells and the spectrum of IgA-associated antibodies found in external secretions provide arguments that support two pathways of stimulation for a secretory humoral immune response. In addition to an explicitly local immune response induced by a topical antigen application, a second mechanism of induction operating through the sensitization of GALT, and possibly BALT, emerges. The latter pathway of stimulation leads to the appearance of specific IgA-associated antibodies in secretions of mammary, salivary, and lacrymal glands (and perhaps other sites), all of which suggests the existence of a common mucosal secretory system. Not yet explained are the mechanisms involved in the homing to secretory glands of cells sensitized in the remote lymphoid tissues (GALT and BALT), the differentiation patterns of these cells, and the regulation of selective IgA expression.