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At least 217 records · Page 12Linked to original sources
PubMed2002

Cytokine profiles in a rat model of otitis media with effusion caused by eustachian tube obstruction with and without Streptococcus pneumoniae infection.

OBJECTIVE: Cytokine expression was studied in a rat model of otitis media with effusion. METHODS: The left eustachian tube was obstructed (eustachian tube obstruction [ETO]) in 84 rats. Forty-two ears were challenged with, and those rats were treated from day 2 to day 7 with ampicillin. Twelve rats (6 per group) were killed on days 1, 2, 7, 21, 35, 56, and 112; mucosa was harvested and assayed for interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), interleukin-10 (IL-10), interferon-gamma (IFN-gamma), transforming growth factor-beta (TGF-beta), monocyte chemoattractant protein-1 (MCP-1), and interleukin-8 (IL-8) gene expression, and effusion was assayed for IL-1beta, TNF-alpha, IL-6, IL-10, and macrophage inflammatory protein-2 (MIP-2) protein. RESULTS: Most cytokines were detectable in the effusion from infected ears with ETO on days 1 and 2 only. MIP-2 exhibited a biphasic response. Only effusion MIP-2 was consistently detected in uninfected ears with ETO. Three patterns of mucosal cytokine messenger RNA (mRNA) upregulation were observed: isolated early (IL-1beta, IL-8), isolated late (TNF-alpha, IFN-gamma), and biphasic (MCP-1, IL-6, TGF-beta) responses. Early cytokine mRNA upregulations were observed only in the infected ears with ETO, whereas late upregulations were observed in both groups. CONCLUSIONS: Early expression of the assayed cytokines occurred only in ears with active infection. For both groups, a late upregulation of cytokine message but not protein was documented. The profile of cytokine expression during otitis media episodes may be useful in defining etiology, disease stage, and prognosis.

Ampicillin↗
PubMed1991

Early onset neonatal group B streptococcus (GBS) infection: associated obstetric risk factors.

An analysis of all early onset neonatal Group B streptococcal (GBS) infections at the Royal Women's Hospital, Melbourne was made for the 10-year period 1979-1988. There were 104 cases with 29 neonatal deaths (28%). One or more predisposing perinatal risk factors was evident in 82% of cases (premature labour 79%, prolonged membrane rupture (greater than 12 hours) 57%, premature rupture of the membranes 69%, maternal sepsis 29%). Overall, 88% of GBS infections were evident within 24 hours of birth, suggesting an intrapartum pathogenesis for infection.

Bacteriuria↗
PubMed1994

Antibody-independent protection in mice against type Ia group B streptococcus lethal infection.

There is ample evidence that protection against group B streptococcal (GBS) disease, both in experimental animals and in humans, is related to the presence of specific antibodies and complement. However, until now the possibility of increasing resistance to GBS infection by potentiating natural cell-mediated immunity in the host, has not been explored. In this study we examine the effect of administering in vivo MVE-2 (a polymer fraction of 1,2-co-polymer of divinyl ether and maleic anhydride) and inactivated Candida albicans (CA) cells on mouse resistance to the reference strain type Ia 090 GBS (GBS-090) lethal infection. MVE-2 and CA, respectively a synthetic and a microbial biological response modifier (BRM), are strong inducers and activators of natural resistance effectors, such as natural killer (NK) cells, macrophages and polymorphonuclear cells (PMN). The results showed that MVE-2 protected 100% CD-1 mice from a systemic lethal challenge with GBS-090 (5 x 10(3) microorganisms/mouse) when administered 3 days before infection at dose of 50 mg kg-1. CA treatment, in five doses (CA-5d) over 14 days protected 100% mice when administered at 2 x 10(7) cells/mouse and when the last CA injection was given 1 day before the GBS-090 challenge. Instead, when the GBS-090 challenge was performed by intraperitoneal route, protection was obtained with CA-5d treatment but not with MVE-2. The possibility that MVE-2 or CA stimulated a rapid production of specific antibodies against GBS-090 infection was excluded by the ELISA assay. Evidence exists that NK cells do not play a primary role as effectors in the MVE-2 and CA conferred protection since the strong reduction in NK activity, due to in vivo administration of anti-asialo GM1 antibodies before GBS-090 infection, did not influence the BRM-induced protection. Besides, high NK activity levels, induced by in vivo rhIL-2 administration, did not protect the mice against GBS-090 infection. Both studies on in vivo clearance and in vitro microbicidal activity, showed that, after 1 h, immunopotentiated effectors were unable to kill GBS-090, but were highly effective against GBS type VI. These results seem to indicate that intracellular GBS-090 killing is a slow process requiring more than 1 h. This study demonstrates that it is possible to increase resistance to GBS-090 lethal infection by BRMs, by potentiating the antibody-independent microbicidal activity of the phagocytes.

Animals↗
PubMed1989

[Penicillin insensitive and resistant Streptococcus pneumoniae infection in children].

Five cases of penicillin insensitive or resistant pneumococcal infection in children were experienced during the period of 2 years since March, 1986. One isolate from middle ear showed the MIC of 4 micrograms/ml against penicillin-G. One isolate of insensitive pneumococcus was isolated from CSF specimen. Between 1976 and 1987, 59 isolates from 88 stocked pneumococcal clinical isolates were alive. These 59 strains were screened by oxacillin disc for insensitive and resistant pneumococcus. Five strains which were insensitive or resistant strains had inhibitory zone under 20 mm. The prevalence rate of insensitive or resistant pneumococcus since 1986 was 18%.

Humans↗
PubMed1995

Experimental Streptococcus pneumoniae infection in mice for studying correlation of in vitro and in vivo activities of penicillin against pneumococci with various susceptibilities to penicillin.

The purpose of the study was to investigate the correlation of in vitro activity with the in vivo effect and the pharmacokinetics of penicillin in the treatment of infections with pneumococci with various susceptibilities to penicillin. We used 10 pneumococcal strains for which penicillin MICs ranged from 0.016 to 8 micrograms/ml. Time-kill curve experiments were performed with all strains. We found that the effect of penicillin in vitro is concentration independent, with a maximum effect at two to four times the MIC for penicillin-susceptible as well as penicillin-resistant pneumococci. The mouse peritonitis model with an inoculum of approximately 10(6) CFU, to which mucin was added, resulted in a reproducible lethal infection with the pneumococci. The 50% effective dose was determined for each strain, and we found a highly significant correlation between the log MIC and the log 50% effective dose of penicillin against these strains (P < 0.01). Furthermore, it was shown that the most important pharmacokinetic parameter determining the effect of penicillin in vivo was the time that the concentration of penicillin in serum was greater than the MIC.

Animals↗
PubMed1994

Transgene-encoded antiphosphorylcholine (T15+) antibodies protect CBA/N (xid) mice against infection with Streptococcus pneumoniae but not Trichinella spiralis.

Immunodeficient CBA/N (xid) mice are highly susceptible to Streptococcus pneumoniae infection. Previous studies indicated that this susceptibility may be attributed to the lack of antibodies to phosphorylcholine (PC) in the circulation of these animals. We now provide direct proof that when these mice are genetically manipulated to produce significant amounts of circulating anti-PC immunoglobulin G antibodies of the T15 idiotype, they can be protected against a lethal challenge with S. pneumoniae. Transgenic mice were also used to investigate whether the transgene-encoded antibodies could protect the animals against another PC-bearing microorganism, Trichinella spiralis; in this case, there was no protection. These results were further supported by experiments with CFW mice which had been immunized to produce high levels of anti-PC antibodies but which were found to be just as susceptible to T. spiralis infection as nonimmunized animals.

Animals↗
PubMed1997

Survey of emm gene sequences and T-antigen types from systemic Streptococcus pyogenes infection isolates collected in San Francisco, California; Atlanta, Georgia; and Connecticut in 1994 and 1995.

The variable 5' emm (M-protein gene) sequences and T-antigen types were determined from 340 systemic group A streptococcal (GAS) isolates taken from hospitalized patients in San Francisco, Calif.; Atlanta, Ga.; and Connecticut in 1994 and 1995. Eighty percent of these isolates had emm sequences and T-antigen types in agreement with previously recorded M- and T-antigen associations. Most of the remaining strains either were T nontypeable (11%) or contained emm genes encoding M proteins for which T-antigen associations have not been made (6%). One newly encountered emm gene, designated ST2974, from each of 13 isolates had the T type 8/25/Imp19. Another new emm gene, ST2967, from 8 of 11 isolates was T nontypeable. Six other unique emm gene sequences from seven isolates were encountered. Sequencing of the variable region of the emm gene of GAS isolates (emm typing) is effective for surveying the sequence variability of the M virulence protein, and combined with T typing, emm typing is useful for monitoring GAS strain diversity.

Amino Acid Sequence↗
PubMed2000

Empyema of lung associated with Streptococcus milleri infection.

Empyema of the lung is a very serious illness which must be detected quickly and treated aggressively. We report an unusual case of empyema of the lung associated with a boating accident while the patient was fishing in a sea loch off the west coast of Scotland.

Anti-Bacterial Agents↗