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[Manifestations of Streptococcus infection resulting from various serologic groups of streptococcus].

44 autopsy cases (from 1985 to 1990) are studied out of which in 38 cases the diseases were produced by streptococcus of group A. In 18 cases there was a pharyngeal or extra-pharyngeal generalized streptococcus infection (scarlet fever). Moderately pronounced local damage, mainly pneumonia, were found in 20 cases. In 3 other cases the disease was produced by group B streptococcus, in 2 cases by streptococcus D and in 1 case by streptococcus of G group. Group A streptococcus was encountered mainly in children older than 6 months (31 cases), B and D at an earlier age (particularly B streptococcus). Morphologically, there were no essential differences connected with different streptococcus groups. The infection in most cases was correlated with a respiratory diseases, more frequently with influenza or respiratory-syncytial infection this favouring more grave course of streptococcus infection.

Child↗

[Pathology of generalized Streptococcus infection].

7 cases of the generalized streptococcus infection in children aged from 1 year 8 months to 12 years are analyzed. The course of the disease was in all cases extremely rapid and terminated by death within 3-4 days. Results of the autopsy material investigation allowed to conclude that the pathology of the generalized streptococcus infection at present does not differ from that described in classical text-books. The attention is drawn to the connection between the generalized streptococcus infection and herpes-like infections since in all cases studied herpes stomatitis, genital herpes, varicella were noted clinically. The presence of herpes-like infections was confirmed morphologically in some cases.

Child↗

Hyporesponsiveness of peripheral blood lymphocytes to streptococcal superantigens in patients with guttate psoriasis: evidence for systemic stimulation of T cells with superantigens released from focally infecting Streptococcus pyogenes.

Throat infection with Streptococcus pyogenes is the most important trigger for acute guttate psoriasis. We examined the in vitro responses of peripheral blood mononuclear cells (PBMC) to streptococcal superantigens, SPEA and SPEC, and staphylococcal superantigens, SEB and TSST-1, in patients with guttate psoriasis, in patients with chronic plaque psoriasis, and in healthy subjects. PBMC from patients with guttate psoriasis responded poorly to SPEA and SPEC at concentrations of 0.1 and 1 ng/ml as compared with those from patients with plaque psoriasis, but showed high responses to SEB and TSST-1. The hyporesponsiveness recovered after improvement of the skin eruption. There was no significant difference between guttate and chronic types of psoriasis in the percentage of circulating T-cell receptor BV2 or BV8-bearing T cells, responsive to streptococcal superantigens, indicating that T-cell clonal anergy was a mechanism underlying the hyporesponsiveness. Our results suggest that superantigens released from focally infecting S. pyogenes induce a transient activation of relevant T cells, leading to the development of skin eruption and, subsequently, temporary T-cell anergy to these toxins.

Adult↗

Severe Streptococcus infection in spotted hyenas in the Ngorongoro Crater, Tanzania.

In a population of spotted hyenas (Crocuta crocuta) monitored between 1996 and 2005 in the Ngorongoro Crater, Tanzania, 16 individuals from five of eight social groups displayed clinical signs of an infection, including severe unilateral swelling of the head followed by abscess formation at the mandibular angle, respiratory distress, mild ataxia, and lethargy. Two (12.5%) of these 16 individuals died within days of developing signs. Clinical signs in hyenas were first noted in 2001, and most cases occurred between September 2002 and February 2003, suggesting an outbreak of infection during this period. Histopathological examination of internal organs from one hyena that died with signs revealed morphological changes consistent with severe bacterial infection. Phenotypic examination and phylogenetic analysis of the 16S rRNA gene of the causative agent of infection revealed a Lancefield group C Streptococcus with a high level of homology to S. equi subsp. ruminatorum, a subspecies of S. equi recently described in domestic sheep (Ovis aries) and goats (Capra hircus) with mastitis in Spain. Strains similar to this bacterium were also isolated from two hyenas without obvious clinical signs, suggesting that hyenas may be 'carriers' of this bacterium, and from a sympatric Burchell's zebra (Equus burchelli), a herbivore species often consumed by hyenas. To our knowledge this is the first report of a Streptococcus infection in these two wildlife species. The high genetic similarity between the hyena and zebra isolates indicates that inter-specific transmission may occur, possibly when hyenas consume infected zebra carcasses.

Animals↗

Cytokine response to group B streptococcus infection in mice.

This study was undertaken to better understand the complex relationship between specific and non-specific host defence mechanisms and group B streptococci (GBS). A comprehensive kinetics analysis of cytokine mRNA expression was performed, by Northern blot assay, in peritoneal exudate cells (PEC) and spleen cells (SC) recovered from CD-1 mice at various times during the course of an intraperitoneal infection with a lethal dose (5 x 10(3) microorganisms/mouse) of type Ia GBS, reference strain 090 (GBS-Ia). Analysis of cytokines involved in the development of a specific TH response shows that GBS-Ia in PEC induce only a weak increase of IL-2 mRNA expression and in SC a cytokine pattern characterized by IL-2, IFN-gamma and IL-12 in the absence of IL-4, IL-5 and IL-10. This selected cytokine pattern could provide appropriate conditions for the development of a TH1 response. Analysis of inflammatory cytokines, which are usually induced early during an in vivo infection, shows that there is a significant expression of mRNA specific for IL-1beta, TNFalpha and IL-6, both in PEC and SC only at 24 h which persists at a high level until 36 h. This delayed cytokine induction, accompanied by the contemporary activation of splenic phagocytic cells, occurs only when the number of GBS-Ia is extremely high. In fact, at 24 h GBS-Ia have heavily colonized all organs. In vitro infection of thioglycollate-elicited peritoneal macrophages confirms that the ability of GBS-Ia to induce a strong inflammatory cytokine response depends strictly on the number of infecting microorganisms. Indeed, macrophages respond to GBS-Ia with a very rapid induction of IL-1beta and TNFalpha mRNA when infected at a ratio of 1:10, but not at 100:1. Two major observations emerged from this study: (1) GBS-Ia, by inducing a cytokine pattern which seems to favour development of a TH1 response, could evade antibody production essential for resistance to GBS; and (2) inflammatory cytokine response is induced when a heavy microbial invasion of the host has already occurred. These novel features of GBS-Ia could contribute to the development and progression of lethal infection in mice.

Animals↗

Clinical triggers to initiate intrapartum penicillin therapy for prevention of group B streptococcus infection.

Despite national recommendations for prophylactic group B streptococci intrapartum penicillin therapy (GBS-IPT), there is little guidance for clinicians regarding to how to achieve the recommended 4 hours of therapy. We sought to identify clinical triggers for effective temporal prompts to initiate GBS-IPT to achieve the recommended duration of therapy. GBS-colonized women who delivered between 37 and 42 weeks were analyzed retrospectively. The clinical record was reviewed for clinical events including rupture of membranes, oxytocin therapy, 4-cm dilation, active labor, narcotic analgesia, epidural analgesia. In addition, combinations of these triggers were evaluated using the first appearance of 4-cm dilation or active labor, narcotic analgesia or epidural, and a composite indicator of each of these four triggers. Antibiotic duration and proportion receiving 4 hours of GBS-IPT for each trigger were compared with the conventional penicillin management the patient actually received (CM). Data were analyzed with Z-test for proportions with Bonferroni correction and one-way analysis of variance. Two hundred thirteen women met study criteria and were reviewed. Using CM, 90.8% of nulliparas and 68.7% of parous women achieved adequate GBS-IPT. In nulliparas, each clinical trigger resulted in equivalent rates of adequate GBS-IPT compared with CM. The duration of therapy was less for 4-cm dilation, epidural, epidural or narcotic analgesia, and 4-cm dilation or active labor triggers in nulliparas, suggesting better identification of the period 4 hours prior to delivery. In parous women, clinical triggers did not perform better than CM. In nulliparous women, clinical triggers to initiate therapy may achieve high rates of GBS-IPT, with a significant decrease in the duration of antibiotic therapy. In nulliparous women, clinical triggers better identify the 4-hour window prior to delivery than CM.

Adult↗