Acute Serogroup A Streptococcal Shock: A Porcine Model

Sætre, T.; Høiby, E. Arne; Aspelin, Trude; Lermark, Gro; Lyberg, Torstein

doi:10.1086/315692

Cited by 17 publications

(15 citation statements)

References 43 publications

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“…Necrotic fibers that had lost their striations appeared in small clumps; the cytoplasm of the individual cells was vacuolated and hypereosinophilic (Fig. 1) Bacterial counts in infected tissues other then the CNS (Table 1) confirmed that Streptococcus iniae type II is responsible for an overwhelming septic disease characterized by large numbers of live bacteria, in accordance with similar models described in warmblooded animals (Saetre et al 2000, Yuste et al 2002. The histopathological findings of the viscera were consistent with acute bacterial infection: there was mild to moderate centrilobular hepatitis with histiocytic infiltration in the liver; hyaline droplets were observed in the cytoplasm of tubular cells in the kidneys, and there was mild lymphocyte depletion of interstitial tissue; and there was severe congestion in the spleen.…”

Section: Resultssupporting

confidence: 80%

Streptococcus iniae type II infections in rainbow trout Oncorhynchus mykiss

Lahav¹,

Eyngor²,

Hurvitz³

et al. 2004

Dis. Aquat. Org.

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Clinical and pathological findings (anorexia, hemorrhage, lethargy, loss of orientation and exophthalmia) indicated that Streptococcus iniae type II is responsible for a fatal disease in rainbow trout. Histopathological findings revealed that S. iniae type II produces a systemic disease, including a diffuse necrotizing myositis. The distribution of viable bacteria in infected tissues substantiated the pathological findings, confirming that S. iniae type II is responsible for a generalized septic disease of rainbow trout. KEY WORDS: Rainbow trout · Streptococcus iniae · Serotype · Pathology Resale or republication not permitted without written consent of the publisherDis Aquat Org 62: [177][178][179][180] 2004 2003). In the present work we assessed the pathological outcomes of infections of rainbow trout by S. iniae serotype II. Our results indicate that Serotype II strains produce an acute septic disease accompanied by multisystem organ involvement. MATERIALS AND METHODSSampling procedure for pathology and bacteriological analysis. Specimens were collected from 2 trout farms located in northern Israel (Upper Galilee) which are supplied with water at a constant temperature of 16°C. At the time of collection both farms were experiencing heavy mortalities, and bacteriological examination (30 fish from each farm, 50 to 350 g each) revealed pure colonies of β-hemolytic Gram-positive cocci. Bacteriological identification (Eldar et al. 1995), authenticated by PCR analysis (Zlotkin et al. 1998), confirmed the presence of arginine dehydrolase-negative isolates of Streptococcus iniae. PCR analysis with the p14 primer did not produce the 750 bp band, indicating that all current isolates were of type II (Bachrach et al. 2001). Tissues (brain, heart, spleen, kidney, liver, intestine, gills and muscle) from 10 diseased rainbow trout were fixed in 10% neutral buffered formalin and stained with hematoxylin and eosin (HE). Gross lesions were recorded.Distribution of bacteria in tissues. Bacterial colonyforming units (CFUs) were counted in the tissues of 20 rainbow trout (100 to 200 g each), infected with Streptococcus iniae type II and showing clinical signs of streptococcosis (darkening of the skin combined with multifocal ecchymoses, lethargy, loss of orientation and ocular pathologies). Organs (brain, heart, spleen, kidney, liver, intestine, gills and muscle) were weighed and blended over a 60-mesh grid. Tissue homogenate samples (1 g) were suspended in 10 ml phosphatebuffered saline (PBS) (15 mM Na 2 HPO 4 , 145 mM NaCl, pH 7.20) supplemented with 0.2% Triton X-100 (Sigma) and serially diluted. The bacterial CFU population was determined by plate counting.The bacterial loads in tissues of rainbow trout infected by Streptococcus iniae type I were assessed with a 2-step cohabitation method. First, 10 naive rainbow trout (50 to 80 g each) were infected by intraperitoneal inoculation of (7.5 × 10 5 CFU fish -1 ) virulent S. iniae Dan-15 (type I strain), as described previously (Eldar et al. 1997a). Then, on Day 10 ...

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Section: Resultssupporting

confidence: 80%

Streptococcus iniae type II infections in rainbow trout Oncorhynchus mykiss

Lahav¹,

Eyngor²,

Hurvitz³

et al. 2004

Dis. Aquat. Org.

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“…In neonatal sepsis or direct lung injury, an immediate increase in circulating inflammatory cytokines, including TNF-␣, IL-1␤, IL-6, and IL-10 (11,37,49) triggers second messenger pathways favoring contraction and smooth muscle proliferation (8). Cyclooxygenase (COX) pathway metabolites are implicated in increased pulmonary vascular tone.…”

mentioning

confidence: 99%

Role of 12-lipoxygenase in hypoxia-induced rat pulmonary artery smooth muscle cell proliferation

Preston

Hill

Warburton

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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The 12-lipoxygenase (12-LO) pathway of arachidonic acid metabolism stimulates cell growth and metastasis of various cancer cells and the 12-LO metabolite, 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE], enhances proliferation of aortic smooth muscle cells (SMCs). However, pulmonary vascular effects of 12-LO have not been previously studied. We sought evidence for a role of 12-LO and 12(S)-HETE in the development of hypoxia-induced pulmonary hypertension. We found that 12-LO gene and protein expression is elevated in lung homogenates of rats exposed to chronic hypoxia. Immunohistochemical staining with a 12-LO antibody revealed intense staining in endothelial cells of large pulmonary arteries, SMCs (and possibly endothelial cells) of medium and small-size pulmonary arteries and in alveolar walls of hypoxic lungs. 12-LO protein expression was increased in hypoxic cultured rat pulmonary artery SMCs. 12(S)-HETE at concentrations as low as 10(-5) microM stimulated proliferation of pulmonary artery SMCs. 12(S)-HETE induced ERK 1/ERK 2 phosphorylation but had no effect on p38 kinase expression as assessed by Western blotting. 12(S)-HETE-stimulated SMC proliferation was blocked by the MEK inhibitor PD-98059, but not by the p38 MAPK inhibitor SB-202190. Hypoxia (3%)-stimulated pulmonary artery SMC proliferation was blocked by both U0126, a MEK inhibitor, and baicalein, an inhibitor of 12-LO. We conclude that 12-LO and its product, 12(S)-HETE, are important intermediates in hypoxia-induced pulmonary artery SMC proliferation and may participate in hypoxia-induced pulmonary hypertension.

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“…In porcine models of endotoxemia, it has been reported that the primary hemodynamic effect of LPS infusion is an increase in pulmonary artery pressure and an increase in systemic vascular resistance, followed by a reduction in cardiac output (CO) [23][24][25][26]. In porcine endotoxemia, an increase in pulmonary vascular resistance is also typical [27], which indicates that the porcine pulmonary circulation is very sensitive to vasoconstrictors, or that it produces considerable amounts of vasoconstrictors such as endothelin-1.…”

Section: Discussionmentioning

confidence: 99%