Inhibitory effects and mechanisms of cinnamaldehyde against Fusarium oxysporum, a serious pathogen in potatoes.

BACKGROUND: Potatoes, a major economic crop, are significantly impacted by Fusarium dry rot, a prevalent postharvest disease. Despite the broad-spectrum antimicrobial properties of cinnamaldehyde, a naturally-derived plant substance, its efficacy against the causal pathogen of potato dry rot (Fusarium oxysporum) and the underlying mechanisms have not been extensively studied. RESULTS: Our study demonstrates that cinnamaldehyde effectively inhibits the growth of Fusarium oxysporum, the pathogen responsible for potato dry rot, and increases its sensitivity to environmental stress factors such as extreme temperatures and high salt stress. Treatment with cinnamaldehyde results in altered fungal mycelium morphology, compromised cell wall stability, and disrupted cell membrane integrity, thereby reducing spore viability. Specifically, it interferes with the cell membrane and cell wall structures of the fungus, potentially disrupting fungal growth by modulating signaling pathways involved in cell wall maintenance, chitin metabolism, and GPI-anchored protein function. Notably, we show that cinnamaldehyde induces a form of regulated cell death in F. oxysporum, which is characterized not as typical apoptosis, as evidenced by Annexin V negative staining. However, the specific cell death type and underlying mechanism still needed to be further explored. CONCLUSION: Cinnamaldehyde, an environmentally friendly plant-based active compound, exhibits strong inhibitory effects on F. oxysporum, indicating its potential use in the prevention and control strategies for potato dry rot. This research contributes to the understanding of novel antifungal mechanisms and offers promising insights into eco-friendly alternatives for managing this economically significant postharvest disease. © 2024 Society of Chemical Industry.

Protective Effects of NaHS/miR-133a-3p on Lipopolysaccharide-Induced Cardiomyocytes Injury.

Objective: The aim of this study was to investigate the effects of sodium hydrosulfide (NaHS) on Lipopolysaccharide (LPS)-induced cardiomyocyte injury in H9c2 cells. Methods: H9c2 cardiomyocytes cultivated with medium containing 10 µg/mL LPS were used to recapitulate the phenotypes of those in sepsis. Two sequential experiments were performed. The first contained a control group, a LPS group, and a LPS + NaHS group, with the aim to assure the protective effects of NaHS on LPS-treated cardiomyocytes. The second experiment added a fourth group, the LPS + NaHS + miR-133a-3p inhibition group, with the aim to preliminarily explore whether miR-133-3p exerts a protective function downstream of NaHS. The adenosine triphosphate (ATP) kit was used to detect ATP content; real-time quantitative polynucleotide chain reaction (qPCR) was used to measure the levels of mammalian targets of rapamycin (mTOR), AMP-dependent protein kinase (AMPK), and miR-133a-3p, and Western blot (WB) was used to detect protein levels of mTOR, AMPK, myosin-like Bcl2 interacting protein (Beclin-1), microtubule-associated protein 1 light chain 3 (LC3I/II), and P62 (sequestosome-1, sqstm-1/P62). Results: Compared with the control group, the expressions of miR-133a-3p (P < 0.001), P62 (P < 0.001), and the content of ATP (P < 0.001) decreased, while the expressions of Beclin-1 (P = 0.023) and LC3I/II (P = 0.048) increased in the LPS group. Compared with the LPS group, the expressions of miR-133a-3p (P < 0.001), P62 (P < 0.001), and the content of ATP (P < 0.001) in the NaHS + LPS group increased, while the expressions of Beclin-1 (P = 0.023) and LC3I/II (P = 0.022) decreased. Compared with the NaHS + LPS group, the expression levels of miR-133a-3p (P < 0.001), P62 (P = 0.001), and the content of ATP (P < 0.001) in the LPS + NaHS + miR-133a-3p inhibition group were downregulated, and the expression levels of Beclin-1 (P = 0.012) and LC3I/II (P = 0.010) were upregulated. The difference was statistically significant. There was no significant difference in the expression of AMPK and mTOR between groups. Conclusion: Our research demonstrated that NaHS relieved LPS-induced myocardial injury in H9c2 by promoting the expression of miR-133a-3p, inhibiting autophagy in cardiomyocytes, and restoring cellular ATP levels.

Anti-Oomycete Effect and Mechanism of Salicylic Acid on Phytophthora infestans.

Pathogenic oomycetes infect a wide variety of organisms, including plants, animals, and humans, and cause massive economic losses in global agriculture, aquaculture, and human health. Salicylic acid (SA), an endogenous phytohormone, is regarded as an inducer of plant immunity. Here, the potato late blight pathogen Phytophthora infestans was used as a model system to uncover the inhibitory mechanisms of SA on pathogenic oomycetes. In this research, SA significantly inhibited the mycelial growth, sporulation, sporangium germination, and virulence of P. infestans. Inhibition was closely related to enhanced autophagy, suppression of translation initiation, and ribosomal biogenesis in P. infestans, as shown by multiomics analysis (transcriptomics, proteomics, and phosphorylated proteomics). Monodansylcadaverine (MDC) staining and Western blotting analysis showed that SA promoted autophagy in P. infestans by probably targeting the TOR signaling pathway. These observations suggest that SA has the potential to control late blight caused by P. infestans.

MCC950 Ameliorates Acute Exogenous Lipoid Pneumonia Induced by Sewing Machine Oil in Rats via the NF-κB/NLRP3 Inflammasome Pathway.

BACKGROUND/AIM: Acute exogenous lipoid pneumonia (AELP) is a rare disorder caused by intake of lipid formulations and is often underdiagnosed. Meanwhile, the mechanism of AELP is still underlying. MCC950, was previously found to significantly suppress the release of inflammatory cytokines IL-18 and IL-1ß. However, the effect of MCC950 on AELP induced by sewing machine oil has not been reported. MATERIALS AND METHODS: The NLRP3, NF-[Formula: see text]B p65, caspase-1 and IL-1ß expression in lung tissues were compared between a rat model of AELP and control rats using western blotting and real-time quantitative assay. Moreover, haematoxylin and eosin (H&E) staining was performed to elucidate the mechanisms by which MCC950 ameliorates sewing machine oil-induced AELP in vivo. RESULTS: MCC950 reduced the expression of NF-[Formula: see text]B p65 in the lung samples of the treatment group and further down-regulated the NLRP3 and caspase-1 levels while inhibited the production of IL-1ß. Besides, decreases in inflammatory cell infiltration in the lung were shown using H&E staining. CONCLUSION: MCC950 ameliorates sewing machine oil-induced acute exogenous lipoid pneumonia in rats through inhibition of the NF-[Formula: see text]B/NLRP3 inflammasome pathway.

Endophytic Bacillus subtilis H17-16 effectively inhibits Phytophthora infestans, the pathogen of potato late blight, and its potential application.

BACKGROUND: As a highly prevalent epidemic disease of potato, late blight caused by Phytophthora infestans poses a serious threat to potato yield and quality. At present, chemical fungicides are mainly used to control potato late blight, but long-term overuse of chemical fungicides may lead to environmental pollution and human health threats. Endophytes, natural resources for plant diseases control, can promote plant growth, enhance plant resistance, and secrete antifungal substances. Therefore, there is an urgent need to find some beneficial endophytes to control potato late blight. RESULTS: We isolated a strain of Bacillus subtilis H17-16 from potato healthy roots. It can significantly inhibit mycelial growth, sporangia germination and the pathogenicity of Phytophthora infestans, induce the resistance of potato to late blight, and promote potato growth. In addition, H17-16 has the ability to produce protease, volatile compounds (VOCs) and form biofilms. After H17-16 treatment, most of the genes involved in metabolism, virulence and drug resistance of Phytophthora infestans were down-regulated significantly, and the genes related to ribosome biogenesis were mainly up-regulated. Moreover, field and postharvest application of H17-16 can effectively reduce the occurrence of potato late blight, and the combination of H17-16 with chitosan or chemical fungicides had a better effect than single H17-16. CONCLUSION: Our results reveal that Bacillus subtilis H17-16 has great potential as a natural fungicide for controlling potato late blight, laying a theoretical basis for its development as a biological control agent. © 2023 Society of Chemical Industry.

Isolation and Screening of Antagonistic Endophytes against Phytophthora infestans and Preliminary Exploration on Anti-oomycete Mechanism of Bacillus velezensis 6-5.

Phytophthora infestans, the notorious pathogen of potato late blight, leads to a severe decline in potato yields and even harvest failure. We isolated 201 endophytic isolates from healthy root tissues of potatoes, among which 41 showed strong antagonistic activity against P. infestans. Further, the tolerance to stress and the potential application against potato late blight of these antagonistic isolates were tested. Most of them were extremely tolerant to stresses such as acid-alkali, temperature, UV, salt, and heavy metal stress. However, some antagonistic isolates with excellent stress tolerance might be pathogenic to potatoes. Combining the screening results, a total of 14 endophytes had excellent comprehensive performance in all the tests. In this paper, the endophyte 6-5 was selected among them for the preliminary exploration of the anti-oomycete mechanism. Analysis of the 16S rDNA sequence revealed that 6-5 had a high homology to the corresponding sequence of Bacillus velezensis (99.72%) from the NCBI database. Endophyte 6-5 significantly inhibited the mycelial growth of P. infestans, with an inhibition rate of over 90% in vitro assays, and deformed the hyphal phenotype of P. infestans. In addition, endophyte 6-5 could secrete protease and cellulase, and produce antagonistic substances with high thermal stability, which might be helpful to its antagonistic activity against P. infestans. Furthermore, it was demonstrated that 6-5 had the ability to improve the resistance of potato tubers to late blight. In short, our study described the process of isolating and screening endophytes with antagonistic activity against P. infestans from potato roots, and further explored the potential of biocontrol candidate strain 6-5 in potato late blight control.

Integrative mRNA and microRNA Analysis Exploring the Inducing Effect and Mechanism of Diallyl Trisulfide (DATS) on Potato against Late Blight.

Potato late blight, caused by Phytophthora infestans, leads to a significant reduction in the yield and value of potato. Biocontrol displays great potential in the suppression of plant diseases. Diallyl trisulfide (DATS) is a well-known natural compound for biocontrol, although there is little information about it against potato late blight. In this study, DATS was found to be able to inhibit the hyphae growth of P. infestans, reduce its pathogenicity on detached potato leaves and tubers, and induce the overall resistance of potato tubers. DATS significantly increases catalase (CAT) activity of potato tubers, and it does not affect the levels of peroxidase (POD), superoxide dismutase (SOD), and malondialdehyde (MDA). The transcriptome datasets show that totals of 607 and 60 significantly differentially expressed genes (DEGs) and miRNAs (DEMs) are detected. Twenty-one negatively regulated miRNA-mRNA interaction pairs are observed in the co-expression regulatory network, which are mainly enriched in metabolic pathways, biosynthesis of secondary metabolites, and starch and sucrose metabolism based on the KEGG pathway. Our observations provide new insight into the role of DATS in biocontrol of potato late blight.

Down-regulation of Xist and Mir-7a-5p improves LPS-induced myocardial injury.

Background: X-inactive specific transcript (Xist) is a lncRNA, which plays a significant role in X-chromosome inactivation, regulates cell proliferation in tumor cells, and inhibits apoptosis in acute myocardial infarction. On the other hand, miR-7a-5p is involved in cardiomyocytes injury in myocardial ischemia/reperfusion. However, their roles in LPS-induced damage remain unclear. Objectives: This study aimed at using siRNA transfection and lentivirus infection to regulate the expression of xist and miR-7a-5p, and to evaluate their effects on LPS-induced myocardial damage. Method: Mice cardiomyocytes (MCM) cells were divided into six groups, namely the control group, the LPS group, the LPS + lncRNA- group, the LPS + lncRNA+ group, the LPS + miRNA- group, and the LPS + miRNA+ group. Quantitative real-time PCR (qRT-PCR) was performed to assay for the RNA expressions of xist, miR-7a-5p, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), and recombinant mitochondrial transcription factor A (Tfam) in all the groups. The ATP level was determined using the adenosine triphosphate (ATP) assay kit according to the manufacturer's instructions. Flow cytometry was performed to estimate the level of apoptosis and proliferation in cells in each group. Results: The level of xist in the myocardial cells was markedly higher in the LPS group compared with the control group; however, it was reduced in the LPS+ lncRNA- group. There was no significant difference in the expression of xist among the LPS+miRNA-, LPS+miRNA+, and LPS groups. Moreover, the expression of mir-7a-5p was significantly reduced in myocardial cells in the LPS group, and moderately reduced in the LPS+ miRNA- group, but remarkably elevated in the LPS+ miRNA+ group (P<0.05). The expression of mir-7a-5p was comparably similar in the LPS+ lncRNA- group, LPS+ lncRNA+ group, and LPS groups. Further, the levels of PGC-1a, and Tfam were determined. In the LPS group, the expression of PGC-1α was significantly reduced but elevated in the LPS+lncRNA- and LPS+ miRNA- groups (P<0.05). There was no significant difference in the level of PGC-1α among the LPS, LPS+ lncRNA+, and LPS+ miRNA+ groups. The expression of Tfam was markedly reduced in the LPS group (P < 0.05), but elevated after the suppression of xist and mir-7a-5p. The expression of Tfam was not significantly different among the LPS group, LPS+ lncRNA+ and LPS+ miRNA+ groups. Notably, overexpression of mir-7a-5p had a mild effect on the expression of Tfam in the LPS+ miRNA+ group compared with the control group. Besides, ATP expression in the LPS group was markedly reduced, but elevated after the inhibition of xist and mir-7a-5p. Suppressing the expression of xist or mir-7a-5p resulted in reduced cell apoptosis and increased cell proliferation. Conclusions: In this study, we established that down-regulation of xist and mir-7a-5p reduces apoptosis in response to LPS.

Pyrrolidine dithiocarbamate and dexamethasone are novel treatments of Acute Exogenous Lipoid Pneumonia.

BACKGROUND: Acute exogenous lipoid pneumonia (AELP) is characterized by pulmonary inflammation. This mainly occur in children who have ingested sewing machine oil or other mineral oils accidentally. Despite emerging evidences revealing that inhibiting inflammation improves acute exogenous lipoid pneumonia, the actual process of inhibiting inflammation remains unknown. This study aimed to evaluate the effects of PDTC and dexamethasone on AELP to gain insight into the mechanism of AELP. METHODS: The experimental rats were randomly divided into 10 groups: NS control group (NS3 group, NS5 group), Oil inhalation group (AE3 group, AE5 group), PDTC intervention group (PDTC3 group, PDTC5 group), DXM intervention group (DXM3 group, DXM5 group), PDTC + DXM combined intervention group (PDTC + DXM3 group, PDTC + DXM 5 group). Enzyme-linked immunosorbent assay (ELISA) was used to determine concentrations of macrophage migration inhibitory factor (MIF), interleukin-6 (IL-6) and tumor necrosis factor-α (TNFα) in bronchoalveolar lavage fluid (BALF) and serum samples. On the other hand, western blotting was used to measure the expression levels of nuclear factor-κB p65 (NF-κB p65) and b-cell leukemia 2 (Bcl-2) in the lungs. Hematoxylin and Eosin (H&E) staining was performed to evaluate changes in the lung tissue. The wet-to-dry lung weight ratio was subsequently used to determine the pulmonary edema of the lungs. RESULTS: There were increased MIF levels in both serum and BALF samples of the AE group. Pyrrolidine dithiocarbamate (PDTC) and dexamethasone (DXM) independently and in combination reduced pulmonary inflammation induced by the sewing machine oil by regulating MIF expression. TNF-α and IL-6 levels in serum and BALF samples of the AE group were higher than those of the NS control animals. However, their levels decreased after treatment with either PDTC, DXM or PDTC + DXM. Similarly, NF-κBp65 expression increased after oil inhalation but decreased after treatment with either PDTC, DXM or PDTC + DXM. PDTC, DXM and PDTC + DXM treatment significantly reduced pulmonary inflammation and pulmonary edema of the lung tissue following induction of acute exogenous lipoid pneumonia. CONCLUSIONS: Individual or combined use of PDTC and DXM can ameliorate pulmonary inflammation induced by inhalation of sewing machine oil by inhibiting the NF-κB pathway in young rats. These findings provide novel insights that will greatly contribute in treatment of AELP.

Efficacy of levofloxacin on macrolide-unresponsive and corticosteroid-resistant refractory Mycoplasma pneumoniae pneumonia in children.

BACKGROUND: This study aimed to summarize the experience in treatment of Mycoplasma pneumoniae pneumonia (MPP) with worsening lung shadow despite treatment with appropriate antimicrobials and corticosteroid in children. METHODS: All patients satisfied refractory MP pneumonia (RMPP) diagnostic criteria were enrolled. The clinical manifestations, laboratory findings, imaging features, treatments, and outcomes were retrospectively reviewed. RESULTS: Six patients with an average age of 7.83±3.13 years old were included in this study. All the patients were non-responsive to macrolide (ML) and glucocorticoids treatment shown by aggravated clinical symptoms and chest radiographies. The average total duration of fever was 19.5±8.34 days and the average time before levofloxacin (LVX) therapy was 10±2.97 days. After LVX treatment, the time of fever was from 1 to 3 days in five cases and 11 days in one case. The MP-DNA copies in the sputum decreased slowly after ML treatment in six patients, while they decreased quickly after LVX treatment in 5 children. A2063G mutation of domain V of 23SrRNA gene was found in five cases. Five patients recovered completely 16-32 days after treatment. One patient developed acute disseminated encephalomyelitis (ADEM) with abnormal brain magnetic resonance imaging and occurred serious sequelae. CONCLUSIONS: The sputum MP-DNA copies and clinical symptoms have a positive correlation with therapeutic efficacy. LVX may be beneficial in treatment of ML-unresponsive and corticosteroid-resistant RMPP in children. RMPP can be gradually cured by effective treatment of LVX, while which can damage the nervous system and lead to severe complications once MP invades brain tissues.

Misdiagnosis of scrub typhus complicated by hemophagocytic syndrome.

BACKGROUND: This study sought to analyze the cases of clinical misdiagnosis of scrub typhus complicated by hemophagocytic syndrome. METHODS: We retrospectively reviewed the medical records for diagnoses, clinical course, chest X-ray findings, laboratory data, and antibiotic therapy. RESULTS: All nine patients were misdiagnosed at the outpatient department between 07/2009 and 07/2017. They were diagnosed with septicemia and hemophagocytic syndrome, sepsis and hemophagocytic syndrome, severe infection, hepatitis and hemophagocytic syndrome, or upper respiratory tract infection. Among the nine patients, hepatic function examination showed decreased albumin and elevated C-reactive protein levels in all patients; alanine aminotransferase was increased and platelets were decreased in eight patients. Weil-Felix reaction was positive in three of nine patients. Indirect immunofluorescence demonstrated positive IgM antibody and EB virus-IgM in all nine patients; Mycoplasma pneumoniae antibody was positive in seven patients. All nine patients underwent chest computed tomography; no abnormality was found in two patients. Patch shadow with increased density was found in seven patients, including four patients with right pleural effusion and two with bilateral pleural effusion. Bone marrow biopsy was performed in all nine patients and hemophagocytic cells were seen. The nine misdiagnosed cases were given multiple broad-spectrum antibiotics either successively or concomitantly before and after admission, but no effective antibiotics against Orientis tsutsugamushi were applied. After diagnosis was corrected to scrub typhus, five patients were switched to chloramphenicol and dexamethasone, two patients were given azithromycin and dexamethasone, and two patients were treated with chloramphenicol. Body temperature returned to normal within 2-3 days and the children were quickly relieved from their condition. CONCLUSION: Hemophagocytic syndrome may be the presenting clinical feature of scrub typhus and initially mask the disease. Initial misdiagnosis is common and includes septicemia and hemophagocytic syndrome. The eschar is a useful diagnostic clue and febrile patients without any localizing signs should be thoroughly examined for its presence.

Clinical characteristics and effective treatments of scrub typhus-associated hemophagocytic lymphohistiocytosis in children.

Hemophagocytic lymphohistiocytosis (HLH) is an uncommon and life-threatening disorder that may rarely complicate the clinical course of Orientia tsutsugamushi disease (scrub typhus). Here, we describe the clinical features, laboratory parameters, management, and outcome of 16 children with scrub typhus-associated HLH. All patients satisfied the HLH-2004 diagnostic criteria. All patients had fever of unknown origin and multisystem damage. Raised hepatic transaminases and abnormalities in routine blood test were observed in all children. Imaging tests showed abnormalities in 10 cases. Six patients were treated with intravenous azithromycin for 5 days, and 10 with intravenous chloramphenicol for 7-10 days because of non-response to 3-day azithromycin treatment. Five patients were treated with intravenous albumin and 3 with intravenous immunoglobulin. Two patients with severe symptoms (shortness of breath, cyanosis) were treated with dexamethasone (0.3 mg/kg/d). Fifteen patients recovered completely after 8-22 days of treatment. One patient died. The occurrence of severe complications draws attention to the need for early diagnosis and effective treatment. Anti-rickettsial antibiotic treatment (azithromycin or chloramphenicol) without the need for chemotherapy may be beneficial in such cases, instead of treatment according to the 2004 HLH protocol.

Protective effects of exogenous NaHS against sepsis-induced myocardial mitochondrial injury by enhancing the PGC-1α/NRF2 pathway and mitochondrial biosynthesis in mice.

This study aimed to examine whether exogenous NaHS can protect myocardial mitochondrial injury from sepsis by enhancing the peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α)/ nuclear factor erythroid-2-related factor 2 (NRF2) pathway and mitochondrial biosynthesis in mice. Animals were divided into sham-operated, sepsis, sepsis + 25 µmol/L NaHS, sepsis + 50 µmol/L NaHS, sepsis + 100 µmol/L NaHS, and sepsis + 200 µmol/L NaHS groups. The myocardial damage was evaluated by hematoxylin and eosin staining for myocardial microstructure and serum cardiac troponin I (cTnI) detection. The myocardial mitochondrial damage was evaluated through transmission electron microscopic observation of mitochondrial microstructure and detection of the degree of myocardial mitochondrial swelling. The adenosine triphosphate (ATP) level was used to appraise the mitochondrial function. The mRNA expression levels of Nrf2, PGC-1α, and Tfam were analyzed to explore the molecular mechanism. RESULTS: In the sepsis group, the structure of myocardial tissue and mitochondria were significantly damaged, the serum cTnI level increased (P < 0.05), the ATP level reduced, the degree of myocardial mitochondrial swelling aggravated, and the mRNA expression levels of Nrf2, PGC-1α, and Tfam increased (P < 0.05). After NaHS treatment, the structure of myocardial tissue and mitochondria improved, the cTnI level reduced, the ATP level increased, the degree of myocardial mitochondrial swelling alleviated, and the mRNA expression level of Nrf2, PGC-1α, and Tfam increased continuously in a dose-dependent manner (P < 0.05). CONCLUSIONS: Exogenous NaHS had a protective effect against myocardial mitochondrial injury in sepsis. The mechanism might lie in enhancing the PGC-1α/NRF2 pathway and mitochondrial biosynthesis.

[Clinical analysis of scrub typhus-associated hemophagocytic syndrome].

OBJECTIVE: To analyze the clinical manifestations and intervention against fulminant scrub typhus-associated hemophagocytic syndrome. METHOD: The medical records for the onset time of hemophagocytic syndrome, the clinical course, the chest radiographic findings, laboratory data, antibiotic therapy, clinical outcome and its prognosis were retrospectively reviewed. RESULT: (1) Four patients were diagnosed as scrub typhus based on clinical manifestations only, while 15 patients met the criteria of laboratory diagnosis. All 19 patients with scrub typhus had hemophagocytic syndrome. Eschar lesion was identified in 12 patients, 7 patients were described as an ulcer. A seasonal pattern (78.9% from June through September in 15 patients) was observed. Clinical misdiagnosis was common (all 19 cases). There were 9 patients with admitting diagnosis of scrub typhus, 10 patients were not diagnosed as scrub typhus after admission. In 5 cases within 3 days after admission diagnosis was corrected as scrub typhus. Until discharge from the hospital, 5 cases were not diagnosed with scrub typhus. In this study, the length of time from the illness onset (beginning of fever) to the occurrence of clinical symptoms was (9 ± 4) days. (2) All 19 patients had changed AST levels (149 ± 37) U/L, albumin levels (23 ± 4) g/L, C-reactive protein levels (103 ± 51) mg/L, and platelet count (48 ± 41) × 109/L; bone marrow aspiration revealed in 16 patients marked hemophagocytosis. Weil-Felix agglutination test revealed positive results in 6 of 15 cases. Diagnostic IFA results were positive for 14 patients; 19 patients had interstitial pneumonitis and 17 patients had pleural effusion. (3) Five cases with failure to diagnose the disease had ineffective antibiotics treatment (imipenem or ß-lactam-based regimens). These patients did not receive appropriate treatment with antibiotics against scrub typhus. Fourteen patients with admitting diagnosis of scrub typhus were successfully treated with appropriate antibiotics, 8 cases with chloramphenicol, 3 cases with azithromycin, and in 3 patients (2 cases of azithromycin and one case of erythromycin), therapy was then switched to chloramphenicol. Four patients were treated with methylprednisolone and 10 patients with dexamethasone. (4) During their hospitalization, the clinical course in five cases with failure to diagnose the disease rapidly developed and progressed to the life-threatening MODS, four of five cases died. However, the course in 14 patients were relieved and did not progress to MODS. CONCLUSION: The diagnosis of scrub typhus was frequently delayed, the early course of scrub typhus could be associated with hemophagocytic syndrome. Serious complications of MODS generally occur without antibiotic treatment. Scrub typhus-associated hemophagocytic syndrome should be taken into consideration among patients with acute systemic febrile illness, significant increases in levels of CRP, hypoalbuminemia, thrombocytopenia, splenomegaly, pneumonitis with pleural effusion, especially those with suspected exposure history. It was not easily recognized without careful observation and was present for a few days in each patient.

[Risk factors for death in children with septic shock].

OBJECTIVE: To identify the risk factors for death in children with septic shock. METHODS: Clinical data of 53 children with septic shock admitted to the Yuying Children's Hospital between January 2006 and July 2008 were retrospectively studied. Risk factors for death were assessed using univariate analysis and logistic regression analysis. RESULTS: Nineteen cases died out of 53 children with septic shock. Univariate analysis and logistic regression analysis showed that arterial blood pH value<7.0 (OR=89.66), hypotension (OR=84.00), the pediatric critical illness score<70 (OR=60.00), the number of organ dysfunction>or=3 (OR=38.98), incompletion of volume resuscitation within 6 hrs after shock (OR=26.41), and no administration of effective antibiotics within 1 hr after shock (OR=11.43) and of vasoactive drugs (OR=75.68) were risk factors for death in children with septic shock. CONCLUSIONS: A low arterial blood pH value (<7.0), hypotension, a pediatric critical illness score (<70) and the number of organ dysfunction>or=3 are related to a high mortality in children with septic shock. If the volume resuscitation can be completed within 6 hrs after shock, effective antibiotics can be administered within 1 hr after shock, and vasoactive drugs can be used properly, the outcome of children with septic shock may be improved.

[Clinical analysis of community-acquired Pseudomonas aeruginosa septic shock].

OBJECTIVE: This study sought to analyze the clinical manifestations and intervention of fulminant septic shock in community-acquired Pseudomonas aeruginosa septicemia. METHODS: We retrospectively reviewed the medical records for diagnosis, antibiotic therapy, clinical course of septic shock, respiratory support, laboratory data etc. RESULTS: Eight of nine cases with P. aeruginosa septic shock died. Fever (nine cases) and cough (three cases) or diarrhea (3 cases) were the 2 most common initial symptoms, three cases developed skin gangrenosum later. Pseudomonas aeruginosa infection was not considered in any of the cases before death or blood culture showed positive result. Only 3 cases were initially treated with susceptible antibiotic regimen but no anti pseudomonas combination therapy was applied, susceptible antibiotic monotherapy was applied in 7 cases after transfer to the ICU. The mean latency of shock occurrence was 5.1 hours (range 0 to 21 hours) after admission, the mean duration from the occurrence of shock to death was 13.8 hours (range, 1 - 32 hours). All the patients were transfer red to ICU for shock, the appropriate resuscitation of shock patients was delayed by 49.3 minutes (range 25 - 80 minutes) by transfer. Only two cases were diagnosed and treated for shock on admission; after transferred to ICU, only 5 patients were diagnosed as having shock, and only 3 received anti-shock treatment. Eight of the patients died of persistent shock. In 6 patients who died, mechanical ventilation was not applied until cardiac arrest occurred. All the patients had hypoalbuminaemia, elevated serum C-reactive protein concentration, leukopenia and 6 cases had DIC. CONCLUSION: The initial presentation of the cases with community-acquired Pseudomonas aeruginosa septicemia was nonspecific with fever and cough or diarrhea. Clinicians often underestimated the severity of the infection, few patients received effective antimicrobial therapy. The authors suggest that an anti-pseudomonas antibiotic should be included in the initial empiric antibiotic regimen to cover P. aeruginosa high-risk patients; the front-line clinician should be educated for early recognition and aggressive resuscitation of P infection. aeruginosa septicemia.

[Three cases of enterovirus 71 infection with pulmonary edema or pulmonary hemorrhage as the early clinical manifestation].

OBJECTIVE: To recognize the clinical features of the enterovirus 71 (EV71) infection with pulmonary edema or pulmonary hemorrhage as a fulminant and often fatal illness. METHODS: We retrospectively reviewed the medical records of the three cases with EV71 infection for clinical manifestation, laboratory data, medications, outcome etc. RESULTS: All the cases were infants and they all died. These infants had no skin or mucosal lesions, however, they had sudden onset of cyanosis and tachypnea 1 to 2 days after the onset of the febrile disease with vomiting. All these 3 cases were misdiagnosed and were treated for shock on admission. Pulmonary hemorrhage was not considered in any of the cases on admission. All the cases received tracheal intubation when foamy secretions were discharged from mouth and nose of the patients and notable cyanosis was noted. After intubation, all had pink foamy fluid flew out from the endotracheal tube. The patients had hyperglycemia and limb weakness, two had tachycardia, and hypertension was found in one case. Chest X-ray showed bilateral or unilateral widespread air space opacity, but the cardiac size and shape were normal. All the patients had leucocytosis. EV71 infection was confirmed by detection of specific sequences of the virus in throat swab and tracheal secretions samples and in one case in cerebrospinal fluid sample. CONCLUSION: Pulmonary edema or pulmonary hemorrhage occurred in the 3 cases with EV71-infected infants. The initial presentation was often nonspecific with fever and vomiting, and sudden appearances of cyanosis, tachypnea, tachycardia, hypertension or hypotension, limb weakness may suggest pulmonary edema or hemorrhage. Excessive fluid resuscitation may deteriorate the illness, on the contrary, fluid restriction and inotropic agents, and early intubation with positive pressure mechanical ventilation may be the proper treatment.