Fatal community-acquired bloodstream infection caused by Klebsiella variicola: A case report.

BACKGROUND: Klebsiella pneumoniae (K. pneumoniae) is an infective microorganism of worldwide concern because of its varied manifestations and life-threatening potential. Genetic analyses have revealed that subspecies of K. pneumoniae exhibit higher virulence and mortality. However, infections with Klebsiella subspecies are often misdiagnosed and underestimated in the clinic because of difficulties in distinguishing K. pneumoniae from its subspecies using routine tests. This case study reports the rapid and fatal effects of K. pneumoniae subspecies. CASE SUMMARY: A 52-year-old male patient was febrile and admitted to hospital. Examinations excluded viral and fungal causes along with mycoplasma/chlamydia and parasitic infections. Bacterial cultures revealed blood-borne K. pneumoniae sensitive to carbapenem antibiotics, although corresponding treatment failed to improve the patient's symptoms. His condition worsened and death occurred within 72 h of symptom onset from sepsis shock. Application of the PMseq-DNA Pro high throughput gene detection assay was implemented with results obtained after death showing a mixed infection of K. pneumoniae and Klebsiella variicola (K. variicola). Clinical evidence suggested that K. variicola rather than K. pneumoniae contributed to the patient's poor prognosis. CONCLUSION: This is the first case report to show patient death from Klebsiella subspecies infection within a short period of time. This case provides a timely reminder of the clinical hazards posed by Klebsiella subspecies and highlights the limitations of classical laboratory methods in guiding anti-infective therapies for complex cases. Moreover, this report serves as reference for physicians diagnosing similar diseases and provides a recommendation to employ early genetic detection to aid patient diagnosis and management.

[Effects of Lidocaine on the Rho/ROCK Signal Transduction of the Posterior Basilar Artery in Rabbit SAH].

OBJECTIVE: To observe the expression of Rho/Rho-associated kinase (ROCK) signaling pathway in the basilar artery and the effect of lidocaine on this signaling pathway after subarachnoid hemorrhage (SAH) in rabbits. METHODS: 24 New Zealand white rabbits were randomly divided into sham operation (sham) group, SAH group, and occipital cisterna lidocaine (CD) group. There were 8 rabbits in each group. Intracisternal injection of non-anticoagulant autologous arterial blood (1 mL/kg) were applied to SAH group and CD group animals to establish SAH model, sham normal saline group was injected with 37 ℃ physiological saline (1 mL/kg); after 30 min, CD group was injected with 0.3 mL 2% lidocaine cisterna, SAH group and sham group were injected with saline. After 72 h, food intake and neurologic function damage were measured. The expressions of Rho associated kinase 2 (ROCK2) and myosin light chain (MLC) and calmodulin (CaM) protein in the basilar artery were measured by Western blot. The ROCK2 and MLC and CaM gene expressions were measured by using real-time quantitative PCR. RESULTS: Compared with sham group, reduced food intake, various degrees of neurological impairment, increased ROCK2 mRNA and protein expressions in basal artery, and decreased MLC and CaM expressions were observed in SAH group and CD group (P<0.05). Compared with the SAH group, there was no statistically significant difference in diet intake and neurological damage in the CD group (P>0.05); the mRNA and protein expressions of ROCK2 in the basilar artery decreased, and the expressions of MLC and CaM increased (P<0.05). CONCLUSION: Intracisternal injection of lidocaine may inhibit the transmission of Rho/ROCK signal in the basilar artery and reduce the basilar artery smooth muscle contraction after SAH.

[Neuroprotection Mechanism of Lidocaine in Rabbits with Early Brain Injury Resulted from Subarachnoid Hemorrhage].

OBJECTIVES: To determine the neuroprotection mechanism of lidocaine on early brain injury resulted from subarachnoid hemorrhage. METHODS: Eighteen New Zealand white rabbits were randomly divided into three groups: Sham group, subarachnoid hemorrhage (SAH) group and lidocaine treatment (LD) group. Operations were performed on all animals under anesthesia. Autologous nonheparinized arterial blood (1 mL/kg, body mass) was injected into cisterna magna of rabbits in the SAH and LD groups, while saline (1 mL/kg, body mass) was given to rabbits in the sham group. Thirty minutes later, intravenous injection of 0.6 mL 20 mg/mL lidocaine was given to those in the LD group, and intravenous injection of 0.6 mL saline was given to those in the Sham and SAH groups. Food intake and neurological impairments of the rabbits were assessed 72 h after the induction of SAH. The protein and mRNA experssions of Caspase-3 and cytochrome-c (Cyt-c) in hippocampus tissues were detected using real-time PCR (RT-PCR) and Western blot. RESULTS: Rabbits in the SAH and LD groups had lower food intake and higher mRNA and protein expressions of Caspase-3 and Cyt-c than those in the sham groups, which was accompanied with varying degrees of neurological impairments. No significant differences in food intake and neurological impairments were found between the SAH and LD groups (P >0.05). However, rabbits in the LD group had lower levels of mRNA and protein expressions of Caspase-3 and Cyt-c than those in the SAH group (P <0.05). CONCLUSION: The neuroprotection mechanism of lidocaine on early brain injury in rabbits with subarachnoid hemorrhage may be associated with inhibition of mitochondrial pathway and downregulated mRNA and protein expressions of Caspase-3 and Cyt-c in brain tissues.

[Comparison of Two Methods of Lidocaine Administrating for Neuroprotection in Rabbit Model of Subarachnoid Hemorrhage].

OBJECTIVES: To compare the neuroprotection effect of two methods of Lidocaine administration in rabbit model of subarachnoid hemorrhage. METHODS: Forty New Zealand white rabbits were randomly divided into sham group, subarachnoid hemorrhage group (SAH), Lidocaine intravenous injection group (L1), and Lidocaine intracisternal administration group (L2). The rabbits were given general anaesthesia, then 1.5 mL autologous nonheparinized arterial blood was injected into cisterna magna to establish SAH model, while 1.5 mL saline was used in sham group. Thirty minutes later, the rabbits in L1 and L2 group respectively received 0.3 mL 2% Lidocaine administration of intravenously and intracisternally injection. All animals were sacrificed at 72 h after SAH. The samples of basilar artery and hippocampus tissue were processed for morphometric analysis. At pre-operation and 72 h after SAH, the level of interleukin-6 (IL-6) in serum was measured. HE staining and C fos immunohistochemical staining were performed in L1 and L2 groups. Artery area and artery diameter of basal arteries, normal neuron density and C-fos positive cell in hippocampus were measured at 72 h after SAH. RESULTS: The baseline level of IL-6 was not significant different in four groups (P>0.05). The level of IL-6 at 72 h after SAH was significantly higher than that at pre-operation in SAH, L1 and L2 groups (P<0.05), while the level of IL-6 in SAH and L1 group was higher than that in L2 group (P<0.05). Compared to sham and L2 group, the cross-section area and diameter of basal artery were smaller in SAH and L1 group, while the normal neuron density of hippocampus was less (P<0.05). CONCLUSIONS: Intracisternal administration of Lidocaine could provide neuroprotection in rabbit model of subarachnoid hemorrhage.

Breaking the reduced glutathione-activated antioxidant defence for enhanced photodynamic therapy.

Photodynamic therapy (PDT) has been applied in cancer treatment by utilizing reactive oxygen species (ROSs) to kill cancer cells. However, a high concentration of reduced glutathione (GSH) is present in cancer cells and can consume ROSs and sharply reduce the PDT activity. To address this problem, herein, we synthesized a thymine modified Zn phthalocyanine (ZnPc, a monomer and an active form for PDT) and prepared its nanoparticle form (an aggregator and an inactive form) with Hg2+ providing the driving force for the "thymine-Hg2+-thymine" interaction. The nanoparticles could remain in the inactive form during the delivery process in blood. Once endocytosed by cancer cells, the nanoparticles are disintegrated, and deprived of Hg2+ by intracellular GSH, which decreases the level of GSH. Simultaneously, the activity of the released monomer ZnPc is recovered and high PDT activity is observed.

[Prevention Effect of Thymosin-alpha1 Aganist Early Ventilator-associated Pneumonia in Patients with Mechanical Ventilation].

OBJECTIVE: To investigate the preventive effects of thymosin-alpha1 against early ventilator-associated pneumonia (VAP) in the patients with mechanical ventilation. METHODS: Fifty two patients with expectancy of mechanical ventilation over 48 h were divided into routine therapy group (n=26) and thymosin therapy group (n= 26) in random. The patients in routine therapy group were given intensive care unit (ICU) conventional treatment, and the patients in thymosin therapy group were given thymosin treatment additionally (1.6 mg subcutaneous injection, qd X 7 d). The incidence and occurrence time of VAP were observed, and the time of mechanical ventilation and ICU stay were recorded. The levels of CD3+, CD4+, CD4+ /CD8+ T lymphocyte, CD14+ mononuclear cell human leukocyte antigens-DR (CD14+ HLA-DR) and procalcitonin (PCT) were detected before mechanical ventilation and at the 3d and 7th d after mechanical ventilation. RESULTS: The base line including the level of immunologic function had no difference between the two groups (P>0.05). The incidence of VAP in thymosin therapy group was lower than that in routine therapy group, but it was not significant difference (P>0.05). The durations of machine ventilation and ICU stay in thymosin therapy group were shorter than those in routine therapy group (P<0.05). The occurrence time of VAP in thymosin therapy group was significantly later than that in routine therapy group (P<0.05). At the 3rd and 7th d after mechanical ventilation, thymosin therapy group achived higher levels of CD3+, CD4+, CD4+ /CD8+ T lymphocyte and CD14+ HLA-DR than routine therapy group did (P<0.05). CONCLUSION: Thymosinal may be able to improve immunologic function and prevent the incidence of early VAP in the patients with mechanical ventilation.

[The effect of Xuebijing injection on immune regulation in SIRS patients].

OBJECTIVE: To investgate the effect of Xuebijing Injection on immune regulation in patients with systemic inflammatory response syndrome (SIRS). METHODS: 56 SIRS patients admitted to the ICU of Guizhou Provincial Hospital from January 2013 to December 2013 were included in this study. The patients were randomly divided into a control (C) and a treatment (T) group. Patients in C group received routine treatment; while patients in T group received additional Xuebijing Injection 50 mL Bid. The following indicators were recorded and compared between the two groups before and 4 and 7 days after treatments: CD4+, CD8+, CD4+/CD8+, monocytes CD14+/human leukocyte antigen-DR (HLA-DR), score of acute physiology and chronic health evaluation II (APACHE II), heart rate, white blood cells, body temperature, respiration rate, and MODS (7 d after treatment only). RESULTS: No differences were found between the two groups before treatments (P > 0.05). T Group had higher levels of CD4+, CD8, CD4+/CD8+ and monocytes CD14+/HLA-DR than C group at 4 and 7 d after treatments (P < 0.05). T group also had higher levels of improvement in vital indicators compared with C group (P < 0.05). No significant difference in incidence of multiple organ dysfunction syndrome (MODS) was found between the two groups (P > 0.05). CONCLUSION: Xuebijing Injection can regulate immune function of patients with SIRS.

[Protective effect of ulinastatin on pulmonary function after cardiopulmonary bypass].

OBJECTIVE: To investigate the effects of Ulinastatin with different doses on pulmonary protection after cardiopulmonary bypass (CPB). METHODS: Ninety patients after CPB were brought into this study and divided into low doses Ulinastatin group (L group, n=30, 5 000 U/kg), high doses Ulinastatin group (H group, n=30, 20 000 U/kg) and control group (C group, n= 30), respectively. When the patients were transferred into ICU after CPB, Ulinastatin was given intravenously to those in L and H group, while saline was given in C group. Blood samples were harvested at the time before the treatments (T0) and 12 hours (T1), 24 hours (T2) after the treatments, for the measurements of arterial pressure of oxygen (PaO2), arterial pressure of carbon monoxide (PaCO2),difference of alveoli-arterial oxygen pressure (PO(2A), oxygenation index (Ol),and tumor necrosis factor-alpha (TNF-alpha) level. Pulmonary dynamic compliance (Cd), plat pressure (Pplat) and peak pressure (Ppeak) were determined at the time of To and wean (Tw). The durations of ventilation and intubation were recorded. RESULTS: At T0, the levels of PaO2, PaCO2, PO2A-a, OI and TNF-alpha in each group showed no significantly difference (P> 0. 05). At T1 and T2, the patients in H group had higher levels of PO2, PO2A-a. and OI, lower level of TNF-alpha, shorter duration of ventilation and intubation than the patients in other two groups(P<0. 05). The parameters in L group were better than those in C group, but the differences were not stastically significant (P>0. 05). There was no significantly difference in the levels of Cd, Pplat, and Ppeak at T0 and Tw between any two groups (P>0. 05). The intubation and ventilation time in H group were shorter than that in L and C group (P<0. 05). CONCLUSION: The application of Ulinastatin could achieve pulmonary protective effect after CPB, and it seems the effect could be better with high dose (20 000 U/kg) of Ulinastatin.