scholarly journals Comparative Efficacies of Antibiotics in a Rat Model of Meningoencephalitis Due to Listeria monocytogenes

1999 ◽  
Vol 43 (7) ◽  
pp. 1651-1656 ◽  
Author(s):  
Christian Michelet ◽  
Stephen L. Leib ◽  
Daniele Bentue-Ferrer ◽  
Martin G. Täuber

ABSTRACT The antibacterial activities of amoxicillin-gentamicin, trovafloxacin, trimethoprim-sulfamethoxazole (TMP-SMX) and the combination of trovafloxacin with TMP-SMX were compared in a model of meningoencephalitis due to Listeria monocytogenes in infant rats. At 22 h after intracisternal infection, the cerebrospinal fluid was cultured to document meningitis, and the treatment was started. Treatment was instituted for 48 h, and efficacy was evaluated 24 h after administration of the last dose. All tested treatment regimens exhibited significant activities in brain, liver, and blood compared to infected rats receiving saline (P < 0.001). In the brain, amoxicillin plus gentamicin was more active than all of the other regimens, and trovafloxacin was more active than TMP-SMX (bacterial titers of 4.1 ± 0.5 log10 CFU/ml for amoxicillin-gentamicin, 5.0 ± 0.4 log10 CFU/ml for trovafloxacin, and 5.8 ± 0.5 log10 CFU/ml for TMP-SMX;P < 0.05). In liver, amoxicillin-gentamicin and trovafloxacin were similarly active (2.8 ± 0.8 and 2.7 ± 0.8 log10 CFU/ml, respectively) but more active than TMP-SMX (4.4 ± 0.6 log10 CFU/ml; P< 0.05). The combination of trovafloxacin with TMP-SMX did not alter the antibacterial effect in the brain, but it did reduce the effect of trovafloxacin in the liver. Amoxicillin-gentamicin was the most active therapy in this study, but the activity of trovafloxacin suggests that further studies with this drug for the treatment ofListeria infections may be warranted.

2021 ◽  
Vol 2 (2) ◽  
pp. 100-106
Author(s):  
Aleksandra I. Pavlyuchkova ◽  
Aleksey S. Kotov

In childhood, various infectious, autoimmune, genetic diseases can manifest. We present a case of fatal encephalomyelopolyradiculoneuritis of unknown etiology in a 9-year-old child. Patient N.K. in February 2019, noted an increase in temperature to subfebrile values, received symptomatic and antibiotic therapy without effect. An increase in protein and lymphocytes was found in the cerebrospinal fluid. According to MRI data, the emergence of more and more foci of the pathological signal in the brain and spinal cord, cranial nerves and nerve roots of the lumbar plexus was noted. Known infectious and autoimmune diseases were excluded. Despite active therapy with glucocorticoids, antibiotics, antiviral drugs, immunoglobulin, the disease continued to progress, and the patient died in April 2020.


2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Leandro Castañeyra-Ruiz ◽  
Ibrahim González-Marrero ◽  
Agustín Castañeyra-Ruiz ◽  
Juan M. González-Toledo ◽  
María Castañeyra-Ruiz ◽  
...  

Neuromyelitis optica is an inflammatory disease characterized by neuritis and myelitis of the optic nerve. Its physiopathology is connected with the aquaporin-4 water channel, since antibodies against aquaporin-4 have been found in the cerebrospinal fluid and blood of neuromyelitis optica patients. The seropositivity for aquaporin-4 antibodies is used for the diagnosis of neuromyelitis optica or neuromyelitis optica spectrum disease. On the other hand, aquaporin-4 is expressed in astrocyte feet in the brain-blood barrier and subventricular zones of the brain ventricles. Aquaporin-4 expression is high in cerebrospinal fluid in hydrocephalus. Furthermore, neuroepithelial denudation precedes noncommunicating hydrocephalus and this neuroepithelial disruption could allow aquaporin-4 to reach anomalous brain areas where it is unrecognized and induce the generation of aquaporin-4 antibodies which could cause the neuromyelitis optica and certain types of hydrocephalus.


2019 ◽  
Vol 43 (5) ◽  
pp. 348-353
Author(s):  
Taishin Chung ◽  
Ki-Cheol Yoon ◽  
Kwang Gi Kim ◽  
Seung Hoon Lee ◽  
Heon Yoo

The increase of intracranial pressure is a life-threatening condition which requires urgent treatment to prevent the further neurologic problem. A design of the brain port is proposed, in which a bi-directional check valve controls the flow of the cerebrospinal fluid depending on the intracranial pressure in accordance with the other devices. Drug administration and cerebrospinal fluid drainage could be performed easily without any additional surgery other than the transplant of a brain port. The intracranial pressure value at which the cerebrospinal fluid should be drained is adjustable by altering the pressure of the drainage bag. The results of the experiment with the simulated brain system are supporting and verifying the substance of this article.


1969 ◽  
Vol 21 (02) ◽  
pp. 294-303 ◽  
Author(s):  
H Mihara ◽  
T Fujii ◽  
S Okamoto

SummaryBlood was injected into the brains of dogs to produce artificial haematomas, and paraffin injected to produce intracerebral paraffin masses. Cerebrospinal fluid (CSF) and peripheral blood samples were withdrawn at regular intervals and their fibrinolytic activities estimated by the fibrin plate method. Trans-form aminomethylcyclohexane-carboxylic acid (t-AMCHA) was administered to some individuals. Genera] relationships were found between changes in CSF fibrinolytic activity, area of tissue damage and survival time. t-AMCHA was clearly beneficial to those animals given a programme of administration. Tissue activator was extracted from the brain tissue after death or sacrifice for haematoma examination. The possible role of tissue activator in relation to haematoma development, and clinical implications of the results, are discussed.


1968 ◽  
Vol 59 (3) ◽  
pp. 479-486 ◽  
Author(s):  
Lars-Ake Idahl ◽  
Bo Hellman

ABSTRACT The combination of enzymatic cycling and fluorometry was used for measuring glucose and glucose-6-phosphate in pancreatic β-cells from obese-hyperglycaemic mice. The glucose level of the β-cells corresponded to that of serum over a wide concentration range. In the exocrine pancreas, on the other hand, a significant barrier to glucose diffusion across the cell membranes was demonstrated. During 5 min of ischaemia, the glucose level remained practically unchanged in the β-cells while it increased in the liver and decreased in the brain. The observation that the pancreatic β-cells are characterized by a relatively low ratio of glucose-6-phosphate to glucose may be attributed to the presence of a specific glucose-6-phosphatase.


1990 ◽  
Vol 122 (2) ◽  
pp. 191-200 ◽  
Author(s):  
C. G. J. Sweep ◽  
Margreet D. Boomkamp ◽  
István Barna ◽  
A. Willeke Logtenberg ◽  
Victor M. Wiegant

Abstract The effect of intracerebroventricular (lateral ventricle) administration of arginine8-vasopressin (AVP) on the concentration of β-endorphin immunoreactivity in the cerebrospinal fluid obtained from the cisterna magna was studied in rats. A decrease was observed 5 min following injection of 0.9 fmol AVP. No statistically significant changes were found 5 min after intracerebroventricular treatment of rats with 0.09 or 9 fmol. The decrease induced by 0.9 fmol AVP was of short duration and was found 5 min after treatment but not 10 and 20 min. Desglycinamide9-AVP (0.97 fmol), [pGlu4, Cyt6]-AVP-(4–9) (1.44 fmol), Nα-acetyl-AVP (0.88 fmol), lysine8-vasopressin (0.94 fmol) and oxytocin (1 fmol) when intracerebroventricularly injected did not affect the levels of β-endorphin immunoreactivity in the cerebrospinal fluid 5 min later. This suggests that the intact AVP-(1–9) molecule is required for this effect. Intracerebroventricular pretreatment of rats with the vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)AVP (8.63 fmol) completely blocked the effect of AVP (0.9 fmol). In order to investigate further the underlying mechanism, the effect of AVP on the disappearance from the cerebrospinal fluid of exogenously applied β-endorphin was determined. Following intracerebroventricular injection of 1.46 pmol camel β-endorphin-(1–31), the β-endorphin immunoreactivity levels in the cisternal cerebrospinal fluid increased rapidly, and reached peak values at 10 min. The disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid then followed a biphasic pattern with calculated half-lifes of 28 and 131 min for the initial and the terminal phase, respectively. Treatment of rats with AVP (0.9 fmol; icv) during either phase (10, 30, 55 min following intracerebroventricular administration of 1.46 pmol β-endorphin-(1–31)) significantly enhanced the disappearance of β-endorphin immunoreactivity from the cerebrospinal fluid. The data suggest that vasopressin plays a role in the regulation of β-endorphin levels in the cerebrospinal fluid by modulating clearance mechanisms via V1-receptors in the brain.


Author(s):  
Walter Ott

Descartes’s treatment of perception in the Optics, though published before the Meditations, contains a distinct account of sensory experience. The end of the chapter suggests some reasons for this oddity, but that the two accounts are distinct is difficult to deny. Descartes in the present work topples the brain image from its throne. In its place, we have two mechanisms, one purely causal, the other inferential. Where the proper sensibles are concerned, the ordination of nature suffices to explain why a given sensation is triggered on the occasion of a given brain motion. The same is true with regard to the common sensibles. But on top of this purely causal story, Descartes re-introduces his doctrine of natural geometry.


2020 ◽  
Vol 12 (1) ◽  
pp. 001-008
Author(s):  
Ting Liu ◽  
Xing-Zhi Liao ◽  
Mai-Tao Zhou

Abstract Background Brain edema is one of the major causes of fatality and disability associated with injury and neurosurgical procedures. The goal of this study was to evaluate the effect of ulinastatin (UTI), a protease inhibitor, on astrocytes in a rat model of traumatic brain injury (TBI). Methodology A rat model of TBI was established. Animals were randomly divided into 2 groups – one group was treated with normal saline and the second group was treated with UTI (50,000 U/kg). The brain water content and permeability of the blood–brain barrier were assessed in the two groups along with a sham group (no TBI). Expression of the glial fibrillary acidic protein, endthelin-1 (ET-1), vascular endothelial growth factor (VEGF), and matrix metalloproteinase 9 (MMP-9) were measured by immunohistochemistry and western blot. Effect of UTI on ERK and PI3K/AKT signaling pathways was measured by western blot. Results UTI significantly decreased the brain water content and extravasation of the Evans blue dye. This attenuation was associated with decreased activation of the astrocytes and ET-1. UTI treatment decreased ERK and Akt activation and inhibited the expression of pro-inflammatory VEGF and MMP-9. Conclusion UTI can alleviate brain edema resulting from TBI by inhibiting astrocyte activation and ET-1 production.


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