Diagnosis of neuroschistosomiasis by antibody specificity index and semi-quantitative real-time PCR from cerebrospinal fluid and serum

2014 ◽  
Vol 63 (2) ◽  
pp. 309-312 ◽  
Author(s):  
Georg Härter ◽  
Hagen Frickmann ◽  
Sebastian Zenk ◽  
Dominic Wichmann ◽  
Bettina Ammann ◽  
...  

We describe the case of a 16-year-old German male expatriate from Ghana who presented with obstipation, dysuria, dysaesthesia of the gluteal region and the lower limbs, bilateral plantar hypaesthesia and paraesthesia without pareses. A serum–cerebrospinal fluid (CSF) Schistosoma spp. specific antibody specificity index of 3.1 was considered highly suggestive of intrathecal synthesis of anti-Schistosoma spp. specific antibodies, although standardization of this procedure has not previously been described. Diagnosis was confirmed by detection of Schistosoma DNA in CSF by semi-quantitative real-time PCR at 100-fold concentration compared with serum. Accordingly the two diagnostic procedures, which have not previously been applied for routine diagnosis, appear to be useful for the diagnosis of neuroschistosomiasis. Clinical symptoms resolved following anthelmintic and anti-inflammatory therapy.

2010 ◽  
Vol 55 (No. 7) ◽  
pp. 325-330 ◽  
Author(s):  
M. Kaevska ◽  
I. Slana ◽  
P. Kralik ◽  
I. Pavlik

Mycobacterium avium subsp. avium (MAA) is the etiologic agent of avian tuberculosis, a chronic contagious disease described in a wide variety of domestic and wild bird species. The aims of this study were to assess the advantages of triplex quantitative real time PCR (qPCR) in comparison with culture testing for distribution of MAA in the organs of hens displaying varying degrees of clinical symptoms of the disease. From one small flock of ten hens and one cock with a history of weight loss, 98 tissue samples were examined in total. Pathological lesions were observed in six hens from which two were clinically ill. A total of 12 samples were positive by culture and 16 were positive by IS901 and IS1245 qPCR, confirming MAA infection. In conclusion, qPCR was a faster and more reliable alternative method in comparison with conventional culture analysis. Due to the detection of MAA in the muscle tissue of one hen, consumption of under cooked meat originating from infected fowl could pose a threat to immunosuppressed individuals.


2004 ◽  
Vol 194 (1-2) ◽  
pp. 7-12 ◽  
Author(s):  
Stephan W. Aberle ◽  
Judith H. Aberle ◽  
Christoph Steininger ◽  
Elisabeth Puchhammer-St�ckl

Author(s):  
Marco Pacifici ◽  
Serena Delbue ◽  
Ferdous Kadri ◽  
Francesca Peruzzi

Author(s):  
Gerhard Dobler

• TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from oth-er forms of viral encephalitis or other diseases. • Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. • Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detec-tion of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. • During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. • Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either Infection with other flaviviruses or with other flavivirus vaccines.


TBE appears with non-characteristic clinical symptoms, which cannot be distinguished from other forms of viral encephalitis or other diseases. Cerebrospinal fluid and neuro-imaging may give some evidence of TBE, but ultimately cannot confirm the diagnosis. Thus, proving the diagnosis “TBE” necessarily requires confirmation of TBEV-infection by detection of the virus or by demonstration of specific antibodies from serum and/or cerebrospinal fluid. During the phase of clinic symptoms from the CNS, the TBEV can only rarely be detected in the cerebrospinal fluid of patients. Most routinely used serological tests for diagnosing TBE (ELISA, HI, IFA) show cross reactions resulting from either infection with other flaviviruses or with other flavivirus vaccines.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yi Wang ◽  
Hongjuan Liao ◽  
Yueheng Wang ◽  
Jinlin Zhou ◽  
Feng Wang ◽  
...  

Abstract Background Cardiovascular diseases have become the leading cause of death worldwide, and cardiac hypertrophy is the core mechanism underlying cardiac defect and heart failure. However, the underlying mechanisms of cardiac hypertrophy are not fully understood. Here we investigated the roles of Kallikrein 11 (KLK11) in cardiac hypertrophy. Methods Human and mouse hypertrophic heart tissues were used to determine the expression of KLK11 with quantitative real-time PCR and western blot. Mouse cardiac hypertrophy was induced by transverse aortic constriction (TAC), and cardiomyocyte hypertrophy was induced by angiotensin II. Cardiac function was analyzed by echocardiography. The signaling pathway was analyzed by western blot. Protein synthesis was monitored by the incorporation of [3H]-leucine. Gene expression was analyzed by quantitative real-time PCR. Results The mRNA and protein levels of KLK11 were upregulated in human hypertrophic hearts. We also induced cardiac hypertrophy in mice and observed the upregulation of KLK11 in hypertrophic hearts. Our in vitro experiments demonstrated that KLK11 overexpression promoted whereas KLK11 knockdown repressed cardiomyocytes hypertrophy induced by angiotensin II, as evidenced by cardiomyocyte size and the expression of hypertrophy-related fetal genes. Besides, we knocked down KLK11 expression in mouse hearts with adeno-associated virus 9. Knockdown of KLK11 in mouse hearts inhibited TAC-induced decline in fraction shortening and ejection fraction, reduced the increase in heart weight, cardiomyocyte size, and expression of hypertrophic fetal genes. We also observed that KLK11 promoted protein synthesis, the key feature of cardiomyocyte hypertrophy, by regulating the pivotal machines S6K1 and 4EBP1. Mechanism study demonstrated that KLK11 promoted the activation of AKT-mTOR signaling to promote S6K1 and 4EBP1 pathway and protein synthesis. Repression of mTOR with rapamycin blocked the effects of KLK11 on S6K1 and 4EBP1 as well as protein synthesis. Besides, rapamycin treatment blocked the roles of KLK11 in the regulation of cardiomyocyte hypertrophy. Conclusions Our findings demonstrated that KLK11 promoted cardiomyocyte hypertrophy by activating AKT-mTOR signaling to promote protein synthesis.


2008 ◽  
Vol 375 (1) ◽  
pp. 150-152 ◽  
Author(s):  
Cheng Xin Yi ◽  
Jun Zhang ◽  
Ka Man Chan ◽  
Xiao Kun Liu ◽  
Yan Hong

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