Concentration of Procalcitonin and C-Reactive Protein in Patients with Human Granulocytic Anaplasmosis and the Initial Phase of Tick-Borne Encephalitis

2005 ◽  
Vol 1063 (1) ◽  
pp. 439-441
Author(s):  
S. LOTRIC-FURLAN
Author(s):  
Djeyne Silveira Wagmacker ◽  
Jefferson Petto ◽  
Fabiano Leichsenring Silva ◽  
Alan Carlos Nery dos Santos ◽  
Ana Marice Teixeira Ladeia

2006 ◽  
Vol 296 ◽  
pp. 69-75 ◽  
Author(s):  
Gernot Walder ◽  
Erdenechimeg Lkhamsuren ◽  
Abmed Shagdar ◽  
Jantsandoo Bataa ◽  
Tsetsegsaikhan Batmunkh ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Bernardo Neme Ide ◽  
Lázaro Alessandro Soares Nunes ◽  
René Brenzikofer ◽  
Denise Vaz Macedo

The purpose of this study was to observe the time course of muscle damage and inflammatory responses following an eccentric overload resistance-training (EO) program. 3 females (23.8 ± 2.6 years; 70.9 ± 12.7 kg; 1.6 ± 0.08 m) and 5 males (23.8 ± 2.6 years; 75.1 ± 11.2 kg; 1.8 ± 0.1 m) underwent thirteen training sessions (4 × 8–10 eccentric-only repetitions—80% of eccentric 1RM, one-minute rest, 2x week−1, during 7 weeks, for three exercises). Blood samples were collected prior to (Pre) and after two (P2), seven (P7), nine (P9), eleven (P11), and thirteen (P13) sessions, always 96 hours after last session. The reference change values (RCV) analysis was employed for comparing the responses, and the percentual differences between the serial results were calculated for each subject and compared with RCV95%. Four subjects presented significant changes for creatine kinase at P2, and another two at P13; six for C-reactive protein at P2, and three at P11; two for neutrophils at P2, P4, and P13, respectively; and only one for white blood cells at P2, P4, P7, and P9, for lymphocyte at P7, P9, and P13, and for platelet at P4. We conclude that EO induced high magnitude of muscle damage and inflammatory responses in the initial phase of the program with subsequent attenuation.


2018 ◽  
Vol 39 (4) ◽  
pp. 200
Author(s):  
Peter Irwin ◽  
Siobhon Egan ◽  
Telleasha Greay ◽  
Charlotte Oskam

It may seem perplexing that there is any uncertainty in Australia about the existence of zoonotic tick-associated infections1–3. Outside this country, particularly in the northern hemisphere, tick-borne diseases such as human granulocytic anaplasmosis, babesiosis, Boutonneuse fever, ehrlichiosis, Lyme borreliosis, and tick-borne encephalitis, have well documented aetiologies, epidemiology, diagnostic methods, and treatments. Why is Australia different and what research is being conducted to address this issue? This article briefly addresses these questions and explains how high-throughput metagenomic analysis has started to shed light on bacterial microbiomes in Australian ticks, providing new data on the presence and distribution of potentially zoonotic microbial taxa.


2008 ◽  
Vol 7 ◽  
pp. 73-77
Author(s):  
V. A. Rar ◽  
N. V. Fomenko ◽  
O. V. Mel’nikova ◽  
N. Ya. Chernousova

Serum samples from patients hospitalized with febrile illnesses occurring after tick bites were investigated for antibodies against agents of human granulocytic anaplasmosis (HGA) and human monocytic ehrlichiosis (HME). Ten from 205 patients were shown to contain HGA-specific antibodies, one patient — HME-specific antibodies, and one patient — both antibodies against agents of HGA and HME. Diagnosis of HGA was serologically and clinically confirmed for four patients. All patients with serologically confirmed HGA were shown to contain also antibodies against Borrelia burgdorferi sensu lato or HME-specific antibodies. Moreover, one patient was shown to be infected with tick-borne encephalitis virus. Thus, it seems reasonable to analyze patients with confirmed tick-borne encephalitis as well as with febrile illness after tick bites on the infection with HGA and HME.


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