Kampylobakterioza
Choroba ta, wywoływana przez bakterie z rodzaju Campylobacter, występuje na całym świecie. Znanych jest około 20 gatunków i podgatunków mikroorganizmów należących do tego rodzaju, z czego obecność C. jejuni lub C. coli stwierdzana jest u większości ludzi i zwierząt, u których wykryto tę chorobę. Bakterie te mają szczególne wymagania środowiskowe (wysoka temperatura, warunki mikroaerofilne, duża wilgotność), dlatego też ich zdolność do przetrwania poza organizmem gospodarza jest bardzo ograniczona. U ludzi żyjących w klimacie umiarkowanym zachorowania na kampylobakteriozę mają charakter sezonowy (wiosna,lato), co może wiązać się z wyższą przeżywalnością bakterii w środowisku w czasie dogodnych dla niej warunków temperaturowych (Bednarski & Wieliczko 2006).U ludzi choroba przebiega najczęściej pod postacią zapalenia jelit i/lub żołądka, a dominującym objawem jest biegunka, często krwawa (Krutkiewicz 2008). Niekiedy przekształca się ona w zakażenie o charakterze ogólnoustrojowym, skutkujące podwyższeniem temperatury ciała, bólami brzucha oraz powiększeniem wątroby i śledziony. Zakażenie mikroorganizmem z rodzaju Campylobacter może u ludzi skutkować również zapaleniem wsierdzia,septycznym zapaleniem stawów oraz zapaleniem opon mózgowo–rdzeniowych. Typowe objawy choroby (zapalenie i biegunka) przeważnie ustępują samoistnie po upływie 3–6 dni (Krutkiewicz 2008). W przypadku, gdy objawy występują dłużej niż tydzień, wskazane jest skonsultowanie się z lekarzem w celu podjęcia odpowiedniego leczenia.
Niektóre szczepy Campylobacter sp. wytwarzają cyto- i/lub enterotoksyny, powodujące rozpad krwinek i/lub uszkodzenie komórek wątroby. Ponadto lipopolisacharydy, będące składnikiem ściany komórkowej tych bakterii, stymulują odpowiedź układu immunologicznego. U niektórych szczepów ich struktura antygenowa jest podobna do struktury antygenów powierzchniowych neuronów człowieka. W wyniku powyższego zjawiska mimikry molekularnej organizm może rozpoznawać własne komórki jako obce i skierować przeciw nim odpowiedź układu odpornościowego, co skutkuje rozwojem chorób autoimmunizacyjnych, takich jak zespół Guillaina-Barrego z zapaleniem nerwów obwodowych i choroba reumatoidalna (Bednarski & Wieliczko 2006).
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Open Neurol J. 2012; 6: 158–178.
Published online 2012 Dec 28. doi: 10.2174/1874205X01206010158
PMCID: PMC3565243
Chronic Lyme Disease and Co-infections: Differential Diagnosis - Walter Berghoff
Campylobacter jejuni
Campylobacter jejuni is a small Gram-negative bacterium whose pathological significance was recognized around 1980. Campylobacter jejuni is among the most frequent pathogens worldwide, causing acute diarrhea. Sources of infection are game and domestic animals, especially poultry, various animal products and contaminated water [286]. The pathogen can persist in a coccoid form, but also in its normal form, for months in unfavorable conditions. It penetrates epithelial cells of the intestine causing their destruction, possibly by means of toxins [287, 288].
The main clinical manifestations of Campylobacter jejuni infection are gastroenteritis and abdominal complications in the early phase and reactive arthritis and Guillain-Barré syndrome in the late phase of the disease.
Campylobacter jejuni has differential diagnostic significance due to the late manifestations of the disease, namely due to reactive arthritis and Guillain-Barré syndrome.
Reactive arthritis in Campylobacter jejuni infections is seldom with a frequency of about 2.6% [289-292]. In connection with a Campylobacter jejuni infection, Guillain-Barré syndrome has an unfavorable prognosis [293]. Its incidence is approximately 1‰ [294]. Reactive arthritis occurs approximately one to two weeks after gastroenteritis [288] and Guillain-Barré syndrome approximately two months after the onset of infection [295].
Antibiotic treatment reduces the duration of gastroenteritis. The drugs of choice are erythromycin (1500 mg/daily), azithormycin (500 mg daily) and ciprofloxacin (1000 mg daily). Macrolides [296] and quinolones are primarily recommended, but resistance to them can occur [297]. Resistance to trimethoprim und beta-lactamases also exists [298].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565243/
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Współistniejąca z boreliozą choroby przeniesione drogą inną niż kleszcze
Mykoplazmoza :
Mycoplasma pneumoniae
Zakażenie kropelkowe, zakażenie przez kontakt
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Chlamydioza :
Chlamydia pneumoniae
Chlamydia trachomatis
Zakażenie kropelkowe, kontakt płciowy
--------------------
Jersinioza (m.in. reaktywne zapalenie stawów i rumień guzowaty)
Yersinia enterocolitica
Droga pokarmowa
----------------------
Parwowiroza
Parvovirus B19
Zakażenie kropelkowe, transfuzja krwi, zakażenie płodu w ciąży
----------------------
Kampylobakterioza
Campylobacter jejuni
Droga pokarmowa
--------------------------------------
Molecular mechanisms of campylobacter infection.
van Putten JP, van Alphen LB, Wösten MM, de Zoete MR.
Source
Department of Infectious Diseases & Immunology, Utrecht University, Yalelaan 1, Utrecht, The Netherlands. j.vanputten@uu.nl
Abstract
Campylobacter jejuni is the principal bacterial foodborne pathogen. A major challenge still is to identify the virulence strategies exploited by C. jejuni. Recent genomics, proteomics, and metabolomics approaches indicate that C. jejuni displays extensive inter- and intrastrain variation.
The diverse behavior enables bacterial adaptation to different environmental conditions and directs interactions with the gut mucosa. Here, we report recent progress in understanding the molecular mechanisms and functional consequences of the phenotype diversity. The results suggest that C. jejuni actively penetrates the intestinal mucus layer, secretes proteins mainly via its flagellar apparatus, is engulfed by intestinal cells, and can disrupt the integrity of the epithelial lining. C. jejuni stimulates the proinflammatory pathway and the production of a large repertoire of cytokines, chemokines, and innate effector molecules. Novel experimental infection models suggest that the activation of the innate immune response is important for the development of intestinal pathology.
PMID: 19812984
--------------------------
J Antimicrob Chemother. 2006 Dec;58(6):1154-9. Epub 2006 Oct 5.
Role of the CmeABC efflux pump in the emergence of fluoroquinolone-resistant Campylobacter under selection pressure.
Yan M, Sahin O, Lin J, Zhang Q.
Source
Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, USA.
Abstract
OBJECTIVES:
The objective of this study was to determine the contribution of the CmeABC efflux pump to the emergence of fluoroquinolone (FQ)-resistant mutants in Campylobacter jejuni under various levels of selection pressure.
METHODS:
The frequency of emergence of ciprofloxacin-resistant mutants was measured in wild-type C. jejuni NCTC 11168 and its isogenic cmeB mutant and cmeR mutant (overexpressing cmeABC) using plates containing various concentrations of ciprofloxacin. Representative ciprofloxacin-resistant mutants were selected for gyrA sequence analysis and MIC determination. Accumulation of ciprofloxacin in Campylobacter cells was measured using spectrofluorometry.
RESULTS:
Mutation of cmeB drastically reduced the frequency of emergence of FQ-resistant mutants at 10x and 32x the MIC of ciprofloxacin, while the cmeR mutant displayed an approximately 17-fold increase in the frequency of emergence of the mutants at 32x the MIC when compared with the wild-type strain. Various point mutations occurred in gyrA in the FQ-resistant mutants selected at 5x and 10x the MIC, while the Thr-86–>Ile mutation was predominant in the mutants selected at 32x the MIC. The Thr-86–>Ile change conferred a high-level resistance to FQs, but other mutations only conferred an intermediate-level FQ resistance. In contrast, all types of gyrA mutations in the CmeABC-overexpressed background conferred high-level resistance to ciprofloxacin. Overexpression of cmeABC significantly reduced the amount of ciprofloxacin accumulated within bacterial cells.
CONCLUSIONS:
CmeABC is not only important for maintaining high-level resistance to FQs but also contributes significantly to the emergence of FQ-resistant mutants. Inhibition of this efflux pump may prevent the emergence of clinically relevant FQ-resistant Campylobacter mutants.
PMID: 17023497
--------------------------
Appl Environ Microbiol. 2011 Aug;77(15):5257-69. Epub 2011 Jun 3.
Investigating antibacterial effects of garlic (Allium sativum) concentrate and garlic-derived organosulfur compounds on Campylobacter jejuni by using Fourier transform infrared spectroscopy, Raman spectroscopy, and electron microscopy.
Lu X, Rasco BA, Jabal JM, Aston DE, Lin M, Konkel ME.
Source
School of Food Science, Washington State University, Pullman, WA 99163, USA.
Abstract
Fourier transform infrared (FT-IR) spectroscopy and Raman spectroscopy were used to study the cell injury and inactivation of Campylobacter jejuni from exposure to antioxidants from garlic. C. jejuni was treated with various concentrations of garlic concentrate and garlic-derived organosulfur compounds in growth media and saline at 4, 22, and 35°C. The antimicrobial activities of the diallyl sulfides increased with the number of sulfur atoms (diallyl sulfide < diallyl disulfide < diallyl trisulfide). FT-IR spectroscopy confirmed that organosulfur compounds are responsible for the substantial antimicrobial activity of garlic, much greater than those of garlic phenolic compounds, as indicated by changes in the spectral features of proteins, lipids, and polysaccharides in the bacterial cell membranes. Confocal Raman microscopy (532-nm-gold-particle substrate) and Raman mapping of a single bacterium confirmed the intracellular uptake of sulfur and phenolic components. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were employed to verify cell damage. Principal-component analysis (PCA), discriminant function analysis (DFA), and soft independent modeling of class analogs (SIMCA) were performed, and results were cross validated to differentiate bacteria based upon the degree of cell injury. Partial least-squares regression (PLSR) was employed to quantify and predict actual numbers of healthy and injured bacterial cells remaining following treatment. PLSR-based loading plots were investigated to further verify the changes in the cell membrane of C. jejuni treated with organosulfur compounds. We demonstrated that bacterial injury and inactivation could be accurately investigated by complementary infrared and Raman spectroscopies using a chemical-based, “whole-organism fingerprint” with the aid of chemometrics and electron microscopy.
PMID: 21642409
------------------------------
foto ze strony : http://www.ecolab.com/expertise-and-innovation/microbial-risks/campylobacter
van Putten JP, van Alphen LB, Wösten MM, de Zoete MR.
Source
Department of Infectious Diseases & Immunology, Utrecht University, Yalelaan 1, Utrecht, The Netherlands. j.vanputten@uu.nl
Abstract
Campylobacter jejuni is the principal bacterial foodborne pathogen. A major challenge still is to identify the virulence strategies exploited by C. jejuni. Recent genomics, proteomics, and metabolomics approaches indicate that C. jejuni displays extensive inter- and intrastrain variation.
The diverse behavior enables bacterial adaptation to different environmental conditions and directs interactions with the gut mucosa. Here, we report recent progress in understanding the molecular mechanisms and functional consequences of the phenotype diversity. The results suggest that C. jejuni actively penetrates the intestinal mucus layer, secretes proteins mainly via its flagellar apparatus, is engulfed by intestinal cells, and can disrupt the integrity of the epithelial lining. C. jejuni stimulates the proinflammatory pathway and the production of a large repertoire of cytokines, chemokines, and innate effector molecules. Novel experimental infection models suggest that the activation of the innate immune response is important for the development of intestinal pathology.
PMID: 19812984
--------------------------
J Antimicrob Chemother. 2006 Dec;58(6):1154-9. Epub 2006 Oct 5.
Role of the CmeABC efflux pump in the emergence of fluoroquinolone-resistant Campylobacter under selection pressure.
Yan M, Sahin O, Lin J, Zhang Q.
Source
Department of Veterinary Microbiology and Preventive Medicine, College of Veterinary Medicine, Iowa State University, Ames, IA 50011, USA.
Abstract
OBJECTIVES:
The objective of this study was to determine the contribution of the CmeABC efflux pump to the emergence of fluoroquinolone (FQ)-resistant mutants in Campylobacter jejuni under various levels of selection pressure.
METHODS:
The frequency of emergence of ciprofloxacin-resistant mutants was measured in wild-type C. jejuni NCTC 11168 and its isogenic cmeB mutant and cmeR mutant (overexpressing cmeABC) using plates containing various concentrations of ciprofloxacin. Representative ciprofloxacin-resistant mutants were selected for gyrA sequence analysis and MIC determination. Accumulation of ciprofloxacin in Campylobacter cells was measured using spectrofluorometry.
RESULTS:
Mutation of cmeB drastically reduced the frequency of emergence of FQ-resistant mutants at 10x and 32x the MIC of ciprofloxacin, while the cmeR mutant displayed an approximately 17-fold increase in the frequency of emergence of the mutants at 32x the MIC when compared with the wild-type strain. Various point mutations occurred in gyrA in the FQ-resistant mutants selected at 5x and 10x the MIC, while the Thr-86–>Ile mutation was predominant in the mutants selected at 32x the MIC. The Thr-86–>Ile change conferred a high-level resistance to FQs, but other mutations only conferred an intermediate-level FQ resistance. In contrast, all types of gyrA mutations in the CmeABC-overexpressed background conferred high-level resistance to ciprofloxacin. Overexpression of cmeABC significantly reduced the amount of ciprofloxacin accumulated within bacterial cells.
CONCLUSIONS:
CmeABC is not only important for maintaining high-level resistance to FQs but also contributes significantly to the emergence of FQ-resistant mutants. Inhibition of this efflux pump may prevent the emergence of clinically relevant FQ-resistant Campylobacter mutants.
PMID: 17023497
--------------------------
Appl Environ Microbiol. 2011 Aug;77(15):5257-69. Epub 2011 Jun 3.
Investigating antibacterial effects of garlic (Allium sativum) concentrate and garlic-derived organosulfur compounds on Campylobacter jejuni by using Fourier transform infrared spectroscopy, Raman spectroscopy, and electron microscopy.
Lu X, Rasco BA, Jabal JM, Aston DE, Lin M, Konkel ME.
Source
School of Food Science, Washington State University, Pullman, WA 99163, USA.
Abstract
Fourier transform infrared (FT-IR) spectroscopy and Raman spectroscopy were used to study the cell injury and inactivation of Campylobacter jejuni from exposure to antioxidants from garlic. C. jejuni was treated with various concentrations of garlic concentrate and garlic-derived organosulfur compounds in growth media and saline at 4, 22, and 35°C. The antimicrobial activities of the diallyl sulfides increased with the number of sulfur atoms (diallyl sulfide < diallyl disulfide < diallyl trisulfide). FT-IR spectroscopy confirmed that organosulfur compounds are responsible for the substantial antimicrobial activity of garlic, much greater than those of garlic phenolic compounds, as indicated by changes in the spectral features of proteins, lipids, and polysaccharides in the bacterial cell membranes. Confocal Raman microscopy (532-nm-gold-particle substrate) and Raman mapping of a single bacterium confirmed the intracellular uptake of sulfur and phenolic components. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) were employed to verify cell damage. Principal-component analysis (PCA), discriminant function analysis (DFA), and soft independent modeling of class analogs (SIMCA) were performed, and results were cross validated to differentiate bacteria based upon the degree of cell injury. Partial least-squares regression (PLSR) was employed to quantify and predict actual numbers of healthy and injured bacterial cells remaining following treatment. PLSR-based loading plots were investigated to further verify the changes in the cell membrane of C. jejuni treated with organosulfur compounds. We demonstrated that bacterial injury and inactivation could be accurately investigated by complementary infrared and Raman spectroscopies using a chemical-based, “whole-organism fingerprint” with the aid of chemometrics and electron microscopy.
PMID: 21642409
------------------------------
foto ze strony : http://www.ecolab.com/expertise-and-innovation/microbial-risks/campylobacter
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