Time for a culture change? Suboptimal compliance with blood culture standards at a district hospital in Cape Town

Background. The benchmark for contaminated blood cultures (BCs) is 3%. The South African (SA) guideline aims to optimise BC yield and reduce contamination. Data on BC collection practices in SA since the publication of the 2010 SA guideline are lacking.Objective. To evaluate compliance with the national guideline for the optimal use of BCs and determine the BC contamination rate at a local district hospital.Method. An audit of compliance with 22 BC standards was conducted at a district hospital in Cape Town, SA. Standards were evaluated by reviewing clinical and laboratory data and by a clinician questionnaire.Results. Of the 425 BCs reviewed, 12.5% had positive growth, and 4.5% grew contaminants. Only 33% of BC bottles contained the recommended fill volume of 8 - 10 mL, and 96.9% of patients had a single BC within a 24-hour period. Of all the BCs, only 7.8% had a combined blood volume of at least 20 mL. The yield of pathogens in BCs collected after antibiotic exposure was 4.9% compared with 7.5% for those cultures with no prior antibiotic exposure (p=0.3). The overall median needle-to-incubator transport time was 11 hours 25 minutes.Conclusion. The BC contamination rate was high and compliance with most standards was variable or not met. The findings may not be generalisable to other hospitals, and we recommend that each institution reviews its own BC practices. Recommendations made to hospital staff included a re-audit following implementation of these recommendations

Chemokine CCL9 Is Upregulated Early in Chronic Kidney Disease and Counteracts Kidney Inflammation and Fibrosis

Inflammation and fibrosis play an important pathophysiological role in chronic kidney disease (CKD), with pro-inflammatory mediators and leukocytes promoting organ damage with subsequent fibrosis. Since chemokines are the main regulators of leukocyte chemotaxis and tissue inflammation, we performed systemic chemokine profiling in early CKD in mice. This revealed (C-C motif) ligands 6 and 9 (CCL6 and CCL9) as the most upregulated chemokines, with significantly higher levels of both chemokines in blood (CCL6: 3–4 fold; CCL9: 3–5 fold) as well as kidney as confirmed by Enzyme-linked Immunosorbent Assay (ELISA) in two additional CKD models. Chemokine treatment in a mouse model of early adenine-induced CKD almost completely abolished the CKD-induced infiltration of macrophages and myeloid cells in the kidney without impact on circulating leukocyte numbers. The other way around, especially CCL9-blockade aggravated monocyte and macrophage accumulation in kidney during CKD development, without impact on the ratio of M1-to-M2 macrophages. In parallel, CCL9-blockade raised serum creatinine and urea levels as readouts of kidney dysfunction. It also exacerbated CKD-induced expression of collagen (3.2-fold) and the pro-inflammatory chemokines CCL2 (1.8-fold) and CCL3 (2.1-fold) in kidney. Altogether, this study reveals for the first time that chemokines CCL6 and CCL9 are upregulated early in experimental CKD, with CCL9-blockade during CKD initiation enhancing kidney inflammation and fibrosis

Interpretation of microbiological reports

The original publication is available at http://www.cmej.org.za/index.php/cmejThe quality of a laboratory report is influenced by many variables such as the quality of the specimen collected, the time of transporting the specimen to the laboratory and the provision of appropriate and correct information on the laboratory request form to guide the laboratory in processing and interpreting the culture results. The laboratory procedures are quality controlled to guarantee relevant, reliable, timely, and correctly interpreted reports that will guide patient management. However, poor-quality specimens may lead to misleading results, inappropriate antimicrobial therapy and delay in diagnosis

Candida species : species distribution and antifungal susceptibility patterns

LetterThe original publication is available at http://www.samj.org.za[No abstract available

Time for a culture change? suboptimal compliance with blood culture standards at a district hospital in Cape Town

CITATION: Abrahams, M. S., Whitelaw, A. C. & Orth, H. 2015. Time for a culture change? suboptimal compliance with blood culture standards at a district hospital in Cape Town. South African Medical Journal, 105(12):1039-1043, doi:10.7196/SAMJ.2015.v105i12.9442.The original publication is available at http://www.samj.org.zaBackground. The benchmark for contaminated blood cultures (BCs) is 3%. The South African (SA) guideline aims to optimise BC yield and reduce contamination. Data on BC collection practices in SA since the publication of the 2010 SA guideline are lacking. Objective. To evaluate compliance with the national guideline for the optimal use of BCs and determine the BC contamination rate at a local district hospital. Method. An audit of compliance with 22 BC standards was conducted at a district hospital in Cape Town, SA. Standards were evaluated by reviewing clinical and laboratory data and by a clinician questionnaire. Results. Of the 425 BCs reviewed, 12.5% had positive growth, and 4.5% grew contaminants. Only 33% of BC bottles contained the recommended fill volume of 8 - 10 mL, and 96.9% of patients had a single BC within a 24-hour period. Of all the BCs, only 7.8% had a combined blood volume of at least 20 mL. The yield of pathogens in BCs collected after antibiotic exposure was 4.9% compared with 7.5% for those cultures with no prior antibiotic exposure (p=0.3). The overall median needle-to-incubator transport time was 11 hours 25 minutes. Conclusion. The BC contamination rate was high and compliance with most standards was variable or not met. The findings may not be generalisable to other hospitals, and we recommend that each institution reviews its own BC practices. Recommendations made to hospital staff included a re-audit following implementation of these recommendations.http://www.samj.org.za/index.php/samj/article/view/9442Publisher's versio

Development, establishment and validation of in vitro and ex vivo assays of vascular calcification

Objective: Vascular calcification (VC) is one major complication in patients with chronic kidney disease, with a misbalance in calcium and phosphate metabolism playing crucial role. The mechanisms underlying VC have not been entirely revealed to date. As studies aiming at the identification and characterization of the involved mediators are highly relevant, we developed a standardized operating protocol for in vitro and ex vivo approaches in this study to aiming at the comparability of these studies. Approach and results: We analyzed in vitro and ex vivo experimental conditions to study VC. Therefore, vascular smooth muscle cells were used for in vitro experiments and rat aorta for ex vivo experiments. The degree of calcification was estimated by quantification of calcium concentrations and by von Kossa staining. As a result, a step-by-step protocol for performing experiments on VC was established. We were able to demonstrate that the degree and the location of VC in vascular smooth muscle cells and aortic rings was highly dependent on the phosphate and CaCl2 concentration in the medium as well as the incubation time. Furthermore, the VC was reduced upon increasing fetal calf serum concentration in the medium. Conclusion: In the current study, we developed and validated a standardized operating protocol for systematic in vitro and ex vivo analyses of medial calcification, which is essential for the comparability of the results of future studies. (C) 2020 The Authors. Published by Elsevier Inc

Development, establishment and validation of in vitro and ex vivo assays of vascular calcification

Objective: Vascular calcification (VC) is one major complication in patients with chronic kidney disease, with a misbalance in calcium and phosphate metabolism playing crucial role. The mechanisms underlying VC have not been entirely revealed to date. As studies aiming at the identification and characterization of the involved mediators are highly relevant, we developed a standardized operating protocol for in vitro and ex vivo approaches in this study to aiming at the comparability of these studies. Approach and results: We analyzed in vitro and ex vivo experimental conditions to study VC. Therefore, vascular smooth muscle cells were used for in vitro experiments and rat aorta for ex vivo experiments. The degree of calcification was estimated by quantification of calcium concentrations and by von Kossa staining. As a result, a step-by-step protocol for performing experiments on VC was established. We were able to demonstrate that the degree and the location of VC in vascular smooth muscle cells and aortic rings was highly dependent on the phosphate and CaCl2 concentration in the medium as well as the incubation time. Furthermore, the VC was reduced upon increasing fetal calf serum concentration in the medium. Conclusion: In the current study, we developed and validated a standardized operating protocol for systematic in vitro and ex vivo analyses of medial calcification, which is essential for the comparability of the results of future studies. (C) 2020 The Authors. Published by Elsevier Inc

Uremic Toxins Affecting Cardiovascular Calcification: A Systematic Review

Cardiovascular calcification is highly prevalent and associated with increased morbidity in chronic kidney disease (CKD). This review examines the impact of uremic toxins, which accumulate in CKD due to a failing kidney function, on cardiovascular calcification. A systematic literature search identified 41 uremic toxins that have been studied in relation to cardiovascular calcification. For 29 substances, a potentially causal role in cardiovascular calcification was addressed in in vitro or animal studies. A calcification-inducing effect was revealed for 16 substances, whereas for three uremic toxins, namely the guanidino compounds asymmetric and symmetric dimethylarginine, as well as guanidinosuccinic acid, a calcification inhibitory effect was identified in vitro. At a mechanistic level, effects of uremic toxins on calcification could be linked to the induction of inflammation or oxidative stress, smooth muscle cell osteogenic transdifferentiation and/or apoptosis, or alkaline phosphatase activity. For all middle molecular weight and protein-bound uremic toxins that were found to affect cardiovascular calcification, an increasing effect on calcification was revealed, supporting the need to focus on an increased removal efficiency of these uremic toxin classes in dialysis. In conclusion, of all uremic toxins studied with respect to calcification regulatory effects to date, more uremic toxins promote rather than reduce cardiovascular calcification processes. Additionally, it highlights that only a relatively small part of uremic toxins has been screened for effects on calcification, supporting further investigation of uremic toxins, as well as of associated post-translational modifications, on cardiovascular calcification processes