Is Clostridioides difficile toxins detection necessary when the glutamate dehydrogenase enzyme is detected?

INTRODUCTION: Clostridioides difficile causes diarrhea and pseudomembranous colitis. Its diagnosis is made with glutamate dehydrogenase (GDH) or toxins A and B detection and is confirmed with nucleic acid amplification tests. OBJECTIVE: To define if GDH determination is redundant to that of toxins. METHODS: Retrospective, observational study in diarrheal stools of patients with suspected Clostridioides difficile infection. Toxins and GDH were determined by immunochromatography. Bayesian simulation was performed with likelihood ratios; a p-value < 0.05 was regarded as significant. RESULTS: 329 GDH and toxin A and B results were analyzed. Clostridioides difficile infection prevalence was 18.2 %. Sensitivity and specificity of the GDH test were 0.90 and 0.89, respectively. Positive likelihood ratio was 8.9, and negative was 0.11. CONCLUSIONS: A negative GDH result considerably reduces the probability of infection but does not rule it out. Clostridioides difficile toxins detection may be necessary in institutions where nucleic acid amplification is not affordable or accessible.

INTRODUCCIÓN: Clostridioides difficile causa diarrea y colitis pseudomembranosa. Su diagnóstico se realiza con la detección de glutamato-deshidrogenasa (GDH) o las toxinas A y B y se confirma con pruebas de amplificación de ácidos nucleicos. OBJETIVO: Definir si la determinación de GDH es redundante a la de las toxinas. MÉTODOS: Estudio observacional retrospectivo de muestras fecales de pacientes con sospecha de infección por Clostridioides difficile. Las toxinas y GDH se determinaron mediante inmunocromatografía. Se realizó una simulación bayesiana con los cocientes de probabilidad; se consideró significativo un valor de p < 0.05. RESULTADOS: Se analizaron 329 resultados de GDH y toxinas A y B. Se encontró una prevalencia de infección de Clostridioides difficile de 18.2 %. La sensibilidad y especificidad de la prueba de GDH fue de 0.90 y 0.89, respectivamente. El cociente de probabilidad positivo fue de 8.9 y el negativo, de 0.11. CONCLUSIONES: Un resultado negativo de GDH disminuye considerablemente la probabilidad de infección, pero no la descarta. La detección de toxinas de Clostridioides difficile puede ser necesaria en instituciones donde la amplificación de ácidos nucleicos no es económica o accesible.

¿La detección de toxinas de Clostridioides difficile es necesaria cuando se detecta la enzima glutamato deshidrogenasa? / Is Clostridioides difficile toxins detection necessary when the glutamate dehydrogenase enzyme is detected?

Resumen Introducción: Clostridioides difficile causa diarrea y colitis pseudomembranosa. Su diagnóstico se realiza con la detección de glutamato-deshidrogenasa (GDH) o las toxinas A y B y se confirma con pruebas de amplificación de ácidos nucleicos. Objetivo: Definir si la determinación de GDH es redundante a la de las toxinas. Métodos: Estudio observacional retrospectivo de muestras fecales de pacientes con sospecha de infección por Clostridioides difficile. Las toxinas y GDH se determinaron mediante inmunocromatografía. Se realizó una simulación bayesiana con los cocientes de probabilidad; se consideró significativo un valor de p < 0.05. Resultados: Se analizaron 329 resultados de GDH y toxinas A y B. Se encontró una prevalencia de infección de Clostridioides difficile de 18.2 %. La sensibilidad y especificidad de la prueba de GDH fue de 0.90 y 0.89, respectivamente. El cociente de probabilidad positivo fue de 8.9 y el negativo, de 0.11. Conclusiones: Un resultado negativo de GDH disminuye considerablemente la probabilidad de infección, pero no la descarta. La detección de toxinas de Clostridioides difficile puede ser necesaria en instituciones donde la amplificación de ácidos nucleicos no es económica o accesible.

Abstract Introduction: Clostridioides difficile causes diarrhea and pseudomembranous colitis. Its diagnosis is made with glutamate dehydrogenase (GDH) or toxins A and B detection and is confirmed with nucleic acid amplification tests. Objective: To define if GDH determination is redundant to that of toxins. Methods: Retrospective, observational study in diarrheal stools of patients with suspected Clostridioides difficile infection. Toxins and GDH were determined by immunochromatography. Bayesian simulation was performed with likelihood ratios; a p-value < 0.05 was regarded as significant. Results: 329 GDH and toxin A and B results were analyzed. Clostridioides difficile infection prevalence was 18.2 %. Sensitivity and specificity of the GDH test were 0.90 and 0.89, respectively. Positive likelihood ratio was 8.9, and negative was 0.11. Conclusions: A negative GDH result considerably reduces the probability of infection but does not rule it out. Clostridioides difficile toxins detection may be necessary in institutions where nucleic acid amplification is not affordable or accessible.

A snapshot of antimicrobial resistance in Mexico. Results from 47 centers from 20 states during a six-month period.

AIM: We aimed to assess the resistance rates of antimicrobial-resistant, in bacterial pathogens of epidemiological importance in 47 Mexican centers. MATERIAL AND METHODS: In this retrospective study, we included a stratified sample of 47 centers, covering 20 Mexican states. Selected isolates considered as potential causatives of disease collected over a 6-month period were included. Laboratories employed their usual methods to perform microbiological studies. The results were deposited into a database and analyzed with the WHONET 5.6 software. RESULTS: In this 6-month study, a total of 22,943 strains were included. Regarding Gram-negatives, carbapenem resistance was detected in ≤ 3% in Escherichia coli, 12.5% in Klebsiella sp. and Enterobacter sp., and up to 40% in Pseudomonas aeruginosa; in the latter, the resistance rate for piperacillin-tazobactam (TZP) was as high as 19.1%. In Acinetobacter sp., resistance rates for cefepime, ciprofloxacin, meropenem, and TZP were higher than 50%. Regarding Gram-positives, methicillin resistance in Staphylococcus aureus (MRSA) was as high as 21.4%, and vancomycin (VAN) resistance reached up to 21% in Enterococcus faecium. Acinetobacter sp. presented the highest multidrug resistance (53%) followed by Klebsiella sp. (22.6%) and E. coli (19.4%). CONCLUSION: The multidrug resistance of Acinetobacter sp., Klebsiella sp. and E. coli and the carbapenem resistance in specific groups of enterobacteria deserve special attention in Mexico. Vancomycin-resistant enterococci (VRE) and MRSA are common in our hospitals. Our results present valuable information for the implementation of measures to control drug resistance.

Efficacy and renal toxicity of one daily dose of amikacin versus conventional dosage regime.

This study assessed the efficacy and renal toxicity of one daily dose of amikacin versus several doses in infected full-term newborns. A clinical trial was conducted with 120 patients who were divided into two groups: group A (n = 60), infants who received amikacin 20 mg/kg/d in one dose; and group B (n = 60), infants who received amikacin 10 mg/kg/d every 12 hours. Both groups also received ampicillin 100 mg/kg/day. Blood levels of amikacin, urinary beta(2)-microglobulin (beta(2)-m), serum creatinine (SCr), and glomerular filtration rate (GFR) were measured in each patient. No significant difference was found in demographic characteristics as well as in their beta(2)-m, SCr, and GFR levels. Infection was resolved in 96% for infants of group A and 91% for group B ( P = 0.254). Renal toxicity was present in 20 versus 31.6%, respectively ( P = 0.211). In both groups no significant difference was found in peak amikacin levels, whereas trough levels were higher for group B ( P = 0.004). No significant difference was found in efficacy or renal toxicity in either group. We recommend using amikacin in one daily dose. It could diminish the manipulation of intravenous access, reducing the risk of nosocomial infections.

Anticuerpos monoclonales en el diagnóstico de la tromboastenia de Glanzmann / Monoclonal antibodies in the diagnosis of Glanzmann's thrombasthenia

La tromboastenia de Glanzmann (TG) es una trombocitopatía causada pro el déficit en la cantidad de glucoproteínas IIb y IIIa (GP IIb/IIIa) de la membrana plaquetaria. Son descritos tres pacientes con TG; todos presentaban un tiempo de sangrado prolongado con recuento plaquetario normal y porcentajes mínimos de agregación plaquetaria cuando se usaron adenosin difosfato, colágena y epinefrina como inductores. Dos de los pacientes eran hermanos y tenían el antecedente de consanguinidad. Dos de los pacientes tenían historia de hemorragia principalmente de mucosas y el otro era asintomático. En los tres se realizaron estudios de inmunocitoquímica con la técnica de la imunoperoxidasa tipo indirecto usando un anticuerpo monoclonal (HPI-1D cortesía del Dr. W.L. Nichols Clínica Mayo, Rochester, Minnesota EUA) específico contra las GP IIb/IIIa. En los pacietnes sintomáticos la captación del anticuerpo fue totalmente negativa y en el que no presentó síntomas el anticuerpo fue parcialmente captado. Esta técnica en nuestra experiencia es más rápida y económica que la agregometría plaquetaria permitiendo realizar el diagnóstico con seguridad. La TG es una entidad aparentemente muy rara en nuestro país; sin embargo, es probable que su diagnóstico no establezca en muchos casos por carecer de la tecnología adecuada