Staphylococcal scalded skin syndrome (SSSS) is the medical term used to define a skin condition induced by the exfoliative toxins produced by Staphylococcus aureus. The disorder is also known as Ritter disease, bullous impetigo, neonatal pemphigus, or staphylococcal scarlet fever. The disease especially affects infants and small children, but has also been described in adults. Prompt therapy with proper antibiotics and supportive treatment has led to a decrease in the mortality rate.
The current case report describes the clinical progress of a patient with generalized erythema and fever, followed by the appearance of bullous lesions with tendency to rupture under the smallest pressure, and with extended areas of denudation.
The patient aged four years and six months was admitted to our clinic to establish the aetiology and treatment of a generalized bullous exanthema, followed by a skin denudation associated with fever and impaired general status.
Based on clinical and paraclinical examinations a diagnosis of Staphylococcal scalded skin syndrome was established which responded favourably to antibiotic treatment, hydro-electrolytic re-equilibration, and adequate local hygiene.
Staphylococcal infection can represent a problem of significant pathological importance sometimes requiring a multidisciplinary approach involving paediatricians, dermatologists, infectious diseases specialists, and plastic surgeons.
In recent years, a new form of medicine has become increasingly significant, namely, personalised medicine (PM). PM is a form of care in which treatment is tailored for an individual patient.
PM is about using multiple data sets to create a digital human mapping. A person’s biological traits are determined by the interactions of hundreds of genes and gene networks, as well as external factors such as diet and exercise. Combining and then investigating these multiple databases with powerful statistical tools, allows a new understanding of how genetic intricacy drives health and disease and so leads to a closer personalised medical approach that targets each individual’s unique genetic make-up.
Sepsis is a systemic inflammatory response to infection, ranging from systemic inflammatory response syndrome (SIRS) to septic shock and multiple organ dysfunction syndromes (MODS). Sepsis is the most common cause of death in intensive care patients. Treatments in an ICU may need to be adapted to the continuous and rapid changes of the disease, making it challenging to identify a single target. PM is thus seen as the future of sepsis treatment in the ICU.
The fact that individual patients respond differently to treatment should be regarded as a starting point in the approach to providing treatment. The disease itself comes secondary to this concept.
As chronic HIV infection is prone to co-infections more than any other infectious condition, many severely immune-depressed patients require advanced diagnostic investigations and complex treatment.
The case of a 30-year-old severely immune-depressed patient with AIDS, who developed neurological impairment and was diagnosed with encephalitis is presented. Multiple diagnostic approaches had to be used in order to identify the etiologic agents responsible for the clinical, immunological and biological evolution. Despite using advanced laboratory investigations and complex treatment, the patient developed multiple organ dysfunction syndromes that led to a fatal outcome.
Establishing etiologic relations and treatment priorities in patients with severe immunodeficiency and co-infections can prove difficult, underlining the need of rapid syndromic testing.
Sepsis is an injurious systemic host response to infection, which can often lead to septic shock and death. Recently, the immune-pathogenesis and genomics of sepsis have become a research topic focusing on the establishment of diagnostic and prognostic biomarkers. As yet, none have been identified as having the necessary specificity to be used independently of other factors in this respect. However the accumulation of current evidence regarding genetic variations, especially the single nucleotide polymorphisms (SNPs) of cytokines and other innate immunity determinants, partially explains the susceptibility and individual differences of patients with regard to the evolution of sepsis. This article outlines the role of genetic variation of some serum proteins which have the potential to be used as biomarker values in evaluating sepsis susceptibility and the progression of the condition.
Pulmonary abscess or lung abscess is a lung infection which destroys the lung parenchyma leading to cavitations and central necrosis in localised areas formed by thick-walled purulent material. It can be primary or secondary. Lung abscesses can occur at any age, but it seems that paediatric pulmonary abscess morbidity is lower than in adults. We present the case of a one year and 5-month-old male child admitted to our clinic for fever, loss of appetite and an overall altered general status. Laboratory tests revealed elevated inflammatory biomarkers, leukocytosis with neutrophilia, anaemia, thrombocytosis, low serum iron concentration and increased lactate dehydrogenase level. Despite wide-spectrum antibiotic therapy, the patient’s progress remained poor after seven days of treatment and a CT scan established the diagnosis of a large lung abscess. Despite changing the antibiotic therapy, surgical intervention was eventually needed. There was a slow but steady improvment and eventually, the patient was discharged after approximately five weeks.
Background. Validating new sepsis biomarkers can contribute to early diagnosis and initiation of therapy. The aim of this study is to evaluate the sepsis predictive capacity of soluble urokinase plasminogen receptor (suPAR) and its role in evaluating the prognosis of bloodstream infections. Material and method. We conducted a prospective pilot study on 49 systemic inflammatory response syndrome (SIRS) patients admitted to the intensive care unit (ICU), that were divided, on the basis of bacteremia in group A (SIRS with bacteremia, n=14) and group B (SIRS without bacteremia, n=35). Hemoculture and blood samples were drawn on the first day to determine suPAR, C-reactive protein (CRP) and procalcitonin (PCT). We set to identify significant cut-off values in estimating bacteremia and mortality in septic patients. Results. In group A, suPAR values were 14.3 ng/mL (range 10-45.5 ng/mL) and in group B, 9.85 ng/mL (range 3.4-48 ng/mL) p=0.008. Area under the curve (AUC) for suPAR was 0.745 (95% CI: 0.600-0.859), for CRP 0.613 (95% CI: 0.522-0.799) and for PCT 0.718 (95% CI: 0.477-0.769). Cut-off value for suPAR in bacteremia prediction was 9.885 ng/mL, with 100% sensibility and 51.43% specificity. Mortality in group A was 85.7% (12/14) and in group B 74.3% (26/39), p>0.05. Area under the curve (AUC) for suPAR was 0.750 (95% CI: 0.455-0.936), for CRP 0.613 (95% CI: 0.413-0.913) and for PCT 0.618 (95% CI: 0.373-0.888). Cut-off value of suPAR in predicting mortality was 11.5 ng/mL, with 66.67% sensibility and 100% specificity. Conclusions. In our study suPAR had a predictive capacity for bacteremia and seems to be an independent factor for mortality prognosis in septic patients.
To date it is unknown if there is a predisposition to sepsis. In this respect, genetic studies have been conducted with the aim to find gene variants which can point out a higher predisposition to developing sepsis. The primary objective of this study is to highlight whether the genetic polymorphism of Angiopoietin-2 gene (ANG2-35G>C) is present mainly in septic patients. As secondary objectives we aimed to evaluate if there are any associations between ANG2-35G>C polymorphism and the severity scores Acute Physiology and Chronic Health Evaluation II (APACHE II) and Simplified Acute Physiology Score (SAPS) as well as routine tests in septic patients such as C reactive protein (CRP), procalcitonin (PCT). We enrolled adult patients admitted to the Intensive Care Unit (ICU). After admission to the ICU and the diagnosis of sepsis, blood samples were collected and the severity scores: APACHE II, SAPS were calculated on the first day of ICU admission. We recorded the following from the blood samples: CRP, PCT, angiopoietine2 (Ang-2). We performed several one-way ANOVA tests to determine any significant mean difference of the analyzed variables. We observed that variant genotypes of ANG2-35G>C gene polymorphism are significantly related to CRP, aspect which increases this biomarker credibility compared with others (i.e., PCT), in septic patients. ANG2-35G>C gene polymorphism is associated with severity scores, APACHE II, and SAPS in sepsis.
Background: Known also as Osler’s triad, Austrian syndrome is a complex pathology which consists of pneumonia, meningitis and endocarditis, all caused by the haematogenous dissemination of Streptococcus pneumoniae. The multivalvular lesions are responsible for a severe and potential lethal outcome.
Case report: The case of a 51-year-old female patient, with a past medical history of splenectomy, is presented. She developed bronchopneumonia, acute meningitis and infective endocarditis as a result of Streptococcus pneumoniae infection and subsequently developed multiple organ dysfunction syndromes which led to a fatal outcome. Bacteriological tests did not reveal the etiological agent. The histopathological examination showed a severe multivalvular endocarditis, while a PCR based molecular analysis from formalin fixed valvular tissue identified Streptococcus pneumoniae as the etiologic agent.
Conclusions: The presented case shows a rare syndrome with a high risk of morbidity and mortality. Following the broad-spectrum treatment and intensive therapeutic support, the patient made unfavourable progress which raised differential diagnosis problems. In this case, the post-mortem diagnosis demonstrated multiple valvular lesions occurred as a result of endocarditis.
Objectives: The goal of the study was to investigate the correlations between the interleukin-6 IL-6 -174 G/C and IL-6 -572 G/C gene polymorphisms and sepsis risk and severity in adult ICU patients.
Materials and Methods: We prospectively assessed 107 septic patients and divided them into two subgroups: organ dysfunction-free sepsis subgroup S (n=60) and septic shock subgroup SS (n=47). A control group of 96 healthy individuals was included. Both patients and controls underwent IL-6 -174 G/C and -572 G/C genotyping and circulating IL-6 in the study group which were measured from samples taken in the first day of sepsis diagnosis.
Results: No differences in the genotype frequencies of the two polymorphisms between study and control groups were identified. The GC genotype and C allele of IL-6 -572 G/C gene polymorphism was statistically significant more frequent in the organ dysfunction-free subgroup (p=0.01, p=0.004 respectively). No statistically significant differences for the IL-6 -174 G/C gene polymorphism were found between the two sepsis subgroups. Circulating IL-6 levels were significantly higher in the septic shock subgroup and among patients with GG genotypes of both studied polymorphisms.
Conclusion: We underline the possible role of IL-6 -572 G/C as a marker of severe evolution. There is no evidence of a direct role of IL-6 -174 G/C gene polymorphism in sepsis risk and outcome. Il-6 levels are correlated with sepsis severity but not with variant genotype of investigated IL-6 gene polymorphisms.