Eleni E. Magira

Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton-Valentine leukocidin genes: A lethal cause of pneumonia in an adult immunocompetent patient

Necrotizing pneumonia and fatal septic shock were caused by Panton-Valentine leukocidin-positive, community-acquired, methicillin-resistant Staphylococcus aureus (CA-MRSA) in a previously healthy, 61-y-old female. This patient did not belong to any high-risk group (e.g. homosexuals, military recruits, sports team members, etc.). CA-MRSA infection should be suspected in any adult with severe pneumonia/sepsis.

Early Response Roles for Prolactin Cortisol and Circulating and Cellular Levels of Heat Shock Proteins 72 and 90α in Severe Sepsis and SIRS

Objective. To evaluate the early heat shock protein (HSP) and hormonal stress response of intensive care unit (ICU) patients with severe sepsis/septic shock (SS) or systemic inflammatory response syndrome (SIRS) compared to healthy subjects (H). Methods. Patients with early (first 48 hrs) SS (n = 29) or SIRS (n = 29) admitted to a university ICU and 16 H were enrolled in the study. Serum prolactin, cortisol, and plasma ACTH were determined using immunoassay analyzers. ELISA was used to evaluate extracellular HSPs (eHSP90α, eHSP72) and interleukins. Mean fluorescence intensity (MFI) values for intracellular HSPs (iHSP72, iHSP90α) were measured using 4-colour flow-cytometry. Results. Prolactin, cortisol, and eHSP90α levels were significantly increased in SS patients compared to SIRS and H (P < 0.003). ACTH and eHSP72 were significantly higher in SS and SIRS compared to H (P < 0.005). SS monocytes expressed lower iHSP72 MFI levels compared to H (P = 0.03). Prolactin was related with SAPS III and APACHE II scores and cortisol with eHSP90α, IL-6, and lactate (P < 0.05). In SS and SIRS eHSP90α was related with eHSP72, IL-6, and IL-10. Conclusion. Prolactin, apart from cortisol, may have a role in the acute stress response in severe sepsis. In this early-onset inflammatory process, cortisol relates to eHSP90α, monocytes suppress iHSP72, and plasma eHSP72 increases.

Acute generalized livedo racemosa caused by Capnocytophaga canimorsus identified by MALDI-TOF MS

Independent of the size of the dog and the type of injury, serious infections may follow a dog bite and these may result in the abrupt onset of multiorgan failure. Early recognition of the warning signs with regard to the underlying severity of the infection is of the utmost importance. Reticulate skin eruptions constitute a precursory phenomenon.

Virus infection and autoimmunity: Is there a cause-and-effect relationship?

A 57-year-old woman was admitted, to the intensive care unit f our tertiary hospital, because of reduced level of consciousess and shortness of breath, required intubation and mechanical entilation. During the previous 3 months she complained of weakess with profound malaise, reduced appetite and loss of weight. week before her admission she suffered two episodes of tranient confusion and diminished level of consciousness that resolved mmediately. There was no past medical history. No chest pain, ough, diarrhea, fever, nausea, rash or arthralgias were reported. n physical examination, the patient was afebrile and appeared hin with marked pallor. The temperature was 36.8 ◦C, the blood ressure 175/99 mm Hg, the pulse 84 beats per minute. Purple disoloration on both hands consisted with Raynaud’s phenomenon as observed (Fig. 1). No skin thickening or other lesions were bserved. Laboratory findings on admission were as follow: hemoglobuin 7.7 g/dl; white-cell count, 7200/mm3 (89 N/8L/6M%); platelet, 7,000/mm3; erythrocyte sedimentation rate, 14 mm; C-reactive rotein, 0.1 mg/dl (normal <0.5 mg/dl); creatinine, 3.92 mg/dl, lood urea nitrogen, 191 mg/dl; lactate dehydrogenase (LDH), 86 IU/l (normal value <255); reticulocyte 9.46%. Peripheral blood

Severe hyperkalemia induced by a short interruption of barbiturate coma

Dear Editor, A 23-year-old woman was admitted to the ICU division of Tzanion Hospital after a motor vehicle crash. Her clinical diagnosis was severe head injury consisting of cerebral edema and traumatic subarachnoid hemorrhage grade 3. Her Glasgow Coma Score (GCS) at the scene was 7, requiring tracheal intubation for airway protection. On admission, pulse was 100 beats/min and blood pressure was 130/75 mmHg. Complete blood count results were normal. Her physical examination was unremarkable except for the finding related to the pupils, which were 2 mm in size, equal, and nonreactive to light. Initial intensive care management included sedation with propofol 2% (2.8 mg/ kg/h) and midazolam (0.46 mg/kg/ h), both of which were held at continuous constant rate for the first 6 days of hospitalization, along with ventilation to almost normocarbia (pCO2 37–38 mmHg), maintenance of normoglycemia, and core body temperature close to 36 C. Total suppression of brain activity by induction of barbiturate coma therapy (BCT) with sodium thiopental at constant infusion rate (2.14 mg/kg/h, interrupted once for 45 min on day 5) was initiated, and electroencephalogram (EEG) was used to determine the optimal depth of barbiturate coma. On the first day following injury (day 1), the patient required norepinephrine (5 lg/min) to achieve the desired mean arterial pressure (MAP) of about 85–90 mmHg. The patient had mild hypokalemia (3.3 mmol/l) on starting sodium thiopental (admission potassium level was 2.9 mmol/l), which responded to potassium supplementation (total 67.5 mmol over 5 h) (Fig. 1). At day 3, despite her neurologically stable clinical condition, she deteriorated, with marked increase in inotrope requirement (23.4 lg/ml). She received also 135 mmol potassium in 10 h. By the end of day 5, the hemodynamic and potassium instability (42.7 lg/ml and 5.8 mmol/l, respectively) were very remarkable. Blood pH was 7.36, and the other electrolyte values were normal. Blood, sputum, and urine cultures on standard media at day 5 were all sterile. Creatine phosphokinase (CPK) was normal. Whole body computed tomography (CT) scan reevaluation was negative, and head CT scan appeared slightly improved. By the middle of day 6, despite no active bleeding or septic shock identified, the hemodynamic parameters were very disturbing, along with the serum potassium level, which was increased to 7.4 mmol/l. Muscle crush injury and rhabdomyolysis were not present. Electrocardiogram (ECG) abnormalities were not found, and troponin I was normal. The possible medications that could have potentially harmed the patient were propofol and sodium thiopental. Since neither the myocardial enzymes nor ECG and transthoracic echocardiogram (TTE) were abnormal, we ruled out propofol infusion syndrome as the causative factor. The findings of refractory hypotension and otherwise unexplained hyperkalemia raised the possibility that sodium thiopental could be the causative factor. A tapering dose of sodium thiopental was initiated by the end of day 5 and completed in the middle of day 6, and the inotrope dose within the next few hours started to decrease. Continuous venous–venous hemodiafiltration dialysis (CVVHDF) was started to reverse the serious hyperkalemia. Twenty-four hours later, the patient

Legionnaire's Disease and Influenza

Legionella pneumophila and influenza types A and B viruses can cause either community-acquired pneumonia with respiratory failure, or Legionella infection could attribute to influenza infection with potentially fatal prognosis. Copathogenesis between pandemic influenza and bacteria is characterized by complex interactions between coinfecting pathogens and the host. Understanding the underlying reason of the emersion of the secondary bacterial infection during an influenza infection is challenging. The dual infection has an impact on viral control and may delay viral clearance. Effective vaccines and antiviral therapy are crucial to increase resistance toward influenza, decrease the prevalence of influenza, and possibly interrupt the potential secondary bacterial infections.