Early-onset sepsis remains a common and serious problem for neonates, especially preterm infants. Group B streptococcus (GBS) is the most common etiologic agent, while Escherichia coli is the most common cause of mortality. Current efforts toward maternal intrapartum antimicrobial prophylaxis have significantly reduced the rates of GBS disease but have been associated with increased rates of Gram-negative infections, especially among very-low-birth-weight infants. The diagnosis of neonatal sepsis is based on a combination of clinical presentation; the use of nonspecific markers, including C-reactive protein and procalcitonin (where available); blood cultures; and the use of molecular methods, including PCR. Cytokines, including interleukin 6 (IL-6), interleukin 8 (IL-8), gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α), and cell surface antigens, including soluble intercellular adhesion molecule (sICAM) and CD64, are also being increasingly examined for use as nonspecific screening measures for neonatal sepsis. Viruses, in particular enteroviruses, parechoviruses, and herpes simplex virus (HSV), should be considered in the differential diagnosis. Empirical treatment should be based on local patterns of antimicrobial resistance but typically consists of the use of ampicillin and gentamicin, or ampicillin and cefotaxime if meningitis is suspected, until the etiologic agent has been identified. Current research is focused primarily on development of vaccines against GBS.

Early-Onset Neonatal Sepsis

To assess the effect of age on cardiac volumes and function in the absence of overt or occult coronary disease, we performed serial gated blood pool scans at rest and during progressive upright bicycle exercise to exhaustion in 61 participants in the Baltimore Longitudinal Study of Aging. The subjects ranged in age from 25 to 79 years and were free of cardiac disease according to their histories and results of physical, resting and stress electrocardiographic, and stress thallium scintigraphic examinations. Absolute left ventricular volumes were obtained at each workload. There were no age-related changes in cardiac output, end-diastolic or end-systolic volumes, or ejection fraction at rest. During vigorous exercise (125 W), cardiac output was not related to age (cardiac output [1/min] = 16.02 + 0.03 [age]; r = .12, p = .46). However, there was an age-related increase in end-diastolic volume (end-diastolic volume [ml] = 86.30 + 1.48 [age]; r = .47, p = .003) and stroke volume (stroke volume [ml] = 85.52 + 0.80 [age]; r = .37, p = .02), and an age-related decrease in heart rate (heart rate [beats/min] = 184.66 - 0.70 [age]; r = -.50, p = .002). The dependence of the age-related increase in stroke volume on diastolic filling was emphasized by the fact that at this high workload end-systolic volume was higher (end-systolic volume [ml] = 3.09 + 0.65 [age]; r = .45, p = .003) and ejection fraction lower (ejection fraction = 88.48 - 0.18 [age]; r = -.33, p = .04) with increasing age. These findings indicate that although aging does not limit cardiac output per se in healthy community-dwelling subjects, the hemodynamic profile accompanying exercise is altered by age and can be explained by an age-related diminution in the cardiovascular response to beta-adrenergic stimulation.

Exercise cardiac output is maintained with advancing age in healthy human subjects: cardiac dilatation and increased stroke volume compensate for a diminished heart rate.

Arrhythmias and the “Holiday Heart”: Alcoholassociated cardiac rhythm disorders

✓ Present knowledge of the still controversial pathogenetic, ultrastructural, diagnostic, and treatment aspects of chronic subdural hematomas is reviewed.

Chronic subdural hematomas" a review

Insulin-dependent diabetes mellitus (IDDM), also known as juvenile diabetes, results from destruction of the insulin-producing beta cells in the pancreas [1]. Both viruses and autoimmunity have been suggested as possible causes. The evidence for viruses comes largely from experiments in animals, but several studies in humans point to viruses as an occasional trigger of this disease.

https://www.nejm.org/doi/pdf/10.1056/NEJM197905243002102?listPDF=true

Virus-Induced Diabetes Mellitus

Coxsackie B viral myocarditis and valvulitis identified in routine autopsy specimens by immunofluorescent techniques

Fifty hearts of infants and children were collected at routine autopsies and were surveyed by means of routine histologic techniques and immunofluorescent antibody staining methods. Twenty-nine hearts had interstitial myocarditis with varying degree of myocardial damage. Seventeen had interstitial reactions with an increase in cellularity and with patchy edema. Coxsackievirus B antigens were found in 12 of these hearts. The high incidence of coxsackievirus B antigen in the myocardium of the infants and children is possibly related to the "myocarditis," labeled variously as Fiedler's, idiopathic, interstitial, isolated, or aseptic myocarditis or chronic rheumatic heart disease. The common occurrence of clinically occult coxsackievirus B infection may possibly be related to the etiology of still-births, congenital anomalies, and sudden, unexpected deaths in infancy and childhood. The need for better diagnostic virological facilities in clinical practice is evident from these studies.

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=JAMA&articleId=337190&pdfFileName=jama_203_1_001.pdf

Interstitial and coxsackievirus B myocarditis in infants and children. A comparative histologic and immunofluorescent study of 50 autopsied hearts.

Hemorrhages into the tissues constitute one of the striking features of heat hyperpyrexia Victims of heat stroke exhibit several alterations of the hemostatic mechanism These include a progressive thrombocytopenia, prolongation of the bleeding and clotting times, lowered plasma fibrinogen and prothrombin levels, and increased fibrinolytic enzyme activity 1,2 A decrease in platelet number and a prolonged prothrombin time also occur in cases of artificially induced fever 3 Many of these alterations in the clotting mechanism are similar to those associated with various disseminated intravascular coagulation syndromes 1 It has been assumed that elevated body temperatures during heat stroke damages the endothelial wall of the small vessels inducing clumping of the platelets at the damaged sites and thus triggering the clotting mechanism 1 Obstruction of the small vessels eventually leads to increased capillary permeability and to petechial hemorrhages The extent of endothelial cell damage in relation to intravascular coagulation during heat

Heat stroke. An electron microscopic study of endothelial cell damage and disseminated intravascular coagulation.

Histologic and ultrastructural changes in the myocardium of mice consuming various concentrations of pure ethanol, beer and wine as their sole liquid intake for 4 to 10 weeks are described. Ultrastructural alterations were seen in the sarcoplasmic reticulum, myofilaments and intercalated discs. The changes were minor but discernible. The pathogenesis of these changes is discussed in terms of a possible direct toxic effect of alcohol on the myocardium.

H.L. Colcolough

Papers

Coxsackie B viral myocarditis and valvulitis identified in routine autopsy specimens by immunofluorescent techniques

Interstitial and coxsackievirus B myocarditis in infants and children. A comparative histologic and immunofluorescent study of 50 autopsied hearts.

Heat stroke. An electron microscopic study of endothelial cell damage and disseminated intravascular coagulation.

The effect of ingestion of ethyl alcohol, wine and beer on the myocardium of mice.

Acute myocardial lesions; following experimentally-induced intracranial hemorrhage in mice: a histological and histochemical study.