These factors include onset of labor before 37 weeks of gestation (premature birth), prolonged rupture of membranes (≥18h before delivery), intra-partum fever (>38 °C,  >100.4 °F), amniotic infections (chorioamnionitis), young maternal age, and low levels of GBS anticapsular polysaccharide antibodies in the mother. Nevertheless, most babies who develop EOD are born to GBS colonized mothers without any additional risk factor. A previous sibling with EOD is also an important risk factor for development of the infection in subsequent deliveries, probably reflecting a lack of GBS polysaccharides protective antibodies in the mother. Heavy GBS vaginal colonization is also associated with a higher risk for EOD. Overall, the case–fatality rates from EOD have declined, from 50% observed in studies from the 1970s to 2 to 10% in recent years, mainly as a consequence of improvements in therapy and management. Fatal neonatal infections by GBS are more frequent among premature infants.GBS LOD affects infants from 7 days to 3 months of age and is more likely to cause bacteremia or meningitis. LOD can be acquired from the mother or from environmental sources. Hearing loss and mental impairment can be a long-term sequela of GBS meningitis. In contrast with EOD, the incidence of LOD has remained unchanged at 0.26 per 1000 live births in the US. S. agalactiae neonatal meningitis does not present with the hallmark sign of adult meningitis, a stiff neck; rather, it presents with nonspecific symptoms, such as fever, vomiting and irritability, and can consequently lead to a late diagnosis.
Lactate accumulation reduces contractility and eventually necroses cardiomyocytes, releasing their troponin storage into the bloodstream. Serum troponin elevation is a characteristic biomarker of MI.Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for Non-ST Elevation Myocardial Infarction, referencing the lack of ST-segment elevation in ECG traces. This is because in NSTEMI, only part of the myocardial wall is infarcted, which does not diagnostically present with ST-elevation. NSTEMI becomes STEMI when the entire myocardial wall is infarcted. Diagnostically, STEMI displays prolonged ST-segment elevation in ECG traces, and is thus named ST-Elevation Myocardial Infarction. Minutes after STEMI, fatal cardiac arrest could occur. STEMI is life-threatening if immediate reperfusion therapy is not initiated. Gangrene
Gangrene, specifically dry gangrene, is caused by an atherosclerotic or thromboembolic arterial occlusion. Gangrene is a complication of prolonged PAD, leading to shriveling, blackening, and infarction of peripheral tissue, commonly in the extremities. In severe cases, amputation of the affected limb is required. Ischemic Stroke
Ischemic stroke is a thrombotic, or rarely, thromboembolic or atherosclerotic complication of arteries supplying the brain. Occlusion of brain arteries leads to rapid ischemic death of neurons, both at the infarct core and ischemic penumbra. Similar to cardiomyocytes, neurons require constant perfusion for proper function. Any interruption of blood supply causes neurons to switch to anaerobic metabolism, exhausting intracellular ATP levels. ATP depletion causes an influx of calcium cations into neurons and efflux of excess glutamate, triggering the apoptosis and necroptosis of neurons.Neuronal necrosis precipitates irreversible brain damage.