Factor H binding protein is key to the pathogenesis of N. meningitidis, and is, therefore, important as a potential vaccine candidate. Porins are also an important factor for complement inhibition for both pathogenic and commensal species. Porins are important for nutrient acquisition. Porins are also recognized by TLR2, they bind complement factors (C3b, C4b, factor H, and C4bp (complement factor 4b-binding protein)). Cooperation with pili for CR3-mediated internalization is another function of porins. Ability to translocate into host cells and modulate reactive oxygen species production and apoptosis is made possible by porins, as well. Strains of the same species can express different porins. Genome
At least 8 complete genomes of Neisseria meningitidis strains have been determined which encode about 2,100 to 2,500 proteins.The genome of strain MC58 (serogroup B) has 2,272,351-base pairs. When sequenced in 2000, it was found to contain 2158 open reading frames (ORFs). Of these, a biological function was predicted for 1158 (53.7%). There were three major islands of horizontal DNA transfer found. Two encode proteins involved in pathogenicity. The third island only codes for hypothetical proteins. They also found more genes that undergo phase variation than any pathogen then known. Phase variation is a mechanism that helps the pathogen to evade the immune system of the host.The genome size of strain H44/76 is 2.18 Mb, and encodes 2,480 open reading frames (ORFs), compared to 2.27 Mb and 2,465 ORFs for MC58. Both strains have a GC content of 51.5%.
If related to pulmonary disorders, the amount of lung damage dictates whether or not treatment is efficacious in reversing newborn lung insufficiency. Other causes for acute pulmonary hypertension include: infection, endocrine disorders, and drug injury.Examples of cases with newborns who with sustained fetal circulation are pulmonary hypoplasia and genetic abnormalities. Treatment
Treatment aims to increase the amount of oxygen in the blood and reverse any causes of hypoxia as well as gain adequate perfusion.Common treatments include:
Oxygen therapy
Mechanical ventilation
Pulmonary vasodilators
Nitrous Oxide Inhalation (iNO)
Sildenafil
Milrinone
GlucocorticoidsThe therapies available to manage PPHN include high frequency ventilation, surfactant instillation, pulmonary vasodilators, and extracorporeal membrane oxygenation.iNO is the preferred medication for PPHN due to its ability to more selectively cause pulmonary vasodilation in comparison to intravenous vasodilators. While this medication decreases the need for extracorporeal membrane oxygenation or extracorporeal life support, it has not been shown to reduce mortality. Intravenous sildenafil has been shown to have similar efficacy and is becoming more commonly used as treatment for PPHN.Assessment of the efficacy of these treatments includes chest radiographs and arterial blood gases. Signs of inefficacious treatments include prolonged capillary filling time, low pulse volume, low blood pressure, and sustained metabolic acidosis.In addition to treating the direct effects of this condition, other management strategies are implemented concurrently to stabilize the newborn.These include, but are not limited to nutritional support, reduction of stressful environment, gentle sedation, monitoring/treating acidosis and establishing normal systemic blood pressure.Challenges in developing countries:
PPHN has been seen more frequently in developing countries or resource-poor areas, though it occurs across the globe.