The accumulation of fluid in the heart creates a higher than normal pressure system that places increasing pressure demands on the pulmonary venous system in order for appropriate oxygenation of blood to occur. This results in what is called pulmonary venous hypertension (PVH), and results in distention and recruitment of pulmonary capillaries to help distribute the increased pressure gradient. At the capillary, there is a microvascular barrier that helps regulate fluid status via molecular pressure forces such as forces that push outward from vessels and pressures that pull or attract into vessels. With increasing PVH, pressure outward overcomes pressure inward, and fluid is distributed to the lung interstitium, preserving oxygen exchange at the capillary. Fluid is transported to the hilum and pleural space, and removed via the lymphatic system. At first, the body is capable of handling excess water. Later, the capillary vasculature is overwhelmed by increased pressure and fluid backs up into the alveolar sac, resulting in pulmonary edema and decreased oxygenation capability. Additionally, increased pressure demands on capillary vasculature result in increases in vascular tone to include remodeling of pre-capillary vessels such as medial wall hypertrophic changes. Overtime, the remodeling efforts of the vessels can progress to hyperplastic changes of the vessels wall construction, and results in increased pulmonary vascular resistance.There is ongoing interest into establishing connections of cardiac asthma to abnormalities in bronchiole anatomy. Current evaluation has proposed multiple mechanisms for increased airway resistance, and focus is on four alternate explanations:

Bronchoconstriction as a result of pulmonary edema.
Disinfectants such as bleach are used to kill bacteria or other pathogens on surfaces to prevent contamination and further reduce the risk of infection. Bacteria in food are killed by cooking to temperatures above 73 °C (163 °F). List of genera and microscopy features
Many genera contain pathogenic bacterial species. They often possess characteristics that help to classify and organize them into groups. The following is a partial listing. List of species and clinical characteristics
This is description of the more common genera and species presented with their clinical characteristics and treatments. Genetic transformation
Of the 59 species listed in the table with their clinical characteristics, 11 species (or 19%) are known to be capable of natural genetic transformation. Natural transformation is a bacterial adaptation for transferring DNA from one cell to another. This process includes the uptake of exogenous DNA from a donor cell by a recipient cell and its incorporation into the recipient cells genome by recombination. Transformation appears to be an adaptation for repairing damage in the recipient cells DNA. Among pathogenic bacteria, transformation capability likely serves as an adaptation that facilitates survival and infectivity. The pathogenic bacteria able to carry out natural genetic transformation (of those listed in the table) are Campylobacter jejuni, Enterococcus faecalis, Haemophilus influenzae, Helicobacter pylori, Klebsiella pneumoniae, Legionella pneumophila, Neisseria gonorrhoeae, Neisseria meningitidis, Staphylococcus aureus, Streptococcus pneumoniae and Vibrio cholerae. See also
Human microbiome project
List of antibiotics
Pathogenic viruses

Notes
References
External links

Bacterial Pathogen Pronunciation by Neal R. Chamberlain, Ph.D. at A.T.