Sandbox:Prince

The only known reservoirs for H. influenzae in humans are the respiratory tract and, to a lesser extent, the conjunctival and genital surfaces. Since carriage of H. influenzae is so common among healthy individuals, its pathogenicity must be examined in the wider context of the conditions that permit its perpetuation on mucosal surfaces, factors that reflect the coevolution of microbe and host-an ongoing relationship. The dynamic nature of this relationship is evidenced by the genetic diversity within natural populations of H. influenzae and the diverse, complex nature of host immune responses among genetically different individuals. The strategies deployed by a microbe-which is highly adapted to its host-to ensure its survival, proliferation, and dissemination may result in no discernable damage to the host (carrier state) or may result in tissue damage of varying severity. Disease may therefore be considered as an accidental (or perhaps incidental) consequence of the microbial factors that permit its survival. These characteristics must be considered in the context of the adaptive potential of H. influenzae in the individual and in the population at large. The potential to adapt

and therefore to compete successfully for essential nutrients, to evade host defenses, to propagate from one host to another, and to cause tissue damage involves phenotypic complexities governed by many genes. The eclectic nature of pathogenicity is well exemplified by H. influenzae, involving as it does the capacity to colonize mucosal surfaces, to spread contiguously (for instance to the middle ear or sinuses) or invade epithelial cells, to disseminate within the bloodstream, and to localize to selected tissues (such as meninges, epiglottis, or synovia of joints). The ability to analyze the "pathogenic personality" of microbes at the molecular level has been greatly facilitated by the application of genetic and recombinant DNA techniques.

s. The first are systemic

infections that occur as a result of, or in association with,
invasion of the bloodstream; examples include meningitis,
epiglottitis, cellulitis, septic arthritis, and pneum

Virulent factors of H. influenza:

Capsular polysaccharide
Lipopolysaccharide
Outer-membrane proteins
Pilus proteins
IgAl proteases
Histamine
Factors affecting ciliat

George Washington, the United States’ first president, 2 yr after leaving office on December 13, 1799, was reported to have “a cold” and mild hoarseness. The next morning, around 2:00 AM, he had difficulty breathing. By 6:00 AM, he was febrile, had throat pain, and experienced respiratory distress. Three physicians were called to his side and tried various remedies, all without success.1 Washington died at 10:20 PM, likely due to bacterial epiglottitis. If he had lived and received care 200 yr later, the outcome might have been different.

Variable	Empyema Thoracis	Lung abscess	parapneumonic effusion	Pneumonia	Lung cancer

Von Willebrand disease (vWD) is the most common genetic coagulation disorder described in humans. It affects up to 1% of the population, although most cases are mild. Symptomatic vWD is much rare, ~1 in 10000. Von Willebrand disease arises from a qualitative or quantitative deficiency of von Willebrand factor (vWF), a large glycoprotein protein that is required for platelets to bind to collagen. vWF is therefore important in primary hemostasis. When the disease comes to medical attention, it usually presents in the typical manner for platelet disorders: mucosal bleeding and easy bruising. The disease is usually inherited in an autosomal dominant manner, although there are recessive forms as well, and it can also be acquired secondary to another disease.

diagnosis hxThe disease is characterized mainly by mucosa-associated bleeding and bleeding after surgery and trauma. The diagnosis is based on a personal or family history of bleeding and laboratory evidence of abnormalities in von Willebrand factor, factor VIII, or both.