Located on skin mucous membranes vagina 20 of healthy women and in

Located on skin mucous membranes vagina 20 of healthy

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-Located on skin, mucous membranes, mouth (30-50%), vagina (20% of healthy women), and in the GI tract -Colonize in the mucous membranes of all humans after birth -Opportunistic organism -Causes local or disseminated infections Disseminated: may involve several internal organs (abscess in the kidney, brain, liver, and heart, characterized by persistent/recurrent fever, gram negative shock like symptoms- hypotension, tachycardia), DIC, and death -Special adhesion factors- allows it to bind to implanted devices, epithelium, ECM, leukocytes, facilitates tissue invasion -Secretes several enzymes that function as -Immunocompromised (cancer, transplant patients, HIV/AIDS) are at an increased risk for acquiring candida infections d/t diminished levels of neutrophils -Invasive candidiasis may also occur from indwelling catheters, IVs, peritoneal dialysis (direct access) -Complications: abscesses in the kidneys, brain, liver, shock DIC, death - Mycotoxicoses - ingestion of fungal toxins (Amanita mushroom produces hepatotoxins, wild mushroom that when eaten causes liver failure, problem in foreign countries, will require liver transplantation & dialysis to remove toxins) - Aspergillus Flavus produces aflatoxins (heptatotoxic, tumor causing)- ingested with spoiled grains and peanuts -Undergoes morphologic changes from unicellular yeast to filamentous hyphal
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virulence factors and contribute to tissue destruction -Disruption by antibiotic therapy can cause Candida overgrowth > vaginitis or oropharyngeal infection (thrush) forms (alters profile of surface antigens and increased resistance to immunologic destruction as well as altered tissue adhesion specificity) INFLUENZA, and MEASELS Viral Infection Clinical Manifestations Pathophysiology Clinical Implications INLUENZA Clinical manifestations include fevers, myalgias, malaise, dry cough and headaches. Complications include secondary bacterial pneumonia, bronchitis, viral pneumonia, febrile seizure, encephalitis and myocarditis. *From LEC. NOTES* The pathogenesis is as follows: • Virus is inhaled → neuraminidase (viral protein, on envelop) → degrades protective mucous layer of respiratory system → using hemagglutinin (viral protein, on envelop) → infects cells of the upper and lower respiratory system → necrosis of superficial respiratory cells and inflammation → leaving host susceptible to bacterial pneumonia. • Neuraminidase also is responsible for the release of viruses from infected cells • Systemic symptoms include myalgias, fever, fatigue are due to the cytokines released not the infection. • Viral infection does not go beyond respiratory system because the viral hemagglutinin is cleaved by proteases located in the respiratory system. • Immunity is a IgA function • Mutations in the virus are due to changes in the neuraminidase and hemagglutinin viral proteins. These are surface proteins on the virus and is how the virus is named (H1N1).
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  • Fall '15
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