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Disease 1
MIP 315 study
| Question | Answer |
|---|---|
| Gram Positive Bacterium Characteristics | B-Lactamase Enzymes located on the exterior of the cell wall Thick outer cell wall Inner plasma membrane |
| LPS | Lipopolysaccharide, Endotoxin |
| Gram Negative Bacterium Characteristics | LPS exterior, Endotoxin released on death Thin cell wall Inner plasma membrane |
| Sepsis | Infection of the blood |
| Septic Shock | Occurs with a large infection of gram negative bacteria. As Inflammation occurs in too many areas leading to a lack of fluid and cardiac issues. |
| Endotoxin | Occurs only in gram negative bacterium. The LPS breaks down when the bacterium die releasing the toxin. All similar |
| Exotoxin | Occurs in either gram positive or negative bacterium. Released by the bacterium while still alive and their is a much larger variety. |
| Prions | Misfolded pathogenic protein. converts normal PrPc into pathogenic PrPsc. Does its harm by forming amyloid plaques. Infection thought to occur through peyer's patches. |
| Amyloid Plaque | Caused by proteins that share specific structural traits causing them to form an aggregate. |
| Virus | DNA or RNA core surrounded by a protein coat. Symptoms involve the infected tissue and the immune response. |
| Viral Reproduction Cycle | 1. Absorption 2. Penetration 3. Uncoating 4. Replication 5. Assembly 6. Release |
| Hemagglutinin (H) | Influenza surface protein class. 17 types, Entry |
| Neuraminidase (N) | Influenza surface protein class. 9 types, Exit |
| Malaria | Caused by protozoan of the genus Plasmodium. Specifically the most common cause of the disease is Plasmodium falciparum. |
| Salmonella | a genus of rod-shaped, Gram-negative, non-spore-forming, predominantly motile enterobacteria. Contacts epithelia in intestines releases proteins that interrupt cyclic amp function stopping ATP synthesis in the intestines. Prevents re-uptake of water. |
| Spongiform Encephalopathies | Brain function wanes after infection |
| Major Prion Diseases | Kuru (humans), Scrapie (sheep), Creutzfelt jakob (humans), Bovine Spongiform Encephalitis (cattle), Chronic wasting disease. |
| Fungi | Eukaryotic microorganisms. Chiton cell wall. Cause disease by producing toxins. Mycoses are infections of the fungi on host surfaces where they digesting underlying cells. |
| Valley Fever | Type of fungal disease that when inhaled can cause a systemic mycoses. This starts with inhalation and then through the blood they infect many areas of the brain. |
| Parasites | Eukaryotic animals and protists. |
| Protozoans | Like malaria. Pathogenesis starts with blood then goes to liver then blood cells. Cyclical destruction of red blood cells causes chills. Mosquito can get to almost half the worlds population. |
| Nematode | Roundworm, filarial. Elephantiasis, mosquito and person to person transmission; blocks liquids, causes enlargement of extremities. Canine heartworm, mosquito transmission; heartworm grows and blocks blood flow. Mechanical issues |
| Innate Immunity | Exists innately and is pre-existing to an encounter with a pathogen. Skin, Inflammation |
| Inflammation | Follows infection or trauma. Meant to destroy dead cells or pathogens and initiate healing process. Macrophages react to LPS. Mast cells surround blood vessels and are excited by cell death, pathogens, and immune cells. Histamine. Overactive= bad |
| Leukotrienes and Prostaglandins | mechanism of inflammation that cause more inflammation and pain. |
| Neutrophils | The most common white blood cells. Have pathogen specific receptors. Allows them to ingest the pathogen, and release enzymes to destroy surrounding cells. |
| Macrophages | Release pro-inflammatory cytokines. Same other functions as neutrophils. Can act as pathogen presenting cell for adaptive immunity. |
| Adaptive Immunity | Takes time. They have memory and specificity. IgG second time not IgM. |
| T- Cells | Lymphocyte. Examine MHC molecules. Helper cells uses CD4 sees MHC 2 and they release cytokines to activate division of B-cells. Killer cells use CD8 sees MHC 4 and destroy infected non antigen presenting cells. |
| B- Cells | Lymphocyte. Can recognise bacteria and bind to pathogens. They are antigen presenting cells, MHC 2. They when activated produce antibodies (Humoral immune response). |
| Antibodies | Neutralizes toxins and viruses. Opsonization coating bacterium allowing for easier phagocytosis. |
| Immune deficiencies | Primary: congenital surprisingly common especially with inbreeding. Acquired: nutritional, stress, microbial. |
| HIV/ AIDS | Uses GP120 binds to CD4. Enveloped retrovirus that uses reverse transcriptase and inserts its DNA into host and goes into a state of sleep. When T-helper cell levels to low opportunistic infections kill host. Transfusions easiest, Sexual most common. |