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MechanismsPathogens
| Question | Answer |
|---|---|
| Disease | Any condition in which the normal structure or functions of the body are damaged or impaired. It can be caused by infection by a pathogen, genetics, environmental causes, or inappropriate immune responses. |
| Infection | The successful colonization of a host by a microorganism (pathogen). |
| Pathogenicity | The potential qualitative ability of an organism to cause disease (i.e., whether it can cause disease or not). |
| Virulence | The degree of pathogenicity or the "disease-producing power" of an organism. It quantifies how severe the disease is within a group of pathogens |
| Median Infectious Dose (ID 50) | The number of pathogen cells or virions required to cause active infection in 50% of inoculated animals. |
| Median Lethal Dose (LD 50) | The number of pathogenic cells, virions, or amount of toxin required to kill 50% of infected animals. |
| Capsule Production | This physical layer prevents immune cells from adhering to and engulfing the bacterium |
| Proteases | These enzymes protect against phagocytosis and can also destroy antibodies |
| Communicable Disease | A disease that can be spread from person to person. If it is very easily spread, it is specifically referred to as a contagious disease (e.g., COVID-19, measles). |
| NOn-Communicable Disease | An infectious disease that is not spread from one person to another (e.g., tetanus). |
| Latrogenetic | Diseases contracted as the direct result of a medical procedure, such as wound infections following surgery. |
| Nosocomial | Diseases acquired specifically in a hospital or healthcare setting, such as MRSA. |
| Zoonotic | Diseases that are transmitted from animals to humans, such as rabies or yellow fever. |
| stages of an acute infectious disease | 1. Incubation period 2. Prodromal period 3. Period of illness 4.Period of decline 5.Period of covalescences |
| Incubation period | Occurs after initial entry; the pathogen begins multiplying, but there are insufficient numbers to cause signs or symptoms. |
| Prodromal Period | The pathogen continues to multiply, and the host begins to experience general signs and symptoms (like tiredness or aches) resulting from immune activation. |
| Period of illness | Signs and symptoms are most obvious and severe; the number of pathogen particles reaches its peak. |
| Period of decline | The number of pathogen particles begins to decrease, and signs and symptoms start to subside. |
| Period of covalescences | The patient generally returns to normal functions, although some permanent damage may remain |
| Koch's Postulates | The suspected agent must be absent from all healthy organisms but present in all diseased organisms. The causative agent must be isolated from the diseased organism and grown in pure culture. The cultured agent must cause the same disease when inoculated into a healthy, susceptible host. The same agent must be re-isolated from the newly diseased host. |
| Significance of Postulates | These are used to determine if a specific microbe causes a specific disease. Molecular Koch's Postulates were later created to address limitations, such as pathogens that cannot be grown in pure culture or are found in asymptomatic carriers. |
| Outcome of Host-parasite relationship | The outcome is determined by the interaction between the pathogen's virulence factors (its ability to cause harm) and the host's defenses. Factors like the host's age (very young or elderly), pregnancy, or compromised immune systems (due to chemotherapy or surgery) significantly increase susceptibility. |
| Virulance factors | Virulence factors allow pathogens to colonize, damage host tissues, and spread |
| Adhesion factors | Allow microbes to attach to specific host cells |
| Exoenzymes | Degrade host tissues to facilitate invasion (e.g., collagenase breaks down connective tissue). |
| Toxins | Directly produce symptoms like fever, cardiovascular problems, diarrhea, and septic shock. |
| Endotoxins | Built into the structure of the bacterial cell (e.g., Lipid A in gram-negative bacteria) and are released only when the cell is damaged or dies. They typically cause general symptoms like fever and inflammation. |
| Exotoxins | Toxic proteins produced and actively secreted by living bacteria into surrounding tissues (soluble in bodily fluids). They are more specific in their action and can destroy host cells or inhibit specific metabolic functions. |
| Effects on the body | Toxins can cause severe systemic issues including toxemia (toxins in the blood) and septic shock |
| Toxigenicity | ability of a microorganisms to produce a toxin |
| Toxemia | Presence of toxin in the host's blood |
| Intoxications | presence of toxin without microbial growth |
| Stages of Pathogenesis | Exposure - contact through mucosal membranes allowing pathogens to enter body (privates/mouth) Adhesion - pathogenic microbes attach to the cells of the body invasion- spreading of pathogen through local tissues or the body. may produce exoenzymes or toxins serving as virulencefactors that allow them to colonize and damage host cells as the spread deeper infection - successful multiplication of the pathogen, can be local focal or systemic |
| local infection | small area of the body typically near entry |
| focal infection | localized pathogen or the toxins produced that spread to secondary location |
| systemic infection | infection spreads throughout the body |
| Glycohydrolases | degrade hyaluronic acid that cements cells together to promote spreading through tissues |
| Nucleases | degrades DNA released by dying sells that trap the bacteria and promote spread |
| Phospholipases | degrade phospholipid bilayer of host cells, causing, sellular lysis, and degrade membrane of phagosomes to enable escape into the cytoplasm |
| Proteases | degrade collegen in connective tissue to promote spread |
Created by:
agk236