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Microbial Infection
| Question | Answer |
|---|---|
| Infection: | The invasion and growth of microorganisms within a host. Expression of disease. |
| Disease: | The damage or disruption of normal body functions caused by infection. Symptoms of infection; deviation from the normal. |
| Pathogens: | Microorganisms that cause disease in a host. |
| Pathogenicity: | The ability of a microorganism to cause disease. (There will be a question about this on the exam!) |
| Virulence: | The degree or severity of a pathogen’s ability to cause disease. (There will be a question about this on the exam!) |
| Virulence Factor: | A molecule or structure produced by pathogens that enhances their ability to infect or damage the host. Ex: capsules, Lipid A (endotoxins), flagella, biofilms, fimbriae |
| Capsules: | Microbial capsules are protective outer layers, most commonly found in bacteria, that are usually made of polysaccharides and help the microbe evade the immune system. |
| Lipid A (endotoxins): | toxic component of gram-negative bacterial endotoxins, anchoring the lipopolysaccharide (LPS) to the outer membrane. |
| Flagella: | flagella are protein-based appendages used for motility. |
| Pili: | Hair-like structures on bacterial surfaces that aid in attachment, movement, and DNA transfer between cells. |
| Biofilms: | Communities of microorganisms attached to surfaces and embedded in a protective matrix, making them more resistant to antibiotics and host defenses. |
| Fimbriae: | Short, thin, bristle-like projections on bacteria that help them adhere to host tissues and surfaces. |
| Measuring Virulence: | virulence can be estimated from experimental studies of the LD50 (lethal dose), the amount of agent that kills 50 percent of the animals in a test group. |
| How Does High Virulence Affect The Kill Rate? | Highly virulent pathogens show little difference in the number of cells required to kill 100 percent of the population as compared to 50 percent of the population. |
| Streptococcus Pneumonia: | highly virulent organism, mortality ~5–7% in healthy adults; higher in elderly or immunocompromised |
| Salmonella Eneterica Typhimuriium: | moderately virulent organism, higher mortality (~5–10%) in immunocompromised or elderly |
| Francisella tularensis: | Comes from infected wild rabbits, highly infectious — even a very small number of bacteria (10–50 organisms) can cause disease — which makes it dangerous, but modern antibiotic treatment is highly effective. |
| The Compromised Host: | The pathogen-host interaction is dependent upon the host and the pathogen. Certain medical procedures (like surgery) or underlying conditions predispose individuals to develop diseases. |
| What are some factors that leave people immunocompromised? | Nosocomial (healthcare-associated) infections affect nearly two million people per year. Infections with viruses, such as HIV, weaken the immune system. |
| Opportunistic Infections: | caused by organisms that do not cause disease in healthy hosts. |
| Adherence: | the enhanced ability of microbes to attach to host tissues. Required but not enough alone to cause disease. Pathogens enter via specific portals of entry and attach using fimbriae (pili), capsules/slime layers, or biofilms. |
| The Infection Process: | — Exposure (to pathogens) — Adherence (to skin or mucosa) — Invasion (through epithelium) — Multiplication (growth and production of virulence factors and toxins). |
| The Disease Process: | — Toxicity (toxin effects are local or systemic) — Invasiveness (further growth at original and distant sites) — Both result in tissue or systemic damage |
| Invasiveness: | ability of a pathogen to grow in host tissue at densities that inhibit host function. |
| Bacteremia: | the presence of bacteria in the bloodstream. |
| Septicemia: | bloodborne systemic infection. May lead to massive inflammation, septic shock, and death. |
| Infection: | any situation in which a microorganism (not a member of the local flora) is established and growing in a host. |
| Virulence Factor: | Molecules produced by pathogens that enhance their ability to cause disease by damaging host tissues or evading immune defenses. |
| Enzymatic Virulence Factors: | Enzymes secreted by pathogens that break down host tissue components, enabling invasion and spread through the body. |
| Hyaluronidase | Breaks down hyaluronic acid (polysaccharide found in connective tissue that provides structural support and integrity) in host tissues, allowing pathogens like Streptococcus pyogenes to spread deeper. |
| Coagulase | Produced by Staphylococcus aureus; forms clots that protect bacteria from immune cells. |
| Streptokinase | Produced by Streptococcus pyogenes; dissolves blood clots, releasing pathogens to spread into the bloodstream and deeper tissues. |
| Collagenase | Breaks down collagen in connective tissues, enabling pathogens to penetrate deeper into muscles and organs. |
| Toxicity | the ability of an organism to cause disease via toxins that disrupt or kill host cells. Exotoxins, released during growth, are classified as cytolytic toxins, AB toxins, or superantigens. |
| Endotoxins: | toxic lipopolysaccharides (LPS) in the outer membrane of most gram-negative bacteria. Unlike exotoxins, they are structural, not proteins, and are released in significant amounts only when bacterial cells lyse. |
| Cytolytic Exotoxins | Toxins that degrade cytoplasmic membrane integrity, causing cell lysis and death. |
| Hemolysins | Cytolytic toxins that specifically lyse red blood cells. |
| Staphylococcal α-toxin | A cytolytic exotoxin that kills nucleated cells and lyses erythrocytes (red blood cells). |
| Superantigen Toxins | Overactivate the immune system by binding directly to T cells and MHC proteins, triggering massive cytokine release and toxic shock (e.g., Staphylococcus aureus toxic shock syndrome toxin. Think about the tampons!) |
| Some Causes of Superantigen Exotoxins: | Produced mainly by Gram-positive bacteria like Staphylococcus aureus and Streptococcus pyogenes. They can cause food poisoning (S. aureus enterotoxins), toxic shock syndrome, or pyrogenic fever. |
| Enterotoxins: | Exotoxins that target the small intestine, causing massive fluid secretion, vomiting, and diarrhea. Example: Cholera toxin, an AB-type exotoxin from Vibrio cholerae, the cause of cholera. |
| A-B Type Exotoxins: | some of the best known and most potent exotoxins are AB toxins, including those expressed in diphtheria, tetanus, botulism, and cholera. |
| What are AB Toxins Made Up Of? | It is made of an active (A) domain and a binding (B) domain. The A-domain adds an ADP-ribosyl group to EF-TU, which prevents its function in translation. |
| Diphtheria Toxin: | An AB toxin that stops protein synthesis in host cells, causing cell death and a thick throat membrane. |
| The Activity of Diphtheria Toxin: | The B subunit binds host cell receptors and facilitates entry of the A subunit into the cytoplasm. The A subunit ADP-ribosylates EF-2, halting protein synthesis and killing the host cell. |
| How Did They Make The Diphtheria Antitoxin? | Produced by injecting horses with increasing doses of diphtheria toxin to stimulate antibody production. The horses’ serum, containing antibodies, is purified and used to treat humans, providing immediate, short-term protection by neutralizing the toxin. |
| A-B Neurological Exotins: | AB exotoxins from Clostridium botulinum and C. tetani that target nervous tissue; botulinum is extremely potent, tetanus is a strong neurotoxin. |
| Botulinum Toxin Activity: | Blocks acetylcholine release at neuromuscular junctions, stopping nerve signals from reaching muscles and causing flaccid (limp) paralysis. |
| Tetanus Toxin Activity: | Blocks glycine release from inhibitory neurons in the spinal cord, preventing muscles from relaxing and causing spastic (rigid) paralysis with continuous contractions. |
| Botulism (specifically): | Botulinum toxin blocks acetylcholine, causing flaccid paralysis (e.g., “floppy baby” syndrome). Often food-borne, with weakness, drooping eyelids, swallowing difficulty, and possible respiratory paralysis. |
| Tetanus (specifically): | Tetanus toxin blocks glycine release, preventing muscle relaxation and causing spastic paralysis. Enters through puncture wounds; symptoms include lockjaw, muscle spasms, back arching, and potential respiratory failure. |
| Vaccines for Botulism: | There is a rarely used toxoid vaccine for high-risk individuals (e.g., lab workers). Not routinely given to the general public. |
| Vaccines for Tetanus: | Tetanus toxoid vaccine (part of DTaP, Tdap, or Td vaccines). Routine childhood immunization with boosters every 10 years. Provides active immunity by stimulating the body to produce antibodies against tetanus toxin. |
| Chemistry Associated with Exotoxins Vs. Endotoxins: | exotoxins are made of proteins (polypeptides) while endotoxins are made of lipopolysaccharides (LPS), specifically the lipid A component of the outer membrane of Gram-negative bacteria. |
| Mode of Action & Symptoms Associated with Exotoxins Vs. Endotoxins: | Exotoxins target specific host cell functions, causing symptoms like paralysis, diarrhea, or tissue damage. Endotoxins trigger a non-specific inflammatory response, leading to fever, shock, and potential organ failure. |
| Can Exotoxins and Endotoxins Be Destroyed With Heat? | Exotoxins can but endotoxins cannot. |
| Fever Potential with Exotoxins Vs. Endotoxins: | exotoxins generally do not cause fever while endotoxins are highly pyrogenic. |
| Genetic Origin of Exotoxins Vs. Endotoxins: | exotoxins are encoded by genes on plasmids, bacteriophages, or chromosomal DNA, while endotoxins are a structural component of the bacterial cell wall. |
Created by:
smurtab