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Transcript
Characteristics of Bacteria Virulence- the degree of pathogenicity; depends on the presence of certain cell structures and on bacterial exo and endotoxins. Flagella- protein filaments that extend like long tail from the cell membranes of some bacteria. The flagella can facilitate movement toward or away from a chemical concentration gradient in a process called chemotaxis. Pili- straight filaments arising from the bacterial cell wall. They are shorter than flagella and do not move. They can serve as adherence factors (adhesins), which may enhance the bacteria’s ability to cause disease. Capsules- protective walls that surround the cell membranes of some bacteria. They are typically composed of simple sugar residues. The bacteria secrete the sugar substances, which then coat the inner cell wall. Capsules “protect” the bacteria from phagocytization by macrophages and neutrophils. o Tests used to visualize capsules India ink stain- the stain is not taken up by the capsule and thus appears as a transparent halo around the cell. Quellung reaction- bacteria are mixed with antibodies that bind to the capsule. When the antibodies bind, the capsule swells to an observable size. Endospores- formed only by two genera: aerobic Bacillus and anaerobic Clostridium. Endospores are metabolically dormant forms of bacteria that are resistant to heat, cold, drying, and chemical agents. They are formed when there is a shortage of needed nutrients; they can lie dormant for years. Biofilm- extracellular polysaccharide network that forms a “bandage” around bacteria. The biofilm allows bacteria to bind to medical devices (like IV catheters), and it protects them from attack by antibodies and the immune system. Ex. Staphylococcus epidermidis tends to form biofilms on IV catheters and can cause sepsis. Exotoxins- proteins released by both Gram + and Gram – bacteria. o Neurotoxins- exotoxins that act on the nerves or motor endplates to cause paralysis. Examples: tetanus and botulinum toxins o Enterotoxins- exotoxins that act on the GI tract to cause diarrhea. Enterotoxins inhibit sodium chloride resorption, activate NaCl secretion, or kill intestinal epithelial cells. The end result is the osmotic pull of fluid into the intestines. Effects of enterotoxins Infectious diarrhea- bacteria colonize and bind to the GI tract. The diarrhea will continue until the bacteria are destroyed by the immune system or antibiotics. Examples include Vibrio cholera, Escherichia coli, Campylobacter jejuni, and Shigella dysenteriae. Food poisoning- bacteria grow in food and release enterotoxins in the food. The diarrhea and vomiting is usually short-lived (<24 hours). Examples include Bacillus cereus and Staphylococcus aureus. o Pyrogenic exotoxins- stimulate the release of cytokines and can cause rash, fever, and toxic shock syndrome. Examples include S. aureus and Streptococcus pyogenes. o Tissue invasive exotoxins- allow bacteria to destroy and tunnel through tissues. This includes enzymes that destroy DNA, collagen, fibrin, NAD, red blood cells, and white blood cells. Endotoxins An endotoxin is lipid A, which is a piece of the outer membrane lipopolysaccharide of Gram – bacteria. Lipid A/endotoxin is very toxic and is released when the bacterial cell undergoes lysis. Endotoxins are also shed in small amounts from living bacteria. o Administering antibiotics to a patient with a Gram – infection may worsen the person’s condition because all of the bacteria will be lysed, releasing large quantities of endotoxin. o Unlike exotoxin, endotoxin is a normal part of the outer portion of the bacteria that sheds off. Septic shock- a common and deadly response to both Gram- and Gram + bacterial infections. Septic shock is a leading cause of death in ICU units. Bacteremia- by definition, bacteria in the bloodstream. The bacteria can be detected by isolating the bacteria in blood cultures. Brushing your teeth causes bacteremia with few effects. However, bacteremia can progress to sepsis. Sepsis- bacteremia that causes a systemic immune response to the infection. Symptoms may include a fever, elevated white blood cell county, and rapid heart rate. Septic shock- sepsis that results in dangerous drops in blood pressure and organ dysfunction. Bacteremia from a localized infection may release toxins that circulate in the bloodstream and stimulate immune cells. The immune cells release proteins, such as tumor necrosis factor (TNF). Septic shock can be fatal (>40%). Mortality rises with every organ system that fails. The table below lists the possible effects of septic shock on various organ systems. System Vascular Effect Vasodilation Result Decreased blood pressure Heart Myocardial depression Kidneys Acute renal failure Liver Hepatic failure Brain Coagulation system Encephalopathy Disseminated intravascular coagulation Decreased cardiac output, decreased blood pressure Decreased urine output, accumulation of toxins Accumulation of metabolic toxins; hepatic encephalopathy Alteration in mental status Clotting, bleeding Effects of specific toxins Clostridium tetanus produces the tetanus toxin, which causes uncontrolled muscle contractions with lockjaw and tetanic paralysis of respiratory muscles. C botulinum produces botulinum toxin, which causes paralysis with respiratory muscle paralysis. Botulinum toxin is the most potent exotoxin. Streptococcus pyogenes produces pyrogenic toxin, which activates the mediators of sepsis and can result in scarlet fever. Staphylococcus aureus- toxic shock syndrome toxin. May produce symptoms such as fever, rash, diarrhea, and shock.