Term
| What color are gram-positive bacteria after gram stain? |
|
Definition
| Gram-positive bacteria are purple (positive) after gram stain (color primarily due to crystal violet). |
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|
Term
| What color are gram-negative bacteria after gram stain? |
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Definition
| Gram-negative bacteria are usually counter-stained with safronin (they do not absorb Gram stain), and are usually reddish. |
|
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Term
| What is the basis of the Gram stain? |
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Definition
| Gram-positive bacteria are able to retain stain after wash because they have a thick cell wall. Gram-negative bacteria have a cell wall only a one or two peptidoglycan-layers thick. |
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Term
| What are some functions of the cytoplasmic membrane besides permeability barrier? |
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Definition
| Besides acting as a permeability barrier, the cytoplasmic membrane is also important for: active transport and facilitated diffusion; electron transport/ATP synthesis; lipid and cell wall synthetic systems; synthesis and explort of membrane and extracellular proteins; anchorage of flagella. |
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Term
| What is the outer membrane? |
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Definition
| In gram-negative bacteria, outside of the thin cell wall is an additional membrane bilayer, which contains lipopolysaccharide (LPS), an important activator of TLRs. |
|
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Term
| What is the peptidoglycan cell wall made of? |
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Definition
| The peptidoglycan portion of the cell wall is a heteropolymer made up of n-acetylglucosamine (NAG) and n-acetylmuramic acid (NAM) linked by beta-1,4 glycosidic bonds. |
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Term
| Why are gram-positive bacteria particularly vulnerable to lysozyme? |
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Definition
| Lysozyme cannot attack the cell wall peptidoglycan of gram-negative bacteria because of the outer membrane. It will attack the cell wall of gram-positive bacteria, since they lack the outer membrane. This is effective at lysing these cells since they have a high internal osmotic pressure. |
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Term
| What cross-links the cell wall polymers together? |
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Definition
| A tetrapeptide forms a cross-bridge between the different cell wall polymers and helps with stability. Some antibiotics act at this linker. The cross-link can be thought of as a molecular sieve, excluding large molecules and antibiotics (>5kd) from accessing the cell membrane and interior. |
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Term
| Do both gram-positive and gram-negative bacteria have capsules? |
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Definition
| Both groups of bacteria have capsules. They are made up of a bulky loose network of usually polysaccharide. They are often important antigenic determinants and antiphagocytic. The capsules can be bigger than the bacteria themselves. They must be identified by negative staining. |
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Term
| Are teichoic acids found in both gram-positive and –negative bacteria? |
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Definition
| Teichoic acid is a feature of gram-positive cell walls and are linked to peptidoglycan or to the membrane through a lipid. |
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Term
| In the gram-negative bacteria, what is the periplasmic space? |
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Definition
| The periplasmic space is the space between the cytoplasmic and outer membrane. The outer membrane acts as a molecular sieve (similar to the cell wall itself), but it has a lower threshold (<700 da). This threshold is created by the porins, which hydrophilic molecules must pass through to enter gram-negative bacteria. In general, gram-negative thus have a narrower spectrum of antibiotics that work on them. |
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Term
| In a gram-negative bacteria, which membrane has symmetrical phospholipids and which doesn’t? |
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Definition
| The cytoplasmic membrane has roughly symmetrical phospholipids (on opposing leaves of the bilayer), while the outer membrane has a very asymmetrical phospholipids. There can also be large oligosaccharides attached to the outer leaflet of the outer membrane (a good example is Lipid A, recognized by a TLR). The repeating subunit in the most extracellular part of the LPS is the “O” antigen. |
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Term
| What else is Lipid A known as? |
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Definition
| Lipid A is the endotoxin which can cause leakage of blood vessels, fever, and decreased blood pressure leading to vasulcar collapse and eventually shock. Thus, gram-negative bacteria can cause death just by being attacked by our body if they’re in high enough amounts. |
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Term
|
Definition
| Flagella are made of flagellin protein and are attached to the cell membrane through the basal body. A motor component imparts a propeller-like movement that drives the bacteria toward nutrients and away from harmful substances (chemotaxis). Flagella proteins are the “H” antigen in a strain name. |
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Term
|
Definition
| Pili are short protein filaments. There are many per cell and can serve as a source of adherence or through bacterial conjugation (sex pili). The type IV secretion system passes the plasmids through the pilus. |
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Term
| How do some bacteria secrete proteins into a host cell? |
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Definition
| The type III secretion system is like a needle that can deliver proteins through the cell membrane of host cells. |
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Term
| What are some antibiotics that act at the three broad steps of cell wall synthesis (the cytoplasmic, cell wall, and periplasmic or exterior steps)? |
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Definition
| Phosphomycin and cycloserine can block in the cytoplasmic phase. Bacitracin can block at the cell wall/cell membrane phase. Vancomycin acts between the cell wall/cell membrane and periplasmic/exterior steps. Penicillin acts at the exterior step. |
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Term
| What are the two broad patterns of time course in inflammation? |
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Definition
| Broadly, inflammation can be “acute,” that is, occurring immediately after an exposure and of short duration. Inflammation can also be “chronic,” that is, having a longer duration and being associated with tissue destruction and repair (scarring and fibrosis). |
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|
Term
| What are the three broad patterns of cellular infiltrate in inflammation? |
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Definition
| The three broad classes are: neutrophils & macrophages; mononuclear cells (lymphocytes and macrophages); and eosinophilic. |
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Term
| What kind of infiltrate is seen in an acute inflammatory reaction? What is it effective against? |
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Definition
| Mostly neutrophils and some macrophages (agents of the innate immune system) are present in acute inflammatory reactions. This type of reaction is effective against extracellular organisms. |
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Term
| What kind of infiltrate is seen in a chronic inflammatory reaction? What is it effective against? |
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Definition
| Lymphocytes (and some macrophages) are seen in chronic inflammation. Here, the reaction can be predominantly humoral (plasma cells), which is effective against extracellular organisms, or cell-mediated (CD8+ cells), which is effective against intracellular organisms. |
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Term
| What kind of organism is an eosinophilic infiltrate typically targeting? |
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Definition
| Eosinophilic reactions are associated with a response to helminths (worms.) |
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Term
| What type of inflammation is exudative? What are some characteristics of it? |
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Definition
| Exudative inflammation is usually associated with acute inflammation (innate immunity) and with a predominantly polymorphonuclear (neutrophil) infiltrate. Increased blood flow and vascular permeability is associated with rubor, dolor, tumor, and calor. Organisms that are being responded to are typically extracellular gram-positive cocci or gram-negative rods. More rarely extracellular fungi are responsible. |
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|
Term
| What are some common clinical examples of exudative inflammation? |
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Definition
| Both tonsillitis and appendicitis are common clinical examples of exudative inflammation. |
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|
Term
| What are the four main outcomes of exudative inflammation? |
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Definition
| The four main outcomes of exudative inflammation are: normal healing; progressive to chronic inflammation; scarring; and tissue destruction (which can lead to abscess formation). |
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Term
| What are some common causes of abscesses? What typically forms around their edges? |
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Definition
| Extracellular bacteria and fungi (especially in immunocompromised hosts) can cause abscesses. With time, the abscess becomes walled off with a rim of fibrosis (the body’s attempt to contain the area of infection and wall off the tissue destruction). |
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Term
| What type of inflammation is mononuclear inflammation? What are some organisms that typically trigger it? |
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Definition
| Mononuclear inflammation is typically chronic and associated with lymphocytes (adaptive immunity) and macrophages. This sort of inflammation can be associated with any organism that is capable of prolonged persistence, but intracellular organisms (viruses, bacteria, parasites) are particularly common triggers. |
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Term
| What is granulomatous inflammation? |
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Definition
| Granulomatous inflammation is a subtype of mononuclear inflammation, where “epitheliod histiocytes” (activated macrophages) rim central necrotic tissue. In this type of inflammation, macrophages are trying to kill a poorly digestible organism, so CD4+ cells secrete large amounts of cytokines trying to increase macrophage killing efficiency. Fibroblasts can try to wall off this site of reaction. |
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|
Term
| What is a classic cause of granulomatous inflammation? |
|
Definition
| Mycoplasma (the cause of tuberculosis) is the most common cause of granulomatous inflammation. Certain fungal organisms (Histoplasma) and rare parasites (the eggs of Schistosomes) can also be causes. |
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|
Term
| In addition to eosinophilic reactions, what other type of inflammatory response is found commonly in response to helminths? |
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Definition
| Granulomatous inflammation can also form around worms. |
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Term
| What organisms typically cause cytopathic responses? |
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Definition
| Viruses induce cytopathic responses. Viral replication can cause aggregates or cells to fuse, forming multi-nucleated cells. The amount of inflammation in this type of reaction is variable. |
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|
Term
| What is necrotizing inflammation? |
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Definition
| Necrotizing inflammation is typically a response to toxins and involves large areas of host tissue death. |
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Term
| Normal microbial flora are usually non-pathogenic. What is the term for how they behave? |
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Definition
| Normal microbial flora behave as commensals. They are adapted to single species and frequently very specific micro-environments (specific locations in the host). |
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|
Term
| What is the difference between transient and resident flora? |
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Definition
| Resident flora includes microorganisms that are unique and (relatively) permanent to a host. A host’s transient flora are highly dependent on the environment. |
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|
Term
|
Definition
| A pathogen is simply a microorganism capable of producing pathology (disease) in a percentage of normal healthy non-immune individuals. In low doses, sub-clinical infection may result. Disease of the host is often associated with propagation of the organism (its goal). |
|
|
Term
| What is an opportunistic pathogen? |
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Definition
| An opportunistic pathogen will not cause disease in a healthy host but only in individuals whose normal defense mechanisms have been compromised. |
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|
Term
| What is an obligate pathogen? |
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Definition
| An obligate pathogen is one that cannot be found anywhere but in association with the host. |
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|
Term
| What is a facultative/opportunistic pathogen? |
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Definition
| A facultative/opportunistic pathogen is one that can grow and survive in the environment as well as the host. |
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|
Term
|
Definition
| Zoonoses are pathogens that are transmitted from animal hosts to humans. |
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|
Term
| What is an obligate intracellular pathogen? |
|
Definition
| An obligate intracellular pathogen (e.g. virus) can only be grown inside host cells and cannot be cultured extracellularly. |
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|
Term
| What is a factultative intracellular pathogen? |
|
Definition
| A facultative intracellular pathogen is an organism that can grow inside or outside of cells and can be cultured on agar surface in the laboratory. |
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|
Term
|
Definition
| Virulence refers to the degree of pathogenicity. This may be defined quantitatively in animal studies or epidemiologically. |
|
|
Term
| What is a virulence factor? |
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Definition
| A virulence factor is a component of a pathogen (such as a toxin) responsible for its ability to cause disease. Virulence factors are multifactorial involving highly regulated pathways. |
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|
Term
| What are virulence factors for enteropathogenic E. coli (EPEC)? |
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Definition
| EPEC causes bloody diarrhea in children in developing countries. Its virulence is due to its ability to intimately associate and damage intestinal walls (through pedestal formation). This occurs through injection of a receptor (Tir) through hollow syringe-like pili, which rearranges the host cytoskeleton, allowing EPEC to attach through an adhesion. These functions are encoded on a pathogenicity island on EPEC. |
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Term
|
Definition
| Host factors affect whether exposure to a pathogen will result in disease, clearance or the carrier state. These include the route and size of the inoculum, prior exposure history, genetic predisposition of the host, breakdown of tissue barriers and immune status. The host has multiple immune and non-immune mechanisms for protection. Successful pathogens have evolved mechanisms to defeat these protective functions in the host. |
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|
Term
| What are the stages in host-pathogen interaction? |
|
Definition
| The stages in host-pathogen interaction are: encounter, entry, colonization, invasion, and transmission. |
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|
Term
| What are the usual points of entry for pathogens? |
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Definition
| Pathogens typically enter through the: skin, GI, respiratory, or urogenital tract. These tracts themselves prevent colonization (e.g. peristalsis, ciliary movement, normal flora). However, some microorganisms can cause disease without ever leaving the mucosal surface. |
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|
Term
| What is the difference between horizontal and vertical spread? |
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Definition
| Horizontal spread occurs from person to person, while vertical spread occurs from mother to child (in the case of certain congenital infections). |
|
|
Term
| Why is gonorrhea recurrent? |
|
Definition
| Neisseria gonorrhea undergoes both phase (on-off switching) and antigenic variation (heterogeneity of epitopes). Pilins (responsible for adhesion) are present in multiple copies, creating antigenic variation. Opacity protein can have in- or out-of-frame reading, also contributing to antigenic variation. |
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|
Term
|
Definition
| An IgA protease (like that produced by Neisseria gonorrhea and many other mucosal pathogens) hydrolyzes human IgA between the Fc and Fab regions, leaving antibody bound but unable to signal to the host immune system. |
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|
Term
| What percentage of antibiotics is unnecessary or inappropriate? |
|
Definition
| 50% of prescriptions for antibiotics are unnecessary or inappropriate. They are the second most commonly used class of drugs. More than $8 billion is spent per annum and half of all patients in hospitals are on antibiotics at any one time. There is a problem with increasing resistance and fewer drugs in the pharmaceutical pipeline. |
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|
Term
| What is the difference between bacteriostatic and bacteriocidal antibiotics? |
|
Definition
| Bacteriostatic agents merely slow the growth of bacteria, while bacteriocidal agents kill the organism. Bacteriostatic agents rely on the immune system to clear the remaining organisms. |
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|
Term
| What is the difference between antibiotics and antimicrobials? |
|
Definition
| Antibiotics are produced by organisms (“against life.”) Antibiotics are largely produced (by bacteria) during stationary phase (after logarithmic growth), when their population is established and their primary concern is to guard against colonies that could displace them. Antimicrobials are a larger class than includes antivirals and antifungals. |
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|
Term
| What are major places that antibiotics act? |
|
Definition
| The major places in a bacteria that antibiotics act are at the cell wall, in DNA replication, during protein synthesis, and in folate metabolism (DNA/RNA precursors). |
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|
Term
| What are the two major classes of antibiotics that act at the cell wall? |
|
Definition
| Beta-lactams (by interfering with transpeptidases) and glycopeptides (by binding to peptidoglycans) act at the cell wall. |
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|
Term
| What are the four major classes of antibiotics that act during protein synthesis? |
|
Definition
| Macrolides, tetracyclines, aminoglycosides, and oxazolidinones all act by interfering with peptidyltransferases to hamstring microbial protein synthesis. |
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|
Term
| What is the major class of antibiotics that act during DNA replication/repair? |
|
Definition
| The fluoroquinolines interfere with DNA replication by hobbling DNA gyrase. |
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|
Term
| What are the two classes of antibiotics that act to interfere with folate metabolism? |
|
Definition
| Trimethacrin and sulfamethoxizole act to interfere with folate metabolism. |
|
|
Term
| How do beta-lactams access their transpeptidase targets? |
|
Definition
| Beta-lactams access the transpeptidases by diffusing through porins in the outer membraneand attach to target transpeptidases located on the outer leaflet of the cytoplasmic membrane. They inhibit crosslinking of the peptidoglycan layer. They’re most active during log-phase growth. |
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|
Term
| What are four subclasses of the beta-lactams? |
|
Definition
| Penicillins, cephalosporins, carbapenems, and monobactams are the four subclasses of beta-lactams. |
|
|
Term
| Some bacteria have become resistant to beta-lactams. What drugs are typically combined with beta-lactams in the same formulary to overcome this? |
|
Definition
| Beta-lactamase inhibitors can allow beta-lactams to overcome beta-lactam resistance. |
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|
Term
| What class of bacteria do the cephalosporins not cover? |
|
Definition
| Cephalosporins are not effective against the entercocci. |
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Term
| Newer (“higher” generation cephalosporins) are better at fighting gram-negative or gram-positive organisms? |
|
Definition
| The newer the cephalosporin, the better at fighting gram-negative bacteria and the worse at fighting gram-positive. They are also less likely to be allergenic to patients who have previously displaced a cephalosporin allergy. |
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|
Term
| Carbapenems and monobactams either have very broad-spectrum antibiotic activity or very little allergy crossover. Which is which? |
|
Definition
| Carbapenems have a very broad-spectrum antibiotic activity but very high allergy crossover in those that are allergic to pencillin. Monobactams have very little allergy cross-over. |
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|
Term
| Glycopeptides (the other class of antibiotics that act at the cell wall) are effective (with emerging resistance) with what class of bacteria? |
|
Definition
| Glycopeptides are especially effective against gram-positive bacteria and especially resistant gram-positive organisms (MRSA). |
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|
Term
| With regard to Staph aureus, are the beta-lactams and glycopeptides –cidal or –static? Which works faster? |
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Definition
| Both the beta-lactams and the glycopeptides are bacteriocidal to Staph aureus. Beta-lactams kill faster. |
|
|
Term
| Why are aminoglycosides not used much anymore? |
|
Definition
| Aminoglycosides are toxic with a very narrow therapeutic window (they can cause nephro- and ototoxicity). |
|
|
Term
| What class of organisms are macrolides active against? |
|
Definition
| Macrolides are predominantly active against gram-positives. |
|
|
Term
| When are streptagramins and oxazolidinones mostly used? |
|
Definition
| Streptagramins and oxazolidinones are active against MRSA and other resistant gram-positives. |
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|
Term
| Why is the one streptagramin rarely used? |
|
Definition
| The one streptagramin is a combination of dalfopristin and quinupristin in a 30:70 ratio (which is hard achieve in vivo) and a relatively common side effect is major pain. |
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|
Term
| What are the fluoroquinolines effective against? |
|
Definition
| Fluoroquinolines are effective against streptococci and have a broad gram-negative spectrum. They can have serious side-effects (rashes, glucose metabolism, long QT interval). |
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|
Term
| How can streptococci be characterized? |
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Definition
| Streptococci are frequently characterized by cell wall antigen. Group A (S. pyogenes) can cause pharyngitis, cutaneous, and invasive infections. Group B can cause maternal and newborn infection, UTIs, and bacteremia and menginitis. Group D is the Enterococcus. Strep pneumoniae is also a member. |
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|
Term
| What is a very helpful identifying characteristic of all Streptococcus pyogenes? |
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Definition
| All Streptococcus pyogenes (Group A Streptococcus) are capable of causing beta-hemolysis of red blood cells. |
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Term
| Do Streptococci make catalase? |
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Definition
| No Streptococci make catalase. They are also quite sensitive to the antibiotic bacitracin and are small white gram-positive cocci that grow in chains. There is no environmental reservoir. |
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Term
| Broadly, what are Streptococci’s virulence factors? |
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Definition
| Virulence factors include the Streptolysins (damage tissue and inhibit clearance), M protein (blocks opsonization and provides antigenic variation), capsule (resists phagocytosis), and hyaluronidase (degrades connective tissue). |
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|
Term
| Why is full immunity not provided after an initial Strep pyogenes infection? |
|
Definition
| There are nearly 80 M-protein types, and they are the major antigenic determinant. M-protein is also anti-phagocytic by blocking opsonization and it can additionally act as an adhesion. |
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|
Term
| How is streptodornase responsible for Streptococcus virulence? |
|
Definition
| Streptodornase can degrade DNA which accumulates in pus from lysed cells and adds to pus’s viscosity. Decreasing viscosity can allow S. pyogenes to spread even at sites of high immune extravasation. |
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|
Term
| What is the main reservoir of S. pyogenes? |
|
Definition
| School-age children are the main reservoir for S. pyogenes in the posterior pharynx on the tonils. It can also colonize the skin. Children less than 5 for some reason are less susceptible to Group A Streptococcus. |
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Term
| What generally must happen to allow skin infection by Group A Streptococcus? |
|
Definition
| Skin generally must be damaged to allow skin infection by Group A Streptococcus. Crowding specifically is a factor in the spread of S. pyogenes (both skin infection and infection of the pharynx). |
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|
Term
| What are two examples of minor skin infections caused by Strep pygoenes? |
|
Definition
| Impetigo (desquamation followed by GAS infection) and erysipelas (cellulitis spreading with the help of toxins) are two minor skin infections caused by Strep pyogenes. |
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|
Term
| What are three examples of disseminated (invasive infections) caused by Group A Streptococcus? |
|
Definition
| Bacteremia, pneumonia, and septic arthritis are examples of invasive infections caused by S. pyogenes. |
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|
Term
| What is the most common infection caused by S. pyogenes? |
|
Definition
| Sore throat (pharyngitis, “strep throat”) is caused by S. pyogenes. patients may also have fevere, malaise, cervical lymphadenopathy and headache. There will be erythematous posterior pharynx with or without acute inflammatory exudate. |
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|
Term
|
Definition
| Scarlet fever is a complication of streptococcal pharyngitis with a red rash on upper chest spreading to the extremities (caused by an erythrogenic toxin). It is accompanied by strawberry tongue but can be treated well with antibiotics. |
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|
Term
| What is necrotizing fascitis? What is the common name? Why does it result? |
|
Definition
| Necrotizing fascitis is also known as infection with “flesh-eating bacteria” (Group A Streptococcus). This is due to the organism’s ability to dissect down through subcutaneous, connective, and muscle tissues. It can then dissect down tissue planes unimpeded. Tissue becomes necrotic and must be debrided quickly before patient death. |
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Term
|
Definition
| Rheumatic fever is a post-infection complication approximately 3 weeks after S. pyogenes infection. There can be fever with carditis, polyarthritis, subcutaneous skin nodules, and/or chorea. It is an autoimmune response and can cause most seriously cause damage to the heart. |
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|
Term
| What post-infection renal complication can Streptococcus cause? |
|
Definition
| A post-infection complication is glomerular nephritis. It is an Type III autoimmune disease in the glomerulus and can cause renal failure. |
|
|
Term
| How can Streptococci cause toxic shock syndrome? |
|
Definition
| Toxin elaboration by Group A Streptococcus presents as “super-antigen,” activating a large minority of host T-cells, leading to hypotension, multi-system organ failure, and generalized erythematous rash. This is toxic shock syndrome. This is similar to TSS caused by Staph infection, except the precipitating Strep infection is usually more disseminated. |
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|
Term
| How is Strep pyogenes typically identified in the laboratory? |
|
Definition
| The best method is to culture the organism in the lab (beta-hemolytic and no catalase activity). However, a quick test can also be reaction against antigen. After infection, antibodies to conserved antigens can also be identified as signs of previous infection (useful in post-infection sequeliae). |
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|
Term
| How is Strep pyogenes typically treated? |
|
Definition
| Group A Streptococcus is still resistant to penicillin but macrolides can also be used if the patient is allergic to peniccilins. Treatment for acute rheumatic fever is supportive (anti-inflammatories) but future episodes must be prevented to avoid serious heart damage. They may need to be on prophylactic long-term antibiotics. |
|
|
Term
| Is Group B Streptococcus always beta-hemolytic? |
|
Definition
| Group B Streptococcus is visually similar to Group A, but is not always beta-hemolytic or sensitive to bacitracin. |
|
|
Term
| Is M-protein present on Group B Streptococcus? |
|
Definition
| M-protein is not found on Group B Streptoocccus. Its main virulence factor is a large capsule effective at resisting phagocytosis. |
|
|
Term
| Where is Group B Streptococus commonly found? What is its role in neonatal infection? |
|
Definition
| It can survive in the bloodstream and cause invasive infection in babies and (less commonly) mothers. It is commonly found in the GI tract and only typically causes complications in vertical transmission. It is the leading cause of neonatal bacterial infection and is common in prematurity (because of paucity of vertical antibody transfer). Pregnant women are screened to see if they’re carriers and are treated prophylactically to prevent vertical transmission. |
|
|
Term
| What are the four basic mechanisms of antimicrobial resistance? |
|
Definition
| The four basic mechanisms of antimicrobial resistance are: enzymatic degradation; prevention of target access; alteration of target sites; activation of efflux pumps. |
|
|
Term
| What are some reasons that antibiotic resistance is increasing in the hospital setting? |
|
Definition
| Abundance of susceptible hosts, inattention to basic infection control measures, selective pressure from antibiotic use, overuse/inappropriate use of antibiotics, plasmid linkage of resistance genes (multiple resistances on a single plasmid), movement of patients and staff between institutions, and unrecognized colonization are all reasons why antibiotic resistance is increasing in the hospital setting. |
|
|
Term
| What are the two most basic types of acquisition of antibiotic resistance? |
|
Definition
| Antibiotic resistance can be intrinsic (on the genome) or it can be acquired (mutation of genes that extend activity or acquisition of resistance determinants). |
|
|
Term
| What are the three major mechanisms for genetic exchange in bacteria? |
|
Definition
| Conjugation (communication of gene between bacteria), transformation (direct uptake of gene), transduction (by bacteriophage) are three major mechanisms for genetic exchange in bacteria. |
|
|
Term
| What is a good example of inactivation of the antibiotic by destruction or modification? |
|
Definition
| Beta-lactamases, enzymes that degrade penicillins, are a good example of this mode of antibiotic resistance. In this way, penicillins cannot bind to the transpeptidases. This allows the bacteria to continue to build a healthy cell wall. Beta-lactamases may be plasmid-mediated or chromosomal and their may be extended spectrum beta-lactamases that include resistance to newer antibiotics. |
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|
Term
| What is an example of the prevention of access to target strategy in antibiotic resistance? |
|
Definition
| A major mechanism of resistance to carbapenems and fluoroquinolines is prevention of access of the antibiotics to the periplasmic space (where their target is) by deletion of the relevant porin. |
|
|
Term
| What is an example of bacterial resistance due to altered target site? |
|
Definition
| Both penicillin-resistance S.pneumoniae and MRSA produce altered target sites. In MRSA, the mecA gene product is an altered binding protein. Thus the active site of the penicciln-binidng protein cannot bind to its target any longer. |
|
|
Term
| What is a common method that S. aureus can acquire vancomycin susceptibility? |
|
Definition
| S. aureus can alter its peptidoglycan, which leads to decreased affinity of vancomycin for target. In this case, vancomycin loses a single H-bond, which reduces binding 1000-fold, leading to VRSA. There have been six cases of this in the US. It is believed that gene transfer from Enterococcus to S. aureus resulted in S. aureus gaining vancomycin resistance. |
|
|
Term
| What antibiotic is typically resisted by efflux pumps? |
|
Definition
| Macrolides and tetracyclines can typically be resisted through the action of efflux pumps. These efflux pumps can be inducible or constitutive. Efflux pumps can give resistance to more than one specific antibiotic (for example macrolides and fluoroquinolines). |
|
|
Term
| What main system of innate immunity do bacterial capsules interfere with? |
|
Definition
| Bacterial capsules interfere with the alternative pathway of complement activation. The classical pathway is still effective, but the host must wait for antibodies to be produced in large numbers. The O-antigen also prevents formation of the MAC. |
|
|
Term
| What are four very important examples of encapsulated bacteria? |
|
Definition
| Streptococcus pneumoniae, Staphylococcus aureus, Neisseria meningitides, and Haemophilus influenza are four very important examples of encapsulated bacteria. |
|
|
Term
| How does the capsule enable organisms to cause meningitis? |
|
Definition
| There needs to be prolonged bacteremia for these organism to colonize the brain. The capsule enables these bacteria to efficiently survive in the bloodstream and cause bacteremia (and be transported to normally sterile tissues). Severe bacteremia is called sepsis. |
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|
Term
| What are three important characteristic of the pneumonococcus that cause its disease burden? |
|
Definition
| Pneumococcus is common (high rate of carriage), occasionally virulent (sepsis, pneumonia, meningitis), and it is adaptable (antibiotic resistance and evasion of vaccine-based immunity). |
|
|
Term
| Is S. pneumonia gram-positive? Cocci? Alpha-hemolytic? Catalase-negative? |
|
Definition
| S. pneumonia (the pneumococcus) is catalase-negative, alpha-hemolytic, gram-positive cocci. Sensitivity to optichin (an unused toxic antibiotic) is characteristic of the pneumococcus. |
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|
Term
| What populations is pneuomococcal bacteremia common in? |
|
Definition
| S. pneuomoniae is a common source of infection throughout all decades of life, but especially so in the young and elderly. |
|
|
Term
| Pneumococcus have carbohydrate capsular antigens that generate a good antibody response. How do they cause serious infections then? |
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Definition
| There are more than 90 unique polysaccharide types, and it takes almost 5 days to rev up an antibody response, when S. pneuomoniae can cause bacteremia. |
|
|
Term
| What is the number one cause of acute otitis media (middle ear infection)? |
|
Definition
| Streptococcus pneumoniae (a normal resident of the upper respiratory tract) can transit the Eustachian tube and cause infection and inflammation of the ear. This tube can become more easily obstructed in a child, causing easier transit. |
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|
Term
| What kind of pneumoniae does the pneumococcus usually cause? |
|
Definition
| S. pneuominae is an important cause of lobar pneumoniae. Patchy areas of alveoli fill with acute inflammatory cells (PMNs). Capillary walls dilate and erythrocytes also fill the space, causing the productive cough. |
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Term
| Through what method has the pneumococcus accumulated resistance to beta-lactams? |
|
Definition
| S. pneumoniae has acquired step-wise penicillin-binding proteins (altered target) mutations. This tends to confer resistance to all agents of this class. |
|
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Term
| What are some characteristics of Haemophilus influenza? |
|
Definition
| H. influenza is a small, nonmotile gram-negative coccobacillus. It is aerobic and requires hemin and NAD. Carriage may be as high as 80% of the population in the upper respiratory tract. |
|
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Term
| What differentiates locally from invasive infectious H. influenza? |
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Definition
| Non-typeable H. influenza don’t have capsules, and cause mostly otitis media, sinusitis, chronic bronchitis and pneumonia. Type B H. influenza has a capsule and can cause bacteremia, cellulites, epiglottitis, and meningitis because they can traverse the blood stream. There is an effective conjugate vaccine. |
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|
Term
| What are characteristics of Neisseria meningitidis? |
|
Definition
| Neisseria meningitidis is a gram-negative, bean-shaped diplocccus. It is not transmitted sexually like N. gonorrhea and has a capsule. |
|
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Term
| What are the two distinct sy ndromes that N. meningitidis causes? |
|
Definition
| N. meningitidis causes meningococcemia (dramatic systemic infection with endovascular damage (skin purpura) and rapid death) and meningitis (much more slowly progressive and treatable). |
|
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Term
| Why are young children (who have not been immunized by the conjugate vaccine) particularly susceptible to H. influenza b? |
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Definition
| Hib has a polysaccharide capsule which is not particularly antigenic in young children. Antibody responses are necessary to clear this infection. |
|
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Term
| What type of sexually-transmitted lesions are painful? Which are painless? |
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Definition
| Chancroid and lesions arising from genital herpes simplex are painful. Syphilis, lymphogranuloma venerum and granuloma inguinale produce painless lesions. |
|
|
Term
| What are basic characteristics of Treponema pallidum? |
|
Definition
| Treponema pallidum is a strict human pathogen and it takes on the appearance of a slim gram-negative spirochete. Darkfield or fluorescent microscopy is necessary for proper visualization under the microscope. |
|
|
Term
| What are the virulence factors with T. pallidum? |
|
Definition
| The virulence factors in syphilis are hard to detect, but there are certainly adherence factors, hyaluronidase, and T. palladium also coats itself with host cell fibronectin, reducing its immunogenicity. |
|
|
Term
| What are some characteristics of primary syphilis? |
|
Definition
| Primary syphilis can present with skin lesions (painless chancres with raised borders), endarteritis and periarteritis. PMNs and macrophages will be present. Regional adenopathy can be present. This may resolve spontaneously within 2 months. |
|
|
Term
| What are some characteristics of secondary syphilis? |
|
Definition
| Secondary syphilis is disseminated disease and can have prominent skin lesions (palms and soles) and protean manifestations. Generally, secondary syphilis is highly infectious and can be a flu-like illness (sore-throat, headache, muscle aches). |
|
|
Term
| What are some characteristics of tertiary syphilis? |
|
Definition
| Tertiary syphilis results in tissue destruction from localized multiplication. Strokes and cardiac lesions, personality disorders and psychiatric disturbances and granulomatous lesions can result. T. palidum can be particularly aggressive in immunocrompomised hosts. |
|
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Term
|
Definition
| Syphilis is spread almost exclusively sexually (except in vertical transmission from mother to child). It can be spread extremely effectively: in a single sexual contact, the risk of transmission can be around 30%. |
|
|
Term
| How long can the latent period last between secondary and tertiary disease last? |
|
Definition
| The latent period can be up to 20-30 years. The spirochetes slow their metabolism and are asymptomatic during this time. |
|
|
Term
| What is the best treatment for syphilis? |
|
Definition
| Penicillin is the best treatment for syphilis. Safer sex should also be encouraged. |
|
|
Term
| What are some basic characteristics of the organism that causes gonorrhea? |
|
Definition
| Gonorrhea is caused by Neisseria gonorrhea. It is a gram-negative diplococcus with fastidious growth requirements. N. gonorrhea is oxidase and catalase positive. |
|
|
Term
| What are some virulence factors that Neisseria gonrorhea have? |
|
Definition
| N. gonorrhea has pili (important for attachment, immunogenic and variable), por proteins (prevent phagolysosome fusion), and opacity protein (mediates binding to epitheliail cells). Iron is essential for growth and metabolism, and N. gonorrhea has a lipooligosaccharide (similar to LPS), which has endotoxin activity. It is inherently resistant to beta-lactams. |
|
|
Term
| Is gonorrhea more common in women or men? |
|
Definition
| Gonorrhea is more common in women. They have around 50% acquisition after a single exposure to an infected man. |
|
|
Term
| What are symptoms of gonorrhea? |
|
Definition
| Urethritis (discharge), cervicitis, salpingitis, pelvic inflammatory disease, proctitis, conjunctivitis, pharyngitis, and rarely bacteremia are all symptoms of gonorrhea. |
|
|
Term
| How is gonorrhea diagnosed? |
|
Definition
| Gonorrhea can be negatively gram-stained and growth on chocolate agar. It can be differentiated from N. meningitides, which oxidizes glucose and maltose. Chlamydia should also be tested for (Chlamydia and gonorrhea frequently travel together). |
|
|
Term
| How can gonorrhea be treated? |
|
Definition
| Gonorrhea is always beta-lactam-resistant and is increasingly growing resistant to fluoroquinolone. Treatment for gonorrhea should always be combined with treatment for Chlamydia. |
|
|
Term
| What are some basic characteristics of Chlamydia? |
|
Definition
| Chlamydia trachomatis is a strict intracellular parasite of humans. It is a small gram-negative bacillus with no peptidoglycan layer in the cell wall. It has an infectious elementary body form and a noninfectious reticulate body form. |
|
|
Term
| Where does C. trachomatis infect? |
|
Definition
| C. trachomatis infects the uretha, endocervix, endometrium, fallopian tubes, anorectum, respiratory tract, and the conjunctiva. |
|
|
Term
| What are host responses to Chlamydia? |
|
Definition
| Sterility can result from vigorous inflammatory response to pelvic inflammatory disease that Chlamydia can cause. Blindness can result if it infects the conjunctiva. |
|
|
Term
| What is the common theme between these three gram-negative bacterial pathogens: Pseudomonas, Helicobacter, and Legionella? |
|
Definition
| Pseudomonas, Helicobacter, and Legionella are all motile. |
|
|
Term
| What are some basic characteristics of Pseudomonas aeruginosa? |
|
Definition
| P. aeruginosa is a motile gram-negative rod with a capsule. P. aeruginosa produce pigmens and capsules, which aid in their formation of mucoid colonies. It is common in the environment and can colonize opportunistically (commonly in cystic fibrosis patients) and cause biofilms. |
|
|
Term
| What are some clinical diseases that Pseudomonas can cause? |
|
Definition
| Pseudomonas can cause pulmonary infections, primary skin infections, urinary tract, ear, and eye infections. Rarely, it can cause bacteremia and endocarditis. |
|
|
Term
| What are the two results of Pseudomonas colonization? |
|
Definition
| Pseudomonas can cause a chronic infection (e.g. CF) where it evades host defenses and causes chronic inflammation. It can also cause an acute short-term infection where high amounts of toxins are produced which leads to tissue damage and organ failure. |
|
|
Term
| How can Pseudomonas be treated and controlled? |
|
Definition
| Pseudomonas is impossible to eliminate in the living environment. It is highly antibiotic resistant but is usually sensitive to gentamicin, amikacin, and imipenem. CF patients require different antibiotics, usually oral ciprofloxacin. |
|
|
Term
| What are some virulence factors that Pseudomonas expresses? |
|
Definition
| Pseudomonas virulence factors include adhesins, capsules, endo- and exotoxins. Antibiotic resistance can come from its ability to form biofilms, as well as more traditional porin mutations and beta-lactamases. |
|
|
Term
| What are some basic characteristics of Helicobacter pylori? |
|
Definition
| H. pylori is a gram-negative curved rod which is highly motile and has high urease activity (to allow it to colonize the human stomach and partially neutralize the low pH in the thick mucus lining of stomach (where the pH isn’t so low)). |
|
|
Term
| What are the clinical diseases that H. pylori causes? |
|
Definition
| H. pylori is highly associated with Type B gastritis and gastric and duodenal ulcers. Infection also increases propensity to gastric adenocarcinoma and gastric MALT B-cell lymphoma. However, H. pylori itself probably does not cause the majority of the symptoms. Host inflammation and hypersecretion probably is responsible. |
|
|
Term
| What is a diagnostic test specific to Helicobacter pylori? |
|
Definition
| H. pylori can be detected with a radioactive urease test. Labelled CO2 indicates presence of H. pylori in gut. Antibody tests are also possible. |
|
|
Term
| What is treatment and control for Helicobacter p.? |
|
Definition
| Monotherapy for H. pylori is ineffective, leading to resistance. Antibiotics plus proton-pump inhibitor (making the stomach less acidic) is always necessary for effective combination therapy. |
|
|
Term
| What are some basic characteristics of Legionella pneumophila? |
|
Definition
| Legionella is a gram-negative motile small coccobacillus. It has distinct phospholipid content in the cell envelope and is poorly stained. |
|
|
Term
| Legionella pneumophila is classified as an accidental pathogen. What is its epidemiology? |
|
Definition
| Legionella is a natural parasite of amoeba and abundant in the natural bodies of water (and water distribution systems). When it becomes aerosolized, it can colonize people with compromised immune systems. They falsely recognize macrophages in the human for its natural host. They can survive in macrophages, multiply, and spread. |
|
|
Term
| What are the two clinical diseases associated with Legionella infection? |
|
Definition
| Legionella pneuomophila can cause Pontiac fever, an acute short-lived self-limiting influenza-like disease. it is non-fatal. Legionnaire’s disease in contrast, has 2-10 days incubation, where couch, pneumonia, high fever eventually leads to multi-organ disease and mortality greater than 15%. |
|
|
Term
|
Definition
| An enterotoxin is merely a toxin that acts in the lumen of the gut. |
|
|
Term
|
Definition
| The DPT immunizes someone against Diptheria, Pertussis, and Tetanus disease by injecting inactivated toxoids from all three organisms. |
|
|
Term
| What are the three current conjugate vaccines? |
|
Definition
| Streptococcus pneumoniae, Neisseria meningitides and Haemophilus influenza type b all have conjugate vaccines available to help reduce their infection. |
|
|
Term
| Many toxins have an A-B subunit structure. Explain this. |
|
Definition
| The B subunit binds to the host. Then the A subunit is then inserted into the cell when it senses a pH change in the endosome, leading to cell toxicity (and, at first, alteration of the behavior of the cell to the benefit of the bacteria). |
|
|
Term
| What are the basic characteristics of Vibrio cholerae? |
|
Definition
| Vibrio cholerae is a gram-negative curved rod with a long flagella that is transmitted via fecal-oral transmission. It causes severe gastroenteritis and death due to dehydration and electrolyte abnormalities. It has an environmental reservoir where it may form biofilms on mollusks. Cholera generally exists in epidemics or pandemics. |
|
|
Term
| Is the cholera toxin an A-B type toxin? |
|
Definition
| The cholera toxin is an A-B type toxin which causes pumping out of Na+, Cl-, K+, and HCO3- into the gut lumen, causing water to follow (severe diarrhea). Death is by dehydration via “rice water” stool. Tetracycline is effective against the bacteria, but rehydration support is most important. E. coli can actually make this same toxin which causes a similar but less severe diarrhea (“traveler’s diarrhea.”) |
|
|
Term
| Why are Clostridium species unlikely to be serendipitiously discovered in culture? |
|
Definition
| Clostridium are anaerobes. |
|
|
Term
| What are basic characteristics of Clostridial species? |
|
Definition
| Clostridial species are spore-forming, anaerobic gram-positive rods. They are ubiquitous in the environment. |
|
|
Term
| What diseases do Clostridium difficile cause? |
|
Definition
| C. dificille causes antibiotic-associated diarrhea and pseudomembranous colitis. When broad-spectrum antibiotics are used which reduce normal bowel flora, C. difficile can overgrow, producing two large protein toxins (entertoxin and cytotoxin). |
|
|
Term
| What are some basic charactistics of Clodtridium tetani? |
|
Definition
| C. tetani is a gram-positive rod that produces spores which reside in the soil. When they arrive in a relatively anaerobic wound (e.g. a puncture), they reproduce rapidly and produce toxins that act on inhibitory neurotransmitters which causes paroxysms of spasms and spastic paralysis. |
|
|
Term
| How is the toxin produced by Clostridium botulinum different than that produced by Clostridium tetani? |
|
Definition
| Botulism produces a flaccid paralysis, where acetylcholine is prevented from being released. It is usually associated with home canning. Frequently, infants can also get botulism but fortunately it has a good prognosis and usually only supportive care is necessary. |
|
|
Term
| What disease does Clostridium perfringens cause? |
|
Definition
| Clostridium perfringens causes gas gangrene. This involves a toxin that causes cell lysis and necrosis. It can cause food poisoning but will rarely be isolated. |
|
|
Term
| What are some basic characteristics of Bordetella pertussis? |
|
Definition
| B. pertussis is a gram-negative coccobacillus which elaborates several toxins, the most important of which is the pertussis toxin. This leads to increased secretion in the upper airway and decreased phagocytic clearance. This is the etiologic agent of “whooping cough.” |
|
|
Term
| What are the three stages of Pertussis? |
|
Definition
| Pertussis first presents with a catarrhal stage, which is indistinguishable from viral upper respiratory infection. It then develops into a paroxysmal stage with episodic coughing, which may or may not have inspiratory whoop following paroxysms of coughing. Convalescence will require weeks with frequent complications. It is believed that it is rising in prevalence because of decreased immunity from vaccinations early in life. |
|
|
Term
| What are some basic characteristics of Corynebacterium diptheriae? |
|
Definition
| C. diptheriae is a club-shaped gram-positive rod which causes both pharyngeal and skin infection. It is a classic toxin-mediated disease that is well-controlled in this country by vaccine. |
|
|
Term
| What are Koch’s postulates? |
|
Definition
| Koch’s postulates say that one should be able to: find the organism in the diseased tissue; grow the organism in pure culture; show that the disease is reproduced when organism is injected into a susceptible animal species; and isolate the organism from the infected animal. |
|
|
Term
| What are some basic characteristics of Mycobacterium tuberculosis? |
|
Definition
| M. tuberculosis is a small, acid-fast (is neither gram-positive nor gram-negative), rod-shaped, non-motile, non-spore-forming bacteria. |
|
|
Term
| What helps explain M. tuberculosis’s extremely long incubation period? |
|
Definition
| M. tuberculosis grows very slowly. It is a strict aerobe and does not produce endotoxins or exotoxins. Tissue damage is related to hypersensitivity of the sensitized host to bacterial products. This small growth is somewhat explained by the extremely complex and lipid-rich (hydrophobic) cell envelope, which forces it to take up and metabolize nutrients slowly. This makes them resistant to most common antibiotics. |
|
|
Term
| For an active tuberculosis infection, how many antibiotics are typically used? |
|
Definition
| For an active tuberculosis infection, 3 or 4 first-line drugs are typically used. For TB prophylaxis, only one drug is typically used. |
|
|
Term
| Is M. tuberculosis a facultative intracellular pathogen? |
|
Definition
| M. tuberculosis is a facultative intracellular pathogen. It can resist digestion through expression of O2 scavengers, by inhibiting lysosome fusion, and by escaping into the cytoplasm. Eventually, infected macrophages will signal to form a granuloma to contain the infection. B- and T- cells will also respond to form part of the granuloma. |
|
|
Term
| After granuloma formation, what happens? |
|
Definition
| In 90-95% of patients, a calcified lesion forms in the lung with viable organisms contained within. In some people, this initial containment fails, and biliary tuberculosis proceeds, leading rapidly to death. Those patients with a good first response can either contain the infection for life, or become reactivated later when their immune system weakens (~10% of these individuals). |
|
|
Term
| What is the preferred tropism of Mycobacterium lepriae? |
|
Definition
| M. lepriae grows best in skin or peripheral nerves. |
|
|
Term
| What are some symptoms of M. lepriae? |
|
Definition
| M. lepriae can either cause tuberculoid or lepromatous leprosy with a continuum between the two. Tuberculoid is less evere with numb macular skin lesions and asymmetric nerve involvement. Lepromatous has nodular skin lesions with slower, symmetric nerve involvement. The difference between these two courses is due to differences in cell-mediated immunity. |
|
|
Term
| What are the three most common causes of diarrhea? |
|
Definition
| Campylobacter, Salmonella, and Shigella are the three most common causes of diarrhea. Patterns vary locally. |
|
|
Term
| What are three main pathogenic mechanisms that cause diarrhea? |
|
Definition
| Diarrhea can be caused by ingestion of a preformed toxin (from S. aureus), by infection by toxigenic organisms (by C. perfringens, ETEC, EHEC, V. cholerae, C. difficile), and by infection by enteroinvasive organisms (C. jejuni, Salmonella, Shigella, EIEC, Listeria). |
|
|
Term
| What bacteria primarily infect the small bowel? |
|
Definition
| V. cholerae, Clostridium perfringens, and ETEC primarily infect the small bowel. |
|
|
Term
| What bacteria primarily infects the colon? |
|
Definition
| Shigella primarily affects the distal colon. It can cause acute mucosal infection with erosion and purulent exudates. It is rarely invasive. |
|
|
Term
| What bacteria can infect both the small and large bowles? |
|
Definition
| Campylobacter jejuni and Salmonella can infect both the small and large bowels. C. jejuni can also infect the appendix. Post-infection, C. jejuni patients can acquire Guillan-Barre syndrome (flaccid paralysis). |
|
|
Term
| What are the six different types of E. coli? |
|
Definition
| Enterotoxigenic (ETEC, produces cholera-like toxin), Enteropathogenic (EPEC), Enterohemorrhagic (EHEC), Enteroinvasic (EIEC, similar to Shigella and Listeria), Enteroaggregative (EAEC), Diffusely adhering (DAEC). |
|
|
Term
| What are some basic characteristics of Clostridium difficile? |
|
Definition
| C. dificile is a gram-positive bacillus. It is an obligate anaerobe which forms spores and is the primary cause of anttibiotic-associated diarrhea and pseudomembranous colitis. It can cause both community and nosocomial infection. It has a high relapsing rate but frequently stopping broad-spectrums to allow normal flora to regenerate may be sufficient. |
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|
Term
| What bacteria is associated with nauseua and vomiting within 1-6 hours of ingestion? |
|
Definition
| S. aureus and B. cereus toxins can cause short-duration nausea and vomiting within 1-6 hours after ingestion. |
|
|
Term
| What bacteria is associated with abdominal cramps and diarrhea within 8-16 hours? |
|
Definition
| C. perfringens and B. cereus can be ingested and produce toxins and cause abdominal cramps and diarrhea within 8-16 hours. |
|
|
Term
| What bacteria need 16-72 hours to cause fever and abdominal cramps (tissue-invasive)? |
|
Definition
| Salmonella, Shigella, Campylobacter, Yersinia, EIEC are major considerations . |
|
|
Term
| What bacteria need 16-72 hours to cause abdominal cramps and watery diarrhea (toxigenic)? |
|
Definition
| E. coli and V. cholera need 16-72 hours to cause abdominal cramps and water diarrhea. |
|
|
Term
| What agents are capable of causing persistent diarrhea (> 14 days)? |
|
Definition
| Giardia, Cryptosporidium, and Entamoeba are capable of causing persistent diarrhea? |
|
|
Term
| What is the most common nosocomial diarrheal-causing bacteria? |
|
Definition
| C. difficile is the most common cause of nosocomial diarrhea. |
|
|
Term
| What is the most common cause of bloody diarrhea? |
|
Definition
| E. coli is the most common cause of bloody diarrhea by far. |
|
|
Term
| Most vector-borne diseases occur because we are an accidental host. What does that mean? |
|
Definition
| The bacteria normally resides in a main reservoir (usually another animal species). However, sometimes a vector, either involved in the normal bacterial life-cycle or not, can transmit the bacteria into humans, causing the accidental host a disease. |
|
|
Term
| What is the infectious agent of Lyme Disease? |
|
Definition
| Lyme disease is caused by the spirochete Borrelia burgdorferi (highly motile extracellular gram-negative corkscrew-shaped). It is transmitted usually (in the northeastern and north-central US) by Ixodes scapularis (the deer tick). The animal reservoir is most usually the white-footed mouse (though they can also feed on deer as adults). Most humans will be bitten and infected in Spring and Summer. |
|
|
Term
| What are the early clinical manifestations of Lyme Disease? |
|
Definition
| The early clinical manifestations are a bull’s eye rash in the majority (but not all) patients. Later, facial palsy and flu-like symptoms can appear. |
|
|
Term
| What are the characteristics of late disseminated Lyme Disease? |
|
Definition
| Inflammation of the joints and more infrequently neurological disease (ataxia, memory loss, mood changes, sleep disturbances) may result from untreated Lyme Disease. |
|
|
Term
| What are some basic characteristics of Rickettsia rickettsii, the pathogen that causes Rocky Mountain Spotted Fever? |
|
Definition
| Rocky Mountain Spotted Fever (which is actually most common in the Appalachians and in North Carolina), is caused by Rickettsia rickettsii, a gram-negative obligate intracellular pathogen. Its vector is the wood tick and the wild reservoir is small wild rodents. Rickettsia is transmitted vertically in the ticks. |
|
|
Term
| What are clinical manifestations of Rocky Mountain Spotted Fever? |
|
Definition
| In Rocky Mountain Spotted Fever, a rash starts on the periphery of the body and spreads to the trunk. This is due to damage to the cell membrane of vascular cells leading to leakage of red blood cells. Untreated, Rickettsia can destroy the blood vessels and cause death. |
|
|
Term
| What are some basic characteristics of Yersinia pestis, the causative agent of plague? |
|
Definition
| Yersinia pestis is a primarily extracellular gram-negative bacterium which looks like safety-pins when stained in blood. Wild rodents are the natural reservoir and the flea is the vector. The flea can then transmit Yersinia upon biting into either domestic rats or humans. |
|
|
Term
| What are the clinical manifestations of plague? |
|
Definition
| Initial manifestations are buboes, huge swelling in lymph nodes. Accompanying boboes are fever, chills, headache, extreme exhaustion. Bacteria can then cause bacteremia and turn skin black. If they spread to the lungs, pneumonic plague results and can be spread through coughing. |
|
|
Term
| Can a virus contain both DNA and RNA? |
|
Definition
| A virus always contains DNA or RNA, never both. It must carry with it or code for a polymerase protein that replicates its genome. The genetic information can be single- (sense or antisense direction) or double-stranded |
|
|
Term
|
Definition
| A virus is enclosed by a capsid which may or may not be ensconced in an envelope of lipid made from host. Encapsulated viruses are more easily inactivated since membranes are so fragile. |
|
|
Term
| What are four ways in which viruses conserve ‘genetic space?’ |
|
Definition
| Viruses can: make a polyprotein that is then cleaved; produce a single transcript which is then spliced; employ overlapping reading frames; and have ribosomal frame-shifting. |
|
|
Term
|
Definition
| Viral tropism is the spectrum of tissues and cell types infected by a given virus. Some viruses have very restricted tropisms while others are more broad. This is often explained by the presence or absence of the appropriate viral receptor. |
|
|
Term
| Why may RNA viruses mutate more frequently? |
|
Definition
| RNA polymerases generally lack proofreading activity (in contrast to DNA polymerases). |
|
|
Term
| What are the three methods by which viruses generate diversity? |
|
Definition
| Viruses generate diversity by simple mutation, recombination (between two genomes), and reassortment (a classical form of recombination that can occur when two segmented viruses infect the same cell). |
|
|
Term
| What is a cytopathic virus? |
|
Definition
| A cytopathic virus replicates quickly, killing the cell and producing new virions. Cytopathic effects are observed: inclusions, syncytia, cell swelling. |
|
|
Term
| What is a noncytopathic virus? |
|
Definition
| A noncytopathic virus infects cells, actively producing new virions without immediately killing the cell. |
|
|
Term
| What is a latent/slow/abortive/transforming virus? |
|
Definition
| This type of virus infects the cell, but do not kill the cell nor produce new virus particles. |
|
|
Term
| What are some characteristics of parvoviruses? |
|
Definition
| Parvoviruses are tiny, single-stranded DNA viruses with an icosahedral capsid without an envelope. They replicate in the nuclei of dividing cells and include the adeno-associated viruses (used for gene therapy). |
|
|
Term
| What are symptoms of parvovirus B19 (“fifth disease”), a common parvovirus? |
|
Definition
| Parvovirus B19 replicates in erythrocyte precursors and antibodies to viral proteins are deposited in the skin and joints. In children, a rash, “slapped cheek” measles, and mild fever and malaise appear. Health adults may get arthritis. In immunocompromised patients, severe anemia can result. |
|
|
Term
| What are some basic characteristics of adenoviruses? |
|
Definition
| Adenoviruses are medium-sized unenveloped icosahedral viruses with many proteins (some involved in immune evasion) that contain a double-stranded linear DNA. |
|
|
Term
| What are some typical infections that adenoviruses can cause? |
|
Definition
| Adenoviruses can cause respiratory infections (URI, pharyngitis, pneumonia, pertussis-like illness), conjunctivitis, gastroenteritis, hemorrhagic cystitis, myocarditis. In immunocompromised patients, infections may become disseminated. |
|
|
Term
| What are some basic characteristics of papillomaviruses? |
|
Definition
| Human Papillomaviruses (HPV) are small non-enveloped viruses with circular double-stranded DNA. They cause epithelial cell proliferation and epithelial cell tumors. All cervical cancers are caused by HPV and a highly effective vaccine has very recently been developed.. |
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