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105 Cards in this Set
- Front
- Back
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What are the four steps every bacteria must accomplish to survive in an environment? |
1. enter environment 2. survive 3. replicate 4. leave environment |
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What are three structural differences between G+ and G- bacteria? |
G+ have a thicker peptidoglycan layer, which is the most external layer G- have an outer membrane as the most external layer, with lipopolysaccharides G- have the periplasmic space between the peptidoglycan layer and the outer membrane |
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Bacteria produce two important cell wall components that are not found in any eukaryotic cell. What are they? |
lipopolysaccharides (specifically Lipid A) and peptidoglycans |
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All classical spore forming bacteria are Gram __ |
Gram positive |
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what are virulence factors? |
bacterial products, or strategies, used tocontribute to the ability of an organism to perpetuate itself and/or causedisease |
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What is the structural protein that composes fimbriae (proteinaceous adhesins)? |
Pillin |
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What do fimbriae help the bacteria achieve? |
Attachment to the host cell. Binding of fimbriae to the host cell is often the initial point of contact between bacteria and host Pili that are shed may also help with immunologic avoidance |
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Capsular polysaccharides help the bacteria evade the immune system through what three mechanisms? |
avoid phagocytosis (antiphagocytic) mimic host antigens (antigenic mimicry) mask pathogen antigens (antigenic masking) |
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Why are biofilms less sensitive to antibiotics? |
The density of the bacteria protects the bacteria in the center (poor diffusion) Bacteria in biofilms are also less rapidly dividing (quiescent), and antibiotics tend to target rapidly dividing cells. |
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What is an example of an endotoxin? |
Lipid A of lipopolysaccharide |
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exotoxins are often bipartite. What does this mean? What are the important functional characteristics of these types of toxins? |
A and B subunits B binds to the target, A is active |
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How could a bacterial bipartite exotoxin be modified for cancer therapy? |
Because the B subunit confers target specificity, if you could find a way to make a B subunit specific to cancer cells, you could pair it with any choice of A subunit to kill those cells. |
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What is a superantigen? |
a protein that can polyclonally activate many T cells, resulting in massive cytokine release |
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_______ from bacteria and ________ from eukaryotic hosts compete for iron within the body. |
_siderophore_ from bacteria and _transferrin (also lactoferrin)_ from eukaryotic hosts compete for iron within the body. |
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If the concentration of iron in the body increases, the number of infecting bacteria required to cause disease dramatically _______ |
decreases |
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Where within a host cell can bacteria survive and grow? |
cytoplasm, endosomes/pre-lysosomes, golgi or ER-like vesicles, full-blown vesicles |
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What are three processes that bacteria use to escape degradation by the host phagosome? |
escape (before lysosome phagosome fusion) tolerance avoidance (prevent lysosome phagosome fusion) |
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A collection of virulence factors that are encoded together and are self-contained determinants of disease is called a _________ |
pathogenicity island |
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What are some general defences the body uses at mucosal membranes? |
lysozyme (digests peptidoglycan) lactoferrin mucus/mucin: interferes with bacterial attachment mucosal epithelial cell shed at a high rate |
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Some pathogens secrete toxins generate adhesins/exotoxins that are ciliostatic. What part of the host are these pathogens most likely colonizing? |
upper respiratory tract. ciliostatic chemicals block the activity of ciliated epithelial cells that move particles to the back of the throat where they can be swallowed |
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the primary goal of the complement pathway is to generate the __________. Evasion of the complement system is particularly important for bacteria that live in the _______ |
membrane attack complex bloodstream |
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How do bacteria evade the complement pathway? |
Block complement by protecting bacteria cell surface ("S layer": like armor) Specifically degrade components of the cascade (ex: strep C5a peptidase, degrades C5a to prevent chemoattractant and evade immune system) |
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What signals are chemoattractants for phagocytic host cells? |
complement products clotting products bacterial LPS |
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What components of bacterial cells can lead to the over-exuberant host immune response leading to sepsis? |
LPS peptidoglycan lipoteichoic acid flagellin unmethylated CpG (DNA form specific to bacteria) |
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Why can antibiotic administration in pseudomonas infections lead to sepsis? |
administering antibiotics stresses the bacteria, leading to dramatic increase in outer membrane (OM) blebbing. These OM blebs are highly immunogenic, with peptidoglycans and other bacterial antigens. This causes huge immune response from the host, leading to sepsis |
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What is the difference between sterilization, disinfection, and antisepsis? If you wanted to make sure your hands were bacteria-free, which one would you use? |
sterilization: getting rid of every living thing in a sample (steam and pressure, dry heat, ethylene oxide) disinfection: getting rid of microbes on an inanimate surface (aldehydes, oxidizing agents, moist heat, pasteurization) antisepsis: getting rid of microbes on a living host (halogens, ammonium compounds, alcohols) |
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What is the difference between germicides and sporicides? |
germicides target typical vegetative bacteria sporicides are typically tougher disinfectants, will kill fungal spores, but not bacterial spores |
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_____ material often interferes with the activity of disinfectants. For this reason _______ is of primary importance. |
_organic_ material often interferes with the activity of disinfectants. For this reason _basic hygiene_ is extremely important. |
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How can a therapy be selective to the target without being toxic to the host? |
target metabolic differences between the host and the pathogen target unique bacterial structures (peptidoglycan, protein and nucleic acid machinery) |
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Why are there so many more anibacterial compounds compared to antifungal or antiviral compounds? |
bacteria are more dissimilar to mammals (fungi are eukaryotic, viruses use host machinery to reproduce) so there are more targets. |
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What is MBC and MIC? How does this relate to bactericidal and bacteriostatic? |
Bactericidal: kills bacteria MBC: minimum bactericidal concentration Bacteriostatic: stops bacterial growth MIC: minimum inhibitory concentration |
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What makes a perfect antibiotic (antimicrobial properties)? |
1. selective toxicity 2. appropriate spectrum of activity (broad or narrow) 3. microbicidal activity 4. does not succumb to resistance mechanisms |
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What makes a perfect antibiotic (pharmacological properties)? |
1. non-toxic to host 2. long plasma half-life 3. good tissue distribution (including CNS) 4.can be administered PO or parenteral (injectable) 5. no interference with other drugs 6. no problems with drug allergies |
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What natural source are most antibacterial compounds found in? Where specifically? |
other bacteria or fungi (penicillin from mold) specifically in Streptomycetes (one genus of bacteria) |
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What are 5 common antibacterial targets? |
cell-wall synthesis DNA replication RNA synthesis Protein synthesis Antimetabolites |
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What are examples of antibacterials that interfere with bacterial cell wall synthesis? |
Beta-lactams penicillin cephalosporins cephamycins |
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what is the common mechanism of all Beta lactams? |
block the terminal assembly (cross-linking) of peptidoglycan, weakening the cell wall |
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Many antibiotics are bacteriostatic instead of bacteriocidal. How do they clear bacterial infections? |
By preventing bacterial growth they allow the host immune system to recover and then clear the infection |
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What is often the determining factor between whether an antibiotic is bacteriostatic or bacteriocidal? |
concentration of antibacterial agent, and amount of time bacteria is exposed to antibiotic |
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While many antibiotic compounds were originally isolated from other microorganisms, these compounds are often modified to form semi-synthetic or synthetic compounds. Why? |
Penicillin G (natural): not resistant to stomach acid, couldn't be given orally. narrow spectrum Penicillin V (semi-synthetic): resistant to acid Ampicillin (synthetic): resistant to acid, and has broader spectrum |
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Aminoglycosides, Tetracyclines, Macrolides, and Chloramphenicol all target what important bacterial process? |
Protein synthesis. Target some aspect of ribosome/mRNA/tRNA interaction |
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What is an example of an antibiotic that inhibits DNA synthesis? |
quinolones (nalidixic acid, ciprofloxacin) inhibit DNA gyrase |
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What is the role of DNA gyrase? What antibiotic class blocks it's activity? |
DNA gyrase: enzyme responsible for supercoiling DNA, allowing it to be packed into bacterial cell quinalones (nalidixic acid, ciprofloxacin) |
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What is the mechanism of actin of the antibiotic Rifampin? |
inhibits RNA synthesis binds RNA polymerase and blocks the initiation of transcription |
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Why is it so easy for bacteria to develop quinalone resistance? |
a single point mutation in DNA gyrase (antibacterial target), makes the antibiotic unable to bind its target |
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How do bacteria develop resistance to Beta-lactams? How have drug manufacturers gotten around this? |
bacteria have beta-lactamase, which cleaves Beta-lactams Administer Beta-lactams (like amoxycillin) with a Beta-lactamase inhibitor (like potassium clavulanate) = Augmentin/Clavamox |
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What antimicrobials work by interfering with nucleic acid functions? |
nitroimidazoles (metranidazole), Nitrofurans |
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What antimicrobials work by inhibiting folic acid synthesis? What is their mechanism of action |
sulfonamides (analogue of bacterial para-aminobenzoic acid) trimethoprim (analogue of folic acid) these drugs block folic acid synthesis by occupying the active site of enzymes crucial in the process = competitive inhibitors |
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What are examples of antibiotics that inhibit membrane integrity and function (not beta-lactams) |
polymixin cyclic cationic peptides these bind to LPS and destabilize membranes |
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what are 3 mechanisms by which bacteria develop antibacterial resistance? What is an example of each? |
altered target (ex: DNA gyrase point mutation, resistance to quinalones) altered uptake (ex: tetracycline efflux pump, tetracycline resistance) drug inactivation (ex: beta-lactamase, resistance to beta-lactams) |
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Many soaps used to have Triclosan added as an antibacterial agent. Why was this a bad idea? |
Low levels of Triclosan created a selective pressure, resulted in bacteria with multidrug resistance via efflux pumps. |
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Antibiotic resistant bugs often can't compete with their antibiotic sensitive relatives in a non-selective media. Why is this? |
antibiotic resistance often comes at a cost to the microbe |
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How can antibiotics be used besides as anti-bacterial agents? |
anti-tumor agents immunosuppressants growth promoters (in production animals) |
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Staphylococcus aerobe? anaerobe? Gram +/-? shape? coagulase _____ catalase _______ what type of pathogen? (facultative, opportunistic, frank) |
aerobic Gram + cocci in clusters coagulase positive catalase positive (except 2 odd species) facultative opportunistic pathogens |
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If you cultured a swab of normal hairy skin, what microbe would you likely find? |
Staphylococcus |
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How well do Staphylococcus and Streptococcus survive in the environment? |
Staph: very hardy, environmentally resistant
Strep: wimpy |
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What staphylococcal species are of greatest importance to veterinary medicine? |
S. aureus: many species
S. intermedius: dog, duck, pigeon, horse, mink S. hyicus: pigs S. pseudointermedius: dogs (S. epidermidis very common, but very low virulence) |
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What leukocyte do Staphylococci have a unique interaction with? How do the bacteria utilize this cell? |
neutrophils colonize and live within the neutrophil, get transported around the body (trojan horse concept) |
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How does Staphylococcus evade the immune system? |
Protein-A dependent immune evasion binds antibody, coats bacteria, hiding it from immune system |
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The hemolytic characteristics of Staph are important for _____, but their ________ significance is not clear. |
The hemolytic characteristics of Staph are important for _diagnostics_, but their _pathogenic_ significance is not clear. |
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What is a common condition caused by S. hyicus? |
Exudative dermatitis in pigs greasy pig disease |
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How does Staph cause damage to the skin (what toxin or process does it use)? |
toxins target desmogleins that connect keratinocytes to one another |
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What skin disease in humans has homologous etiology to greasy pig disease? What pathogen causes this disease? |
staphylococcal scaled skin syndrome S. aureus (produces similar toxins to S. hyicus in pigs) |
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S. pseudointermedius infections in dogs cause ____ |
pyoderma |
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What Staph toxin has superantigen activity? |
Toxic shock syndrome toxin (TSST) |
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Many species can develop pustular dermatitis from Staph infections. What is this condition called? |
Impetigo |
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Staphylococcal mastitis of cows, goats, and ewes, is primarily caused by which Staph species? |
S. aureus |
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What does MRSA stand for? What does VRSA stand for? How could VRSA develop? Why is this so terrifying? |
Methicillin Resistant S. aureus Vancomycin Resistant S. aureus S. aureus could get a vancomycin resistance pathogenicity island from closely related Enterococcus species (strains currently exist that are Vancomycin resistant). Vancomycin is currently our best defense against MRSA. |
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What is the best way to prevent Staph infections? |
HYGIENE!! |
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An animal gets a Staph infection and then recovers. What is the likelihood that the animal will be protected against further Staph infections? |
zilch there is no lasting immunity from any staphylococcal infections |
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______-acquired MRSA developed first, but now _______-acquired MRSA is being seen as well |
_hospital_-acquired MRSA developed first, but now _community_-acquired MRSA is being seen as well |
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Streptococci anaerobe? aerobe? G+/-? catalase ______ motile? shape? What kind of pathogen (facultative, opportunistic, frank)? |
facultative anaerobe G+ (like staph) catalase negative (unlike staph) non-motile cocci, clusters most are commensals, some can be frank pathogens |
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What is the difference between a facultative and an opportunistic pathogen? |
Facultative: commensal in one tissue, causes disease at another site in healthy animals Opportunistic: cause disease in compromised patients |
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How do we test for Streptococci clinically? What part of the bacteria is this test detecting? |
Lancefield testing kit looks at cell wall carbohydrate antigens |
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What is unique about the Strep capsule? How is the capsule a virulence factor? |
great example of molecular mimicry: capsule consists of eukaryotic sugar groups that tricks the body into thinking it is host material non-immunogenic, antiphagocytic |
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What is Strep M protein? How is it a virulence factor? |
antiphagocytic, anticompementary, adherence, invasion |
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Necrotizing fasciitis is caused by what bacterial enterotoxin? |
toxic shock syndrome toxin from Strep |
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What is strangles? What is the causative species? |
highly contagious upper RT infection of horses Streptococcus equi equi |
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How is Streptococcus typically transmitted? |
from animal to animal, only occasionally via fomite |
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You see a horse with painful, swollen, purulent submandibular lymph nodes. What's your primary differential? |
Strangles caused by Streptococcus equi equi |
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In S. equi equi, the M protein is highly conserved, whereas it may be more variable in other species. Why is this important? |
Once an animal recovers from strangles it is usually immune to repeat infections, because it has antibodies against the conserved M protein |
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What are possible complications from S. e. equi infections? |
purpura haemorrhagica (immune-mediated, immune complex associated) bastard strangles (abscesses involving lymph nodes in unusual organs) |
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What characteristics does a pathogen need to have for eradication to be possible? |
1. narrow host specificity 2. have to be able to identify all infected animals 3. most animals that clear the pathogen have to be 100% immune 4. pathogen survives poorly in the environment |
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Why is controlling Strangles difficult? |
carrier horses can have latent S. e. equi infections in the guttoral pouch |
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How is S. e. zooepidemicus distinct from S. e. equis? |
zooepidemicus has a lot of genetic variability (unlike equi) usually a mucosal commensal, but can cause secondary infections infects many species |
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What strep species is significant to the pig industry? What symptoms does it cause? |
S. suis systemic disease: meningitis, arthritis, septicaemia, brochopneumonia |
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Where do enterococcus species usually live? when does it cause pathology? |
abundant gut commensal opportunistic pathogens in immune compromised individuals |
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What bacterial agent should be suspected when a wound has been contaminated with fecal material? |
Enterococcus |
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Anthrax is what type of bacteria? |
Bacillus |
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Bacillus G+/-? aerobe? anaerobe? shape? catalase +/-? where are they normally found? |
G+ aerobic or facultative anaerobe rods in chains catalase + environmental soil microbes |
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You come upon a dead cow with dark tarry blood coming out of it's orifices. How do you proceed? |
gear up (PPE) culture it (likely anthrax) burn it! |
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What are the three routes of infection for anthrax? What is the prognosis for each type? |
cutaneous: easy to identify, catch early, best prognosis pulmonary: nonspecific symptoms, progresses farther before diagnosis, more likely fatal intestinal: highly fatal. death occurs after 2-5 days |
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Bacillus species are __________ forming bacteria, allowing them to survive in many environments for a long time |
spore |
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How do anthrax vaccines act? |
Bacillus anthracis has two virulence plasmids strains lacking either of the plasmids are not virulent pasteur's original vaccine: remove toxin producing plasmid modern vaccine: remove capsid producing plasmid |
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What is the structure of Anthrax toxin? |
one B subunit 2 different A subunits: Edema factor (EF) or Lethal factor (LF) |
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What are the actions of the two different A subunits of Anthrax toxin? |
Edema factor (EF): targets calmodulin-dependent adenylate cyclase -> disrupts fluid regulation Lethal factor (LF): serine proteinase that affects host cell cytokine release -> systemic toxic shock |
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Bacillus cereus is like the poor cousin to Bacillus antracis. What clinical symptoms does it cause in people? |
food poisoning |
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What important disease is caused by Rhodococcus? |
Rhodococcus equi chronic suppurative bronchopneumonia of foals high mortality death typically by sepsis |
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What virulence factor is critical to Rhodococcus pathogenicity? |
survival inside of macrophages |
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Where does Rhodococcus typically live? |
soil organism. common in soil and in equine intestinal material/feces. However the vast majority of Rhodococcus isolates do not carry the virulence plasmid |
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How are Rhodococcus virulence genes regulated? |
temperature sensitive turn on virulence genes when exposed to increased temperature inside host |
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What are examples of opsonins that bind bacteria and other parasites in the body? |
LPS-binding protein C3b receptor (from the complement cascade) Antibodies (acquired immune response) |
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Catalase is a common test used to differentiate bacterial species. What role does catalase have in the bacteria? |
Catalase neutralizes reactive oxygen intermediates released from host phagocytic cells |
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Many systemic pathogens produce extracellular DNAse, while nonpathogenic species do not. Why? |
NETs: neutrophil extracellular traps. NETs contain chromatin (DNA), histones, and enzymes. NETs are sticky and immobilize bacteria. Bacterial DNAse helps bacteria get free. |
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What are examples of some inflammatory mediators (products that induce inflammation)? |
complement cascade products fibrinopeptides from clotting cytokines bacterial products (endotoxin, peptidoglycan) |
