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Pathogenic Microbiology > Test 1 > Flashcards

Test 1 Flashcards

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Biology 101 flashcards
1
Q

Define virulence factor

A

Traits that enhance the ability of bacteria to remain in and harm the body to cause disease; often mechanisms used to maintain a niche or by-products of growth and colonization that can cause damage and problems to a human host

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2
Q

Define the ID50

A

The infectious dose for 50% of the population

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3
Q

Define the LD50

A

The lethal dose for 50% of the population

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4
Q

Describe the key difference between an endotoxin and an exotoxin

A

Endotoxins are usually proteins, while exotoxins are typically lipids/glycoproteins; only gram negative bacteria make endotoxins

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5
Q

What is the biggest difference between gram positive and gram negative bacteria?

A

Gram positive bacteria have a thicker cell wall made of peptidoglycan, while gram negative bacteria have a more “complex” system for their cell wall (only gram negative bacteria make endotoxins)

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6
Q

Differentiate between transformation, transduction, conjugation, and transposition as mechanisms of DNA transfer between cells

A

Transformation: Uptake of exogenous DNA
Transduction: Phage mediated DNA transfer
Conjugation: Type IV secretion; sex pilus mediated DNA transfer
Transposition: Jumping genes/transposons

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7
Q

How do commensal flora benefit human hosts?

A

They: make vitamins, digest food, prevent pathogen colonization, and prime innate immunity

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8
Q

Define pathogenicity and relate it to virulence

A

Pathogenicity is the ability to cause disease, while virulence is the extent of pathogenicity

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9
Q

How do microbes cause direct damage?

A

They disrupt host cell function, produce waste products, and/or produce toxins that are detrimental to the host

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10
Q

How do microbes adhere to host cells?

A

They use adhesins/ligands that bind to receptors (glycocalyx, fimbriae, and/or M proteins; they can also form biofilms

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11
Q

What are the cell wall components, and what do they do?

A

M protein resists phagocytosis
Opa protein inhibits T helper cells
Mycolic acid (waxy lipid) resists digestion

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12
Q

What enzymes help bacteria to survive?

A

Coagulase: Coagulates fibrinogen
Hyaluronidase: Hydrolyzes hyaluronic acid
Collagenase: Hydrolyzes collagen
IgA proteases: Destroy IgA antibodies
Invasins: Penetrate into the host cell cytoskeleton

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13
Q

Define toxin, toxigenicity, toxemia, toxoid, and antitoxin

A

Toxin: A substance that contributes to pathogenicity
Toxigenicity: Ability to produce a toxin
Toxemia: Presence of toxin in the host’s blood
Toxoid: Inactivated toxin used in a vaccine
Antitoxin: Antibodies against a specific toxin

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14
Q

What are the pathogenic properties of fungi?

A

Waste products may cause symptoms, chronic infections can provoke an allergic response, tichothecene toxins inhibit protein synthesis, proteases can degrade host proteins, and the capsule prevents phagocytosis

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15
Q

What are the four methods of diagnosis for a pathogen?

A

1) Culture based techniques
2) Microscopic methods
3) Molecular based techniques
4) Serologic based techniques

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16
Q

What is the minimum inhibitory concentration (MIC)

A

The lowest concentration of antibiotic able to inhibit the growth of the bacteria

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17
Q

What is the primary difference between S. aureus, S. epidermidis, and S. saprophyticus?

A

S. aureus is positive for both catalase and coagulase, while S. epidermidis and S. saprophyticus are only positive for catalse.

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18
Q

What are some of the major diseases that S. aureus causes?

A

Food poisoning, Toxic Shock Syndrome (TSS), scalded skin syndrome, pyogenic diseases (folliculitis/wound infections), and other systemic diseases

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19
Q

What are the two main types of a S. epidermidis or S. saprophyticus infection?

A

Infection of foreign bodies (catheter, prosthetic valves, etc) and urinary tract infections (UTI)

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20
Q

What are the main virulence factors for Staphylococcus species?

A

A polysaccharide capsule, group specific carbohydrates (A or B antigen), and type specific proteins/carbohydrates

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21
Q

What should be the treatments for infections of Staphylococcus?

A

Trimethoprim, vancomycin, proper wound cleaning, and draining the wound. There is no fully approved vaccine

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22
Q

What is the primary difference between Streptococcus pyogenes, agalactiae, and pneumoniae?

A

Pyogenes is Group A, agalactiae is Group B, and pneumoniae is Group NT

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23
Q

What are the main facets of Streptococcus?

A

Gram + cocci or diplococci in chains, catalase negative, facultative anaerobes, fermenters, present in upper respiratory tract and skin

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24
Q

What are the main facets of Staphylococcus?

A

Gram + cocci arranged in clusters, catalase positive, facultatively anaerobic (?), common on skin and mucus

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25
Q

What virulence factors are important for Streptococcus pathogenicity?

A

Capsules, peptidoglycan, Pili M protein antigens, streptolysins, etc.

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26
Q

What purpose does Lancefield grouping serve?

A

Classifying streptococci based on the presence of group-specific carbohydrates

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27
Q

What diseases do each of the major Streptococcus species cause?

A

S. pyogenes: Can be suppurative or nonsuppurative; scarlet fever versus necrotizing fasciitis
S. pneumoniae: Pneumonia, meningitis
S. agalactiae: Chronic bovine mastitis, neonatal meningitis

28
Q

How should you diagnose and treat S. pyogenes?

A

Diagnosis: Look at nose/throat and blood/wound cultures, should show Bacitracin sensitivity, examine anti-streptolysin O titers, and look for an M Lancefield type
Treatment: Amoxicillin, prophylactic bicillin for rheumatic fever; no approved vaccine yet

29
Q

How should you diagnose and treat S. pneumoniae?

A

Treat with penicillin, vancomycin, cephalosporin, or fluoroquinolone; vaccines (PCV7, 13, and 23) are available

30
Q

How should you diagnose and treat S. agalactiae?

A

Treat with penicillin + aminoglycoside or vancomycin; polyvalent vaccine exists but no licensed vaccine yet

31
Q

Describe the general attributes of enterococcus

A

Gram positive cocci/diplococci, facultatively anaerobic, arranged in pairs/short chains, grows under adverse conditions, obtains drug resistance easily

32
Q

What are the virulence factors for enterococcus?

A

Secreted proteins: Cytolysin, gelatinase, serine proteases
Surface adhesions: Asa, Esp, Ace, Pili
Cell wall polymers: Capsule, LTA, cell wall antigen

33
Q

How should you diagnose and treat Enterococcus infections?

A

Diagnose: Look for optochin and bile resistance and growth even in harsh conditions
Treatment: Antibiotic combination therapy is recommended (aminoglycosides + ampicillin); caution in hospital setting is also helpful to reduce spread

34
Q

Enterococcus causes what diseases?

A

Surgical site infections, nosocomial (acquired in hospital) UTIs, and infective endocarditis

35
Q

Generally describe Listeria monocytogenes

A

Gram + small uniform rods, aerobic, can grow at 4 degrees, tumbling motility at room temperature, facultative intracellular pathogen, actin-directed intracellular motility

36
Q

What are the major diseases that Listeria causes?

A

Listeriosis in neonates, elderly, and immunocompromised; also meningitis and bacteremia

37
Q

How should Listeria infections be diagnosed and treated?

A

Cold enrichment is a good indicator of Listeria as well as motility
Gentamicin with either penicillin or ampicillin should be used to kill Listeria; there is no vaccine

38
Q

Describe the Corynebacterium genus

A

Gram + pleomorphic bacilli (appears as a Y or in clumps), aerobic or facultatively anaerobic, catalase +, metachromatic granules

39
Q

What are the three species of Corynebacteria that we studied?

A

C. diphtheriae, C. jeikeium, and C. urealyticum

40
Q

Describe C. jeikeium and the diseases it can cause

A

Often has multiple antibiotic resistances, common for opportunistic infections in immunocompromised individuals; carried on skin

41
Q

Describe C. urealyticum and the diseases it can cause

A

Rare but important bacteria; causes UTIs by hydrolyzing urea with urease; the hydrolysis releases NH+, increases pH, and creates alkaline urine

42
Q

Describe C. diphtheriae

A

3 biotypes (we care about mitis), causes respiratory and cutaneous diphtheria; prototype A-B exotoxin acts systemically. The diphtheria toxin is introduced to the bacterium by a lysogenic bacteriophage

43
Q

How does the diphtheria toxin work?

A

The A-B exotoxin disrupts peptide formation in ribosomes by inactivating elongation factor-2. This causes cell death

44
Q

How do you diagnose C. diphtheriae and what are the treatments?

A

An ELEK test identifies presence of diphtheria toxin by precipitation reactions
Penicillin, erythromycin, or passive immunotherapy by antitoxin are the best treatments; the DPT/DTaP vaccine is available as prevention

45
Q

Describe the Clostridia genus

A

Gram + rods, endospore forming, obligate anaerobes, catalase negative, generally 4 types of pathogenesis: histotoxic (tissue infections), enterotoxigenic (gastrointestinal disease), tetanus, and botulism

46
Q

Describe the botulism toxin and how it works

A

7 different subtypes of botulinum toxin (A, B, E, and F cause disease), vary in structure and toxicity, but same general mechanism; the botulinum neurotoxin inactivates the proteins that regulate the release of acetylcholine, blocking neurotransmission; this causes flaccid paralysis (looseness of muscles)

47
Q

How is botulism diagnosed and treated?

A

Symptoms include weakness, difficulty in swallowing and speaking, and respiratory issues; finding toxin in bodily fluids

Treatment includes ventilatory support, trivalent antitoxin to bind free toxins in bloodstream, administering a gastric lavage, and penicillin or metronidazole to eliminate organisms from GI tract

48
Q

Describe C. tetani

A

“Tennis racket” spores, obligate anaerobe, motile, nonfermentive, spores in soil, bacteria in GI tract

49
Q

What are the virulence factors for C. tetani?

A

Tetanus toxin (tetanospasmin) - AB toxin with A-endopeptidase activity to cleave proteins involved in neurotransmitter release

Hemolysin (Tetanolysin) - Inhibited by oxygen

50
Q

Describe tetanus and how the toxin functions

A

4 types: Generalized, Cephalic, Localized/Wound, and Neonatal tetanus (high mortality)

Tetanus toxin moves to CNS by axons; it blocks release of inhibitory neurotransmitters (GABA and glycine) at inter neuron junctions by preventing the conduction of electrical signals. This leads to a continuous excitation response and muscle rigidity

51
Q

How is tetanus diagnosed and treated?

A

Mostly clinical presentation, no toxin or antibodies are usually detected

Metronidazole, passive immunization with antitoxins, and vaccine with tetanus toxoid are treatments/preventions

52
Q

Describe C. perfringens

A

Rectangular gram + rod, spores are rare, catalase negative, subdivided based on production of one or more lethal toxins

53
Q

What diseases do C. perfringens cause?

A

Cellulitis, fasciitis, myositis, myonecrosis (gas gangrene); it can also cause food poisoning and necrotizing enteritis

54
Q

How are C. perfringens infections diagnosed and treated?

A

Direct examination of wound smears and Nagler reaction in yolk media (lecithinase reacting with lipids in egg yolk)

Wound debridement, antibiotic therapy, antiserum against alpha toxin, and hyperbaric oxygen treatment are the best options

55
Q

Describe C. difficile

A

Anaerobic rod, spore former, “barnyard” smell; produces an enterotoxin and a cytotoxin but requires further conditions to actually cause problems; can be part of normal flora

56
Q

What diseases does C. difficile cause?

A

Pseudomembranous colitis and antibiotic associated diarrhea

57
Q

How do you diagnose and treat C. difficile infections?

A

By isolating organisms or detecting toxins in stool samples

Stopping current antibiotics and treatment with vancomycin or metronidazole, expecting relapse since spores are not cleared out, and stool replacement therapy for extreme cases are the best treatments

58
Q

Generally describe the Bacillus genus

A

Gram + or Gram variable bacilli, produce endospores (can be infectious for decades), catalase positive, aerobic or facultatively anaerobic

59
Q

Describe Bacillus anthracis

A

Commonly obtained from farm stock, inhalation, or ingestion; generally requires pXO1 and pXO2 plasmids to be virulent for the anthrax toxin, and poly-D-glutamic acid capsule is quite unique

60
Q

Describe cutaneous, inhalation, or gastrointestinal anthrax

A

Cutaneous: Most common human cases, slow-healing painless ulcer with black covering occurs 1-5 days after contact; ~20% mortality if left untreated

Inhalation: Via spores, virtually 100% fatal, fever, body aches, labored breathing and chest pain, pharyngitis, neck swelling, and organ failure; spores will transport to the lymph nodes to grow

Gastrointestinal (ingestion): Virtually 100% fatal, abdominal pain, ulcers at points of contact, etc.

61
Q

How does the anthrax toxin work?

A

Three factors are needed: Protective Antigen (PA) forms a pore in cells to allow the Edema Factor or Lethal Factor to enter the cell; the Edema Factor raises cAMP levels to cause swelling and fluid secretion, while the Lethal Factor cleaves protein kinases to impact signaling cascade and cause cell death

62
Q

How is anthrax treated?

A

Penicillin, erythromycin, chloramphenicol, doxycycline, ciprofloxacin, or the Bio Thrax vaccine (limited to laboratory workers and active military members); proper vaccination of farm animals should also be done

63
Q

Generally describe B. cereus

A

Opportunistic pathogen, in almost all environments, two major enterotoxins are heat-stable and heat-labile, spore forming, can have a very short incubation period

64
Q

What diseases does B. cereus cause?

A

Food poisoning (by the heat-stable enterotoxin) and diarrheal/gastroenteritis (by the heat-labile enterotoxin)

65
Q

How do you diagnose and treat B. cereus infections?

A

Taking a sample from human cultures or clinical criteria

Vancomycin, ciprofloxacin, gentamicin, and clindamycin can be used to treat; penicillins are ineffective

Pathogenic Microbiology (4 decks)

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