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microbiology > Micro lecture exam 3 > Flashcards

Micro lecture exam 3 Flashcards

1
Q

what are two Bacillus species?

A

Bacillus anthracis and Bacillus cereus

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2
Q

what is the action of the botulin toxin?

A

causes a flaccid paralysis by inhibiting acetylcholine release in the neuromuscular junction

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3
Q

Gas gangrene is caused by…

A

Clostridium perfringens

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4
Q

Which of the following is not classified as an unevenly staining non-spore forming Gram-positive bacilli?
Corynebacterium
Propionibacterium
Mycobacterium
Listeria
Nocardia

A

Listeria

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5
Q

Leprosy is a communicable disease, however, approximately 95% of the human population have a natural immunity?
True or False

A

True

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6
Q

What is the name of the human anthrax vaccine?

A

Biothrax

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7
Q

The genera of human pathogens that produce endospores include…

A

Bacillus and Clostridium

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8
Q

The human anthrax vaccine is readily available for travelers and civilians.
True or False

A

False

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9
Q

Bacillus cereus is a gram positive motile rod.
True or False

A

True

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10
Q

______ are often _______ to prevent the spread of Erysipelothrix rhusiopathiae which causes a specific type of cellulitis.

A

Pigs/vaccinated

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11
Q

what are the 2 gram-positive regular non-sporeforming bacilli?

A

Listeria monocytogenes and Erysipelothirx rhusiopathiae

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12
Q

Genus Bacillus fill in the blank
1. primary habitat is _____
2. ____ and ___ positive
3. source of _______
4. versatile in degrading ______ _______
5. gram-____
motile or nonmotile?
endospore-forming or nonendospore-forming?

A
  1. soil
  2. aerobic/catalase
  3. antibiotics
  4. complex macromolecules
  5. gram positive
    motile/endospore forming
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13
Q

Central spores in Bacillus anthracis develop under all conditions except in…

A

the living body

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14
Q

what are the virulence factors of Bacillus anthracis?

A

polypeptide capsule and exotoxins

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15
Q

what was anthrax thought of for years and how can humans get anthrax?

A

was thought of as a Zoonotic disease and it is acquired through contact with animals (sheep, cattle, goats) and their hides

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16
Q

what organism did Robert Kich work with for his postulates and proving the germ theory?

A

Bacillus anthracis

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17
Q

Human infection for anthrax depends on what 3 different portal of entries?

A

cutaneous- spores enter through the skin; least dangerous
pulmonary- inhalation of spores; most deaths
gastrointestinal- ingested spores; least common

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18
Q

what are the symptoms of cutaneous anthrax?

A

small papule or blisters that may itch; progress to a black eschar
20% fatality

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19
Q

what is pulmonary anthrax also called and what are it’s signs and symptoms?

A

also called woolsorter’s disease
early symptoms: fatigue, malaise, fever, aches, cough
late symptoms: high fever, labored breathing, shock
rapid death in 99% of untreated cases
causes- capillary thrombosis/cardiovascular shock

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20
Q

what is gastrointestinal anthrax’s symptoms and fatality rate?

A

symptoms: flu-like symptoms with fever and tiredness, sore throat, neck swelling, difficulty swallowing, nausea, anorexia, abdominal pain, vomiting & diarrhea

25% - 60% fatality
no cases reported in US

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21
Q

what are the antibiotic treatments for Bacillus anthracis and do they counteract the toxin?

A

ciprofloxacin or doxycycline and it does not

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22
Q

Name 3 facts regarding Bacillus anthracis and animals

A
  1. animals that have died from anthrax are burned or chemically decontaminated before burial
  2. vaccine for animals
  3. imported products composed of animal hides and hair should be gas-sterilized (ethylene oxide)
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23
Q

what is the the new drug approved by FDA for pulmonary anthrax and what does it do?

A

Raxibacumab; monoclonal antibodies bind to exotoxin

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24
Q

what happened in history regarding Bacillus anthracis?

A

2001- mailing of anthrax- containing envelopes
Destination: journalists offices and government offices

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25
Q

This Bacillus is commonly airborne and dustborne. The usual methods of disinfection and antisepsis are ineffective.

A

Bacillus cereus

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26
Q

where does bacillus cereus multiply and survive?

A

multiplies readily in cooked foods like rice, potato, and meat dishes
spores survive cooking (short periods) and reheating
food stored at room temperate spores germinate and produce enterotoxin

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27
Q

what are the symptoms of Bacillus cereus if ingested and how long do these symptoms last?

is there any treatment?

A

symptoms: nausea, vomiting, abdominal cramps, diarrhea; 24-hour duration

no treatment

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28
Q

where has Bacillus cereus been increasingly reported?

A

in immunosuppressed, intubated patients and drig addicts

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29
Q

what causes listeriosis?

A

Listeria monocytogenes

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30
Q

What are the initial symptoms of Clostridium perfringens?

A

pain, edema, bloody exudate in lesion w/ fever, tachycardia, blackened necrotic tissue w/ gas bubbles

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31
Q

What is the difference between Anaerobic cellulitis and Myonecrosis?

A

both are bacteria spreading in necrotic muscle tissue but Myonecrosis can invade healthy healthy tissue and Anaerobic cellulitis remains localized

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32
Q

How can you get infected with C. perfringens

A

-surgical incision
-puncture
-gunshot wound
-crushing trauma
-compound fracture
-diabetic sore
-frostbite
-septic abortions

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33
Q

What is the treatment for C. perfringens?

A

immediate cleaning of wound, debridement, or amputation
-large doses of cephalosporin or PCN
-no vaccine available

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34
Q

Describe Genus Clostridium

A

Gram +, spore forming rods
-strict anaerobic; oval/spherical spores
-synthesize organic acids, alcohols, exotoxins
cause wound & tissue infx and food intoxication

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35
Q

What does Clostridium tetani cause and what are the symptoms

A

causes tetanus

Symptoms: clenching of jaw, arching of back, flexion of arms, extension of legs; death due to paralysis in respiratory mucles

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36
Q

What is the action of neurotoxin Tetanospasmin

A

blocking the release of inhibitory neurotransmitters
-causes paralysis by binding to motor nerve endings in spinal cord
-rigid paralysis (muscles contract uncontrollably)

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37
Q

How do you treat C. tetani and what is the vaccine you get?

A

Control infection with PCN or tetracycline, and muscle relaxers

Toxoid vaccine DTaP (2, 4, 6, 15 months, 5yrs, booster q10yrs)

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38
Q

What is the fatality of C. tetani?

A

10-70%

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39
Q

What does Clostridium difficile-Associated Disease (CDAD) cause?

A

causes antibiotic-associated (pseudomembranous) colitis

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40
Q

Where does C. difficile usually reside and how do you acquire it?

A

-Normal resident of colon; kept in low numbers

Acquired: treatment with broad-spectrum antibiotics kills other bacteria, allowing C. diff to overgrow=superinfection

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41
Q

What are the symptoms of C. diff?

A

diarrhea, abdominal cramps, fever, patches of colon lining sloughs off

*common in community-acquired diarrhea

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42
Q

what does C. diff produce?

A

enterotoxins

43
Q

What is the treatment and prevention for C. diff?

A

Mild: fluid & electrolyte replacement; withdrawal of antimicrobials

Severe: oral vancomycin or metronidazole & replacement cultures

Prevention: bleach cleaners

44
Q

What are the 2 Clostridial Food poisoning?

A

C. botulinum & C. perfringens

45
Q

What are the 3 type of Botulism?

A

-Foodborne
-Infant
-Wound

46
Q

How do you get Foodborne botulism and what are the symptoms?

A

eating home canned food

Symptoms: double vision, difficulty swallowing & speaking, nausea, vomiting, muscular & respiratory paralysis

47
Q

How would Infant botulism occur and what are the symptoms?

A

affects ages 2 weeks-6 months
-ingest spores: raw honey, dust, vegetables

Symptoms: appear lethargic, feeding poorly, weak cry, appearing “floppy”

48
Q

What is wound botulism and who is at risk?

A

spores enter wound and cause food poisoning symptoms

At risk: injection drug uses, traumatic wound, surgery

49
Q

What is the treatment and mortality rate for C. botulinum?

A

-PCN and CDC has antitoxin
-Respiratory & cardia support

5% mortality rate

50
Q

Describe Botox (botulin A or B)

A

-initially used for crossed eyes & uncontrollable muscle spasm in back
-“lunch hour facelift” before FDA approval 2002
-helps with headaches & migraines (approval 2012)
-temporary paralysis in facial muscles to prevent wrinkles

51
Q

Aside from gas gangrene what else does C. perfringens cause?

A

Clostridial gastroenteritis

52
Q

Describe clostridial gastroenteritis

A

most common foodborne illness in US (1 million cases a year)

53
Q

How do spores contaminate food for C. perfringens?

A

commonly raw meat and poultry that hasn’t been cooked thoroughly
-spores germinate and multiply if unrefrigerated

54
Q

Where does the toxin produced in C. perfringens (clostridial gastroenteritis)?

A

toxin is produced in the intestine; acts on epithelial cells

55
Q

What is the treatment for Clostridial gastroenteritis?

A

Rapid recovery and no abx needed, but may need fluid and electrolytes

56
Q

Genus Mycobacteria: Acid-Fast Bacilli (fill in the blank)
Acid-fast staining
1. Gram-_____, _______ bacilli
2. strict _______
3. produce ________
4. Possess ______ acids and a waxy cell wall
5. Do not form _______, ______, or spores
6. Grow ______

A
  1. positive, irregular
  2. aerobes
  3. catalase
  4. mycolic
  5. capsules, flagella
  6. slow
57
Q

What does Mycobacterium tuberculosis produce?

A

no exotoxins or enzymes that contribute to infectiousness

58
Q

What are the virulence factors of M. tuberculosis?

A

contain complex waxes= mycolic acids and cord factor prevent destruction by lysosomes or macrophages

59
Q

What are predisposing factors of M. tuberculosis? How is it transmitted?

A

-inadequate nutrition, debilitation of the immune system, poor access to medical care, lung damage, and genetics

-airborne respiratory droplets; 5-10% of infected people develop disease

60
Q

the primary reservoir for Listeria monocytogenes is..
what can it contaminate?

A

…soil and water/animal intestines
contaminate foods and grow during refigeration

61
Q

what is the virulence for Listeria monocytogenes?

A

ability to replicate in the cytoplasm of cells after inducing phagocytosis; avoids humoral immune system

62
Q

Listeria monocytogenes cases are mostly associated with….

A

consuming dairy products, poultry, and meat

63
Q

what are the treatment and prevention for Listeria monocytogenes?

A

RX: Ampicillin (pcn) or trimethoprim/ sulfamethoxazole (Bactrim)

Prevention: pasteurization and cooking

64
Q

what are the 3 groups of individuals who acquire Listeria monocytogenes (1-4 weeks after eating food)?
what are the symptoms?

A
  1. often mild or subclinical in healthy adults: fever, diarrhea, sore throat
  2. immunocompromised patients: headache, stiff neck, confusion, loss of balance, convulsions; affects brain and meninges; 20% fatality
  3. pregnant women: flu-like symptoms
    crosses the placenta or through the birth canal
    affects fetuses and neonates- can cause miscarriage, stillbirth, premature delivery, or life-threatening infection of the newborn
65
Q

what does Erysipelothrix rhusiopathiae cause?

A

erysipeloid (cellulitis)

66
Q

what is Erysipelothrix rhusiopathiae’s portal of entry and what does it produce? and who is most at risk?

A

enters through skin abrasion and multiplies to produce dark red lesions
most at risk who handle animals, carcasses and meats

67
Q

how do you treat Erysipelothrix rhusiopathiae?

A

PCN or erythromycin

68
Q

Erysipelothrix rhusiopathiae is gram_____
Distributed in animals and the environment mostly _____, _____, ______

A

positive
pigs, fish, poultry

69
Q

what are the 5 medically important gram-positive irregular non-spore-forming bacilli?

A

Corynebacterium
Propionibacterium
Mycobacterium
Actinomyces
Nocardia

70
Q

what causes acne?

A

Propionibacterium acnes

71
Q

name the treatment for
mild acne-
moderate acne-
severe acne-

A

mild acne- salicylic acid
moderate acne- antibiotics clindamycin, acne creams benzoyl peroxide
severe acne- isotretinoin

72
Q

Propionibacterium acnes is gram positive _____ rods; ______ arrangement

A

pleomorphic/ palisade

73
Q

Propionibacterium acnes is common resident of _______ and it secretes enzymes that….

A

pilosebaceous glands
…damage the hair follicle that can lead to scaring

74
Q

Propionibacterium acnes are aerotolerand or anaerobic
true or false

A

true

75
Q

what does Corynebacterium diphtheriae cause and how is it acquired?

A

diphtheria
acquired: respiratory droplets from healthy carriers or actively infected individuals

76
Q

what are the 2 stages of Corynebacterium diphtheriae-diphtheria and describe them.

A
  1. local infection- upper respiratory tract infection
    symptoms: sore throat, nausea, vomiting swollen lymph nodes
    bacteria grow and produce diphtherotoxin
    Diphtherotoxin destroys healthy tissues in the respiratory system. 2-3 days pseudomembrane is formed (thick, gray coating) and builds up in nose and throat
    covers tissues in nose, tonsils, voice box, throat-making it very hard to breath
  2. systemic effects by diphtherotoxin-
    myocarditis with abnormal rhythms, leads to heat failure
    neuritis
    paralysis of soft palate, eye muscles, limbs, diapgram= respiratory failure
    secondary pneumonia
77
Q

what is the treatment for Corynebacterium diphtheriae- diphtheria?

A

*PCN or erythromycin
*antitoxin (from CDC)
*Surgically open blocked airway or tracheostomy
*vaccine: DTaP (diphtheria vaccine used in early thirties)

78
Q

what is cutaneous diphtheria?

A

*caused by a strain of Corynebacterium diphtheriae without the gene to make diphtheria
*mostly seen in the tropics/ US homeless people
*Symptoms: scaling rash/ulcers with clearly demarcated edges
*sometimes maybe coinfect with other species

79
Q

Clinical tuberculosis divided into:

A

-Primary TB
-Secondary TB (reactivation or reinfection)
-Disseminated (extrapulmonary) TB

79
Q

What is another name for Primary TB

A

Latent TB infection

80
Q

What’s the chance of primary TB to develop to secondary TB?

A

only 5-10%

81
Q

What is the infectious dose of primary TB?

A

10 cells

81
Q

After 3-4 weeks after being infected with primary TB the immune system attacks, forming tubercles. What happens if the tubercle breaks down?

A

If it breaks into necrotic caseous lesions, they gradually heal by calcification

82
Q

What are the symptoms of primary TB?

A

there’s no symptoms, cannot spread TB bacteria, but will have a positive skin test

83
Q

what are symptoms for secondary TB (TB disease)

A

violent coughing greenish or bloody sputum, fever, anorexia, weight loss, fatigue, night sweats

84
Q

If TB is untreated, what is the mortality rate?

A

60%

85
Q

TB bacteria remains in the lungs for majority of 85% patients, what happens to the other 15%?

A

bacteria moves to the other parts of the body

86
Q

What happens to the tubercules in secondary TB?

A

tubercules expand and drain into the bronchial tubes and upper respiratory tract

86
Q

What’s another name for disseminated TB?

A

Extrapulmonary TB

87
Q

True or False
During secondary TB, bacilli disseminate to regional lymph nodes, kidneys, long bones, genital tract, brain, and meninges. They create tubercle in these organs

A

True

88
Q

What tests are done to diagnose TB?

A
  1. In vivo or tuberculin testing
    -Mantoux test (PPD)
  2. x-rays
  3. direct identification of acid-fast bacilli in specimen
  4. cultural isolation and biochemical testing
89
Q

What is the management and prevention of M. tuberculosis?

A

-treat 8 weeks with4 drugs
-one pill regimen called Rifater = isoniazid (INH), rifampin (RIF), pyrazinamide (PZA), plus ethambutol (EMB
-then 18 weeks of INH and RIF

90
Q

What vaccine is for M. tuberculosis?

A

BCG vaccine

91
Q

What are two types of resistant M. tuberculosis?

A

*MDR-TB - multidrug-resistant TB
*XDR-TB - extremely drug resistant TB
-resistant to INH and RIF

92
Q

what is tuberculoid leprosy?

A

asymmetrical, shallow lesions, damage nerves- results in local loss of pain receptors
have fewer complications and more easily treated.

93
Q

what are skin lesions?

A

thin granulomas fewer bacilli, not progressive

94
Q

what is lepromatous leprosy?

A

*a deeply nodular infection that causes severe disfigurement of the face and extremities, widespread dissemination
*advanced cases have loss of feeling and tissues waste away in hand and feet due to loss of nerve function
*cooler region of body- thick granulomas= lepromas with more bacilli

95
Q

how do you diagnose tuberculoid leprosy and lepromatous leprosy?

A

*detection of acid-fast bacilli in skin lesions, nasal discharges, and tissue samples
*numbness in hands and feet, loss of heat and cold sensitivity, muscle weakness, thickened earlobes, chronic stuffy nose
*patient history

96
Q

how do you treat tuberculoid leprosy?

A

Rifampin + dapsone for 12 months

97
Q

how do you treat lepromatous leprosy?

A

1.) Rifampin + dapsone + clofazimine for minimum of 2 years
2.) then dapsone for 10 years

98
Q

Is there a vaccine for tuberculoid leprosy and lepromatous leprosy?

A

no vaccine available
India and Brazil use the tuberculosis vaccine for Hansen’s disease.

99
Q

What is Mycobacterium leprae?

A

causes Hansen’s Disease (leprosy)
strict parasite- has not been grown on artificial media or tissue culture.
slowest growing of all species; 30 degrees Celsius
100 cases per year in US; in the south, Cali, Hawaii
common: temperate, tropical and sub-tropical climates

100
Q

what is the course of infection for Mycobacterium leprae?

A

macrophages phagocytize the bacilli, but a weakened macrophage or slow T cell response may not kill bacillus.
incubation from 2-5 years years; if untreated, bacilli grow slowly in the skin macrophages and Schwann cells of peripheral nerves.

microbiology (7 decks)

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