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M2.2 Flashcards

1
Q

spore-forming gram positive
rods
aerobic, nonmotile, box-car-shaped

A

Bacillus anthracis

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2
Q

spore-forming gram positive
rods
aerobic, motile,
reheated fried rice

A

Bacillus cereus

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3
Q

Bacillus anthracis

Capsule?
Motility?
Hemolysis?
Sensitivity to Penicillin?

A

Capsule Present
Motility Non-Motile
Hemolysis Non-hemolytic
Sensitivity to Penicillin
Susceptible
String of pearls
reaction on Mueller
Hinton agar with
Penicillin

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4
Q

Bacillus cereus

Capsule?
Motility?
Hemolysis?
Sensitivity to Penicillin?

A

Absent

Motile

Wide zone of beta
hemolysis

Resistant

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5
Q

BACILLUS ANTHRACIS
CHARACTERISTICS

A

• aerobic, gram-positive box-car like rods
• nonmotile
• spore-forming
• Medusa head morphology
o dry “ground glass” surface and irregular edges with
projections along lines of
inoculation

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6
Q

BACILLUS ANTHRACIS

HABITAT AND TRANSMISSION

A

Soil

contact with infected animals or inhalation of
spores from animal hair and wool

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7
Q

BACILLUS ANTHRACIS

PATHOGENESIS: VIRULENCE FACTORS

A

antiphagocytic capsule
Edema factor (EF)
Lethal factor (LF)
Protective antigen (PA)

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8
Q

BACILLUS ANTHRACIS

antiphagocytic capsule

calmodulin-dependent adenylate cyclase

inhibits a signal transduction in cell division

mediates the entry of the other two components into cell

A

poly-D-glutamate
Edema factor (EF)
Lethal factor (LF)
Protective antigen (PA)

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9
Q

BACILLUS ANTHRACIS

SPECTRUM OF DISEASE

A

Cutaneous, Inhalational, Gastrointestinal Anthrax

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10
Q

BACILLUS ANTHRACIS

Cutaneous Anthrax

A

direct epidermal contact with spores causes formation of a
malignant pustule with subsequent eschar and central
necrosis
o 20% mortality rate

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11
Q

BACILLUS ANTHRACIS

Inhalational Anthrax

Chest X-ray?

A

woolsorter’s disease
1. inhaled spores from animals
2. weaponized preparations (bioterrorism)
o prolonged latent period (2 mos) before rapid deterioration

hemorrhagic mediastinitis
-germination of spores in the mediastinal lymph nodes

Mediastinal widening
o pulmonary hemorrhage, pleural effusion, meningeal
symptoms

o 100% mortality rate without immediate treatment

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12
Q

BACILLUS ANTHRACIS

Gastrointestinal Anthrax

A

UGI ulceration, edema and
sepsis (rapidly progressive course)
o mortality rate approaches 100%

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13
Q

cutaneous anthrax

TREATMENT

A

DOC is ciprofloxacin

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14
Q

inhalational/gastrointestinal anthrax

TREATMENT

A

DOC is ciprofloxacin or doxycycline with one or two
additional antibiotics (rifampin, vancomycin, penicillin, imipenem, clindamycin, clarithromycin)

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15
Q

Which of the following is an important virulence factor of Bacillius
anthracis?
A. Calcium dipicolinate
B. Pili
C. Lipopolysaccharide
D. Protective antigen

A

D. Protective antigen

mediates the entry of the other two
components into cell

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16
Q

BACILLUS CEREUS

HABITAT AND TRANSMISSION

A

grains

reheated fried rice

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17
Q

BACILLUS CEREUS

PATHOGENESIS

A

Heat-Labile Enterotoxin
Heat-Stable Enterotoxin

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18
Q

BACILLUS CEREUS

PATHOGENESIS

A

Heat-Labile Enterotoxin
Heat-Stable Enterotoxin

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19
Q

BACILLUS CEREUS

cholera-like enterotoxin causes ADP-ribosylation,
increasing cAMP

A

Heat-Labile Enterotoxin

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20
Q

BACILLUS CEREUS

staphylococcal-like enterotoxin functions as superantigen

A

Heat-Stable Enterotoxin

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21
Q

BACILLUS CEREUS

SPECTRUM OF DISEASE

A

Food poisoning
Emetic form, diarrheal form
Ophthalmitis

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22
Q

BACILLUS CEREUS

EMETIC FORM

Implicated food?
Incubation period (hours)?
Symptoms?
Duration?
Enterotoxin?

A

Implicated food Rice

Incubation period (hours) < 6 (mean, 2)

Symptoms
Vomiting, nausea,
abdominal cramps

Duration
(hours) 8 – 10 (mean, 9)

Enterotoxin Heat-stable

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23
Q

BACILLUS CEREUS

DIARRHEAL FORM

Implicated food?
Incubation period (hours)?
Symptoms?
Duration?
Enterotoxin?

A

Meat, vegetables

> 6 (mean, 9)

Diarrhea, nausea,
abdominal cramps

20 – 36 (mean, 24)

Heat-labile

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24
Q

BACILLUS CEREUS

Ophthalmitis

A

after traumatic penetrating eye injuries with
a soil-contaminated object

complete loss of light perception within 48 hours of injury

vancomycin, clindamycin, ciprofloxacin or gentamicin

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25
spore-forming gram positive rods anaerobic, tennis-racket-like
Clostridium tetani
26
spore-forming gram positive rods anaerobic, bulging cans
Clostridium botulinum
27
spore-forming gram positive rods anaerobic, bulging cans
Clostridium botulinum
28
spore-forming gram positive rods anaerobic, lecithinase gas-forming
Clostridium perfringens
29
spore-forming gram positive rods anaerobic, pseudomembranes
Clostridioides difficile
30
CLOSTRIDIUM TETANI CHARACTERISTICS
• anaerobic, gram-positive, spore-forming rods • spore is at one end (terminal spore) so organism looks like a tennis racket
31
CLOSTRIDIUM TETANI HABITAT AND TRANSMISSION
soil • entry through traumatic implantation into tissues with low oxygenation
32
CLOSTRIDIUM TETANI PATHOGENESIS
tetanus toxin (tetanospasmin) o Prevents release of GABA from Renshaw cells in spinal cord by cleaving of synaptobrevin
33
Tetanospasmin SITE OF ACTION
Presynaptic terminals Neuromuscular junction
34
Tetanospasmin SITE OF ACTION
Presynaptic terminals Neuromuscular junction
35
Tetanospasmin Presynaptic terminals MECHANISM OF ACTION and RESULT?
Inhibits release of GABA by cleavage of proteins critical for proper function of synaptic vesicle release Rigidity: trismus, risus sardonicus, opisthotonos, apnea/laryngospasm, dysphagia, ↑DTRs
36
Tetanospasmin Neuromuscular junction MECHANISM OF ACTION and RESULT?
Blocks neurotransmitter release Weakness or paralysis
37
Wound infection, multiplication of Clostridium tetani
No symptom
38
Tetanus toxin uptake into nervous system and VAMP cleavage in GABA inhibitory neurons After how many days? Initial symptoms?
7 - 10 days Muscle aches, trismus, myslgia
39
widespread disinhibition of motor and autonomic nervous system of tetanus toxin After how many hours? Clinical symptoms?
24 - 72 hrs Muscle spasm: local and generalized Cardiovascular instability: labile BP, tachy-/bradycardia Pyrexia, increased respiratory and Gl secretions
40
TETANUS PROPHYLAXIS Clean, minor wound
Uncertain or <3 doses Toxoid (TeANA) >3 doses Toxoid (TeANA) last dose >10 years
41
TETANUS PROPHYLAXIS Contaminated wound
Uncertain or <3 doses Toxoid (TeANA) TIG (ATS) >3 doses Toxoid (TeANA) last dose >5 years
42
CLOSTRIDIUM BOTULINUM CHARACTERISTICS
anaerobic, gram-positive, spore-forming rods
43
CLOSTRIDIUM BOTULINUM HABITAT AND TRANSMISSION
soil improperly preserved food o alkaline vegetables such as green beans, peppers, and mushrooms o smoked fish o canned goods (bulging) o honey
44
botulinum toxin
(heat-labile neurotoxin) blocks acetylcholine release causing flaccid paralysis (descending pattern) • eight immunologic types of toxin
45
most common in humans among eight immunologic types of botulinum toxin
types A, B, and E
46
a commercial preparation of exotoxin A uses?
Botox wrinkle removal, torticollis
47
CLOSTRIDIUM BOTULINUM SPECTRUM OF DISEASE: TOXIGENIC
Food-Borne Botulism Infant Botulism Wound Botulism
48
TRIAD OF BOTULISM
1. Symmetric descending flaccid paralysis (with prominent bulbar involvement) 2. Absence of fever 3. Intact sensorium
49
CLOSTRIDIUM BOTULINUM Food-Borne Botulism symptoms? bulbar signs? Sympa/para effects? paralysis?
eye symptoms § BOV, diplopia, ptosis, mydriasis bulbar signs (4 Ds): diplopia, dysphonia, dysarthria, dysphagia anticholinergic effects § dry mouth, constipation, abdominal pain bilateral descending flaccid paralysis respiratory paralysis
50
Infant Botulism
Floppy Baby Syndrome ingest spores found in household dust or honey
51
CLOSTRIDIUM BOTULINUM TREATMENT
TREATMENT • adequate ventilatory support • elimination of the organism from GIT o judicious use of gastric lavage and metronidazole or penicillin • trivalent botulinum antitoxin (types A, B, E)
52
Contamination of wound or punctured skin (common in IV drug users)
C. botulinum
53
CLOSTRIDIUM TETANI TREATMENT
• debridement of primary wound • Metronidazole (400mg rectally or 500 mg IV every 6 h for 7 days) is the preferred antibiotic. An alternative is penicillin (100,000– 200,000 IU/kg per day), although this drug theoretically may exacerbate spasms (Harrisons) • TIG (at the wound site) • Vaccination with tetanus toxoid o given in childhood and every 10 years thereafter
54
CLOSTRIDIUM PERFRINGENS Hemolysis? Growth on the?
• double hemolysis on blood agar • growth on egg-yolk agar o nonmotile but with rapidly spreading growth on culture media
55
CLOSTRIDIUM PERFRINGENS HABITAT AND TRANSMISSION
soil and human colon contamination of wound with soil or feces transmitted by ingestion of contaminated food
56
CLOSTRIDIUM PERFRINGENS SPECTRUM OF DISEASE: TOXIGENIC
Gas Gangrene Food Poisoning
57
CLOSTRIDIUM PERFRINGENS Gas Gangrene Toxin? Manifestation?
alpha toxin, a lecithinase o pain, edema and cellulitis with crepitation o hemolysis and jaundice are common
58
CLOSTRIDIUM PERFRINGENS Food Poisoning Toxin? characterized by? Known as?
production of enterotoxin which acts as superantigen characterized by watery diarrhea with cramps & little vomiting Stormy fermentation of milk
59
CLOSTRIDIUM PERFRINGENS TREATMENT
• wound debridement and penicillin for gas gangrene • supportive management for food poisoning
60
CLOSTRIDIOIDES DIFFICILE HABITAT AND TRANSMISSION
colon o 3% of the general population o up to 30% of hospitalized patients fecal-oral route hospital personnel
61
CLOSTRIDIOIDES DIFFICILE HABITAT AND TRANSMISSION
colon o 3% of the general population o up to 30% of hospitalized patients fecal-oral route hospital personnel
62
CLOSTRIDIOIDES DIFFICILE PATHOGENESIS
antibiotics o clindamycin, 2nd & 3rd gen cephalosporins, ampicillin exotoxins A (enterotoxin) and B (cytotoxin) inhibit GTPases, leading to apoptosis and death of enterocytes
63
CLOSTRIDIOIDES DIFFICILE exotoxin in stool detected by what effect where final phase by which viral cells infect cells? on what diagnostics?
cytopathic effect cultured cells or ELISA
64
pseudomembranes are the visual result of what toxins?
exotoxins A (enterotoxin) and B (cytotoxin) inhibit GTPases, leading to apoptosis and death of enterocytes
65
CLOSTRIDIOIDES DIFFICILE infection can precipitate ____ of ulcerative colitis
flare-ups
66
CLOSTRIDIOIDES DIFFICILE SPECTRUM OF DISEASE: TOXIGENIC
Pseudomembranous Colitis o Non-bloody diarrhea associated with pseudomembranes (yellow-white plaques) on the colonic mucosa o toxic megacolon can occur
67
CLOSTRIDIOIDES DIFFICILE TREATMENT
oral metronidazole oral vancomycin
68
OTHER CLOSTRIDIA Nontraumatic myonecrosis in immunocompromised patients
C. septicum
69
OTHER CLOSTRIDIA Toxic shock syndrome associated with septic abortion
C. sordellii
70
OTHER CLOSTRIDIA Traumatic wound infections
C. tertium
71
CORYNEBACTERIUM DIPHTHERIAE Also known as Motility? Shape? Granules? Culture?
Klebs-Loeffler bacillus non-motile club or comma-shaped rods arranged in V or L shape looks like Chinese characters metachromatic granules Reddish metachromatic (Babes-Ernst / Volutin) Potassium tellurite: dark black colonies Loeffler’s medium: after 12 hours of growth, stain with methylene blue.
72
for detection of toxigenicity CORYNEBACTERIUM DIPHTHERIAE
modified Elek test
73
injection of diphtheria exotoxin into the skin, to determine whether a person is susceptible to infection by diphtheriae
Schick test
74
CORYNEBACTERIUM DIPHTHERIAE HABITAT AND TRANSMISSION
• habitat is human throat • transmission via respiratory droplets
75
CORYNEBACTERIUM DIPHTHERIAE PATHOGENESIS
exotoxin inhibits protein synthesis by adding ADP-ribose to elongation factor-2 (EF-2) o subunit A, has ADP-ribosylating activity o subunit B, binds the toxin to cell surface o exotoxin encoded by b-prophage pseudomembranes death of mucosal epithelial cells
76
CORYNEBACTERIUM DIPHTHERIAE PATHOGENESIS
exotoxin inhibits protein synthesis by adding ADP-ribose to elongation factor-2 (EF-2) o subunit A, has ADP-ribosylating activity o subunit B, binds the toxin to cell surface o exotoxin encoded by b-prophage pseudomembranes death of mucosal epithelial cells
77
ABCDEFG of Diphtheria
ADP-ribosylation Beta-prophage Corynebacterium Diphtheriae Elongation Factor-2 Granules (metachromatic)
78
ABCDE of beta-prophage- encoded toxins
ShigA-like toxin (EHEC) Botulinum toxin Cholera toxin Diphtheria toxin Erythrogenic toxin (S. pyogenes)
79
CORYNEBACTERIUM DIPHTHERIAE SPECTRUM OF DISEASE
prominent thick, gray, pseudomembranes over tonsils and throat
80
pseudomembranes complications
o airway obstruction o Myocarditis - A-V conduction block, dysrhythmia o Neural involvement: peripheral nerve palsies, GBS, palatal paralysis, neuropathies, cranial nerve and/or muscle paralysis
81
CORYNEBACTERIUM DIPHTHERIAE TREATMENT
Erythromycin Macrolides Penicillin G
82
LISTERIA MONOCYTOGENES Shape? Motility? Hemolysis? Paradoxical growth in?
• aerobic, non-spore-forming, gram-positive rods • arranged in V- or L-shape • tumbling motility • narrow zone of beta-hemolysis • cold enhancement: paradoxical growth in cold temperature
83
LISTERIA MONOCYTOGENES HABITAT
• colonizes GI and female GUT • widespread in animals, plants, and soil
84
LISTERIA MONOCYTOGENES TRANSMISSION
• across placenta or by contact during delivery • ingestion of unpasteurized milk products, e.g., cheese
85
LISTERIA MONOCYTOGENES PATHOGENESIS
• internalin: interacts with E-cadherin on the surface of cells • Listeriolysin: escape from phagosomes • actin rockets (actin polymers): propels the bacteria through the membrane of one human cell and into another
86
LISTERIA MONOCYTOGENES SPECTRUM OF DISEASE
Early-Onset Neonatal Listeriosis Late-Onset Neonatal Listeriosis Adult Listeriosis
87
Early-Onset Neonatal Listeriosis Aka? Transmission? Characterized by? Complicated by?
(granulomatosis infantiseptica) o transplacental transmission o characterized by late miscarriage or birth complicated by sepsis, multiorgan abscesses, and disseminated granulomas
88
Late-Onset Neonatal Listeriosis Transmission? manifests as?
transmitted during childbirth meningitis or meningoencephalitis
89
Adult Listeriosis
o bacteremia, sepsis, or meningitis in pregnant, elderly, or immunocompromised individuals
90
LISTERIA MONOCYTOGENES TREATMENT PREVENTION
ampicillin with or without gentamicin pregnant women and immunocompromised patients should not ingest unpasteurized milk products or raw vegetable
91
ERYSIPELOTHRIX RHUSIOPATHIAE catalase, oxisdase, and indole? H2S?
• gram positive rod • negative • H2S producer- unique among gram positive rods
92
ERYSIPELOTHRIX RHUSIOPATHIAE TRANSMISSION Highest risk?
Distributed in land and sea animals worldwide Acquired by direct inoculation from a contaminated source Highest risk : fishermen, handlers, abattoir workers
93
Ersipeloid Aka? Pus?
ERYSIPELOTHRIX RHUSIOPATHIAE Seal finger or Whale finger Pus is not present (to differentiate from Staphylococcal/ Streptococcal infection)
94
Ersipeloid TREATMENT
Penicillin G– drug of choice for severe infections • Intrinsically resistant to vancomycin
95
ACTINOMYCES ISRAELII CHARACTERISTICS
GRAM POSITIVE BACTERIA WITH BRANCHING FILAMENTS anaerobe (normal oral flora)
96
ACTINOMYCES ISRAELII SPECTRUM OF DISEASE
local trauma (broken jaw or dental extraction) Lumpy Jaw- cervicofacial actinomycosis Abscesses that drain through sinus tracts Pelvic inflammatory disease in those with IUDs Physical exam reveals hard, non-tender swelling with sinus tracts draining sulfur granules
97
ACTINOMYCES ISRAELII TREATMENT
prolonged treatment with Penicillin G • consider surgical excision and drainage
98
NOCARDIA ASTEROIDES CHARACTERISTICS
aerobic (normal oral flora) weakly acid fast • setting aerobic, filamentous gram-positive rods with aerial hyphae
99
NOCARDIA ASTEROIDES HABITAT and TRANSMISSION
Habitat: soil and water Transmitted by inhalation of particles from soil
100
NOCARDIA ASTEROIDES main manifestation Immunocompromised Immunocompetent
Subacute to chronic pulmonary infection Pulmonary infection; Mimics TB with negative PPD Cutaneous infection after trauma; spreads to CNS as brain abscesses
101
NOCARDIA ASTEROIDES TREATMENT
Cotrimoxazole Tmpsmx
102
Identified by McFadyean Reaction
Bacillus anthracis
103
A 28/M worker has a 2 day history of fever, cough, dyspnea. He presents in the ER in tripod position, altered sensorium with O2 sat of 86% at room air. ABG showed metabolic acidosis. Patient was intubated but still unstable. Patient then expired at the ER. PMHx (+) DM uncontrolled (+) asthma. Personal Hx: alcoholic drinker, worker in a factory of linen and fabric from sheep fleece. What is the most likely diagnosis? a. CAP b. Asthma exacerbation c. Diabetic ketoacidosis d. Anthrax
d. Anthrax
104
Anthrax In relation to the case above, what is the MOST LIKELY cause of death? a. Pulmonary hemorrhage b. Pleural effusion c. Hemorrhagic stroke d. Cardiac tamponade
a. Pulmonary hemorrhage
105
Anthrax What radiologic finding would be compatible with the case above? a. Meniscus sign b. Widened mediastinum c. “Thumbprint sign” d. Lemon shaped hyperdensity
b. Widened mediastinum
106
T o which of the following clinical entities is the expected cause of the death of the patient in the above case similar to? a. Weil’s syndrome b. Congenital rubella c. Legionnaires disease d. All of the above
a. Weil’s syndrome
107
Which of the following drugs have coverage for the causative agent of Woolsorter’s disease? a. Penicillin and Ciprofloxacin b. Monoclonal antibody c. Doxycycline d. All of the above
d. All of the above
108
Muscles affected: Sardonic smile Lock jaw Opisthotonus
Orbicularis oris Muscles of mastic Lateral pterygoid Temporalis muscle Spinalis muscles Errector spinal
109
Possesses an alpha-toxin (lecithinase)
Nagler’s reaction
110
Which of the following drugs can precipitate pseudomembranous colitis? a. Clindamycin b. Cephalexin c. Amoxicillin d. All of the above
d. All of the above
111
What is the drug of choice in treating pseudomembranous colitis? a. Vancomycin IV b. Vancomycin PO c. Clindamycin d. All of the above
b. Vancomycin PO
112
Causes bull neck diphtheria
Corynebacterium
113
Psychrophile
LISTERIA
114
Causes of neonatal meningitis
- Group B strep - E. coli - Listeria
115
Meningitis - Very young (neonate) and very old: - Children: - Adolescent: - Adult:
Meningitis - Very young (neonate) and very old: E. coli - Children: Haemophilus influenzae - Adolescent: Neisseria meningitidis - Adult: Pneumococci

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