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Y3 Medical Micro > L7.2 Anaerobic +ve and Atypical organisms > Flashcards

L7.2 Anaerobic +ve and Atypical organisms Flashcards

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USMLE® Step 1 flashcards
1
Q

why is a mollicute an atypical organism

A

very small

no cell wall

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2
Q

why are rickettsia, coxiella and chlamydia atypical organisms

A

very small

obligate intracellular

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3
Q

what bacterium are in the mollicutes

A

mycoplasma

ureaplasma

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4
Q

what phylum of bacteria are mollicutes

A

tenericutes
low GC
soft skinned no cell wall

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5
Q

are mollicutes sensitive to antibiotics

A

resistant to those targeting cell wall as haven’t got one

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6
Q

what shape are mollicutes

A

pleomorphic

coccoid and rod

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7
Q

what is important to consider for mollicutes contamination

A

very small so can pass through filters - cell culture contaminants

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8
Q

what do mollicutes require

A

sterols
vitamins
nucleic acid precursors

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9
Q

are mollicutes saprophytic or parasitic

A

both

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10
Q

what is characteristic of mycoplasma pneumoniae

A

extracellular - smallest free living bacterium

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11
Q

where does mycoplasma pneumoniae infect

A

mostly mild upper respiratory tract infections
less opften atypical pneumonia and tracheobronchitis
other manifestations are rare (cardiac, neurologic, skin)

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12
Q

who does mycoplasma pneumoniae infect

A

worldwide; primarily infects school age children

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13
Q

what are the virulence factors for m. pneumoniae

A

P1 adhesin protein
superantigen proteins in cell membrane
toxins

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14
Q

how is mycoplasma pneumoniae spread

A

nasal secretions

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15
Q

how can mycoplasma pneumoniae infect again

A

immunity not life-long- can get again as adult

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16
Q

where do Mycoplasma hominis, Mycoplasma genitalium and Ureaplasma urealyticum colonise

A

genitourinary tract

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17
Q

how many people carry Mycoplasma hominis

A

15%

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18
Q

how many people carry Ureaplasma urealyticum

A

45-75%

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19
Q

what does M. genitalium and U. urealyticum cause

A

non-gonococcal urethritis

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20
Q

what does M. hominis cause

A

pelvic inflammatory disease (female upper genital tract infection) pyelonephritis (kidney inflammation)

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21
Q

what group are rickettsiaceae and anaplasmataceae in

A

rickettsiales - alpha proteobacteria

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22
Q

what group are coxiellaceae in

A

gamma proteobacteria

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23
Q

what is the difference in the cell wall for orientia

A

no peptidoglycan

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24
Q

what is the difference in the cell wall for rickettsia

A

minimal peptidoglycan

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25
Q

what do orientia and rickettsia cause

A

various forms of typhus and related diseases, depending on species

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26
Q

what is the reservoir for orientia and rickettsia

A

animals/arthopods

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27
Q

how do orientia and rickettsia invade cells

A

phagocytosis
escape from phagosome (phospholipase!)
Multiply in cytoplasm until cell dies (typhus group) or are constantly released (spotted fever group)

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28
Q

how if orientia and rickettsia diagnosed

A

microscopy
microimmunofluorescence (uses antibodies against LPS and OM proteins)
PCR-based assays, depending on species

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29
Q

what is the treatment for orientia and rickettsia

A

tetracycline, fluoroquinolones, chloramphenicol, depending on species

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30
Q

what does coxiella burnettii cause

A

causes Q fever
most are asymptomatic or mild flue-like symptoms
5% hepatitis, pneumonia, fevers
Chronic Q fever: can lead to endocarditis (significant mortality; mostly predisposed patients, e.g. immuno-suppressed)

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31
Q

what are the different coxiella burnettii variants

A

small cell variants (stress resistant)

large cell variants (metabolically active)

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32
Q

how is coxiella burnettii diagnosed

A

serological methods (immunofluorescence antibody and ELISA)

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33
Q

what type of pathogen is coxiella burnettii

A

intracellular

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34
Q

what are the reservoirs for coxiella burnetti

A

arthropods
birds
mammals: farm animals and pets

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35
Q

how is coxiella burnetti spread

A

resistant form can survive for years in soil, milk, faeces

infection via inhalation of contaminated material

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36
Q

what is an infectious dose of coxiella burnetti

A

≤10 bacteria

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37
Q

how is coxiella burnetti diagnosed

A

serological methods immunofluorescence antibody and ELISA

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38
Q

what is the treatment for coxiella burnetti

A

doxycyline; vaccines for humans and animals available

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39
Q

what is chlamydiaceae

A

obligate intracellular parasite

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40
Q

how do chlamydiaceae get energy

A

believed to use host ATP

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41
Q

what size are chlamydiaceae and why is this important

A

small can pass through 0.45uM filters

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42
Q

what are the 2 forms of chlamydiaceae in the lifecycle

A

elementary bodies

reticulate bodies

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43
Q

what is the chlamydiaceae lifecycle

A

elementary bodies invade in vacuole/phagosome, multiply in there convert to reticulate bodies
all in RB state = inclusion bodies (as vacuoles so big)
convert back to EB
cell lyse infect
cycle start again

44
Q

what is the biovars of chlamydia trachomatis

A 
trachoma (and urogenital infections)
lymphogranuloma venereum (LVG)
45
Q

what infection does chlamydia trachomatis cause

A

trachoma: infection of the eye (conjunctiva)

urogenital infections

46
Q

what is the chlamydia trachomatis trachoma infection cause

A

scar inner surface of eye lids = eyelids turn inwards = erosion/ulceration of cornea = blindness

47
Q

what is the chlamydia trachomatis urogenital infection cause in men

A

urethritis, epididymitis, infertility

48
Q

how is chlamydia trachomatis transmitted

A

sexual transmission

49
Q

what are the symptoms of chlamydia trachomatis

A

mainly asymptomatic
80% women
25% men

50
Q

what is the chlamydia trachomatis disease spread in body like

A

progressive - genital ulcer may lead to, swelling of lymph nodes which may rupture, forming fistulas

51
Q

what is the chlamydia trachomatis, chlamydia pneumoniae and chlamydia psittaci diagnosis

A

culture (requires viable cells)
serology, now routinely nucleic acid amplification tests (NAATs)
glycogen accumulation in inclusions of C. trachomatis

52
Q

what does chlamydia pneumoniae cause

A

community acquired pneumonia

53
Q

who does chlamydia pneumoniae infect

A

may be subclinical but more severe in elderly and asthmatics

60-80% of people worldwide become infected, but uncommon in childhood

54
Q

what does chlamydia psittaci cause

A

ornithosis – from birds
flu-like symptoms
more severe systemic infection

55
Q

what is the treatment for chlamydia trachomatis, chlamydia pneumoniae and chlamydia psittaci

A

doxycycline

macrolides

56
Q

are clostridium spore forming

A

yes

57
Q

what metabolism do mollicutes have

A

saccharolytic or proteolytic

58
Q

what are the clinical manifestations of clostridium

A

gas gangrene
food poisoning
tetanus
antibiotic associated diarrhoea

59
Q

where is clostridium perfringens a commensal

A

human and animal gut

60
Q

what is the shape of clostridium perfringens

A

rod

61
Q

what is the growth of clostridium perfringens like

A

rapid- fastest growing organism

62
Q

what does clostridium perfringens make

A

toxins

haemolytic enzymes

63
Q

what are the lethal toxins of clostridium perfringens

A

alpha
beta
epsilon
iota toxin

64
Q

what is the the effect of clostridium perfringens type A

A

causes most human infections

largest amount of alpha toxin

65
Q

effect of clostridium perfringens alpha toxin

A

lecithinase (phospholipase C), lyses many cell types - causes massive haemolysis, tissue destruction etc.

66
Q

what causes clostridium perfringens double zone haemloysis

A

alpha and theta toxins

67
Q

where does clostridium perfringens infect

A

soft tissue

68
Q

what is cellulitis

A

localised gas formation in soft tissue

69
Q

what is suppurative myositis

A

pus in muscle planes

70
Q

what is myonecrosis

A

rapid muscle tissue destruction, gas gangrene

71
Q

how can you become infected by clostridium perfringens

A

food poisoning

meat products with high spore (type A) numbers - survive heating and germinate if food not cooled

72
Q

what does clostridium perfringens type C cause

A

clostridial necrotizing enteritis

tissue destruction in jejunum

73
Q

what is the treatment for myositis and myonecrosis

A

must be initiated immediately

surgical removal of tissue and high dose penicillin

74
Q

how is myositis and myonecrosis diagnosed

A

microscopy/culture (rapid growth)

75
Q

what is the metabolism of clostridium tetani

A

proteolytic

76
Q

what is clostridium tetani sensitive to

A

oxygen

77
Q

what are the spores of clostridium tetani like

A

highly heat resistant

ubiquitous in soil, manure

78
Q

what toxin does clostridium tetani have

A

tetanospasmin - heat labile neurotoxin

79
Q

what is the lethal dose of clostridium tetani

A

2.5ng/kg

80
Q

what does the clostridium tetani tetanospasmin do

A

blocks neurotransmitter release of inhibitory synapses = spastic paralysis
death by asphyxia/sudden cardiac arrest

81
Q

what is the treatment for clostridium tetani

A

tetanus immunoglobulin, antibiotics (penicillin)

potent vaccine exists

82
Q

where is clostridium tetani

A

ubiquitous

83
Q

what does clostridium tetani contaminate

A

water food

84
Q

what are the clostridium tetani toxins

A

7 main toxin types A-G

85
Q

which clostridium tetani toxins are associated with human disease

A

A, B, E, F

86
Q

how are clostridium tetani protected in digestive tract

A

complexed with non toxic proteins

87
Q

effect of clostridium tetani toxin

A

inactivates proteins needed for acetylcholine release = no n=muscle excitation = flaccid paralysis = respiratory failure

88
Q

what are the types of clostridium tetani infection

A

foodborne botulism
infant botulism
wound botulsim

89
Q

what is infant botulism from

A

spores in honey, dust

90
Q

what is the treatment for clostridium tetani

A

removed undigested food, give antitoxin and intensive therapy

91
Q

what does clostridium difficle cause

A

antibiotic associated diarrhoea

92
Q

how does clostridium difficle infect

A

spores spread infection

93
Q

where is clostridium difficle a normal part of flora

A

gut of healthy individuals
2/3 babies
3% young adults

94
Q

what disrupts the clostridium difficle to cause infection

A

heavy colonisation of gut following disruption of microflora:
antibiotics
chemotherapy
colonic obstruction

95
Q

what toxins does clostridium difficle make

A

toxin A - enterotoxin

toxin B - sytotoxin

96
Q

what is the effect of the clostridium difficle toxins

A

mucosal inflammation
apoptosis
diarrhoea

97
Q

what is different about the clostridium difficle toxins

A

synergistic, but A or B-negative isolates both appear to be able to cause disease

98
Q

what are the clostridium difficle diagnostics

A

immunoassay for toxin in stool/ nucleic acid amplification tests (NAATs)

99
Q

what is the treatment for clostridium difficle

A 
discontinue antibiotics (mild cases)
metronidazole or vancomycin
faecal transplants are an option! microflora from healthy = injected into gut
100
Q

what makes an organism atypical

A

size
cell wall
life cycle

101
Q

which group is

clostridium

A

low GC

firmicutes

102
Q

what is the ‘respiration’ of clostridium

A

strictly anaerobic - oxygen tolerance varies

103
Q

anaerobic cocci examples

A

Peptostreptococcus

104
Q

how are chlamydia trachomatis biovars grouped

A

subdivided in serovars (based on Major Outer Membrane proteins), associated with specific diseases

105
Q

what are bacterial stain are rickettsia, coxiella and chlamydia

A

negative

106
Q

what is the chlamydia trachomatis urogenital infection cause in women

A

women: urethritis, cervicitis, pelvic inflammatory disease, infertility or ectopic pregnancy

107
Q

what is the chlamydia trachomatis urogenital infection cause in babies

A

transmission to baby at birth: infant pneumonia, conjunctivitis, middle ear infection

Y3 Medical Micro (16 decks)

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