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Microbiology > Exam2Lec4Neisseria, Haemophilus, & Anaerobes > Flashcards

Exam2Lec4Neisseria, Haemophilus, & Anaerobes Flashcards

1
Q

What is the morphology of the genus Neisseria ?

A

Gram negative cocci

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2
Q

What are the two important species of neisseria?

A

Gonorrhoeae

meningitidis

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3
Q

Where is neisseria found?

A

around and inside of neutrophils

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4
Q

What is the spectrum of the disease (neisseria)?

A

Systemic, life-threatening disease

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5
Q

neisseria meingococci is found where?

A

Upper respiratory tract

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6
Q

neisseria gonococci is found where?

A

Genital tract

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7
Q

Details of neisseria species

A

gram negative, non-motile encapsulated, diplococcus, kidney shaped

aerobic but can grow without oxygen as a facultative anaerobe

fastidious growth

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8
Q

What media does neisseria species grow on? and for how long?

A

modified Thayer-martin medium or chocolate agar for 48 hours

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9
Q

What is the host of neisseria meningitidis ?

A

humans are the only natural hosts

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10
Q

What is the portal of entry of neisseria meningitidis?

A

nasopharynx

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11
Q

What are 3 major factors/ virulence factors of n. meningitidis?

A

Pili: colonization of nasopharynx–> become transient flora

Capsule–>systemic spread: bacteremia and meningitis

lps/los

No Man Picks Chick Last

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12
Q

What are the diseases of neisseria meningitidis ?

A

SPAMS Baby Daddy
Purpura fulminans
Meningitis
Septicemia
bacteremia
Arthritis
Shock
Death

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13
Q

What causes systemic spread of neisseria meningitidis ?

A

capsule

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14
Q

How can we classify N. meningitidis ?

A

Serogroups
–polysaccharide capsule: A,B, C, Y, W-135

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15
Q

What is the importance of serogroups of N.meningitdis?

A

Relation to disease:
-certain serogroups relate to disease
-public health tracking of outbreaks
-Development of vaccines

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16
Q

Protection of N.meningitidis requires what?

A

antibodies and complement

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17
Q

What is the N.meningitidis vaccine?

A

-Groups A,C, Y and W-135 polysaccharide conjugated to protein carrier (diphtheria toxoid Menactra®)
-Recommended for all 11-12 year olds, others based on risk factors
-Separate group B vaccine

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18
Q

What is the age recommendation for n.meningitdis vaccine?

A

11-12 years old

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19
Q

Clinical case :
- 3 year old baby is taken to the ER -fever & lethargy for 1 day, petechial rash & purpuric lesions, listless
- Blood cultures, IV antibiotics, hospital
- Lumbar puncture - CSF – white blood cells, (94% PMNs)
- Blood cultures positive for Gram negative diplococci,

A

N. meningitdis

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20
Q

What is the treatment of N.meningitis

A

antibiotics: penicillin, third generation cephalosporin (vefotazime, ceftriaxonr)

MEDICAL EMERGENCY

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21
Q

What is the symptoms of N. Meningitis?

A

Stiff neck
petechial rash
purpuric lesions
WBC in CSP
Gram negative diplococci in blood

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22
Q

What are the virulence factors of N. gonorrhoeae?

A

CROP LIP
Pili: responsible for attachment to host epithet cells

IgA protease: cleaves IgA molecule

Capsule

OPA: assist piling attachment

LOS: endotoxin activity

Por proteins: forms pores through outer membrane

Rmp proteins: inhibits cidal activity of serum

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23
Q

What are the surface factors of N. gonorrhoeae ?

A

Pili
IGA protease
Capsule
Opa
LOS

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24
Q

Role of pili in N. gonorrhoeae

A

Responsible for attachment to host epithelial cells

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25
Q

Role of IgA protease in N. gonorrhoeae

A

Cleaves IgA molecule

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26
Q

role of capsule in N. gonorrhoeae

A

avoid phagocytosis

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27
Q

role of opa in N. gonorrhoeae

A

assist in pili in attachment

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28
Q

role of LOS in N. gonorrhoeae

A

Endotoxin activity

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29
Q

Why is neisseria gonorrhoeae such a successful pathogen

A

antigenic variation

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30
Q

Example antigenic variation

A

Multiple copies (10-15) of pilin gene

Recombination (splicing) of one of the copies of the pilin gene (pilS) with the control regions (pilE)

Recombination within PilS

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30
Q

What is the clinical presentation of N. gonorrhoeae ?

A

Urethritis
Cervicitis
Salpingitis
proctitis
Pharyngitis
Arthritis
conjunctivitis
PID
Septicemia

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31
Q

What is the reservoir for N. gonorrhoeae

A

humans only reservoir-asymptomatic carrier

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32
Q

Who is at the highest risk for n. gon?

A

Teens and young adults

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33
Q

What is the transmission of N. gonorrhoeae

A

Sexual contact primary

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34
Q

What is the clinical presentation in men of N. gonorrhoeae ?

A

-usually symptomatic

-2 to 7 days post infection:
urethral discharge “the drips”
dysuria

complications are rare

rectal and pharyngeal infections

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35
Q

Female or male have higher chance of complication of n. gonorrhea

A

female

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36
Q

Female or male are more symptomatic

A

males

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37
Q

What is the clinical presentation of n. gonorrhea in WOMEN?

A

-frequently mild or asymptomatic
-vaginal discharge, dysuria, abdominal pain
-complications are common (10-20% of cases)
-ascending genital infection causes salpingitis, and PID
-rectal and pharyngeal infections

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38
Q

Both male and females infected with N. gonorrhea can get?

A

rectal and pharyngeal infections

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39
Q

What is PID (N. gonorrhea)?

A

Pelvic inflammatory disease

Complication of untreated N. gonorrhea

painful and may require surgical drainage or in severe causes hysterectomy

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40
Q

What is DGI ( N. gonorrhea )?

A

Disseminated gonococcal infection

N. gonorrhea in cirulatory system

Commonly includes septic arthritis

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41
Q

What is opthhalmia neonatorum (N. gonorrhea)? IMP

A

conjuctivitis resulting from vaginal delivery with infected mother

prevented with eye drops

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42
Q

How do we diagnosis gonorrhea

A

Direct Gram stain - effective for urethral discharge in symptomatic men

Gram (-) diplococci

Culture on chocolate agar or selective media

Oxidase +

Utilization of glucose confirmatory

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43
Q

What is the oxidase result of n. gonorrhea

A

positive–> purplish

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44
Q

What is the oxidase result of n. gonorrhea

A

positive–> purplish

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45
Q

What is the treatment of n. gonorrhea?

A

3rd generation cephalosporin with azithromycin and doxycycline

penicillin resistance now common due to mutated PBP and plasmid encoded beta-lactamase

sexual contacts should be treated to prevent “ping pong” infections

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46
Q

What is n. gonorrhea resistant to

A

penicillin resistance now common due to mutated PBP and plasmid encoded beta-lactamase

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47
Q

n. gonorrhea can be prevented through what ?

A

education and safe sex

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48
Q

What is the morphology of haemophilus influenzae ?

A

Gram negative coccobacilli

Fastidious

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49
Q

H. influenzae can have strain that contain what?

A

may have polysaccharide capsule which determines serotype (a-f) -invasive disease

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50
Q

what version of H. influenzae is not as invasive

A

non-encapsulated

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51
Q

What are the virulence factors of H. influenzae

A

Capsule
Endotoxin
IgA protease
Pili for adherence

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52
Q

Where do non encapsulated varieties of H. influenzae colonize? where does it spread?

A

upper respiratory tract

spread locally- otitis media, sinusitis, bronchitis, pneumonia

53
Q

What does non-encapsulated H.influenzae cause

A

otitis media, sinusitis, bronchitis, pneumonia

54
Q

Where do we see encapsulated varieties of H.influenzae?

A

disease in unimmunized children

55
Q

What do the cell wall components of encapsulated H.influenzae cause?

A

impair ciliary function-damage of respiratory epithelium, enter blood

56
Q

Encapsulated H.influenzae causes what?

A

meningitis, epiglottis, cellulitis

57
Q

What is the old H.influenzae vaccine?

A

polysaccharide vaccines

58
Q

why do we not use H.influenzae polysaccharide vaccines ?

A

because there was not a good immune response

59
Q

What is the new H.influenzae vaccine?

A

Conjugated vaccine

60
Q

What are the symptoms of H. influenzae epiglottitis?

A

Cherry red swollen epiglottis
Fever
score throat
hoarseness
barking and cough

progresses rapidly into medical emergency

61
Q

What is the treatment of H. influenzae epiglottitis

A

antibodies treatment (3rd generation of cephalosporin)

Airway maintenance needed

62
Q

What is the carrier rates of H. influenzae?

A

as high as 80% in children

20-50% in adults

Humans only source

63
Q

If there is a breakout of H. influenzae, what are people treating with?

A

Rifampin

64
Q

Professor said when you see childcare/daycare to think of…

A

H. influenzae

65
Q

Where is the energy derived from in anaerobic bacteria

A

fermentation

66
Q

What is toxic to anaerobic bacteria

A

oxygen

67
Q

Anaerobic bacteria are normal flora where?

A

oral cavity and GI tract

68
Q

Anaerobic wound infection are often ____

A

polymicrobial

synergism

69
Q

What is the morphology of clostridium

A

gramp positive rods-spore formers

Extra detail: Ubiquitous

70
Q

Why clostridium can cause disease?

A

Spore formation

Some have rapid growth in nutritionally enriched, oxygen-deprived environments

Exotoxins

71
Q

What is the morphology of C. perfringens?

A

Large rectangular gram positive rod

72
Q

does C. perfringens grow fast or slow

A

fast

73
Q

what are virulence factors of C. perfringens

A

Alpha-toxin
Beta toxin
Epsilon toxin
Iota toxin

ALL EXOTOXINS

74
Q

C. perfringens’s exotoxins can act as ___

A

superantigens

Binds to outside of MHC Class II cleft to stimulate T cell activity

75
Q

What is C. perfringens clinical disease?

A

Cellulitis: Swollen, red area of skin that feels hot and tender

Fasciitis: Inflammation of connective tissue

Myonecrosis: Localized death of muscle cell fibers

Food poisoning: most common

76
Q

is C. perfringens always dangerous?

A

No: Colonize wounds with no clinical significance
BUT
—1 week after exposure can lead to intense pain, extensive muscle necrosis, shock, renal failure and death – within 2 days.

77
Q

How do we diagnosis C. perfringens?

A

Culture for 1 day

some immunoassays

78
Q

How do we treat C. perfringens skin infections?

A

Antibiotics – penicillin

Debridement

Hyperbaric oxygen

79
Q

How do we treat C. perfringens food poisoning

A

maintain hydration

80
Q

What is the morphology of c. tetani

A

Large, spore-forming rod
Terminal spores

extra detail: Ubiquitous

81
Q

Is C. tetani easy or hard to grow ?

A

hard- very sensitive to oxygen

82
Q

What are the virulence factors of C. tetani

A

Spores

2 toxins:
Tetanolyisin
Tetanospasmin

83
Q

What is tetanolysin in C. tetani

A

toxin

oxygen labile hemolysis

84
Q

What is tetanospasmin in C. tetani ⭐️

A

Oxygen-labile neurotoxin
Produced during stationary growth phase
Responsible for the clinical manifestations of tetanus, spastic and rigid paralysis

85
Q

What does the tetanospasmin do in C. tetani?⭐️

A

blocks the release of inhibitor transmitters (ex.GABA) so if we block this we will have constant excitatory transmitters

TOXIN BINDING IS IRREVERSIBLE

86
Q

tetanus disease relate to ____

A

to distance of wound from the CNS

87
Q

What is generalized tetanus ? ⭐️

A

Most common form
-Masseter muscles (trismus or lockjaw)

-Sustained contraction of the facial muscles is called risus sardonicus

-Drooling, sweating

88
Q

What is localized tetanus

A

Disease confined to musculature at site of primary infection

Example is cephalic tetanus

89
Q

What is neonatal tetanus

A

Infection of the umbilical stump
Developing countries
90% fatal

90
Q

How do we diagnosis c. tetani

A

Confirmational

Tissue debridement

91
Q

How do we treat c. tetani

A

Antibiotics – metronidazole

Passive immunization with human tetanus Ig

92
Q

what preventive measures do we have for c. tetani

A

Vaccination (toxoid)

93
Q

What is the morphology of C. botulinum

A

Large Gram positive spore forming rod

93
Q

What is the morphology of C. botulinum

A

Large Gram positive spore forming rod

94
Q

what is the virulence factor of C. botulinum ?

A

botulinum toxin

95
Q

what does the botulinum toxin result in? ⭐️

A

Result is flaccid paralysis

96
Q

how does the botulinum toxin work?

A

Large progenitor protein (A-B toxin)

Complexed with non-toxic proteins – protects in digestive tract

Heavy chain binds sialic acid receptors and glycoproteins on motor neuron surfaces and stimulates endocytosis of the toxin

Botulinum neurotoxin remains at the neuromuscular junction

Inactivation of proteins regulating release of acetylcholine, blocking neurotransmission at peripheral cholinergic synapses

97
Q

what are the clinical diseases of c. botulism

A

Classic or food borne

infant

wound

inhalation

98
Q

What causes food borne botulism

A

Home canning - one taste leads to disease – eating toxin

Usually an intoxication

99
Q

What are the symptoms of food borne botulism

A

Blurred vision, dry mouth, abdominal pain

Bilateral descending weakness – flacid paralysis

100
Q

what causes infant botulism

A

infection of spores

consumption of honey with spores then they germinate

101
Q

What is the treatment of c. botulinum

A

Ventilatory support

Use of trivalent botulinum antitoxin

Antibiotics for wound infection

102
Q

C. difficile is considered what?

A

antibiotic-associated GI diseases
-Treat with antibiotics – kills some normal flora
-Result can be an overgrowth of Clostridium difficile
——-Benign, self-limited diarrhea
——-Severe, life-threatening pseudo-membranous colitis

103
Q

The benign version of C.difficile causes what?

A

self limited diarrhea

104
Q

The severe version of C.difficile causes what?

A

life-threatening pseudo-membranous colitis

105
Q

What are the two toxin in C.difficile?

A

Enterotoxin (Toxin A)
—–Chemotactic for neutrophils
—-Cytopathic effect – disrupts tight cell-cell junctions, leading to greater permeability of the intestinal wall and diarrhea

Cytotoxin (Toxin B)
—–Actin depolymerization - destruction of the cellular cytoskeleton

106
Q

Toxin A of C.difficle is what

A

enterotoxin

Chemotactic for neutrophils

Cytopathic effect – disrupts tight cell-cell junctions, leading to greater permeability of the intestinal wall and diarrhea

107
Q

Toxin B of C. difficile is what

A

cytotoxin

Actin depolymerization - destruction of the cellular cytoskeleton

108
Q

What percentage of people have c.diff as normal flora

A

5% but higher in hospitalized patients

109
Q

How is c.diff diagnosis is confirmed by____

A

by enterotoxin or cytotoxin detection

110
Q

What is the morphology of c.diff

A

Anaerobic Gram+ spore-forming bacillus

111
Q

What does C.diff cause?

A

Clostridium difficile-associated disease (CDAD)

Pseudomembranous colitis, toxic megacolon, sepsis, and death

112
Q

what is the C.diff transmission

A

Fecal-oral transmission through contaminated environment and hands of healthcare personnel

113
Q

What is a major risk factor for disease with c.diff

A

Antimicrobial exposure

Acquisition and growth of C. difficile
Suppression of normal flora of the colon

114
Q

What is the mutant of c.diff in health care facilities?

A

NAP1 mutant
-Increased toxin production
-Produces new toxin
-Also causes community associated diarrhea

115
Q

How is c.diff diagnosis ?

A

Isolation of bacterium from stool by anaerobic culture

Identification of toxin from stool

116
Q

How is C.diff treated?

A

Discontinue antibiotic therapy

Vancomycin or metronidazole for severe disease

Bacteriotherapy aka fecal transplant

117
Q

Clinical example:
An 80-year-old woman was treated for a UTI with ampicillin. Several days later she developed fever and diarrhea. The stool sample was positive for the toxin associated with which of the following bacteria?

A.Clostridium botulinum
B. Neisseria meningitidis
C. Clostridium difficile
D. Haemophilus influenzae
E. Staphylococcus aureus

A

C

118
Q

A 5-year-old boy wakes his parents in the middle of the night. He had a high fever (40C) and shortness of breath. The child was brought to the hospital and an X-ray of the lateral neck revealed swelling of the epiglottis. Which of the following bacteria is MOST LIKELY to be the etiological agent of his illness?

a.Haemophilus influenzae
b. Streptococcus pneumoniae
c. Streptococcus pyogenes
d. Neisseria meningitidis
e. Clostridium tetani

A

a

119
Q

Which one of the following is NOT an important characteristic
of either Neisseria gonorrhoeae or Neisseria meningitidis?
(A) Polysaccharide capsule
(B) IgA protease
(C) M protein
(D) Pili

A

c

120
Q

Three organisms, Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae, cause the vast majority of cases of bacterial meningitis. What is the MOST important pathogenic
component they share?
(A) Protein A
(B) Capsule
(C) Endotoxin
(D) β-Lactamase

A

b

121
Q

Each of the following statements concerning Clostridium
perfringens is correct EXCEPT:
(A) It causes gas gangrene.
(B) It causes food poisoning.
(C) It produces an exotoxin that degrades lecithin and causes
necrosis and hemolysis.
(D) It is a gram-negative rod that does not ferment lactose.

A

d

122
Q

Each of the following statements concerning Clostridium tetani
is correct EXCEPT:
(A) It is a gram-positive, spore-forming rod.
(B) Pathogenesis is due to the production of an exotoxin that
blocks inhibitory neurotransmitters.
(C) It is a facultative organism; it will grow on a blood agar plate
in the presence of room air.
(D) Its natural habitat is primarily the soil.

A

c

123
Q

Each of the following statements concerning gonorrhea is correct EXCEPT:

(A) Infection in men is more frequently symptomatic than in
women.
(B) A presumptive diagnosis can be made by finding gram-
negative kidney bean-shaped diplococci within neutrophils in a urethral discharge.
(C) The definitive diagnosis can be made by detecting antibodies
to Neisseria gonorrhoeae in the patient’s serum.
(D) Gonococcal conjunctivitis of the newborn rarely occurs in
the United States, because silver nitrate or erythromycin is
commonly used as prophylaxis.

A

c

124
Q

Each of the following statements concerning neisseriae is correct EXCEPT:
(A) They are gram-negative diplococci.
(B) They produce IgA protease as a virulence factor.
(C) They are oxidase-positive.
(D) They grow best under anaerobic conditions.

A

d

125
Q

Each of the following statements concerning wound infections
caused by Clostridium perfringens is correct EXCEPT:
(A) An exotoxin plays a role in pathogenesis.
(B) Gram-positive rods are found in the exudate.
(C) The organism grows only in human cell culture.
(D) Anaerobic culture of the wound site should be ordered.

A

c

126
Q

Each of the following statements concerning Neisseria
meningitidis is correct EXCEPT:
(A) It is an oxidase-positive, gram-negative diplococcus.
(B) It contains endotoxin in its cell wall.
(C) It produces an exotoxin that stimulates adenylate cyclase.
(D) It has a polysaccharide capsule that is antiphagocytic.

A

c

127
Q

CASE: Your patient is a 20-year-old woman with the sudden onset of fever to 104°F and a severe headache. Physical examination reveals nuchal rigidity. You suspect meningitis and do a spinal tap. Gram stain
of the spinal fluid reveals many neutrophils and many gram-negative diplococci. Of the following bacteria, which one is MOST likely to be the
cause?

(A) Haemophilus influenzae
(B) Neisseria meningitidis
(C) Streptococcus pneumoniae
(D) Pseudomonas aeruginosa

A

b

128
Q

CASE: Your patient is a 70-year-old man with a long history of smoking who now has a fever and a cough productive of greenish sputum. You suspect pneumonia, and a chest X-ray confirms your suspicion.
596. If a Gram stain of the sputum reveals very small gram-negative rods and there is no growth on a blood agar but colonies do grow on chocolate agar supplemented with NAD and heme, which one of the following bacteria is the MOST likely cause?
(A) Chlamydia pneumoniae
(B) Legionella pneumophila
(C) Mycoplasma pneumoniae
(D) Haemophilus influenzae

A

d

129
Q

CASE: Your patient is a 70-year-old man with a fever of 40°C and a
very painful cellulitis of the right buttock. The skin appears necrotic, and there are several fluid-filled bullae. Crepitus can be felt, indicating gas in the tissue. A Gram stain of the exudate reveals large gram positive rods. Of the following, which one is the MOST likely cause?
(A) Clostridium perfringens
(B) Bacillus anthracis
(C) Corynebacterium diphtheriae
(D) Actinomyces israelii

A

a

Microbiology (18 decks)

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