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Pathology > Neisseria, Haemophilus and Bordetella > Flashcards

Neisseria, Haemophilus and Bordetella Flashcards

1
Q

What Gram are Neisseria?

A

Gram Negative

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2
Q

What part of N. meningitidis results in septic shock?

A

The lipopolysaccharide (endotoxin) of Neisseria meningitidis is a potent stimulator of inflammation resulting in the septic shock syndrome.

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3
Q

What are the 4 general characteristics of Neisseria?

A
  1. Gram-negative “kidney bean” diplococci
  2. Endotoxic lipopolysaccharide complexed with protein in outer membrane
  3. Growth enhanced in CO2
  4. Fastidious species require enriched media (chocolate agar)
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4
Q

Are Neisseria oxidase positive or negative?

A

OXIDASE POSITIVE

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5
Q

What is the only sugar N. gonorrhea oxidizes?

A

Glucose

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6
Q

What sugars does N. meningitidis oxidize?

A

Glucose and Maltose

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7
Q

What immune component is required to fight Neisseria?

A

Complement

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8
Q

What 2 structures confer virulence to Neisseria menigitidis?

A

Pili - attachment

Capsule - bloodstream invasion and survival and possibly CNS penetration

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9
Q

What is the pathogenesis of Neisseria meningitidis?

A
  1. Attachment - microvilli of nonciliated nasopharyngeal cells via pili
  2. Traverse cell in vesicle to submucosa
  3. Damage ciliated cells
  4. Bloodstream survival enhanced by antiphagocytic
    polysaccharide capsule
  5. Endotoxin mediated activation of complement leading to shock and hemorrhage
  6. CNS inflammation generated by cell wall peptidoglycan, LPS, other bacterial products and is mediated by IL-1 and TNF
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10
Q

What are the clinical manifestations of N. meningitidis infection?

A
  1. Respiratory colonization followed by overt disease or transient carrier state
  2. Meningitis
  3. Skin: petechiae → purpura
  4. Meningococcemia: shock, hemorrhage and purpura,
    destruction of adrenals
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11
Q

What are the identifying features of N. meningitidis in the lab?

A
  1. Gram smear- Cerebrospinal fluid (CSF)
  2. Cultures- CSF, blood, skin
  3. Cultures – Oxidase positive, oxidize glucose and maltose
  4. Nonselective media (blood or chocolate agar)
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12
Q

What is the main treatment for N meningitides?

A

Penicillin - resistance uncommon

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13
Q

What serotype is not used in N. meningitides vaccines?

A

Serogroup B cannot be used in the vaccine as it is non-immunogenic

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14
Q

What is PorB of N. gonorrhea?

A

PorB - Outer membrane protein I (Por proteins) – Porin

a. Pores (channels) in organism
b. Facilitates epithelial cell invasion

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15
Q

What is Opa of N. gonorrhea?

A

Opa - adherence proteins confer opaque appearance to colony which results from Opa-mediated adherence between cells

Opaque associated with localized
Transparent disseminated

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16
Q

What 2 things contribute to the antigenic diversity of N. gonorrhea?

A

Pili - Antigenic variation

Opa – Phase variation

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17
Q

How does pili antigen variation occur in N. gonorrhea?

A

Genetic recombination by transfer of variable sequences form unexpressed (silent) loci, pilS to expression locus, pilE

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18
Q

How does Opa phase variation occur in N gonorrhea?

A

Can switch on and off as many as 11 different Opa

genes throughout the genome creating variation

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19
Q

What is the transmission of N. gonorrhea?

A

Mucosal transmission (genital, mouth, anus, eye) by direct contact

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20
Q

What is the pathogenesis of N. gonorrhea?

A
  1. Attachment via pili and Opa
    Genetic variation of ligands evades immune responses
  2. Invasion and damage
    a. Epithelial cell invasion involves PorB and other outer membrane proteins
    b. Epithelial cell invasion has been demonstrated in salpingitis, but role in uncomplicated mucosal infection not demonstrated
    c. Lipopolysaccharide and peptidoglycan fragments incite inflammatory response
  3. Spread
    a. Prostate, epididymis and paracervical glands by direct
    extension
    b. Possibly carried by sperm to fallopian tubes
    c. Serum resistant strains invade the bloodstream and
    disseminate to skin, joints
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21
Q

What are the clinical manifestations of N. gonorrhea?

A

Urethritis
Cervicitis
Prostatitis and pharyngitis - often asymptomatic
Conjunctivitis

22
Q

How does N. gonorrhea evade the immune system?

A

a. Antigenic and phase variation evade immune response
b. Resist phagocytosis (Opa and pili)
c. IgA 1 protease
d. Evade serum antibody and complement mediated killing
e. Bind “blocking antibodies” to Rmp – Reduction Modifiable Protein

23
Q

What are the methods for the identification of N. gonorrhea?

A

Gram Stain (95% sensitive in men; less in women)
Culture
Gene Amplification

24
Q

What is the treatment for N. gonorrhea?

A

Ceftriaxone PLUS azithromycin

Antibiotic resistance is a BIG problem with N. gonorrhea

25
Q

What are the characteristics of Haemophilus influenzae?

A

It is a small Gram-negative coccobacilli

Grows on chocolate agar (lysed blood)

26
Q

What factors does H. influenzae require to grow?

A 
X factor (hematin)
Y factor (NAD)
27
Q

What is the main virulence factor of H. influenzae?

A

Type B capsule - polyribitol phosphate (PRP)

28
Q

What led to the drastic decrease in the rate of H. influenzae infection?

A

Type B decreased the rate of it by 94%

29
Q

What is the transmission of H. influenzae?

A

Respiratory droplets

30
Q

What is the transmission of N. meningtidis?

A

Respiratory droplets

31
Q

What is the pathogenesis of H. influenzae?

A
  • Adhere - Pili, OMPs
  • Transcytose like Neisseria
  • Encapsulated strains invade bloodstream
  • Endotoxin - local and systemic inflammation
32
Q

What are the clinical manifestations of Type B H. influenzae?

A

a) Meningitis - children

33
Q

What are the manifestations of unencapsulated H. influenzae?

A

a) Otitis media
b) Acute and chronic sinusitis
c) Bronchitis

34
Q

What is the treatment for H. influenzae?

A

Ampicillin
Cephalosporins

Vaccine as preventative measure

35
Q

H. parainfluenzae Disease

A

Respiratory

36
Q

H. aegyptius Disease

A

Conjunctivitis

37
Q

H. (Aggregatibacter) aphrophilus Disease

A

Endocarditis

38
Q

H. ducreyi Disease

A

Chancroid (STD)

39
Q

What are the characteristics of Bordella pertussis?

A

Aerobic

Gram-negative coccobacilli

40
Q

What are the main virulence factors of B. pertussis?

A
  • Adhesins
  • Pertussis Toxin
  • Tracheal cytotoxin - peptidoglycan fragment
41
Q

What is the function of Pertussis Toxin?

A

AB subunit - A - S1 enzymatic, B – S2-S5 binding Subunits

A catalyzes ADP (from NADP) ribosylation of a
cellular regulatory protein (G- protein) which prevents inactivation of activated adenylate cyclase

B subunits bind to receptors on ciliated respiratory cells and phagocytic cells

Biologic effects of PT include: Increased respiratory secretions, mucus production and lymphocytosis

42
Q

What is the function of Tracheal cytotoxin?

A

Tracheal cytotoxin – fragment of peptidoglycan that binds to and causes extrusion of ciliated respiratory epithelial cells. The toxin also stimulates IL-1 release (fever)

43
Q

What is the function of Dermonecrotic toxin?

A

Dermonecrotic toxin – causes ischemic necrosis

44
Q

What is B. pertussis transmitted by?

A

Spread by airborne droplets, highly infectious

45
Q

What is the reservoir of B. pertussis?

A

Sub-clinical adults

46
Q

What is the pathogenesis of B. pertussis?

A
  1. B. pertussis attaches to ciliated epithelial cells by adhesins
  2. Tracheal cytotoxin and possibly other toxins destroy ciliated
    cells, extrude them from border
  3. Adenylate cyclase exerts inhibitory effects on phagocytic cells
  4. Pertussis toxin produces systemic manifestations including enhanced respiratory secretions and mucus production
    contributing to cough as well as lymphocytosis
  5. Lipopolysaccharide – stimulates cytokine release
47
Q

What are the clinical manifestations of B. pertussis?

A

Catarrhal stage - rhinorrhea, fever, sneezing, anorexia

Paroxysmal cough - up to 50 times a day for 2-4 weeks.
Inspiratory whoop, vomiting, mucoid secretions, marked
lymphocytosis

Convalescent stage - cough gradually fades

48
Q

What is required for B. pertussis culture?

A

Specialized media – Regan-Lowe charcoal medium

49
Q

What is the treatment for B. pertussis?

A

Azithromycin, clarithromycin, erythromycin

50
Q

What are the vaccines available for B. pertussis?

A

DTaP, which contains one of the acellular pertussis vaccines, made from purified, detoxified pertussis toxin (PT), filamentous hemagglutinin (Fha), and Pertactin (Pn).

A dose of vaccine containing a reduced amount of pertussis antigens, Tdap, is recommended for all adults in place of a routine.

Pathology (203 decks)

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