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FM 2 > Non-enteric GN Bacteria > Flashcards

Non-enteric GN Bacteria Flashcards

1
Q

Neisseria meningitidis: Sources

A

human nasopharynx; part of normal microbiota

Obligate human pathogen

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2
Q

Neisseria meningitidis: types of infection

A

Nasopharyngeal colonization

Meningitis
• Leading cause of acute bacterial meningitis in teens, young adults

Sepsis
• Sequelae: gangrene, ampuatation

Disseminated intravascular coagulation (DIC) with petechial rash progressing to purpurae

Waterhouse-Friderichsen syndrome: adrenal infarction

Sequelae (of meningitis):
• Cranial nerve damage: deafness (CV VIII), blindness
• Brain damage and cognitive dysfunction: seizures, learning disorders, speech problems

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3
Q

Haemophilus influenzae: sources

A

o Source: nasopharynx

• Aerosol transmission via respiratory droplets

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4
Q

Haemophilus influenzae: types of infection

A
  • Meningitis
  • Sepsis
  • Cellulitis
  • Mastoiditis
  • Epiglottitis
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5
Q

Moraxella catarrhalis: sources

A

asymptomatic colonization of nasopharynx (especially in children)

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6
Q

Moraxella catarrhalis: types of infection

A
  • Upper respiratory infection

* Otitis media

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7
Q

Bordetella pertussis: source

A

aerosol transmission (highly contagious)

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8
Q

Bordetella pertussis: types of infection

A
  • Tracheobronchitis

* Whooping cough

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9
Q

Pseudomonas aeruginosa: source

A

ubiquitous in environment

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10
Q

Pseudomonas aeruginosa: types of infection

A

usually aerobic sites
Skin, nail, and soft tissue infections
• Ex: folliculitis after pool or hot tub use

Otitis externa
• Complication: malignant otitis externa: disease extends to surrounding tissues and bones

Burn and wound infections
• Loss of protective barrier function
• Tissue damage disturbs vascular supply → diminished host immune response

Ocular infections (ex. From contact lens solution)
• Keratitis (corneal inflammation)
• Ulceration
• “Corneal melt” from hydrolytic enzymes

Bacteremia
• If have hematogenous dissemination → Ecthyma gangrenosum
• Deep ulcerative and necrotic skin lesions
• Usually in neutropenic host

Infective endocarditis

Lung infections
Hospital acquired pneumonia; ventilator associated pneumonia
Mucoid strains colonizing CF patients (leading cause of death)
• Genotypically and phenotypically distinct strains
• Establish a persistent biofilm
• By ages 3-7, nearly all CF patients have Pseudomonas colonized in oropharynx and upper respiratory tract
Contributing factors:
o Thick viscous mucous secretions
o Decreased mucociliary clearance
o Decreased host phagocyte function
o Mutant CFTR may serve as Pseudomonas receptor (attachment effect)
Long term therapies:
o Chest percussion = loosen secretions
o Continuous or intermittent antibiotic prophylaxis

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11
Q

Neisseria meningitidis: Risk factors

A

High incidence in “meningitis belt” of sub-Saharan Africa; during Muslim pilgrimage (Hajj) to Mecca

B lymphocyte or Ab deficiencies

Anatomic or functional asplenia
• From trauma, sickle cell disease

Deficiency in 1 or more terminal complement components (C5-9) [Also a risk factor for disseminated gonococcal infection]

Communal living conditions
• Promotes aerosol spread
• Nasopharyngeal colonization
• Bloodstream invasion and meningitis

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12
Q

Neisseria meningitidis: pathogenesis

A

o Invades bloodstream
o Transits to CNS
o Results in sepsis and meningitis
o High morbidity and mortality = death may occur within hours

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13
Q

Neisseria meningitidis: virulence factors

A

Capsule = anti-phagocytic
• Serogroups expressing different capsular polysaccharides: A, B, C, Y, W-135, etc.
• Specific anticapsular Ab fosters opsonization and phagocytosis of encapsulated microbes

Pili and other adhesions

Cell wall components LPS/ endotoxin and peptidoglycan
• Damage host mucosal cells
• Facilitates bloodstream invasion
• Neisserial LPS has few side chains = “Lipo-oligosaccharide” or LOS

Immune evasion
• Surface proteins (pilin and Opa), capsule, and LOS = antigenic variation
• Variability interferes with host immune response
• IgA protease secretion = degrades IgA

Readily takes up/releases DNA → phenotype switching

Iron acquisition
• Via surface proteins
• Bind host iron-containing proteins (transferrin, lactoferrin)

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14
Q

Prevention of Neisseria meningitidis

A

Acquired humoral immunity protects from invasive disease (not from colonization)
o Specific Abs against capsule or other surface component → opsonization and phagocytosis or complement-mediated bactericidal activity
• Maternal Abs in neonates from passive acquisition
• Ab derived from vaccine (capsular polysaccharides)
• Ab derived from nasopharyngeal colonization
• By meningococcal
• By related microbiota (ex: N. lactamica) with cross-reactive epitopes

Functional spleen
• Major lymphoid organ
• Lots of B lymphocytes and macrophages

Functional terminal complement components (C5-9)
• Form membrane attack complex (MAC) → complement-mediated lysis

Vaccination with MCV4 quadrivalent serogroup A/C/Y/W-135 capsular polysaccharide protein (diphtheria toxin) conjugate vaccine
• Does not cover serogroup B

Prophylactic antibiotics for close contacts of index cases:
• Rifampicin
• Fluoroquinolone
• Cephalosporin
• Essential features: efficacy against meningococci and good penetration into mucosal secretions

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15
Q

Treatment of Neisseria meningitidis

A

o Typically broad spectrum treatment with initial presentation
• Cover other potential etiologic agents
o Penicillin or cephalosporin
o Chloramphenicol (in parts of world where low cost and easy storage are important; but has side effects of bone marrow suppression and aplastic anemia)
o Additional treatment:
• IV fluids
• Vasopressors
• Ventilator assistance
• Some cases: glucocorticoid replacement and anticoagulants

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16
Q

Neisseria meningitidis vs. Neisseria gonorrhoeae

A

Neisseria meningitidis
Host: Humans only
Transmission: Aerosol
Location: Nasopharynx
Virulence: Most determinants; including capsule
Sequelae: Sepsis; meningitis; significant morbidity and mortality
Invasion: Invasion leads to disease (sepsis, meningitis)
Incidence: Rare
Vaccine: Against some

Neisseria gonorrhoeae
Host: Humans only
Transmission: Sexually
Location: UG tract 
Virulence: Most determinants; NO capsule
Sequelae: PID, fallopian tube scarring, infertility, ectopic pregnancy, and cervicitis in females; neonatal ocular infection; urethritis in males
Invasion: Seldom invades (can cause rare disseminated gonococcal infection, septic arthritis) 
Incidence: Common (2nd bacterial STI)
Vaccine: none
17
Q

Encapsulated Haemophilus influenzae variants

A

Encapsulated = mainly type B H. influenza (Hib)
o Small GN coccobacillus (rod)

Transmission: aerosol via respiratory droplets

Pathogenesis: 
•	Entry from nasopharynx → blood → CNS
•	Results in sepsis and meningitis 
•	Rapid disease
•	Considerable mortality and morbidity

Virulence factors:
• Anti-phagocytic polysaccharide capsule
• Serotype b has capsule of polyribosyl ribitol phosphate

History:
• Formerly: main (70%) cause of meningitis in kids < 5 years
• Now: relatively rare (< 5 years
• Humoral immunity deficient (immunoglobulin or complement)
• Anatomic/functional asplenia

18
Q

Non-typable Haemophilus influenzae variants

A 
Diseases:
Nasopharyngeal colonization
•	Asymptomatic
•	Very common 
Vaginal colonization 
Sinusitis
Conjunctivitis
•	Major cause in older children
Otitis media
•	Along with S. pneumonia = most common causes
Bronchitis 
Pneumonia 
•	2nd most common cause of CAP in adults (after S. pneumonia)
Perinatal and neonatal infections:
•	Premature birth 
•	Chorioamnionitis
•	Postpartum sepsis in mother
•	Pneumonia, sepsis and meningitis in neonate
19
Q

Identify the infections caused by Moraxella catarrhalis

A

Upper respiratory tract infections in children
• Sinusitis
• Otitis media
• 3rd most common cause (after pneumococcus and NTHi)

Lower respiratory tract infections
• Bronchitis
• Pneumonia
• In people with underlying lung conditions (viral URI in kids, COPD in adults)

Infections: sepsis, meningitis, other disseminated infections
• In immunocompromised patients
• Ex: CF, neutropenia, SLE, leukemia

Nosocomial infections
• Especially in pulmonary or pediatric ICUs

20
Q

Characteristics of Bordetella pertussis

A

GN bacillus
o Slow growing
o Nutritionally fastidious (requires blood agar or synthetic media with growth factors like nicotinamide)
• Obligate human (primate) pathogen

No other environmental reservoir
o Adults = main reservoir for infection
• If unimmunized
• If vaccine immunity has waned since childhood

21
Q

Bordetella pertussis: virulence factors

A

Adhesins: Attachment to respiratory ciliated epithelial cells
• Filamentous hemagglutinin (FHA)
• Fimbriae/ pili
• Pertussis toxin

Tracheal cytotoxin (TCT)
•	Peptidoglycan fragment
•	Causes ciliostasis and ciliated epithelium damage/death

Pertussis toxin (PTx)
• A/B subunit exotoxin
• ADP ribosylation of a G protein → disrupts cAMP regulation → interferes with cell signaling
Local and systemic effects:
• Acts as an adhesin
• Disordered host phagocyte and lymphocyte function
• Decreased transit of lymphocytes from blood → lymph nodes = lymphocytosis
• Decreased bacterial clearance → Frequent secondary infections

Adenylate cyclase toxin
• Interferes with host signaling
Lethal toxin

22
Q

Bordetella pertussis: diagnosis

A

o Culture, PCR, Gram stain (during Catarrhal stage)

23
Q

Bordetella pertussis: prevention

A

Vaccination!
Old: Inactivated whole cell vaccine
• Part of DTP/DPT vaccines
• Associated with side effects
Newer vaccine: acellular bacterial component vaccines
• Has multiple purified bacterial components
• Part of DTaP/Tdap vaccines
• Low level of side effects
• Less durable/shorter-lasting immune response
• May be contributing to increased rates of pertussis

Current recommedations:
• DTaP series in infants and young children
• Tdap booster at 11-12 years
• Single pertussis booster in all adults (regardless of prior immunization or infection status)
• Tdap vaccination of women during each pregnancy

24
Q

Bordetella pertussis: treatment

A

Antibiotics for patient (macrolide like erythromycin)
• Useful during catarrhal stage
• May also decrease transmission to others
• Start treatment in symptomatic patient only when cough duration < 3 weeks

Respiratory isolation (only during catarrhal stage)

Antibiotic prophylaxis for close contacts if within 3 weeks of exposure

Supportive care once late whooping stage
•	Maintain respiratory status (oxygen or ventilator)
•	Nasal suctioning
•	Hydration
•	Nutrition 
•	Monitor for secondary infections
•	Hospitalization if necessary
o	Report to public health department
25
Q

Bordetella pertussis: pathogenesis

A

Catarrhal stage (1-2 weeks):
• Similar to common cold; non-specific symptoms:
• Fever
• Coughing
• Malaise
• Bacterial products damage respiratory epithelium
• Organism is present = antibiotics useful

Spasmodic, paroxysmal, toxemic, or whooping stage (weeks-months):
• Usually when diagnosed
• Intense cough with characteristic “whoop” (inspiratory gasp)
• “100-day” cough
• Respiratory epithelium denuded; ciliary ladder absent
• Organism may be present or cleared
• Antibiotics may be of little use

Convalesent stage:
• Gradual fading of cough
• Regeneration of respiratory epithelium, cilia, ciliary function

26
Q

Bordetella pertussis: Children vs. Adults

A 
Adult infections:
o	Less severe symptoms
•	Prolonged cough with nocturnal exacerbation
o	Easy transmission 
o	Main reservoir for infection

Childhood infections:
o Respiratory compromise: hypoxia, anpnea
o Dehydration from post-tussive vomiting
o Susceptibility to secondary infections (from loss of mucociliary ladder, damaged epithelium, and toxic effects on immune system)
• Pneumonia
• Otitis media
o Complications: seizures, encephalopathy, malnutrition, weight loss, failure to thrive

27
Q

Describe Pseudomonas aeruginosa

A

GN bacilius (rod) with aerobic predilection
o Simple nutritional requirements, not fastidious
o Oxidase positive
o Does not ferment lactose
o Flagellar motility
o Forms biofilms (quorum sensing)
o Blue-green pigments, UV fluorescence, fruity odor
• Ubiquitous in environment
• Resistant to broad range of disinfectants and antimicrobial agents
• Frequent exposures but rare infections
o Opportunistic pathogen = requires some breakdown in host defenses
o Typically very susceptible to host defenses

28
Q

Pseudomonas aeruginosa: virulence factors

A

Secreted exotoxins
• Ex: exotoxin A = protein synthesis inhibitor

Secreted hydrolytic enzymes (ex: elastase, phospholipase)

Pili

Polysaccharide capsule

Exopolysaccharide alginate slime = in mucoid stains from CF patients

29
Q

Name the 3 antibiotic classes used to treat Pseudomonas.

A
  • Fluoroquinolones (ciprofloxacin)
  • Beta-lactams (ceftazidine, imipenem, cefepime, meropenem, piperacillin)
  • Aminoglycosides (tobramycin)
30
Q

Describe the vaccines for Neisseria meningitidis, Haemophilus influenzae, and Bordetella pertussis, their target populations, and their role in preventing disease.

A

Neisseria meningitides
o MCV4 quadrivalent serogroup A/C/Y/W-135 capsular polysaccharide protein (diphtheria toxin) conjugate vaccine
o Does not cover serogroup B
• Has a capsule made of polysialic acid
• Not immunogenic in humans (similar to E. coli K1 capsule)
Vaccinate children: 2 months – 10 years with high-risk conditions:
• Complement deficiency
• Anatomic/functional asplenia
• Children 9 months and older residing or traveling in hyerendemic or epidemic areas, or present during outbreaks
Universal vaccination age 1-12 years
o Universal booster vaccination age 16 years
o Booster every 5 years with complement deficiency or anatomic/functional asplenia

Haemophilus influenza
o Hib polysaccharide conjugate vaccine
o Given 2-4 months; 2nd at 12-15 months

Bordetella pertussis
Old: Inactivated whole cell vaccine
• Part of DTP/DPT vaccines
• Associated with side effects
Newer vaccine: acellular bacterial component vaccines
• Has multiple purified bacterial components
• Part of DTaP/Tdap vaccines
• Low level of side effects
• Less durable/shorter-lasting immune response
• May be contributing to increased rates of pertussis
Current recommedations:
• DTaP series in infants and young children
• Tdap booster at 11-12 years
• Single pertussis booster in all adults (regardless of prior immunization or infection status)
• Tdap vaccination of women during each pregnancy

FM 2 (7 decks)

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