Gram-negative non-enteric bacteria Flashcards

1
Q
  1. Identify the sources of infection and types of infection caused by Neisseria meningitidis, Haemophilus influenza, Moraxella catarrhalis, Bordetella pertussis, and Pseudamonas aeruginosa.
A

N. meningitides: nasopharyngeal colonization, meningitis, sepsis
H. flu: meningitis, sepsis, cellulits, mastoid tis, epiglottis; non-typable: naspharyngeal colonization, vaginal colonization, sinusitis, conjunctivitis, OM, bronchitis, pneumonia (#2), perinatal and neonatal infections
Moraxella: URI, OM
B. pertussis: tracheobronchitis

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2
Q
  1. Describe how meningococi cause disease, how is prevented.
A

gram negative diplococcus
nasopharyngeal colonizer, aerosol transmission, humans are only host

causes fulminant bacteremia and septic shock with high fatality, characteristic disseminated intravascular coagulation (DIC) and petechial rash

sequelae: cranial nerve damage, brain damage, cognitive dysfunction, amputation

available tetravalent capsular polysaccharide conjugate vaccine (does not cover serogroup B- polysialic acid)

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3
Q
  1. Explain the pathogenesis and clinical features of Haemophilus influenza infection, distinguishing between serotype b encapsulated and nontypable variants.
A

H. flu: meningitis, sepsis, cellulits, mastoid tis, epiglottis; non-typable: naspharyngeal colonization, vaginal colonization, sinusitis, conjunctivitis, OM, bronchitis, pneumonia (#2), perinatal and neonatal infections

small gram neg. coccobacillus, now relatively rare cause of sepsis, meningitis, pneumonia, periorbital cellulitis, mastoiditis (elephant ear), epiglottitis

vaccine for type B, cases of illness mostly in children under 5

invasive infection as an extension from upper respiratory tract, epiglottis will produce stridor, thumb sign which is very serious (requires IV steroids)

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4
Q
  1. Identify the infections caused by Moraxella catarrhalis.
A

URI, OM (#3), sinusitis

usually in younger, immunocompromised, CF

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5
Q
  1. Describe how Bordetella pertussis infection is transmitted, diagnosed, prevented and treated.
A

gram negative bacillus, obligate human host

highly contagious via aerosol transmission, damage that persists considerably beyond clearance of bacteria

presents as a cold with worsening cough

prevented with vaccine

prevention: DTaP in infants and children, Tdap booster 11-12 yrs, single booster in adults, Tdap with pregnancy

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6
Q
  1. Compare and contrast pertussis in adults and children.
A

children have more potential complications, esp young children, including

respiratory compromise, susceptibility to secondary infections (pneumonia), dehydration from post-tussive vomiting
seizures, encephalopathy

adults usually have a prolonged cough with nocturnal exacerbation, although still transmissible, adults serve as a reservoir (unvaccinated or waned immunity)

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7
Q
  1. Explain how Pseudomonas aeruginosa acts as an opportunistic pathogen and list common sites of infection.
A

gram-negative rod with aerobic predilection, not fastidious
opportunistic lung, skin (nail soft tissue, otitis externa), eye (corneal inflammation esp with contacts), burn/wound, blood infection, infective endocarditis

often nosocomial

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8
Q
  1. Identify the characteristics of Pseudomonas aeruginosa that make it troublesome once infection is established.
A

secreted exotoxin A (protein synthesis inhibitor)
secreted hydrolytic enzymes (elastase, etc)
mucoid strains from CF patients

destroys vascular supply, diminishing host response

which have a natural resistance to disinfectants and many antibiotics (quinolones, some B-lactams)

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9
Q
  1. Name the 3 antibiotic classes used to treat Pseudomonas.
A

4th and 5th gen cephalosporins- cephapime
aminoglycosides- gentamyacin
floroquinolones- ciprofloxicin (except moxi)

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10
Q
  1. Describe the vaccines for Neisseria meningitidis, Haemophilus influenza and Bordetella pertussis, their target populations and their role in preventing disease.
A

N. men and H flu are based on a polysaccharide coat of the bacteria

Bordetella comes through the “tetanus” vaccine combo Tdap or TDaP

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11
Q

What is the major virulence factor of N. meningitides and relative host defense?

A

capsule that is antiphagocytic

capsule specific antibodies
functional spleen (B cells and macrophages)
Functional terminal complement components- MAC for complement-mediated lysis

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12
Q

How is meningitis treated and what are risk factors for development?

A
Risks:
B cell or antibody deficiencies
anatomic or functional asplenia
deficiency in terminal complement
communal living

epidemics in Africa (sub-Saharan) and Asia
on pilgrimage

Prevention: MCV4 (doesnt cover serogroup B), earlier vaccination with at risk groups, universal vaccine at 11-12 and 16 yrs, prophylactic antibiotics: rifampin, quinolones

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13
Q

How are N. meningitides and gonorrhoeae different?

A

NG seldom invades, and is much more common, NM have capsule, NG do not

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14
Q

What are the major virulence factors of B. pertussis. Explain the pathogenesis of whooping cough.

A

adhesions: attachment to respiratory ciliated epithelium (pertactin, FHA, fimbriae)

tracheal cytotoxin: epithelial damage

pertussis toxin: endotoxin causing decreased transit of lymphocytes from blood into lymph nodes, resulting in lymphocytosis

adenylate cyclase toxin (cell signaling)

bacterial products damage the respiratory epithelium in the catarrhal stage and spasmodic phase follow ending in the convalescent stage when epithelium is replaced

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15
Q

What is the treatment protocol for pertusis?

A

erthyromycin and others are only useful in catarrhal stage (may decrease transmission)

tx. <3 weeks since symptoms started, after only supportivee care (maintain respiratory status, nasal suctioning, hydration, nutrition)

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16
Q

Decribe how the pertusis vaccine has changed since its development?

A

inactivated whole cell vaccine in ’50s had substantial side effects

newer acellular bacterial component vaccines: less immunogenic, low side effects

recently there has been an unexpected waning of immunity- B. pertussis is also not lacking pertactin sometimes

17
Q

What is the causative agent of Ecthyma gangrenous?

A

deep ulcerative and necrotic skin lesions as a result of hematogenous dissemination form bacteremia of Pseudomonas (usually in a neutropenic host)