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Path > 2: Other URT infections > Flashcards

2: Other URT infections Flashcards

1
Q

what URT infections are caused by normal flora? mechanism by which this happens?

A

sinusitis, OM - secondary to blockage of sinus ostia, eustachian tube, by virally-induced or allergic inflammation

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2
Q

what are the four main normal flora dudes that cause URT infections? can these dudes cause meningitis? why or why not?

A

S. pneumoniae - G(+)
S. aureus - G(+)
H. influenzae, non type B - G(-)
M. catarrhalis - G(-)

no meningitis! b/c no capsule

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3
Q

symptoms of sinusitis

A
  • fever
  • pain to sinus palpation
  • purulent drainage at back of throat (can trigger asthma)
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4
Q

how can sinusitis/OM spread to become meningitis?

A

local infection -> invasive disease -> bacteremia -> systemic disease (inflammation of vessels allows crossing of BBB) -> once in CSF, no complement/opsonization -> grows -> meningitis

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5
Q

most common cause of invasive URT disease/meningitis in neonates

A
  • E. coli

- GBS

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6
Q

most common cause of invasive URT disease/meningitis in kids 1-5 y/o

A

now S. pneumoniae

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7
Q

most common cause of invasive URT disease/meningitis in adolescents/ young adults

A

N. meningitidis

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8
Q

most common cause of invasive URT disease/meningitis in all age groups

A

S. pneumoniae

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9
Q

what is the key to pathogenicity that allows some organisms to become systemic and cause meningitis?

A

ENCAPSULATION

  • allows persistence (evasion of immune system) to where it can reach blood (bacteremia), then dissemination, then endothelial cell/macrophage activation by LPS, then vascular leakage -systemic disease + through BBB and proliferate in CSF (no complement):
  • shock, DIC (disseminated intravascular coagulation)
  • meningitis
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10
Q

what actually kills the patient when they get meningitis from one of these guys?

A

the sepsis, DIC, shock

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11
Q

asplenia increases susceptibility to what organisms

A

encapsulated

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12
Q

describe capsule nature and implications for each:

  • pneumococcus
  • N. meningitidis
  • N. gonorrhea
  • H. influenzae type b
A
  • pneumo: PspC capsule: sepsis, meningitis
  • meningitidis: LPS capsule: DIC, sepsis, meningitis
  • gonorrhea: LOS capsule: septic arthritis
    * no sepsis, DIC, or meningitis!!
  • influenzae: LPS capsule: sepsis, meningitis
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13
Q

describe sepsis/shock

A

LPS stimulates TLRs (TLR4) to induce systemic cytokine secretion and endothelial cell activation -then increased vascular permeability, hypovolemia, shock, organ failure

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14
Q

describe DIC

A
  1. systemic activation of coagulation by bacteria

2. results in systemic microthrombi followed by hemorrhage after coagulation factors are used up - petechiae/purpura

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15
Q

what bug causes 95% of CA-pneumonias?

A

S. pneumoniae

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16
Q

what types of infections does S. pneumoniae cause?

A

normal flora -> secondary to obstruction/ other disease

MOPS: 
Meningitis 
OM 
Pneumonias (CA-lobar - often secondary to flu in elderly) 
Sinusitis
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17
Q

what is the most common cause of meningitis?

A

S. pneumoniae

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18
Q

lab findings in S. pneumoniae meningitis

A

in CSF:

  • bacteria
  • increased protein
  • increased PMNs
  • decreased glucose
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19
Q

what virulence factor of S. pneumoniae allows colonization of nasal mucosa?

A

IgA protease

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20
Q

what factors are associated with S. pneumoniae infections?

A
  • impaired immunity
  • malnutrition
  • alcoholism
  • age less than 2
  • sickle cell disease
  • any form of respiratory passage obstruction
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21
Q

what virulence factor of S. pneumoniae allows it to evade the immune system?

A

polysaccharide capsule (PspC) - antiphagocytic

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22
Q

other virulence factors of S. pneumoniae

A
  • pneumolysin (pore-forming and adherence)

- pspA (inhibits alternate complement pathway)

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23
Q

with S. pneumoniae, vaccines are effective for what age groups?

A

high risk groups: young and old

*different vaccines for young (conjugated) and old (not)

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24
Q

what does lobar pneumonia look like on XRay?

A
  • opaque (alveoli filled with pus, fibrin, and macrophages)

- fills entire lobe

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25
Q

talk to me about the pneumococcal conjugate vaccine (PCV13)

A

-for all kids 5 y/o or less + adults at risk

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26
Q

what vaccine should kids 2 y/o or less + high risk patients also get in conjunction to PCV13?

A

pneumococcal polysaccharide vaccine (PPSV23)

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27
Q

what vaccine(s) should all adults 65 or older + those 19 and older at risk receive?

A

PPSV23 only!

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28
Q

risk factors for S. pneumoniae

A
  • chronic diseases
  • immunodeficiency
  • asplenia
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29
Q

general characteristics about neisseria:

  • G(?)
  • capsule or no?
  • O2?
  • cofactors?
  • stable or labile in envt?
  • normal flora or no?
  • sensitivity?
A 
G(-) 
encapsulated 
aerobic/facultative anaerobe 
needs Fe 
labile in environment 
not normal flora 
sensitive to penicillin
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30
Q

entry and incubation of N. meningitidis

A

enters nasopharynx and colonizes mucosa, then invades
incubation less than 1w

associated with cluster outbreaks - dorms, military

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31
Q

what happens when N. meningitidis gets into blood?

A

bacteremia, then - purulent meningitis, sepsis:

  • DIC with petechiae, particularly on earlobes, extremities
  • ischemic necrosis/gangrene in limbs (amputation)
  • vascular collapse
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32
Q

diagnostic confirmation of N. meningitidis

A
  • examine CSF
  • gram stain!!!**
  • look at joint effusions for diplococci inside monocytes
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33
Q

what is an adrenal complication of N. meningitidis sepsis?

A

Waterhouse-Friderichson Syndrome:

  • adrenals fill w/ blood
  • if survive, end up with adrenal insufficiency b/c clot has compressed normal adrenal tissue
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34
Q

describe immune response to N. meningitidis

A

(antiphagocytic capsule) - Ab and complement-mediated phagocytosis

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35
Q

are vaccines effective for N. meningitidis

A

yes, for adolescents and adults

-but doesn’t cover B serotype, which is most common cause of disease in neonates

36
Q

describe entry of N. gonorrhea

A

attaches to columnar and transitional epithelia (pili) - mucosal membranes of the genital tracts, rectum, nasopharynx

37
Q

virulence factors for N. gonorrhea

A
  • LOS

- IgA protease (evades nasal mucosal immunity)

38
Q

diseases caused by N. gonorrhea + pathophysiology

A
  • gonorrhea
  • cystitis

supporative inflammation of mucosal surfaces and subepithelial tissues (grossly purulent lesions and discharge)

can cause supporative arthritis (knees, ankles) following bacteremia

39
Q

what has prevented an effective vaccine for N. gonorrhea?

A

antigenic variability between strains

40
Q

general characteristics of H. influenzae

A

G(-)
pleomorphic
type B = invasive, others noninvasive

41
Q

what does non-invasive H. influenzae cause?

A

URT infections, sinusitis, OM

  • most unencapsulated
  • form part of normal URT flora (40-60% for kids, 35% for adults)
42
Q

what does invasive H. influenzae cause?

A

meningitis, most commonly seen 1-6 y/o

  • most encapsulated
  • type B like an endotoxin - DIC
  • less than 10% have this as normal flora
43
Q

describe two other hemophilus species and what they cause

A

H. parainfluenzae: normal flora of mouth, may cause endocarditis

H. ducreyi: chancroids

44
Q

what is the window of susceptibility for invasive disease by H. influenzae type b?

A

3 mo - 3 y

-kids can’t make a good protective Ab response to type B capsular Ag’s

45
Q

general characteristics of M. catarrhalis

A

G(-)
diplococcus
normal flora of URT
LPS endotoxin, but rarely causes septicemia and meningitis

46
Q

why does M. catarrhalis not cause septicemia/meningitis even though it has LPS?

A

b/c capsule doesn’t evade immunity like Neisseria can

47
Q

what is the third most common cause of secondary bacterial infections such as sinusitis and OM?

A

M. catarrhalis

48
Q

mechanisms of pathogenesis for diphtheria

A
  • local epithelial necrosis (pseudomembrane formation)

- absorption and systemic release of exotoxin A (damage to distant organs - heart)

49
Q

mechanisms of pathogenesis for pertussis

A
  • cell-bound toxin with local epithelial inflammation
  • NO necrosis
  • swelling (narrowed epiglottis) - whooping of cough
50
Q

what is a pseudomembrane composed of?

A

coagulation of:

  • dead cells (neutrophils)
  • blood
  • pus
51
Q

general characteristics of bordetella pertussis

A

G(-)
pleomorphic coccobacillus
aerobic
highly communicable, but self-limiting

52
Q

histologic characteristic of pertussis

A

lymphocytosis!

53
Q

tropism of pertussis, how this plays in with pathology

A

brush border: exotoxin leads to local ciliary paralysis with secondary inflammation

54
Q

pertussis vaccine

A

gives immunization to exotoxin

  • DTaP 7 y/o or less
  • Tdap 10 y/o or more
55
Q

general characteristics of corynebacterium diphtheria

A

G(+)

rod

56
Q

action of diphtheria toxin when it goes systemic

A
  • inhibits protein synthesis in eukaryotic cells

- leads to fatty myocardial changes, myofiber necrosis, and polyneuritis

57
Q

what is the most common cause of death from diphtheria?

A

cardiac failure from exotoxin, NOT respiratory obstruction

58
Q

what two main diseases do you think of with G(-) rods?

A

UTIs

intra-abdominal infections

59
Q

general characteristics of G(-) rods

A

endotoxins: LPS
frequent drug resistance
has replaced pyogenic cocci as bulk of hospital-acquired and opportunistic infections

60
Q

G(-) rods UTIs

A

non-obstructive:
-E. coli

obstructive:
- Klebsiella
- Edwardsiella

61
Q

G(-) rods abdominal infections

A
  • perforation
  • appendicitis
  • cholecystitis
  • diverticulitis

last three are by obstruction

62
Q

two main ways of getting G(-) infections

A
  • spread of organisms that have colonized GI tract

- contamination of tissues and materials from the hospital

63
Q

when do E. coli cause disease?

A

when they gain access to tissues (peritoneum, urinary tract, sepsis) or secondary to tissue inflammation in abdomen (appendicitis, obstruction)

64
Q

can E. coli ferment lactose?

A

yes - coliform

65
Q

what are two GI non-coliforms?

A

S and S - Salmonella and Shigella

66
Q

E. coli types of infections

A
  • UTIs/cystitis
  • supporative infections of abdominal cavity (secondary to obstruction, or via perforation/trauma)
  • hemorrhagic bronchopneumonia in debilitated patients (due to aspiration)
  • G(-) sepsis - DIC/shock
67
Q

what is the cause of most uncomplicated UTIs in the absence of obstruction?

A

E. coli

68
Q

what pneumonia is associated with aspiration in the hospital setting?

A

Klebsiella

69
Q

infections caused by Klebsiella and Enterobacter

A
  • UTIs secondary to obstruction*
  • septicemia: associated with thick mucoid capsule
  • pulmonary infections that may result in necrotizing abscesses
70
Q

proteus mirabilis characteristics and infections

A

G(-)
rod
facultative anaerobe

UTI/pyelonephritis
pneumonia (debilitated patients)

71
Q

virulence factor of proteus mirabilis and implications

A

secretes urease (urea to ammonia)

  • alkaline urine
  • in chronic pyelonephritis, get staghorn calculi (bladder)
72
Q

serratia marcescens infections

A

pneumonia (debilitated patients)

UTIs

73
Q

pseudomonas aeruginosa general characteristics

A 
G(-) 
rod 
pyocyanin, pyoverdin
motile, flagellum 
aerobic 
no spores 
ubiquitous in hospitals - nosocomial/opportunistic 
associated with conditions w/ decreased phagocytic fxn
74
Q

pseudomonas virulence factors

A
  • endotoxin LPS
  • exotoxin A (shock)
  • leukocidin
75
Q

infections caused by pseudomonas

A

“superinfections” replace antibiotic suppressed organisms

PSEUDOHmonas

  • pneumonia (cystic fibrosis)
  • sepsis (black lesions)
  • external otitis (swimmer’s ear)
  • UTI
  • Drug use - osteomyelitis and endocarditis
  • Osteomyelitis in diabetics
  • Hot tub folliculitis

also corneal keratitis in contact wearers

76
Q

describe where pseudomonas localizes in tissues

A

overgrows around blood vessels - ‘blue haze’

77
Q

legionella pneumophilia general characteristics

A 
G(-) 
rod 
flagella 
associated w/ water vapors- then causes epidemics 
community outbreaks
78
Q

infections that legionella causes

A

90% get pontiac fever
10% get Legionaire’s disease

can get fibrinopurulent necrosis leading to scarring of pulmonary tissues

79
Q

in what organisms do you see fibrinopurulent necrosis of pulmonary tissues?

A

ONLY staph and legionella

strep pneumonias do not cause this

80
Q

helicobacter pylori general characteristics

A 
G(-)
spiral/helical 
acid stable 
motile - moves through mucous secretions 
urease
81
Q

function of urease in H. pylori

A

creates protective layer of ammonia around organism to protect it from acid

82
Q

what does H. pylori cause?

A

90% of duodenal ulcers and 80% of chronic gastric ulcers

83
Q

how often does H. pylori go asymptomatic

A

about 50% of affected adults

84
Q

modes of infections for bacteroides and peptostreptococcus

A
  • aspiration
  • trauma
  • fecal leakage
85
Q

describe infections of bacteroides and peptostreptococcus

A
  • ischemic, devitalized tissues
  • mixed infections
  • foul-smelling pus
86
Q

two bacteroides

A

fusobacterium and peptococcus

87
Q

what is peptostreptococcus known for?

A

gingival infections

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