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Pathology: Infectious disease section > Bacteria II > Flashcards

Bacteria II Flashcards

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1
Q

what can lead to otitis media and sinusitis?

A

UPT (normal flora)

-its secondary to blockage of sinus ostia, ET, by virally induced or allergic inflammation (allergic rhinitus)

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2
Q

common colonizers

A
  • Step. pneumoniae
  • staph. aureus
  • H. influenza (non type B, G-)
  • Moraxella catarrhalis (G-)
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3
Q

pathogenesis of sinusitis/OM

A

primary inflammatory response from an UPT or allergies, results in blockage or sinus ostia or ET

  • secondary overgrowth of colonizing bacteria
  • fever,pain, purulent drainage
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4
Q

what are some potential complications from Sinusitis/OM

A

abscess formation, invasion of cribiform plate, damage to middle inner ear

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5
Q

process of UPT infection

A

inflammation->obstruction-> overgrowth of normal flora

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6
Q

how can an UPT infection lead to systemic disease?

A

exposure to virulent organisms-> local infection-> invasive disease-> bacteremia-> systemic disease, meningitis
-Strep. pneumoniae, N. meningitis, H. influenza type B, E.coli (all have capsules)

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7
Q

In neonates, what are the organisms to cause invasive UPD/meningitis

A

E. coli, strep group B

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8
Q

In children 1-5, what are the organisms to cause invasive UPD/meningitis

A

H. influenza type B

-conjugated vaccine

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9
Q

In adolescents and young adults, what are the organisms to cause invasive UPD/meningitis

A

N. meningitidis

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10
Q

In all other age groups, what are the organisms to cause invasive UPD/meningitis

A

Strep. pneumoniae

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11
Q

what is the key to pathogenesis?

A

encapsulated

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12
Q

how does meningitis develop?

A

organism gets in bloodstream-> activate endothelial and macrophages cells-> breaks down the blood brain barrier by increasing the vascular permeability

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13
Q

what is usually always seen with E. coli

A

sepsis

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14
Q

meningitis from an upper respiratory infection

A

starts as a URT-> secondary invasion of bacteria into deeper tissues-> bloodstream-> bacteremia with dissemination of bacteria-> endothelial cell and macrophage activation by LPS leads to vascular leakage

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15
Q

what is more deadly that the actual meningitis?

A

shock, disseminated intravascular coagulation (DIC)

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16
Q

what do infections with encapsulated organisms require?

A

antibodies and/or complement to provide defense against deep invasion of tissues
-also associated with sepsis and DIC

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17
Q

Upper respiratory bacteria: Pneumococcus

A

NF
-G+, diplococcus
virulence: capsule, PspC
invasive disease: sepsis, meningitis

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18
Q

Upper respiratory bacteria: N. meningitis

A

exogenous (rare carries)
-G(-), diplococcus
virulence: Capsule, LPS
invasive disease: DIC, sepsis, meningitis

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19
Q

Upper respiratory bacteria: N. gonorrhea

A

exogenous
-G(-), diplococcus
virulence: capsule, LOS
invasive disease: septic arthritis

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20
Q

Upper respiratory bacteria: H. influenza (type B)

A 
NF
-type B: exogenous
-G(-), pleomorphic
Virulence: capsule, LPS
invasive disease: sepsis, meningitis
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21
Q

what are the 4 things that encapsulated bacteria are able to do?

A
  1. )anti-phagocytic
  2. )invasive disease-> bacteremia
  3. ) increased vascular permeability-> entry to tissue
  4. ) proliferated in CSF-> no complement
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22
Q

why is being encapsulated helpful?

A

evade immune responses and cause more severe infection

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23
Q

what part of the capsule triggers systemic inflammation?

A

LPS or PspC

-sepsis, DIC

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24
Q

what are consequences of bacteremia from encapsulated bacteria?

A

Sepsis/shock

DIC

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25
how is Sepsis/shock stimulated?
LPS stimulates toll-like receptors-> induce systemic cytokine secretion and endothelial cell activation-> increased vascular permeability, loss of intravascular volume, systemic shock and organ failure
26
what is DIC?
systemic activation of coagulation by bacteria | -results in systemic microthrombi followed by hemorrhage after coagulation factors are used up
27
why doesn't Gonococci cause sepsis/DIC/meningitis?
only has LOS | -can evade pahgocytosis and get into bloodstream and into joints (usually in lower half of body)
28
common diseases from Strep. P
NF, causes disease secondary to obstruction or other disease process - upper respiratory (2 to obstruction, viral, allergies)-> Sinus/OM - lower respiratory-> lobar pneumonia (2 to influenza, common community pneumonia) - meningitis (most common)
29
what are infections with strep. P associated with?
impaired immunity, malnutrition, alcoholism, age <2, sickle cell, any form of obstruction of respiratory process
30
virulence factors for strep. P
- polysaccharide capsule, PspC - pneumolysin - pspA (inhibits alternate complement pathway)
31
what are the two pneumococcal vaccination
PCV13 PPSV23 -risk factors include chronic disease, immunodeficiency, and asplenia
32
pneumococcal conjugate vaccine (PCV13)
for young kids, younger than 5 and for adults with certain risk factors
33
pneumococcal polysaccharide vaccine (PPSV23)
- adults 65 or older - 19 or older with risk factors - children 2 years with high risk of pneumococcal diseases
34
Neisseria
LPS - aerobic or facultative anaerobes - need IRON - not NF
35
How does Neisseria get into body?
``` enters nasopharynx-> colonizes mucosa -Sepsis, DIC, petechial hemorrhages -purulent meningitis -sensitive to penicillin cluster epidemics ```
36
neisseria meningits
- microhemorrhages in capillaries-> petechial rash (extremities/ear lobes) - microthrombi-> ischemic necrosis (gangrene in limbs) - vascular collapse-> fatal
37
how does body fight N.m
complement mediated phagocytosis | -vaccines available
38
what is the mechanism of tissue for N.gonorrhea
attaches columnar and transitional epithelial (pili)-> mucosal membrane of the gential tract, rectum, and nasopharynx -IgA protease-> evades mucosal immunity
39
what kind of inflammation does N.g cause?
suppurative inflammation of mucosal surfaces and subepithelial tissues - suppurative arthritis - antigenic variability
40
non-invasive diseases of H. influenza
upper respiratory, sinusitis, OM - encapsulated most common to cause URT - non-encapsulated forms part of NF (children 40-60%, 35% adults)
41
invasive diseases of H. infleunza
meningitis (most common but rare now b/c vaccine) - invasive form encapsulated - type B->endotoxin, cause DIC - H. parainfluenza (NF mouth)-> endocarditis - H. ducreyi-> chancroid
42
what is the window of susceptibility for invasive disease with H. influenza type B
3 months-3 years - newborns protected from maternal antibodies 3-6months - young children unable to make protective antibody response
43
Moraxella catarrhalis (N. catarrhalis)
G-, diplococcus - NF of upper respiratory tract - 3rd most common cause of secondary bacterial infections such as sinusitis/OM - LPS (rarely causes sepsis/meningitis tho)
44
Diphtheria pathogenesis
corynebacterium -local epithelial necrosis (pseuodomembrane formation) ->systemically released exotoxin A-> damages distant organs (exotoxin causes necrosis of upper membrane-> coagulation)
45
pathogenesis to whooping cough (Bordetella pertussis)
cell-bound pertussis toxin with local epithelial inflammation - strong tropism for brush border - exotoxin leads to local ciliary paralysis with secondary inflammation
46
Bordetella pertussis-Whooping cough
pleomorphic G-, aerobic coccobacillus | -characteristic lymphocytosis
47
Pertussis vaccine
Tdap
48
Corynebacterium Diphtheria
G+, rod | ulcerative lesions of respiratory mucosa
49
what causes the pseudomembrane associated with Diphtheria?
necrotic coagulative exudate
50
what causes the disease with diphtheria?
- disease is due to absorption and dissemination of exotoxin - inhibits protein synthesis in eukaryotic cells - leads to fatty myocardial changes, myofiber necrosis, and polyneuritis
51
what is the most common cause of death in diphteria?
due to cardiac failure from exotoxins
52
what do gram negative rods cause?
- urinary tract infections - intra-abdominal infections - rare pneumonias (nosocomial)
53
general characteristics of G- rods
- endotoxins: LPS - frequent drug resistance - replaced pyogenic cocci as bulk of hospital acquired infections
54
Gram negative infections
- UTI's - Abdominal infections: perforation, appendicitis, cholecystitis, diverticulitis - aspiration pneumonia - nosocomial infections
55
what are the two main types of gram negative infections?
1. ) spread of organism that have colonized the GI tract (E. coli) -> overgrowth following obstruction, perforations, aspiration 2. ) contamination of tissue and materials from the hospital environment-> catheters, wounds
56
is E. coli invasive?
No, non-invasive commensual - cause disease when gain access to tissue or secondary to tissue inflammation in abdomen - ferments lactose (coliform)
57
types of infection from E. coli?
1. ) urinary tract infections/cystitis-> uncomplicated UTI, no obstruction 2. ) suppurative infections of abdominal cavity-> secondary to obstruction 3. ) G- hemorrhagic bronchopneumonia in debilitated patients-> aspiration 4. ) g- sepsis-> DIC shock
58
Klebsiella and enterobacter associated diseases
pneumonia UTI -urinary tract infections secondary to obstruction -septicemia: thick mucoid capsule -pulmonary infections-> necrotizing abscesses
59
klebsiella pneumonia
aspiration in hospital setting
60
Proteus/Serratia
- proteus mirabilis | - serratia marcescens
61
proteus mirabilis
G-, facultative anaerobic rod - UTI pyelonephritis; pneumonia (debilitated patients) - secretes urease, alkaline urine-> chronic pyelonephritis: staghorn calculi
62
serratia marcescens
pneumonia in debilitated patients | UTI's
63
Pseudomonas aeruginosa infections
1. ) Skin infections/sepsis for burns 2. ) pneumonia for CF 3. ) chronic UTI from obstruction
64
Pseudomonas aeruginosa
G- rod, pyocyanin and pyoverdin (green pigment) - non spore, aerobic, flagellum, motile - opportunistis, in hospitals - phagocytosis effective in protecting from infection->associated with conditions which decrease phagocytic function - burns, CF patients (pneumonia)
65
virulence factors from Pseudomonas aeruginosa
endotoxin-> LPS exotoxin A-> shock -leukocidin (kill neutrophil response) -antibiotic resistant to number of them (penicillin) -lung infections: fulminant pneumonias -found in walls of blood vessels as blue haze
66
other forms of infections from Pseudomonas aeruginosa
- co-infection with Burkholderia cepacia complex - burns, endocarditis and osteomyelitis (drug abusers) - corneal keratitis (contact wearers) - external otitis (swimmers ear, especially in diabetics) - severe external otitis in diabetes
67
Legionella pneumophilia
pneumonia -G-, flagellate rod -contaminated water -Pontiac fever (90%) -Legionaire's disease (10%)-> get necrotic pneumonia fibrinopurulent necrosis-> leads to scarring of pulmonary tissues
68
Helicobacter pylori
- Gastritis/peptic ulcer disease - spiral/helical G- bacterium - can survive in acid environment of stomach - secretes urease-> creates protective layer of ammonia - lives in mucous layer of stomach
69
anaerobic G- bacterial infections
Bacteroides: fusobacterium, peptococcus peptostreptococcus-> gingival infections modes of infection: aspiration, trauma, fecal leakage -ischemic, devitalized tissues, foul-smelling pus
70
what kind of rare pneumonias do G- give?
aspiration pneumonia
71
who gets aspiration pneumonia
- alcoholics (worse on right side) | - obtunded (decrease of reactivity of reflexes, tend to not swallow all excretions, anesthesia)
72
number one cause of UTI's
Gram negatives
73
what is sepsis
over-whelming infection involving septic bacteremia
74
what is sepsis shock
systemic inflammatory response
75
most common cause of sepsis in septic shock
Gram + and Gram -
76
LPS in blood triggers
septic shock and DIC
77
3 most common bacteria causing UTI's
E. coli pseudomonas aeruginosa enterococcus

Pathology: Infectious disease section (11 decks)

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