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Pathology: Infectious disease section > Bacteria II > Flashcards

Bacteria II Flashcards

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
Q

how is Sepsis/shock stimulated?

A

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

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26
Q

what is DIC?

A

systemic activation of coagulation by bacteria

-results in systemic microthrombi followed by hemorrhage after coagulation factors are used up

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27
Q

why doesn’t Gonococci cause sepsis/DIC/meningitis?

A

only has LOS

-can evade pahgocytosis and get into bloodstream and into joints (usually in lower half of body)

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28
Q

common diseases from Strep. P

A

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)
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29
Q

what are infections with strep. P associated with?

A

impaired immunity, malnutrition, alcoholism, age <2, sickle cell, any form of obstruction of respiratory process

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30
Q

virulence factors for strep. P

A
  • polysaccharide capsule, PspC
  • pneumolysin
  • pspA (inhibits alternate complement pathway)
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31
Q

what are the two pneumococcal vaccination

A

PCV13
PPSV23
-risk factors include chronic disease, immunodeficiency, and asplenia

32
Q

pneumococcal conjugate vaccine (PCV13)

A

for young kids, younger than 5 and for adults with certain risk factors

33
Q

pneumococcal polysaccharide vaccine (PPSV23)

A
  • adults 65 or older
  • 19 or older with risk factors
  • children 2 years with high risk of pneumococcal diseases
34
Q

Neisseria

A

LPS

  • aerobic or facultative anaerobes
  • need IRON
  • not NF
35
Q

How does Neisseria get into body?

A 
enters nasopharynx-> colonizes mucosa 
-Sepsis, DIC, petechial hemorrhages
-purulent meningitis 
-sensitive to penicillin
cluster epidemics
36
Q

neisseria meningits

A
  • microhemorrhages in capillaries-> petechial rash (extremities/ear lobes)
  • microthrombi-> ischemic necrosis (gangrene in limbs)
  • vascular collapse-> fatal
37
Q

how does body fight N.m

A

complement mediated phagocytosis

-vaccines available

38
Q

what is the mechanism of tissue for N.gonorrhea

A

attaches columnar and transitional epithelial (pili)-> mucosal membrane of the gential tract, rectum, and nasopharynx
-IgA protease-> evades mucosal immunity

39
Q

what kind of inflammation does N.g cause?

A

suppurative inflammation of mucosal surfaces and subepithelial tissues

  • suppurative arthritis
  • antigenic variability
40
Q

non-invasive diseases of H. influenza

A

upper respiratory, sinusitis, OM

  • encapsulated most common to cause URT
  • non-encapsulated forms part of NF (children 40-60%, 35% adults)
41
Q

invasive diseases of H. infleunza

A

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
Q

what is the window of susceptibility for invasive disease with H. influenza type B

A

3 months-3 years

  • newborns protected from maternal antibodies 3-6months
  • young children unable to make protective antibody response
43
Q

Moraxella catarrhalis (N. catarrhalis)

A

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
Q

Diphtheria pathogenesis

A

corynebacterium
-local epithelial necrosis (pseuodomembrane formation) ->systemically released exotoxin A-> damages distant organs
(exotoxin causes necrosis of upper membrane-> coagulation)

45
Q

pathogenesis to whooping cough (Bordetella pertussis)

A

cell-bound pertussis toxin with local epithelial inflammation

  • strong tropism for brush border
  • exotoxin leads to local ciliary paralysis with secondary inflammation
46
Q

Bordetella pertussis-Whooping cough

A

pleomorphic G-, aerobic coccobacillus

-characteristic lymphocytosis

47
Q

Pertussis vaccine

A

Tdap

48
Q

Corynebacterium Diphtheria

A

G+, rod

ulcerative lesions of respiratory mucosa

49
Q

what causes the pseudomembrane associated with Diphtheria?

A

necrotic coagulative exudate

50
Q

what causes the disease with diphtheria?

A
  • 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
Q

what is the most common cause of death in diphteria?

A

due to cardiac failure from exotoxins

52
Q

what do gram negative rods cause?

A
  • urinary tract infections
  • intra-abdominal infections
  • rare pneumonias (nosocomial)
53
Q

general characteristics of G- rods

A
  • endotoxins: LPS
  • frequent drug resistance
  • replaced pyogenic cocci as bulk of hospital acquired infections
54
Q

Gram negative infections

A
  • UTI’s
  • Abdominal infections: perforation, appendicitis, cholecystitis, diverticulitis
  • aspiration pneumonia
  • nosocomial infections
55
Q

what are the two main types of gram negative infections?

A
  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
Q

is E. coli invasive?

A

No, non-invasive commensual

  • cause disease when gain access to tissue or secondary to tissue inflammation in abdomen
  • ferments lactose (coliform)
57
Q

types of infection from E. coli?

A
  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
Q

Klebsiella and enterobacter associated diseases

A

pneumonia
UTI
-urinary tract infections secondary to obstruction
-septicemia: thick mucoid capsule
-pulmonary infections-> necrotizing abscesses

59
Q

klebsiella pneumonia

A

aspiration in hospital setting

60
Q

Proteus/Serratia

A
  • proteus mirabilis

- serratia marcescens

61
Q

proteus mirabilis

A

G-, facultative anaerobic rod

  • UTI pyelonephritis; pneumonia (debilitated patients)
  • secretes urease, alkaline urine-> chronic pyelonephritis: staghorn calculi
62
Q

serratia marcescens

A

pneumonia in debilitated patients

UTI’s

63
Q

Pseudomonas aeruginosa infections

A
  1. ) Skin infections/sepsis for burns
  2. ) pneumonia for CF
  3. ) chronic UTI from obstruction
64
Q

Pseudomonas aeruginosa

A

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
Q

virulence factors from Pseudomonas aeruginosa

A

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
Q

other forms of infections from Pseudomonas aeruginosa

A
  • 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
Q

Legionella pneumophilia

A

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
Q

Helicobacter pylori

A
  • 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
Q

anaerobic G- bacterial infections

A

Bacteroides: fusobacterium, peptococcus

peptostreptococcus-> gingival infections

modes of infection: aspiration, trauma, fecal leakage
-ischemic, devitalized tissues, foul-smelling pus

70
Q

what kind of rare pneumonias do G- give?

A

aspiration pneumonia

71
Q

who gets aspiration pneumonia

A
  • alcoholics (worse on right side)

- obtunded (decrease of reactivity of reflexes, tend to not swallow all excretions, anesthesia)

72
Q

number one cause of UTI’s

A

Gram negatives

73
Q

what is sepsis

A

over-whelming infection involving septic bacteremia

74
Q

what is sepsis shock

A

systemic inflammatory response

75
Q

most common cause of sepsis in septic shock

A

Gram + and Gram -

76
Q

LPS in blood triggers

A

septic shock and DIC

77
Q

3 most common bacteria causing UTI’s

A

E. coli
pseudomonas aeruginosa
enterococcus

Pathology: Infectious disease section (11 decks)

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