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Pathogenic Microbiology > Exam #2 > Flashcards

Exam #2 Flashcards

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1
Q

Discovery of Lobar Pneumonia

A

1882 Friedlander discovers Klebsiella

1881 Fraenkel discovers Streprococcus

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2
Q

Streptococcus Genus Division

A

divided in 1919 based on blood agar hemolysis patterns

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3
Q

Streptococci:

Characteristics

A 
gram + spheres
-pairs/chains, non-motile, catalase negative
diverse group
-some normal flora
hemolytic pattern on blood agar
-alpha/beta/gamma
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4
Q

Streptococci:

Pathogenesis

A

extracellular infection
-bacteria killed within phagocytes
tend to produce purulent lesions

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5
Q

Streptococci:

Major Diseases

A 
bacteremia/ impetigo/ glomerulonephritis
pneumonia/ wound infections/ endocarditis
meningitis/ pharyngitis/ UTIs
cellulitis/ necrotizing fasciitis
rheumatic fever/ scarlet fever/ TSST
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6
Q

Streptococcus pneumoniae:

pneumococcus

A 
major respiratory pathogen
-most common cause of pneumonia in US
pathology (lobar pneumonia)
-sudden chills, fever, pleuritic pain, rusty sputum
-complications: lung abscess/ bacteremia
-morbidity/mortality: 40,000 <10% cases
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7
Q

Streptococcus pneumoniae:

Risk Factors

A

10-30% healthy people colonized
viral infection of upper respiratory tract
compromised pulmonary function/alcoholism
increased incidence over 50 years old
impaired immunity (sickle cell anemia, splenectomy, granulocytopenia)
males at greater risk
serotype

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8
Q

Streptococcus pneumoniae:

Other Infections

A 
upper respiratory
-otitis media
-mastoiditis
-sinusitis
extrapulmonary
-meningitis
-septic arthritis
-endocarditis
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9
Q

Streptococcus pneumoniae:

Pathogenesis

A
  • organism colonizes pharynx
  • gains access to lung (aspiration)
  • bacteria move into alveoli
  • bacteria multiply in edematous fluid
  • exudate spills into bronchioles
  • inflammatory response; air displaced
  • centrifugally spreading lesion
  • resolution or death
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10
Q 
Streptococcus pneumoniae:
Virulence Factors (Polysaccharide Capsule)
A

anti-phagocytic (blocks C3b deposition)
absolute requirement for virulence
highly antigenic but variable (90 serotypes)
antibody provides type-specific protective immunity

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11
Q 
Streptococcus pneumoniae:
Virulence Factors (Pneumolysin)
A

membrane-bound toxin (pore forming)
mutation in gene increases lethal dose in animal models
target may be pulmonary endothelium

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12
Q 
Streptococcus pneumoniae:
Virulence Factors (Neuraminidase)
A

cleaves sialic acid in mucin, glycolipids, glycoproteins

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13
Q 
Streptococcus pneumoniae:
Virulence Factors (Choline-Binding Proteins)
A

facilitates

  • colonization of nasopharynx
  • sepsis
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14
Q

Streptococcus pneumoniae:

Laboratory Identification

A

alpha-hemolytic on blood agar
catalase negative
latex bead agglutination

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15
Q

Streptococcus pyogenes:

Characteristics

A

‘Group A Strep’
-based on cell wall carbohydrate composition
causes majority of all streptococcal diseases
-normal flora in 5-10% of healthy humans
beta-hemolysis on blood agar
-two hemolysins; streptolysin O and S
-no hemolysis under aerobic conditions if no S
facultative anaerobe

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16
Q

Streptococcus pyogenes:
Extracellular Virulence Factors
Streptolysin O

A

pore forming cytotoxin; lyses WBCs

antigenic: antibodies can be quantitated

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17
Q

Streptococcus pyogenes:
Extracellular Virulence Factors
Streptolysin S

A

cell-associated and cell-free

leukocidal activity and other cells

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18
Q

Streptococcus pyogenes:
Extracellular Virulence Factors
Pyrogenic Exotoxins

A

family of 9 proteins; ‘SPEs’
superantigenic properties
may enhance invasion
primary determinant of Scarlet fever and TSST

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19
Q

Streptococcus pyogenes:
Extracellular Virulence Factors
Complement Protease

A

C5a peptide

disrupts chemotaxis of phagocytes

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20
Q

Streptococcus pyogenes:
Extracellular Virulence Factors
Streptokinase

A

dissolves fibrin clots

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21
Q

Acute Group A Strep Diseases:

Pharyngitis

A

‘strep throat’

  • most common cause in kids 5-15
  • very contagious- large aerosol droplets
  • fomites are not a factor in transmission
  • asymptomatic carrier state (<1%)
  • bacteria persists 1-4 weeks post-symptomatic stage of disease
  • complications: peritonsillar abscesses; scarlet fever; cervical adenitis; otitis media; TSST
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22
Q

Acute Group A Strep Diseases:

Impetigo

A

different M serotype than respiratory strain
associated with insect bites
fomites are factor

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23
Q

Acute Group A Strep Diseases:

Wound and Puerperal Infections

A

not very common

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24
Q

Acute Group A Strep Diseases:

Streptococcal Toxic Shock-Like Syndrome

A 
SPEs involved
'flesh eating' Group A Streptococcus
soft tissue invasion; multi-organ involvement
necrotizing fasciitis and myositis
extremely rapid course
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25
Q

Non-Suppurative Sequelae:

Rheumatic Fever

A

after throat infection
autoimmune mechanism
-cross-reactivity between anti-M abs and heart tissue

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26
Q

Non-Suppurative Sequelae:

Acute Glomerulonephritis

A
  • after throat or skin infection

- renal injury due to deposition of antigen-Ab complexes in glomeruli

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27
Q

Group A Strep Lab ID

A 
beta-hemolytic on blood agar
catalase negative
latex agglutination
PYR- pyrrolidonyl arylamidase
-test positive
bacitracin
-96-99% of strains sensitive
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28
Q

Treatment:

Streptococcal pneumonia

A 
penicillin drug of choice
vancomycin for resistant strains
vaccine available
-capsule from 23 most common serotypes
-recommended for >65 years, immunocompromised, chronic heart/liver/kidney conditions
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29
Q

Treatment:

Group A Streptococcal Infections

A

penicillin or penicillinase-resistant antibiotic if mixed infection (Staph)

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30
Q

Group B Streptococcus:

GBS

A

exp. S. agalactiae
first isolated from bovine mastitis
this and E. coli are most common causes of neonatal meningitis
normal flora of the gut

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31
Q

Group B Streptococcus:

Mother to Infant Transmission

A
  • 50% of offspring of colonized mothers will be affected

- of those, 2% experience early onset sepsis, pneumonia, or meningitis

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32
Q

GBS:

General

A

late onset, sometimes 1-3 months
risk factors: premature birth, ruptured amniotic membrane
transplancental IgG is protective

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33
Q

GBS:

Virulence Factors

A 
Capsule-Polysaccharide
-sialic acid moeity binds factor H in serum
*facilitates degradation of C3b
Component Protease
-C5a peptidase
-disrupts PMN chemotaxis
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34
Q

GBS:

Virulence Factors - Blr

A

expressed by some GBS strains
‘LRR’ protein (leucine-rich-repeats)
structurally similar to internalin A-type proteins
‘buried’ under under the GBS capsule (in vitro)
likely functions as an adhesin

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35
Q

GBS Diseases:

Neonatal Sepsis

A

fever, lethargy
CNS involvement, 5-10% of cases
20% mortality

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36
Q

GBS Diseases:

Adults

A

uncommon
peripartum chorioamnionitis/ bacteremia
pneumonia, skin, soft tissue infections

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37
Q

GBS:

Lab Identification

A 
beta-hemolytic
bacitracin resistant
CAMP test
-hemolytic zone when cross streaked with S. aureus
-CAMP factor: cytolysin
serogroup typing
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38
Q

GBS Diseases:

Therapeutics

A 
antibiotics
-same as group A
-beta-lactam+aminoglycoside (synergy)
screen for GBS colonization
-third trimester
-prophylaxis during labor
vaccine under development
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39
Q

Viridans Streptococci

A 
alpha-hemolytic streptococci
-many different species
normal flora-mouth, nasopharynx, URT
not typable by carbohydrate antigens
typically don't cause disease
-lack identifiable virulence determinants
-possible adhesins: glucans, other sugars
-low virulence species exist
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40
Q

Viridans Streptococci:

Diseaes - Endocarditis

A 
S. sanguis, S. salivarius
colonization of valves
subacute- slow progression (weeks/months)
responds well to penicillin
fatal if untreated
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41
Q

Viridans Streptococci:

Diseases - Dental Infections

A

S. mutans
adherence+colonization= plaque formation
-pellicle: film of salivary macromolecules

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42
Q

Viridans Streptococci:

Diseases - Dental Caries

A

progressive destruction of enamel –> pulp

  • glycolytic end product: organic acids
  • dietary monosaccharides/disaccharides
  • bacterial polyglycans synth. from sucrose
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43
Q

Viridans Streptococci:

Diseases - Gingivitis/Periodontitis

A

inflammation of the gums
resorption of bone and ligament
-tooth support lost

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44
Q

Group D Streptococci

A 
Enterococcus spp., S. bovis, S. equinus
intestinal commensals
may be alpha, beta, gamma hemolytic
no virulence factors
-Enterococcus can kill nematode elegans
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45
Q

Group D:

Diseases

A
  • urinary tract infections
  • wound and soft tissue infections
  • 10-15% of all nosocomial UTIs, intra-abdominal infections and bacteremia
  • pneumonia is rare
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46
Q

Group D:

Bacteremia

A

most common type of strep sepsis in adults
often follows GI tract infection or manipulation
serious sequelae is endocarditis
-10-20% of all bacterial endocarditis

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47
Q

Group D;

Treatment of Infections

A
  • most Enterococcus spp. are resistant to penicillin
  • combined antibiotics sometimes effective
  • E. faecalis endocarditis is very difficult to treat
  • imipenum/ciprofloxacin may be effective
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48
Q

Group D:

Lab Identification

A 
bacitracin resistant
hydrolysis of bile-esculin
-growth in 40% bile
-esculin--> esculetin
Enterococcus spp. can grow in 6.5% NaCl
-Group D Streptococcal spp. cannot
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49
Q

E. coli:

History

A 
1885
-Theodore Escherich isolates from infant feces
1884
-Gaffkey isolates the 'typhoid' bacillus
1898
-Kiyoshi Shiga isolate agent of bacillary dysentery
1903
-soluble toxin of one Shigella
1900-1915
-periodic epidemics of typhoid fever in NYC
1970's
-E. coli toxins characterized
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50
Q

Enteric Intestinal Infections:

Watery Diarrhea

A

large volume, no white cells, fever, vomiting

proximal small intestine

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51
Q

Enteric Intestinal Infections:

Dysentery (Inflammatory Diarrhea)

A

small volume stools, blood, pus, fever, tenesmus

colon is primary target

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52
Q 
Enteric Intestinal Infections:
Enteric Fever (Systemic)
A

origin is GI tract- small bowel

spread to biliary tract; liver; other RE organs

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53
Q

Enteric Diseases:

Gastritis and Peptic Ulcers

A

Helicobacter pylori
can be asymptomatic for decades
can lead to gastric adenocarcinoma

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54
Q

Enteric Diseases:

Extraintestinal (Opportunistic)

A 
UTIs
gram negative species
meningitis
wound infections
pneumonia
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55
Q

Pathogenesis of Enteric Infections

A 
CNS infections
entry via contaminated device
-inhalation, surgical site, ect.
bloodstream infections
entry via IV catheter/fluids
pneumonias
colonization of colon; perineum; urethra
UTIs
entry via urinary catheter
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56
Q

Laboratory Analysis

A 
primary isolation media
-MacConkey (+lactose)
-enrichment broth, Salmonella/ Shigella
ID of isolate
-sugar fermentation, citrate
-metabolic end products (indole; ammonia)
Serotyping: agglutination w/ anti-sera
-O somatic antigen: polysaccharide LPS sidechain
-H antigen: flagella (heat liable)
capsule
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57
Q

Pathogenic Escherichia coli

A 
produce intestinal/extraintestinal diseases
5 classes of 'diarrheagenic'
-Enterotoxigenic (ETEC)
-Enteropathogenic (EPEC)
-Enteroinvasive (EIEC)
-Enterohemorrhagic (EHEC)
-Enteroaggregative (EAEC)
evolved from commensal
grouped by serotype: O and H carbohydrates
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58
Q

Enterotoxigenic E. coli:

ETEC

A

causes acute secretory diarrhea
-high volume fluid/electrolyte secretion into lumen
-no leukocytes, no blood
‘traveler’s’ diarrhea, ‘deli-belly’, ‘Montezuma’s Revenge’
major cause of diarrhea in children in developing countries
transmitted by fecal contamination of food/water

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59
Q 
ETEC Virulence Factors:
Colonization Pili (Fimbriae)
A

colonization factor antigens (CFAs)
associated with certain serotypes
can vary morphologically

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60
Q

ETEC Virulence Factors:

Heat Labile Toxin (LT)

A

immunologically cross-reactive with cholera toxin
ADP ribosyltransferase
-activates adenylate cyclase–> cAMP
-mediated through modification of G protein of the membrane-bound cyclase complex

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61
Q

ETEC Virulence Factors:

Heat Stabile Toxin 1

A

ST-I
low molecular weight protein
same mechanism as LT (different receptor)
-activates guanylate cyclase–> cGMP

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62
Q

ETEC Virulence Factors:

Heat Stabile Toxin 2

A

ST-II
about 3x larger than ST-I
unknown mechanism of action
-might be similar to ST-I, different receptor

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63
Q

ETEC Virulence Factors

A

in most strains of ETEC, the CFAs and toxins are plasmid-encoded

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64
Q

ETEC:

Treatment

A

improved sanitation is key!
bottled water for travelers/military
infection may provide protective immunity
-secretory IgA primary component
antibiotics may shorten duration of illness

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65
Q

ETEC:

Prevention

A

licensed vaccines

  • formalin-killed whole cell (oral) + CT b-subunit
  • protection from immunity to CFA;s
  • oral live-attenuated
  • ACE527: three recombinant strains
  • Phase I clinical trials completed
  • human volunteer challenge study
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66
Q

Enteropathogenic E. coli:

EPEC

A
  • produces acute or chronic diarrhea in infants-up to 14 days; rare in adults
  • accounts for diarrhea in up to 20% bottle-fed infants < 1 year old
  • adults can be carriers; fecal-oral transmission
  • fomites are a factor in nursery outbreaks
  • watery stool; no blood; white cells
  • forms ‘attaching and effacing’ lesions through alteration of target cell actin filaments
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67
Q

EPEC:

Virulence Factors

A 
encoded from large pathogenicity 'island'
bundle forming pili (BFP)
-plasmid-encoded adhesins
-not required for A/E lesion formation
intimin
-adhesin
-required for A/E lesion formation
exported secretion proteins (Esps)
-enzymatic ('effector') virulence proteins
-translocated into host target by TTSS
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68
Q

Enteroinvasive E. coli:

EIEC

A

produces dysentery IDENTICAL to Shigellosis
-low volume, bloody stools; neutrophils
large virulence plasmid
-IDENTICAL to Shigella spp.
-encodes virulence proteins which induce invasion of non-phagocytic cells (epithelial)
-proteins which facilitate cell-cell spreading
world-wide distribution; developing countries
-common in kids
-person-person transmission; fecal-oral

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69
Q

Enterohemorrhagic E. coli (EHEC):

Diseases

A 
mild diarrhea
hemorrhagic colitis
-copious bloody diarrhea; no white cells
-severe abdominal cramping; no fever
-non-invasive
hemolytic uremic syndrome (HUS)
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70
Q

EHEC:

Pathogenesis

A

A/E cytophathalogy identical to EPEC
has intimin and other similar secreted proteins
tropism different: colonic (EPEC is small bowel)
-long polar (LP) fimbrial and ‘curli’ adhesins

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71
Q

EHEC:

Serotype O157:H7

A 
associated with the most outbreaks
extremely low infectious dose (100-200 cells)
farm animals are carriers
contaminated food (or water)
-undercooked hamburger biggest culprit
-veggies and fruits also a source
72
Q

EHEC:

Virulence/Prevention

A

key virulence factor is Shiga toxin
-correlates with severity of diarrhea and HUS
vaccines are under development

73
Q

EHEC:

Disease Spectrum

A

mild diarrhea/hemorrhagic colitis

  • abdominal pain
  • no fever
  • bloody diarrhea
  • few PMNs in stools
74
Q

EHEC:

HUS

A

hemolytic uremic syndrome

  • microangiopathic hemolytic anemia
  • thrombocytopenia
  • glomerular thrombosis
75
Q

Enteroaggregative E. coli:

EAEC

A

produces acute/chronic diarrhea in children
pathogenic mechanisms unclear
-produce a ‘stacked brick’ adherence pattern

76
Q

EAEC:

Virulence Factors

A

encoded on medium molecular weight plasmid
at least two different pili
at least two toxins: ST-like, LT-like
AspU- unknown function

77
Q

Diarrheagenic E. coli:

Laboratory Identification

A

Lac + (except EIEC)
serotyping -includes detection of toxin
DNA probes -virulence loci (toxins, ect.)
O157:H7 -SMAC

78
Q

Treatment:

ETEC, EIEC, EPEC

A

antibiotics may shorten duration

79
Q

Treatment:

EHEC

A

antibiotics do not alter course of HUS
-may actually enhance disease
supportive: fluid management
hemodialysis; hemopheresis

80
Q

Uropathogenic E. coli:

UPEC

A 
commensals of the urinary tract
infections caused by
-minor trauma
-sexual intercourse
-catheterization
-prostate enlargement
-diseases (<10 serotypes)
*cystitis, pylonephritis, prostatitis
81
Q

Cystitis

A

dysurea; frequency; urgency

-hematuria (50%)/ turbid urine

82
Q

Pylonephritis

A

flank pain; fever

-leading cause of GNS

83
Q

Prostatitis

A

lower back, perirectal, testicular pain

-chronic form is leading cause of recurrent bacteruria in males

84
Q

UPEC:

Virulence Factors

A

alpha-hemolysin
p pili
type 1 pili

85
Q

UPEC:

P Pili

A
  • primary adhesin w/affinity for uroepithelial receptor (digalactoside)
  • facilitates ascending colonization/infection
86
Q

UPEC:

Type 1 Pili

A

somatic (common) pili

  • ubiquitous surface structure of enterics
  • difficult to express in vitro
  • mannose-resistant hemmagglutination
  • may be involved in colonization of the perineum and bladder
87
Q

UPEC:

Treatment

A

bacterial loads variable
-higher counts favor ascending infection (pyelonephritis)
-presence of pathogen and symptoms diagnostic
empiric treatment is common
-antibiotic sensitivity profiling recommended
-different antibiotics effective alone/in combination
-recurrent infections may be benefited by long-term, low-dose chemoprophylaxis

88
Q

Shigella:

Species/Serogroups

A

A: S. dysenteriae; rare in US; most severe
B: S. flexneri; native americans; developing countries
C: S. boydii; rare
D: S. sonnei; most common in US; developing countries
-very closely related to E. coli
-NOT normal gut flora

89
Q

Shigella:

Diseases

A

wide range: asymptomatic to bloody diarrhea

HUS is a complication (Shiga toxin)

90
Q

Shigella:

Pathogenesis

A

transit through stomach (refractory to low pH)
transient multiplication in small intestine
invasion of colonic epithelium
cell to cell spread

91
Q

Shigella:

Gross Pathology

A 
jejunum
-electrolyte/fluid loss
colon
-invasion of epithelium
-colitis
-electrolyte/fluid loss
92
Q

Shigella:

Cellular Pathology

A

1) release from dead cells into lamina propria and reinvasion through basolateral surface of epithelial cells
2) direct passage between cells w/o exposure to extracellular environment
- bacteria-generated protrusions

93
Q

Shigella Virulence:

Most on Large Virulence Plasmid

A 
(identical in EIEC)
invasion plasmid antigens (IPAs A-D)
-induce phagocytosis in epithelial cells
-transported by a TTSS - mxi/spa genes
VirG: facilitates intercellular spread
94
Q

Shigella Virulence:

Chromosomal Determinants

A 
Luc: aerobactin
-iron scavenging (siderophore)
Stx: Shiga toxin
-inhibits host protein synthesis
-binds to vascular endothelium
-expression induced by low Fe++
95
Q

Shigella:

Epidemiology…

A 
no animal reservoirs
food, flies, feces, fomites
infectious dose only 10-100 organisms
17,000-30,000 cases in US a year
risk factors: 1-4 years age, poor sanitation and crowding
self-limiting, no treatment
96
Q

Salmonella Diseases:

Enteric Fever

A

inc. period 7-20 days
weeks duration
early constipation, then bloody diarrhea

97
Q

Salmonella Diseases:

Septicemia-Compromised CMI

A

inc. period variable; variable duration
no GI symptoms
may include ‘metastatic’ infection

98
Q

Salmonella Diseases:

Enterocolitis

A

inc. period 1-2 days
2-5 day duration
vomiting, diarrhea

99
Q

Salmonella:

Overview

A

only one species (S. enterica)

  • sub species based on O, H, K serotypes
  • typhi, typhimurium, choleraesuis, parathyphi (A/B), enteriditis
100
Q

Salmonella:

Groups

A

thyphoidal: S. typhi, S. parathyhi
-human primary host, fecal-oral
non-typhoidal: all others
-reptiles, birds, mammals
-animal fecal-human oral

101
Q

Salmonella Virulence Factors:

Encoded Pathogenicity Islands

A

virulence ‘effectors’ and secretion accessory proteins

TTSS involved

102
Q

Salmonella Virulence Factors:

Cryptic Plasmid

A

large, in S. typhi

  • required for virulence; gene functions unknown
  • DNA homology w/ large plasmid of Yersinia pestis
103
Q

Salmonella Virulence Factors:

Vi Capsule

A

N-actyl galactosaminuronic acid

  • inhibits complement-mediated lysis/chemotaxis
  • antibodies against capsule protective
104
Q

Salmonella Epidemiology:

Typhoidal

A 
-infectious dose = 10000 (low end)
humans sole reservoir
many asymptomatic carriers
persists in gall bladder
major cause of morbidity and mortality in developing countries
105
Q

Salmonella Epidemiology:

Non-Typhoidal

A

poultry, poultry products primary source

50,000 cases a year in US

106
Q

Salmonella:

Treatment

A 
enterocolitis
-fluid/electrolyte replacement
-antibiotics not required
typhoid fever
-chloroamphenicol/ampicillin
-cephalosporins and fluoroquinolones
licensed vaccine available for typhoid
-Ty21a, live-attenuated, oral
animal vaccines for non-typhoidal strains
107
Q

Yersinia Species

A

-Y. pestis: not GI, clonal to Y. pseudotuberculosis
-Y. enerocolitica:GI pathogen
-Y. pseudotuberculosis: GI pathogen
disease vie feces-contaminated food/water
facultative anaerobes; prefer room temp, motile

108
Q

Yersiniae Diseases:

Enterocolitis

A

mainly caused by Y. enterocolitica

fever, diarrhea, blood and white blood cells in stool

109
Q

Yersiniae Diseases:

Reiter’s Syndrome

A

‘aseptic polyarthritis’

can occur weeks to months after diarrhea

110
Q

Yersiniae Diseases:

Septicemia

A

rare

111
Q

Yersiniae Diseases:

Mesenteric Adenitis

A

mimics appendicitis
fever, lower right quadrant pain, enlarged lymph nodes
Y. pseudotuberculosis or Y. enterocolitica

112
Q

Yersinia:

Pathogenesis

A
  • invasion on epithelial cells, intestinal M cells initial target
  • can replicate within and destroy macrophages
  • lymphotropic: can penetrate ileal mucosa to lymph nodes
  • numerous virulence determinants: chromosomal and plasmid-mediated
113
Q

Yersinia Virulence Factors:

Chromosomal

A

Inv
Ail
-required for invasion

114
Q

Yersinia Virulence Factors:

Plasmid-Encoded

A

‘75 kb pLcr’
low calcium response (LCR) genes
expression up-regulated by high temp and low calcium
gene products

115
Q

Yersinia Virulence Factors:

Yersinia Outer Proteins Effectors

A

enzymatic activity

  • YopE
  • YopH
  • YopJ
  • YopM
  • YopN
  • YpkA
  • YadA (YopA)
  • LcrV
116
Q

Yersinia Virulence Factors:

Yersinia Outer Proteins Translocators

A

part of a TTSS, numerous components

  • Syc’s: Yop effector chaperones
  • YopB and YopD: docking complex
  • YscC: injectisome
  • YscF: injectisome
  • others: injectisome
117
Q

Yersinia Virulence Factors:

LcrV = V Antigen

A

also encoded on the Lcr plasmid (pLcr)
mutants of LcrC are avirulent
required for translocation of YOP effectors into target cells
binds TLR-2 and CD-14 –> increases IL-10
binds TLR-4 –> apoptotic cascade

118
Q

Yersinia Epidemiology and Treatment

A

Y. enterocolitica endemic in Europe
infections usually self-limiting
-septicemia treated w/aminoglycosides
experimental oral vaccines

119
Q

Cholera History

A

1563- first outbreak described (India)
1817- first cholera pandemic
1854- mode of disease transmission identified
1883- Koch isolates etiologic agent

120
Q

Vibrionaceae:

Overview

A

‘comma-shaped’ rods, ferment glucose, abundant in marine and surface waters
V. cholerae O139 and O1
-endemic and pandemic cholera
V. cholerae Non-O
-diarrhea and extraintestinal infections
V. parahaemolyticus
-gastroenteritis and extraintestinal infections
other Vibrio species
-ear, wound, soft tissue, extraintestinal

121
Q

V. cholerae

A

actively motile- single polar flagellum
grows well in high salt/high pH
oxidase positive
strain classification
-O1: 2 biotypes- classical, El Tor; 3 sub-types: Ogawa, Inaba, Hikojima
-O139: ‘endemic’ possesses a polysaccharide capsule
-O2-O138: diarrheagenic; CT-

122
Q

El Tor

A

spreads at higher rate
longer post-infection carriage
longer extra-intestinal survival

123
Q

Cholera

A

acute diarrheal disease
-primary effect from entertoxin CT
-non-invasive
-spectrum: asymptomatic to ‘cholera gravis’
1-4 days incubation, high infectious dose
nausea, vomiting, ‘rice-water’ stool
-rapid fluid/electrolyte loss (1L/hr)
-death in 1-4 days due to dehydration, acidosis, shock

124
Q

V. Cholerae Virulence Factors:

Fimbriae

A

toxin co-regulated pili (Tcp)

-facilitates colonization of small bowel

125
Q 
V. Cholerae Virulence Factors:
Cholera Toxin (CT)
A 
heat labile, phage-encoded
A-B subunit structure
-binds GM1 ganglioside
-ADP-rebosylation of GTP binding protein
-increase cAMP--> increase fluid/electrolytes
25 ug purified CT = 20 L fluid loss
126
Q

Cholera:

Epidemiology

A 
seven pandemics since 1817
-El Tor cause of latest
kids 2-9 years greatest risk
-no age bias in previously 'sterile' area
risk to travelers in endemic countries
endemic in US gulf coast
127
Q

Cholera:

Treatment

A 
oral rehydration therapy (ORT)
intravenous fluid and electrolytes
antibiotics (tetracycline)
-shortens duration
prevention
-water sanitation
-no licensed vaccine available
128
Q

Vibrio parahaemolyticus

A

disease: acute watery diarrhea; severe cramping; vomiting
-short incubation: 15 hours
pathogenesis: unclear, possibly toxigenic
epidemiology
-endemic in coastal waters; world-wide
-undercooked/raw seafood primary source
-very common in Japan
-U.S. outbreaks associated with shellfish

129
Q

Vibrio Vulnificus

A

diseases: gastroenteritis; wound infections; bacteremia
raw oysters primary source in U.S.
possess high-affinity siderophores
-scavenge iron from lactoferrin and transferrin
higher risk host: alcoholics, iron overload disorders

130
Q

Campylobacter Species

A 
gram negative tiny 'gull-shaped' rods
microaerophilic; oxidase positive
motile- polar flagella
gut commensal in many animals
most common cause of bacterial diarrhea
-particularly in humans
131
Q

C. jejuni Diseases:

Enteritis

A

diarrhea, abdominal pain, fever

  • stools loose, watery to dysentery-like (blood, fecal leakocytes)
  • 2-4 days incubation, 5-8 days duration
  • bacteremia in 1% GI infections
132
Q

C. jejuni Diseases:

Reiter’s Syndrome

A

reactive arthritis

133
Q

C. jejuni Diseases:

Guillain Barre Syndrome (GBS)

A

demyelination disorder (neuromuscular paralysis)
40% have infection prior to onset of GBS symptoms
cross-reactive anti-LPS antibodies

134
Q

Campylobacter Pathogenesis

A

passage through stomach
colonize upper small bowel
colon ultimate target
-invasive but remain vacuolated

135
Q

Campylobacter:

Virulence Factors

A

cytolethal distending toxin (CDT)
-arrests host cells in G2 growth phase
flagella and pili
others?

136
Q

Camopylobacter:

Epidemiology and Diagnosis

A 
2 million cases in US
developing countries
-undercooked poultry, unpasteurized mile
special selective medium
-vancomycin, polymyxin B, trimethoprim, cephalothin
42 degrees decrease oxygen, increase CO2
stool cults positive after 48-72 hours
treatment: antibiotics reduce duration
137
Q

Helicobacter pylori

A 
formerly 'Campylobacter'
first isolated in 1980's
motile, spiral shaped, microaerophilic
ureases positive
cause of >90% of peptic ulcers
-early link controversial
-possible cause of duodenal ulcers
-source of infection unclear
risk factor for gastric carcinoma
138
Q

Chronic Atrophic Gastritis

A

‘CagA’
protein secreted into target epithelial cell by type IV secretion system
interacts with/inhibits SH2 phosphatase
disrupts receptor tyrosine kinase sig. pathways
-actin skeleton rearragnement
-loss of tight junction integrity
-loss of cell differentiation
-polarity, adhesion, migration inhibition

139
Q

Helicobacter pylori:

Epidemiology and Diagnosis

A

over 80% of children in developing countries colonized
-<20% in industrialized contries
large asymptomatic population
biopsy and culture of gastric mucosa
-incubated at 37 degrees
-urease detected directly from gastric fluids
serological tests: serum IggG and salivary IgA

140
Q

Helicobacter pylori:

Treatment

A
  • bismuth subsalicylate + amoxycellin + metronidazole for at least 14 days
  • H2 receptor antagonists (Zantac)
  • do not cure, only relieve symptoms
141
Q

Chlamydia:

General Characteristics

A 
obligate intracellular bacterium
(doesn't grow in artificial media)
contains DNA, RNA, 'normal' ribosomes
small genome
gram negative envelope (no peptidoglycan)
susceptible to antibiotics (in vivo)
harbors plasmids and phages
142
Q

Chlamydia:

Species

A

C. pneumonia: respiratory
C. psittaci: respiratory
C. trachomatis –> VD
trachoma
-serovars: A, B, Ba, C (cause trachoma)
-serovars: D-K (STD, urethritis, cervicitis)
lymphogranuloma venereum (LGV, urethritis, cervicitis)

143
Q

Chlamydia:

Elementary Body

A 
small, dense
.25 uM
extracellular (infectious)
not fragile
not metabolically active
outer membrane proteins cross-linked
144
Q

Chlamydia:

Reticulate Body

A 
large, homogeneous
0.6-1.0 uM
intracellular (replicative)
fragile
metabolic activity
outer membrane proteins not cross-linked
145
Q

Chlamydia Pathogenesis

A

direct cytopathic effects
-invasion/inhibition of phagolysosomal fusion (apoptosis is inhibited)
-infected host cells vacuolate and degenerate
-De-ciliation of epithelia
-disruption of processing and packaging functions of secretory cells
immune pathology
-acute and chronic inflammation
-tissue damage: conjunctival scarring, ect.

146
Q

Chlamydia Virulence Factors:

Adhesins

A

major outer membrane protein (MOMP)

heparin sulfate-like glucosaminoglycan (GAG)

147
Q

Chlamydia Virulence Factors:

Heat Shock Protein

A

Hsp70

inflammatory responses

148
Q

Chlamydia Virulence Factors:

Cysteine-Rich Protein (CRP)

A

functionally equivalent to peptidoglycan

facilitates intracellular replication and extracellular survival

149
Q

Chlamydia psittaci:

Psittacosis

A 
'ornithosis'
primary atypical pneumonia
-bilateral interstitial pneumonia
-fever, headache, myalgia, dry couch
-occasional systemic complications
inhalation of respiratory secretions/ droppings of infected birds
zoonotic infection
-increased risk to poultry workers and pet bird owners
150
Q

Chlamydia pneumonia:

Walking Pneumonia

A

pharyngitis/LRT involvement w/persistent cough
clinically similar to Mycoplasma pneumoniae
human-to-human transmission via respiratory droplets
6-10% of hospital cases of pneumonia
40% of population had antibodies by 19 years

151
Q

Chlamydia pneumonia:

Associated w/ Coronary Heart Disease

A

detection of microorganism in lesions
serologic evidence
unknown cause-effect linkage

152
Q

Chlamydia trachomatis:

Trachoma

A 
(serovars A, B, Ba, C)
conjunctival innoculum
-self-limiting or chronic infection
-pannus -superficial vascularization of cornea
-secondary infection/blindness
leading cause of preventable blindness
endemic in developing countries
problem in US Appalachia, reservations
153
Q

Chlamydia trachomatis:

Inclusion Conjunctivitis

A

(sero’s D-K)
resembles trachoma but no pannus
copious mucopurulent discharge
newborns and adults

154
Q

Chlamydia trachomatis:

STDs

A

(serovars D-K and L1-L3)

will include neonatal infection associated with STD’s

155
Q

Chlamydia:

Diagnosis

A

growth in cell culture expensive and slow
serology: >4 fold rise in titer is positive
staining/detection of intracellular inclusion bodies
-specimens from eye or genital tract
-inclusions contain glycogen
immunofluorescence of infected tissue

156
Q

Chlamydia:

Detection with DNA

A

PCR
nucleic acid hybridization
reliability –> questionable

157
Q

Chlamydia:

Treatment

A 
Trachoma:
-antibiotics at early stage of infection
-surgical intervention for ocular damage
-no immunity to re-infection
Psittacosis and Pneumonia:
-tetracycline and erythromycin
158
Q

Neiserria Species

A

gram negative diplococci
many species non-pathogenic
-commensals of URT in humans
-N. gonorrhea, N. meningitidis transient flora w/o causing disease, pathogenic

159
Q

Meningitis Species by Age:

<1 Month Old

A

group B streptococci
E. coli
Lesteria monocytogenes

160
Q

Meningitis Species by Age:

1-23 Months

A

S. pneumoniae

N. meningitidis

161
Q

Meningitis Species by Age:

2-18 Years

A

N. meningitidis

S. pneumoniae

162
Q

Meningitis Species by Age:

19-59 Year

A

S. pneumoniae

N. meningitidis

163
Q

Meningitis Species by Age:

60 Years and Up

A

S. pneumoniae

L. monocytogenes

164
Q

Neiserria:

Characteristics

A

non-motile, non-spore-forming
aerobic, oxidase positive, fastidious
pathogens: don’t grow at 22 degrees or on agar w/o blood, does produce CO2
non-pathogenic: grows at 22 degrees and on agar w/o blood, doesn’t produce CO2

165
Q

N. meningitidis Virulence Factors:

Polysaccharide Capsule

A 
absent on gonococcus
anti-phagocytic
13 serogroups
-group-specific antibody is protective
-group A associated with epidemics
-group B, C, and Y most common
antigen present in blood and CSF in severe infections
166
Q

N. meningitidis Virulence Factors:

LPS (LOS)

A

immune evasion
-structure mimics host sphingolipids found in brain
O-side chains integrate host sialic acid to inhibit complement deposition

167
Q

N. meningitidis Virulence Factors:

Outer membrane Proteins

A

‘Opa’ (Opacity) proteins
-may facilitate invasion
sub-divide the serogroiups
antibodies to these proteins are bactericidal

168
Q

N. meningitidis Virulence Factors:

Pili

A

adherence to nasopharyngeal epithelium

bind CD46 glycoprotein on host cells

169
Q

N. meningitidis Virulence Factors:

Pili and Opa

A

‘high level antigenic variation’
multiple gene copies
pili
-positioned downstream of different promoters by recombination ‘on’ (pilE) or ‘off’ (pilS
-pili w/ altered function, incomplete pili,ect.
opa’s
-‘on’ or ‘off’ via translational frame shift in mRNA
-different combinations of proteins expressed under different conditions

170
Q

N. meningitidis:

Pathogenesis

A

pathogenesis different than gonococcus
-meningitis (ability to cross blood-brain barrier)
-toxic septicemia
possesses eight unique pathogenicity islands in its chromosome
-‘region 8’ required for bacteremia: encodes a siderophore receptor and a disulfide oxidoreductase

171
Q

N. meningitidis Disease Spectrum:

Asymptomatic Carrier State

A

5-25% of population (higher in closed population)
reservoir for disease
carrier state enhances immunity

172
Q

N. meningitidis Disease Spectrum:

Meningococcemia

A 
'bacteremia'
may have cutaneous manifestations
Water-Friedrichsen syndrome
meningitis- mortality 85% w/o treatment
chronic form: associated w/ complement deficiency
173
Q

N. meningitidis:

Histopathogenesis

A

mucosal colonization by bacteria
bacterial invasion of and survival within bloodstream
penetration of blood-brain barrier and into CSF
local release of inflammatory cytokines in CSF
adhesion of leukocytes to brain endothelium and diapedesis into CSF
exudation of albumin through opened intercellular junctions of meningeal venules
brain, edema, increased intracranial pressure, altered cerebral blood flow
cranial nerve injury, seizures, hypoxic-ischemic brain damage, herniation

174
Q

N. meningitidis:

Epidemiology

A 
spread human to human
asymptomatic carrier focus of infection
seasonal variation
-highest attack rate in late Winter, early Spring
age
-incidence greatest 6 months to 3 years
-correlates w/decline of maternal antibody and acquired immunity
5000,000 cases/yr
-world wide distribution, sporadic in US
175
Q

N. meningitidis:

Lab ID and Treatment

A

gram stain is presumptive from CSF or blood
culture on blood/chocolate, 37 degrees + 5% CO2
-can use Thayer-Martin if normal flora present
latex agglutination for capsule serotype
penicillin G drug of choice, resistance rare
rifampin, minocycline, sulfonamides used to eliminate pharyngeal carriers

176
Q

N. meningitidis:

Prevention

A

acquired immunity with age
-exposed by transient colonization w/ different capsular serogroups
vaccines available
-mixed capsular prep: A, C, Y, W-135 (not effective if under 2 years)
-serogroup B vaccine in clinical trials (outer membrane vesicles, intranasal administration)

Pathogenic Microbiology (3 decks)

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