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Pathogenic Microbiology > Exam #3 > Flashcards

Exam #3 Flashcards

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1
Q

Neisseria gonorrhoeae:

Outline

A

gram negative diplococci
fastidious- requires blood and increased CO2
naturally competent for DNA transformation
capable of conjunction- large plasmid
-may possess antibiotic resistance genes
-encoded transposons

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2
Q

Neisseria gonorrhoeae:

Epidemiology

A

transmitted via mucosal surfaces and infected secretions

-nonsexual transmission rare

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3
Q

Neisseria gonorrhoeae:

Disease Presentations

A 
asymptomatic infection
urethritis
cervicitis
-inflammation of endocervical canal
-mucopurulent discharge
-abscess formation in paracervical (Bartholin's) glands
vulvovaginitis
-pre-adolescent women and post-menopausal
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4
Q

Neisseria gonorrhoeae:

Diseases

A

opthalmia neonatorum
-acute purulent conjunctivitis in newborns
-acquired via passage through the infected birth canal
epididymitis/prostatitis
-common in males under 35
-sterility is post-infection complication
pelvic inflammatory disease (PID)
-peritoneal spread (Curtis-Fitz-Hugh Syndrome)
-infertility is a complication (fallopian tube damage)

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5
Q

Disseminated Gonococcal Infection (DGI)

A

hematogenous spread
-effects skin and joints
*hemorrhagic papular lesions- fingers, wrists, feet
*arthritis- #1 cause of septic arthritis in adults
-endocarditis and meningitis (rare)
complement deficiency is higher risk

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6
Q

DGI:

Diseases

A 
rectal infection
-generally asymptomatic
-can result in tenesmus, local pain, pus on defecation
pharyngeal infection
-generally asymptomatic
-can result in sore throat
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7
Q

Gonococcal Pathogenesis:

Adherence

A

adheres and invades the epithelial cells

  • non-ciliated cells of fallopian tubes
  • cilitated cells damaged through indirect process
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8
Q

Gonococcal Pathogenesis:

Bacterial Phase Shift

A

antigenic variation: pili and opacity proteins
phase variation: ability to quickly turn genes on and off
-reversible and non-reversible
-Pili and Opa proteins

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9
Q

Gonococcal Virulence Factors:

Pili

A

mediate adherence to eptihelial cells and spermatozoa

subunit (pilin) is component of structure that varies: immune avoidance strategy

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10
Q

Gonococcal Virulence Factors:

Opacity (Opa) Proteins

A

mediate adherence and kinvasion
12 different
each undergoes phase variation
-open reading frame (ORF)- shift mechanism

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11
Q

Opa Phase Variation

A

facilitates survival in high progesterone levels
-Opa+ bacteria isolated during proliferative stage of the menstral cycle
-Opa- bacteria isolated during luteal stage
in vitro studies
-Opa+ more sensitive to progesterone than Opa- variants

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12
Q

Gonococcal Virulence Factors:

Lipooligosaccharide (LOS)

A

shorter form of LPS
membrane blebs of GC contain this component
phase and antigenic variation

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13
Q

Gonococcal Virulence Factors:

Iron-Binding Proteins

A

expressed under low iron

compete w/ transferrin, hemoglobin, lactoferrin

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14
Q

Gonococcal Virulence Factors:

IgA Protease

A

cleaves IgA1 (secretory IgA) at mucosal surfaces

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15
Q

Gonococcal Lab Identification

A 
chocolate agar + increased CO2
growth after 1-2 days incubation
carbohydrate utilization
-both glucose
-both can't use lactose
-meningitidis can use maltose, gonorrhoeae cannot
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16
Q

Gonococcal Treatment:

Penicillin

A

no longer drug of choice

  • penicillinase-producing N. gonorrhoeae (PPNG) exists
  • acquired from H. ducreyi plasmid
  • resistance via mutated PBPs
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17
Q

Gonococcal Treatment:

Tetracycline

A

resistance gene carried by transposon on large conjugative plasmid
some strains resistant to both penicillin and tetracycline

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18
Q

Gonococcal Treatment

A

ceftriazone is drug of choice
some isolates also resistant to other classes of antibiotics
-fluoroquinolones
-spectinomycin
vaccine unavailable due to lack of capsule and Ag variation being problematic

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19
Q

C. trachomatis

A

trachoma serovars A, B, Ba, C
adult inclusion conjunctivitis sero’s D-K
most common VD in US
non-gonococcal urethritis: acute epididymitis
-irritation and discharge
persistant urethral leukocytosis

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20
Q

C. trachomatis:

Serovars D-K

A

acute urethral syndrome; cervicitis; PID
-most females asymptomatic
-symptoms are subtle
-sterility, ectopic pregnancies, miscarriages, low birth weight
neonatal infections
-ocular: acute mucopurulent eye discharge
-most common form of neonate conjunctivitis in US
-interstitial pneumonia- gradual onset; no fever

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21
Q

C. trachomatis:

L1, L2, L2a, L3

A

lymphogranuloma venereum (LGV)

  • tropism of lymphoid tissue
  • primary lesion: small painless vesicle on or near genitalia
  • regional lymphadenopathy after several weeks
  • buboes w/fever, headache, myalgia, arthralgia
  • late phase sequelae
  • perirectal ulcers, fistulas, urethral strictures, fibrosis, elephantiasis
  • many infections inapparent
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22
Q

Treponema spp.:

General Characteristics

A

genus composed of three pathogenic spirochete species
-T. pallidum; T. pertenue; T. carateum
corkscrew motility via axial filaments
-can move through high viscosity media
difficult to visualize microscopically
-too thin, need to use dark field
T. pallidum cannot be grown outside tissue culture or live animals

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23
Q

Syphilis:

Epidemiology

A 
12 million cases per year
highly infectious
-aggressively infets mucous membranes
-sexual and congenital transmission
-can infect by direct contact
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24
Q

Syphilis:

Primary Pathogenesis

A

formation of a chancre at site of infection

  • 2-10 weeks
  • painless ulcer
  • heals spontaneously
  • infection systemic at this point
  • genital sites–> increased risk of HIV
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25
Q

Syphilis:

Secondary Pathogenesis

A

multiple lesions, 2-10 weeks post chancre
-skin- papulosquamous rash
-mucosal lesions- condylomata lata
systemic infection becomes asymptomatic after disappearance of rash
resolution of disease in 1/3 of infected
rare sequelae of secondary syphilis
-meningitis, iritis, hepatitis

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26
Q

Syphilis:

Latent Pathogenesis

A 
asymptomatic
can last years post-infection
secondary lesions in 25%
infectivity of body fluids declines
resolution of disease n 1/3 of infected
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27
Q

Syphilis:

Tertiary Syphilis

A

*neurological (CNS)
meningovasculitis and parenchymal degeneration
chronic meningitis
-fever, headache, ocular involvement, cortical degeneration of brain tissue
-behavioral disturbances - paresis
*cardiovascular
medial necrosis and loss of arterial elasticity
-aortic valve disfunction, aneurysm
*lesions
gummas (syphilomas) and/or syphilids

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28
Q

T. pallidum:

Virulence Factors

A 
poorly characterized
lacks numerous surface-expressed proteins
tpr genes
-12 proteins
-adhesions and/or porins
hemolysins
-5 genes
-products my be cytolytic
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29
Q

T. pallidum:

Virulence Factors cont.

A 
gcp gene
-encodes a sialoglycoprotease (degrades host glycoproteins)
ankA and ankB
-encode homologs of mammalian ankyrin 3
iev
-encodes an integral membrane protein
-possible immunosuppressive effects
30
Q

T. pallidum:

Diagnostic Procedures

A 
direct observation of bacteria from lesions
-dark field microscopy
serology
-RPR: Rapid Plasma Reagin
*non-treponemal-based on cross-reaction of anti- T. pallidum with cardiolipin from beef heart
*not very specific
-FA: fluorescent antibody staining
*confirms RPR
31
Q

T. pallidum:

Treatment and Immunity

A
  • penicillin drug of choice for all stages of the disease
  • tetracycline or erythromycin also effective
  • antibody response to OMPs
  • contributes to host resistance to re-infection
  • CMI resolves lesions but does not clear bacteria
32
Q

Haemophilus ducreyi

A 
gram negative coccobacillus
-may be pleomorphic and gram 'variable'
non-motile
fastidious- needs hemin
-chocolate agar will support growth
-elevated CO2 better
33
Q

H. ducreyi:

Disease

A

ST etiology of chancroid or ‘soft chancre’
10x’s more prevalent in males
short incubation: 2-5 days
-ragged ulcer on genitalia with marked swelling and tenderness
-regional lymph nodes enlarged
associated with poor hygiene and poor socioeconomic conditions

34
Q

H. ducreyi Virulence Factors:

HdCDT

A

Haemophilus ducreyi cytolethal distending toxin

-progressive apoptosis of antigen presenting cells

35
Q

H. ducreyi Virulence Factors:

Outer Membrane Proteins

A

LspA1, LspA2

  • 456 and 543 kDa
  • anti-phagocytic properties
36
Q

H. ducreyi Virulence Factors:

DltA

A

ducreyi lectin A

-serum resistance

37
Q

H. ducreyi Virulence Factors:

flp Gene Cluster

A

15 genes
type IV secretion
tadA: reduced lesion formation if mutated

38
Q

H. ducreyi Virulence Factors:

SOD

A

superoxide dismutase

-may also be involved in iron acquisition

39
Q

H. ducreyi Virulence Factors:

pCb

A

low molecular weight plasmid

-encodes beta-lactamases

40
Q

Ureaplasma urealyticum

A 
single species in genus
related to mycoplasma
large: 0.2-0.3 mm; pleomorphic
-no cell wall- has a three layer membrane
*contains sterols- scavenged from hose
*slow growers on enriched mediea
14 serotypes
produces urease- primary virulence factor
41
Q

Ureaplasma:

Diseases

A

urethritis in males - very common
chorioamnionitis and postpartum fever in females
tetracycline is drug of choic
-will also work against Chlamydia

42
Q

Mycoplasma hominus

A

numerous species - only two pathogenic
-M. pneumoniae, M. hominus
M. hominus associated with genitourinary tract
-commonly causes postpartum fever (self-limiting)
-also, pelvic inflammatory disease
-CNS and joint involvement, but rare
responds to tetracycline

43
Q

Borrelia Species:

Principle Pathogenic Species

A

B. recurrentis: epidemic relapsing fever
B. hermsii: endemic relapsing fever
B. burgdorferi: Lyme disease
-12 other species associated with human disease

44
Q

Borrelia Species:

Morphology

A

‘classic’ spirochete
long: 10-30um
more axial filaments than treponemes
visualized by Giemsa or Wright stain

45
Q

Borrelia Species:

Cultivation

A

some can be cultivated
fastidious: require long-chain fatty acids, ect.
microaerophilic

46
Q

B. hermsii

A 
etiologies of relapsing fever
tick (ornithodoros species)
-'endemic' rf
*rodent primary reservoir
*ticks will also maintain bacteria transovarially
47
Q

B. recurrentis

A 
etiology of relapsing fever
louse-borne
-'epidemic' rf
*humans are the only host
*areas of poor hygiene and dire poverty
48
Q

Relapsing Fever

A

average incubation time = 7 days
bacteremia w/febrile episodes (days)
-each relapse duration: 2-4 days
-one to 4 cycles before resolution (afebrile intervals: 7-9 days)
mortality
-tick-borne: very low!
-louse-borne: up to 40%! (due to myocarditis, hepatic failure, ect.)

49
Q

Relapsing Fevers

A

total systemic involvement
no bacteria in blood during ‘down time’
relapsing cycles correlate with antibody production
antigenic phase-shift

50
Q

B. recurrentis and B. hernsii:

Virulence Factors

A

OMPs and lipoproteins

  • phase vary at high frequency (~40 different phenotypes/proteins)
  • mechanism: recombination between genes on linear plasmids
  • protective humoral immunity when bacterium exhausts phenotypic repertoire
51
Q

B. burgdorferi

A 
etiology of Lyme disease
-follows sylvatic cycle
growth in vitro
-slow, doubling time 8-24 hours
-may take days to weeks to isolate
10 different sub-species
52
Q

B. burgdorferi:

Epidemiology

A

localized distribution in US due to anthropogenic factors
tick-vectored
-most common arthropod-vectored infection in US
-eggs–>larvae–>white-footed mouse–>nymphs–>deer–>maturation/mating

53
Q

B. burgdorferi:

Disease Presentation

A

erythema chronicum migrans (ECM)
-at bite sites, small papule, turns into bull’s eye
fever, fatigue, myalgia, headache that last more months
secondary rash half the time
‘stage #2’ day to weeks post-infection: neurologic/cardiac symptoms
weeks, months, years post-infection: chronic arthritis; encephalitis

54
Q

B. burgdorferi:

Virulence Factors

A 
OspA-->OspC
adhesins
-targets integrins, platelets, and collagen
LPS
peptidoglycan
-inflammatory properties
immune-mediating toxins
55
Q

Relapsing Fever:

Diagnosis and Treatment

A

direct examination of blood
serologic tests
tetracycline or erythromycin effective at a single dose

56
Q

Lyme Disease:

Diagnosis and Treatment

A

clinical findings
direct examination, PCR/serology
doxycycline IV; ceftrioxone for more serious
-response to treatment is slow –> requires 30-60 days

57
Q

Borrelia Vaccine

A 
discontinued
insufficient consumer demand
recombinant OspA... the tick protein
antibodies target the arthropod mid-gut localized bacteria
pathogen is killed at point of enetry
58
Q

Leptospira Species

A 
L. interrogans in humans (over 200 serotypes)
other species are free-living
more 'tightly-wound' spirochete
-very thin-viewed in dark field only
-single axial filament
can be cultivated in vitro
-aerobic; fastidious
-killed in an acidic environment
-survival for weeks in water
59
Q

Leptospirosis:

‘Swamp Fever’

A

occurs world-wide (100-200 in US yearly)
zoonotic disease
-wild and domestic animals (rodents, cattle, dogs)
-transmitted to humans through contaminated water
-farmers and slaughterhouse workers at highest risk

60
Q

Leptospirosis:

Pathogenesis

A

site of inocculation is through break in skin or mucosal surface
rapid systemic spread to include CSF
-also renal tubules and kidneys in animals

61
Q

Leptospirosis:

Virulence Factors

A

23 potential virulence genes by subtractive hypbridization

evidence for apoptotic effectors

62
Q

Leptospirosis:

Disease Presentation

A 
most infections asymptomatic
7-13 days incubation time
flu-like symptoms
-fever, chills, headache, myalgia
-associated w/bacteremia and CSF inflitration (1 week duration)
63
Q

Leprospirosis:

Stage 2

A 
*bacteremia disappears
aseptic meningitis
-usually 3 weeks in duration
-resembles viral meningitis
-other generalized symptoms
*myalgia, rash, renal and hepatic involvement
-severe form: Weil's disease
*extensive vasculitis; jaundice; renal damage; hemorrhagic rash
*10% mortality
64
Q

Leptospirosis:

Diagnosis and Treatment

A

serologic tests (including slide agglutination)
culture not useful as it takes weeks
organism sensitive to beta-lactams or tetracylcine

65
Q

Corynebacterium Species

A 
pathogenic
-C. diptherieae
-C. ulcerans and C. pseudotuberculosis
-C. jeikeium (on immunosuppressed)
-group D-2 coryneforms/ UTIs (C. urealyticum)
low virulence
-'diptheroids'
66
Q

C. diphtheriae:

Characteristics

A 
humans are reservoirs- URT and skin
gram+, club shaped, non-motile
non-spore forming, catalase +
stained organisms resemble Chinese letters
three biotypes
-gravis, mitis, intermedius
67
Q

C. diphtheria:

Diseases

A

URT infection: toxinogenic strains
-low-grade fever and sore throat
-adherent pseudomembrane (tonsils/pharynx)
cutaneous infection: Tox+ or Tox- strains
-insect bites, wounds, co-infected lesions
-tropical climate
toxic complications
-myocarditis/ polyneuritis

68
Q

C. diphtheria:

Pathogenesis

A

non-invasive
respiratory symptoms from local effects of toxin
-pseudomembrane from back of throat to trachea
-cervical adentitis/edema/’bull neck’
-respiratory obstruction
-systemic effects
*myocarditis- arrythmia, congestive heart failure
*CNS- paralysis

69
Q

C. diphtheria:

Diphtheria Toxin

A

encoded by toxin-converting phage
expression under low iron
-repressor upregulated in presence of iron
A/B subunit toxin
-its expressed as a single polypeptide
-B fragment- receptor binding
-A fragment- internalized enzymatic activity

70
Q

C. diphtheria:

Other Virulence Factors

A

iron acquisition proteins and siderophores

Pathogenic Microbiology (3 decks)

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