Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IBI Test 2 > B3.027 Chronic Infections > Flashcards

B3.027 Chronic Infections Flashcards

1
Q

what are chronic infections

A

infections that are not efficiently cleared by either the innate or adaptive immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

examples of viruses that cause chronic/persistant diseases

A

HIV-retroviral integration into host
CMV- persistent infection of glands and kidneys
HSV- episomal latency in neuronal cells, inhibition of apoptosis
EBV- dormancy in B cells with reactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are 6 major bacterial persistence mechanisms

A

antigenic variation or surface antigens (usually immunodominant/serotype defining)
colonization of immunopriveleged niches
modification of intracellular environment
host mimicry
resistance to immune effector mechanisms (opsonization or complement pathway inhibition)
selective gene deactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

bacteria that uses antigenic variation of surface antigens as a mechanism

A

borrelia burgdorferi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

bacteria that use modification of intracellular environment as a mechanism

A

facultative and obligate intracellular bacteria

deactivate lysosome or something else

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

bacteria that uses host mimicry as a mechanism

A

treponema pallidum (host proteins, limited antigens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

bacteria that use resistance to immune effector mechanisms as a mechanism

A 
encapsulated pathogens
borrelia burgdorferi (complement factor sequestration, prevent MAC formation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

spirochetal human diseases

A

syphilis: treponema pallidum
leptospirosis: leptospira interrogans
relapsing fever: several borrelia species
lyme borreliosis: borrelia burgdorferi
periodontal disease: treponema denticola

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe the spirochetal envelope structure

A

periplasmic flagella- hide flagella from the immune system within the periplasm
outer membrane and cytoplasmic membrane
thin and long
predestined for penetration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

leptospira host-pathogen interface

A

LPS and lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treponema pallidum host-pathogen interface

A

no major surface antigens, no LPS

stealth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

borrelia host-pathogen interface

A

abundant lipoproteins which play major roles in pathogenesis

no LPS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

t. pallidum virulence factors

A

no culture in medium (only in rabbit testicles)
hyaluronidase (sticks to extracellular matrix)
fibronectin coat
few surface proteins (Tromp1)
lipoproteins
stealth pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what causes the symptoms of t.pallidum?

A

the immune responses to tissue damage

NOT toxicity of the pathogen itself

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe the stages of syphilis

A

primary at 2 weeks
secondary at 23 weeks
long latency before a tertiary stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the symptoms associated with primary syphilis?

A

chancre at the site of pathogen entry
painless
heals spontaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the symptoms associated with secondary syphilis?

A

maculopapular, desquamative rash
alopecia
papules and plaques in groin
erythematous mucous patches in mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the symptoms associated with tertiary syphilis?

A

gummatous (benign gumma lesions in skin, bone, brain)
cardiovascular (aortic aneurysms)
neurosyphilis (syphilitic meningitis within 2 yrs of infection, vascular syphilis, general paresis, spinal cord damage with demyelination of dorsal roots)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is congenital syphilis?

A

infection in utero after 4th month of gestation
stillborn
rhinitis, secondary and tertiary syphilis
Hutchinsonian teeth and saddleback nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

syphilis epidemiology

A

total US cases 88,000
incidence rising
8:1 males to females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

microscopy diagnostics for syphilis

A 
darkfield of fresh skin lesions (not oral)
DFA staining (fluorescent delabeled antibody)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

nontreponemal serology diagnostics for syphilis

A

VDRL
RPR (rapid plasma antigen)- tests for regain antibodies against cardiolipin (host cell wall component, released due to tissue damage and then an Ab is developed against it)
sensitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

treponemal serology diagnostics for syphilis

A

specific
FTA-ABS
TP-PA

24
Q

DOC for syphilis

A 
penicillin G (single shot IM)
if allergy: doxycycline, tetracycline, azithromycin, ceftriaxzone
25
Q

Jarisch Herxeheimer reaction

A

NOT penicillin allergy
happens in 25% of patients
abrupt onset of fever, chills, myalgias, tachycardia, vasodilation, with flushing, skin rash, or mild hypotension
due to massive release of proinflamm cytokines, triggered by release of endotoxin like substances from bacteremic organisms (lipoproteins)

26
Q

describe the physical structure of leptospira interrogans

A

free living spirochetes
large genomes
several serovars
different LPS on surface

27
Q

asymptomatic hosts of leptospira

A

rodents
dogs
animals
act as resevoirs and shed and contaminate soil/water

28
Q

where do spirochetes persist in the body?

A

renal tubules
shed in urine
contamination of soil and water

29
Q

pathogenesis of leptospirosis

A
  1. infection via intact mucosa or broken skin (via water uptake)
  2. septicemia
  3. damage of small blood vessel endothelium
    - meningitis
    - hepatitis
    - nephritis
    - hemorrhage
  4. exit
30
Q

leptospirosis epidemiology

A 
<100 cases/ year worldwide
occupational exposures
peak in warm months
no human to human transmission
can be fatal
31
Q

microscopy diagnostics for leptospirosis

A

insensitive, nonspecific bc number of spirochetes too low to see
except DFA

32
Q

culture diagnostics for leptospirosis

A

special media, slow growth (2 wks to 4 mo)
blood, CSF: positive during first 10 days
urine: positive after first week

33
Q

serology diagnostics for leptospirosis

A

gold standard: agglutination test

enzyme linked dot IgM immunoassay

34
Q

DOC for leptospirosis

A 
severe: IV penicillin
oral doxycycline (preventative), ampicillin, amoxicillin
35
Q

how are borrelia sp transmitted?

A

soft Ornithodoros ticks
B.hermsii in NW
B.turicatae in SW

36
Q

differentiate between TBRF and LBRF

A

tick borne relapsing fever: endemic

louse borne relapsing fever: epidemic

37
Q

TBRF transmission

A

tick infested rodents nests
Ornithodoros ticks are fast feeders, thus bites are usually not noticed
RF Borrelia are present in salivary glands and quickly transmitted with the saliva upon feeding
ID=1

38
Q

LBRF transmission

A

crushing of louse (rub louse feces into bite wound)

humans the only host

39
Q

describe the mechanism behind recurrent fever

A

recombination of silent genes into single expression site
different genes expressed every few weeks
each serotype is defined by the expression of a different single immunodominant surface lipoprotein

40
Q

microscopy diagnostics for RF

A

detection of spirochetes in blood smears during febrile periods
sens 70%

41
Q

culture diagnostics for RF

A

complex medium

slow growth

42
Q

serology diagnostics for RF

A

western blot for B.turicatae

tests for other spirochetal diseases can show cross reactivity

43
Q

DOC for RF

A

tetracycline (LBRF)
doxycycline (TBRF)
erythromycin

44
Q

species causing Lyme disease

A

Borrelia burgdorferi

45
Q

what types of ticks transmit B.burgdorferi

A

Ixodes

46
Q

describe the epidemiology of Lyme in the uS

A

300,000 cases/year
most common vector borne disease
2 major foci: NE and Great Lakes

47
Q

discuss the transmission of Lyme

A

humans are incidental dead end hosts
Ixodes ticks feed for several days
transmission within 48 hours unlikely
-spirochetes travel from midgut to salivary gland

48
Q

early localized symptoms of Lyme disease

A 
days to weeks at site of tick bite
erythema migrans (EM)
-bulls eye rash
-expanding, self resolving
-appears in most
->5 cm diagnostic
49
Q

early diffuse symptoms of Lyme

A 
malaise
fever
headache
fatigue
chills
MSK pain
lymphadenopathy
50
Q

weeks to months disseminated Lyme symptoms

A 
secondary EMs
neuroborreliosis
-bell's palsy (facial nerve paralysis)
-meningitis
-encephalitis
-radiculopathy
-cranial neuritis
cardiac dysfunction
-myocarditis
-pericarditis
-AV nodal block
51
Q

Late disseminated Lyme symptoms

A

acrodermatitis chronicum atrophicans (paper like skin)
encephalopathy
oligoarticular arthritis (large joints, on only one side)

52
Q

what are two major classes of B.burgdorferi virulence factors

A

tick colonization and survival

mammalian colonization/persistence

53
Q

virulence factor associated with tick colonization and survival

A

OspA binds to tick midgut receptor and protects other bacterial proteins from tick proteases

54
Q

virulence factors associated with mammalian colonization/ persistence

A

OspC binds immunomodulary tick saliva protein, blocks phagocytosis by macrophages, and binds complement component C4b
Adhesins
broad complement resistance family of proteins binding complement regulatory Factor H from different species
antigenic variation allows for persistent infection of reservoir hosts

55
Q

CRASPs

A

complement regulator acquiring surface proteins
block MAC formation
render bacteria serum resistant

56
Q

lyme arthritis pathogenesis

A
  1. invasion and colonization
  2. inflammatory host response to bacterial lipoproteins
  3. bacterial numbers are reduced
  4. persistence/immune evasion
  5. lipoproteins: constant source of inflammatory stimulus in joints (edema associated with neutrophil infiltration)
  6. antibiotic treatment-refractory arthritis: autoimmune response to OspA epitope
57
Q

1st generation Lyme vaccine

A

recombinant lipidated OspA
was approved, but taken off market in 2002
transmission blocking vaccine: needs to generate high titers

IBI Test 2 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions