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Microbio Exam 1 > Vector borne agents > Flashcards

Vector borne agents Flashcards

1
Q

3 diseases caused by vector borne bacterial agents

A
  1. Lyme Disease
  2. Rocky Mountain Spotted Fever
  3. Plague
    - arthropod vector
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2
Q

At least 3 closely related species can cause Lyme disease: Borrelia burgdorferi, Borrelia garinii, Borellia afzelii. Which is found in the US?

A

B. burgdorferi

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3
Q

What is the B. burgdorferi vector?

A

-black legged tick (Ixodes)

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4
Q

Why is simple removal of the Ixodes tick enough to prevent Lyme disease if it has already bitten you?

A

-takes 2-3 days for transmission of bacteria

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5
Q

Ticks have 2 year life cycles and what are the 4 stages?

A
  • eggs hatch into larvae
  • larvae develop into nymphs
  • nymphs progress to adults
  • female adults lay eggs
  • blood meal between each stage of maturation*
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6
Q

Characteristic rash of Lyme Disease

A

-Erythema migrans: bull’s eye rash

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7
Q

Borrelia burgdorferi is what shape of bacterium?

A

-spirochete

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8
Q

Species of ticks and regions they infect with Lyme Disease

A
  • Ixodes scapularis (deer tick) in NE and North central US

- Ixodes pacificus on pacific coast

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9
Q

Which phase of the tick life cycle is most likely to bite humans?

A

-nymph

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10
Q

In the East and Midwest, the most common animal reservoir for B. burgdorferi is…

A
  • white footed mouse

- deer are also important but only because they are the principal host for adult tick

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11
Q

Why do most cases of Lyme Disease occur in the summer?

A

-nymphs feed during late spring and early summer and are the form of tick most likely to transmit bacteria to humans

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12
Q

I.neotomae is the main vector for Lyme Disease on the West coast. What is the reservoir and why does this not get to humans?

A
  • woodrat

- I. neotomae doesnt bite humans

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13
Q

T/F: I. Pacificus prefers to eat lizards, which are not a reservoir for B. borgdorferi, but occasionally will feed on a woodrat and become infected and transmit to humans this way.

A

true

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14
Q

Why aren’t lizards susceptible to Borrelia infection?

A

-due to complement-mediated killing of the bacteria in lizard blood

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15
Q

What can explain the increase in Lyme Disease prevalence?

A
  • increased exposure to agent

- increased awareness/diagnosis of the disease

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16
Q

Lyme Disease is a good example of an _______ disease.

A

-emerging

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17
Q

Who is at risk for Lyme Disease?

A
  • people whose jobs involve landscaping, brush clearing, forestry, or park management in endemic areas
  • work or play in yard or hike, camp, and hunt
  • people living or work in residential areas surrounded by tick-infested woods or brush
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18
Q

Structure and physiology of B. burgdorferi

A
  • spirochete, gram negative, extracellular
  • helical, flexible cylinder with 7-11 periplasmic flagella and an outer membrane that is loosely associated with underlying structure
  • highly motile
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19
Q

T/F: B. burgdorferi causes disease via toxins

A

-false; causes disease due to its ability to migrate through tissues, adhere to host cells, and evade host immune system

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20
Q

What is unique about B. burgdorferi’s genome?

A
  • about 40% on plasmids

- huge proportion dedicated to lipoproteins which are located on bacterial surface

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21
Q

________ is the key step in Borrelia infection in both arthropod vector and mammalian host. What probably mediates this?

A
  • Attachment

- outer surface proteins (Osps) A-F

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22
Q

Explain how tick feeding induced an adaptive response that facilitates spread of Borrelia from tick to host.

A
  • OspA is used to attach to tick midgut by binding TROSPA protein on luminal side of tick gut epithelial cells
  • in unfed ticks, expression of OspA and TROSPA are high
  • during feeding, production of OspA decreases and OspC increases
  • spirochete migrates to tick salivary glands where it can be passed to host
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23
Q

Function of OspC in lyme disease

A
  • may help mediate attachment of bacteria to tick salivary glands, ready for transfer to mammalian host
  • OspC also binds to tick salivary protein (Salp15) and coats bacteria with this tick protein
  • salp15 is immunosuppressive in mammalian host
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24
Q

How is Salp15 immunosuppressive?

A

-protects bacteria from neutralizing antibodies in bloodstream of mammalian host

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25
Q

T/F: In mammalian host, Borrelia spirochete uses same set of surface molecules to bind to host cells and to ECM

A

-false

26
Q

Early clinical manifestations of Lyme Disease

A
  • Erythema migrans at site of tick bite
  • rash appears 7-14 days after tick bite
  • accompanied by fever, fatigue, headache, muscle ache
27
Q

Spirochetes disseminate from site of tick bite in lyme disease by what 3 routes?

A

-cutaneous, lymphatic, and blood-borne routes

28
Q

Signs of early disseminated Lyme Disease

A
  • may appear days to weeks after solitary EM lesion

- secondary EM, muscle aches, fever, facial palsy, headaches, fatigue

29
Q

Late Disseminated Lyme Disease

A
  • may progress to this weeks or months later
  • more commonly seen as intermittent swelling and pain of one or a few joints (often knee)
  • may also cause neurological disease
30
Q

What neurological disease may late disseminated Lyme Disease cause?

A
  • Ataxia
  • Memory loss
  • Mood changes
  • Sleep disturbances
31
Q

4 ways B. burgdorfori persists in host

A
  1. protection from neutralizing antibodies via OspC/SalP15 interaction
  2. avoidance of complement-mediated killing by binding a HOST negative regulator of complement cascade (CRASP)
  3. antigenic variation of surface molecules
  4. hiding in immune privileged sites
32
Q

CRASP and _______ interactions likely contribute to host range.

A
  • factor H

- CRASP must not bind lizard Factor H and why lizard isnt host

33
Q

Mechanism of antigenic variation of bacterial surface of B. burgdorfori

A

-VlsE (surface lipoprotein) undergoes antigenic variation by recombination of 15 silent cassettes into vlsE expression locus

34
Q

2 methods to detect B. burdorfori in the host

A
  1. Cultivation: from vertebrate host or arthropod in Barbour-Stoenner-Kelly medium; slow grower needs 2-6 weeks; recovered from biopsy of EM, large vols of blood early in untreated disease, rarely CSF and NEVER from joint fluid
  2. PCR: can find evidence of organism in joint fluid using PCR
35
Q

Diagnosis of Lyme Disease

A
  • EM rash of 5 or more cm
  • headache, muscle or joint pain IN SUMMER without respiratory or GI symptoms
  • lab confirmation with ELISA followed by Western
36
Q

Why are positive antibody tests not the best for detecting infection?

A
  • take 1-2 weeks to make them

- cannot tell current infection or previous infection

37
Q

Treatment of Lyme Disease

A
  • Doxycycline for early localized or disseminated infection (Amoxicillin is 2nd choice)
  • Intravenous antibiotic for late disseminated disease involving neurologic abnormalities
38
Q

Why is treatment resistant arthritis following Lyme Disease treatment and eradication thought to be autoimmune?

A
  • months or even several years AFTER antibiotic treatment

- PCR negative for organism in joint fluid

39
Q

Rickettsia rickettsii structure and physiology

A
  • gram negative, obligate intracellular pathogen

- causes rocky mountain spotted fever

40
Q

Where and when do most cases of RMSF occur?

A
  • Southeastern and South central states

- summer

41
Q

Season occurrence of a diseases suggests what?

A

-vector spread illness

42
Q

Vectors of RMSF

A
  • West: wood tick

- East: dog tick

43
Q

In the tick containing RMSF, bacteria are transmitted how?

A
  • transovarially from mother to offspring in eggs

- takes pressure off of need to keep bacteria alive in nature

44
Q

Rickettsia rickettsii bacteria are deposited on skin by feeding ticks and enter via ______.

A

-scratching

45
Q

RMSF is characterized by what?

A
  • sudden headache, fever, chills, muscle aches, and characteristic rash
  • rash starts on periphery of body and spreads to the trunk
46
Q

How is R. ricketsii spread throughout the body? Describe their interaction with host cells

A
  • blood stream
  • attach to vascular endothelial cells and induce their own uptake
  • next, rapidly escape from vacuole and reach host cytosol where they replicate
  • use localized polymerization of host actin to spread to adjacent cells or exit host by lysing finger-like projections
47
Q

4 other intracellular bacteria that use actin polymerization to spread

A
  • listeria
  • shigella
  • rickettsia
  • vaccinia
48
Q

RMSF treatment and prevention

A
  • doxycycline (first choice) or chloramphenicol (second choice)
  • no vaccine
  • prevent by wearing protective clothing, using insect repellents, and by monitoring and promptly removing ticks
49
Q

What is the cause of the plague

A

-Yersinia pestis

50
Q

Structure and physiology of Yersinia pestis

A
  • gram negative bacterium, baccilus
  • primarily extracellular growth, but can grow in macrophages
  • looks like safety pins in blood
51
Q

What is the natural reservoir for Yersinia pestis? What is the vector?

A
  • wild rodents

- main vector is rat flea

52
Q

Transmission of Y. pestis from flea to mammalian host

A
  • when flea bites rodent with plague, the bacteria multiple in gut of flea
  • bacteria form biofilm that blocks the flea’s digestive tract so fleas cannot ingest more blood
  • hungry fleas keep biting, each time regurgitating blood and some plague bacteria into the new bite wound and spreading Y. pestis
  • *growth of of bacteria within flea vector alters the behavior of the fleas and aids in transmission of bacteria to mammalian host
53
Q

As with all of these diseases today, humans are accidental hosts. What is the main host for Y. pestis?

A

-rats, but when they die from plague, feed on humans

54
Q

Clinical disease of plague

A
  • plague bacilli spread to LNs, causing them to swell and become hemorrhagic forming buboes
  • accompanying fever, chills, headache, extreme exhaustion
55
Q

If not treated immediately with antibiotics, Y. pestis can spread throughout bloodstream and produce _______.

A
  • septicemic plague: systemic infection

- often fatal

56
Q

What happens if Y. pestis invades lungs? what is now unique about transmission?

A
  • cause pneumonic plague
  • at this point, bacteria do not need fleas to spread and can be spread from humans to humans via airborne transmission
  • creates very dangerous epidemic conditions
57
Q

How does Y. pestis evade the immune system?

A

-prevents phagocytosis via capsule and TTSS effectors

58
Q

TTSS of Y. Pestis: what are the effectors and what do they do?

A
  • YopH, YopT, YopE, YopO
  • prevent phagocytosis of bacterium by macrophages (disrupts host cytoskeleton)
  • slows inflammatory response of host by decreasing INF gamma and TNF
59
Q

How to diagnose the plague

A

-Giema or gram stain of smears from bulboes and/or blood
-fluorescent antibody test against unique envelope antigen
-

60
Q

Treatment and prevention of the plague

A
  • streptomycin or tetracycline
  • isolate individuals with pneumonic plague
  • rat control and insecticides

Microbio Exam 1 (13 decks)

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