Vector-Borne Transmission Flashcards

1
Q

Describe the structure of Borrelia

A

Long spirochete
0.4uM (big enough for light microscope)
Stain G-, but NO LPS
Inflamm. lipoproteins in outer membrane

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2
Q

Four indicators of sepsis?

A

Hypotension
Fever
Heightened HR/BR
Infection Signs

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3
Q

Clinical Presentation of Borrelia recurrentis, hermsii, and 20 others

A

Bacteremia within week of inoculation
Fever, Intense Headache, Muscle Pain for 3-5 days
Symptoms Recurr after 5-10 days latency
May eventually form necrotic foci at parenchymatous organs

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4
Q

Why does Borrelia recurrentis keep on coming back?

A

Antigenic variation (may go through 5-10 cycles)

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5
Q

Borrelia burgdorferi (and 9 others in Eurpose) cause…

A

Lyme Disease

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6
Q

Symptoms of Lyme Disease?

A

Early – Flu-like, Bull’s Eye Rash
Early Disseminated – Facial Nerve Palsy, Meningitis, Carditis
Chronic – Arthritis, Joint Pain, Affect Heart/Nerves

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7
Q

Classy name for Bull’s Eye Rash?

A

Erythema chronicum migrans

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8
Q

How is Borrelia recurrentis spread?

A

Human Louse

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9
Q

How is Borrelia hermsii spread?

A

Soft bodied ticks with a rodent reservoir

– Transovarian and through bite

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10
Q

How is Borrelia burgdorferi spread?

A

Deer tick nymph with deer, mouse, or bird reservoir

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11
Q

Pathogenesis of Borrelia recurrentis and hermsii

A
Uses VMP (variable major protein) antigen
Mostly the same, with a few mutants
Abs select for the mutants
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12
Q

What leads to Borrelia recurrentis latency? relapse?

A

Latency – Most of the population killed

Relapse – Mutant variety grows to repopulate

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13
Q

Pathogenesis of Borrelia burgdorferi

A

Multiple rounds of symptoms probably means multiple infections with difference burgdorferi strains

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14
Q

How is Borrelia controlled?

A
  • Avoid Vectors

- No effective vaccine

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15
Q

How is Borrelia treated?

A

Doxycycline or synthetic penicillins

can use 3rd gen cephalosporins

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16
Q

Describe the structure of Rickettsiae

A

Small G- Rods

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17
Q

Growth conditions required for Rickettsiae?

A

Obligate intracellular parasite

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18
Q

How is Rickettsiae cultured?

A

Yolk sac of embryonated egg

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19
Q

Four groups of Rickettsiae?

A

Typhus group
Spotted Fever Group
Enlichia, Anaplasma
Coxiella burnetti

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20
Q

Which of the four Rickettsiae groups isn’t really a Rickettsiae, but is likely classified that way according to our shelf materials

A

Coxiella burnetti

21
Q

Who is in the Rickettsiae Typhus group?

Where do they grow?

A

prowazekii, typhi, akari

Cytoplasm of Host Cell

22
Q

Who is in the Rickettsiae Spotted Fever group?

Where do they grow?

A

rickettsii

Cytoplasm of host cell

23
Q

Describe the lifecycle of Rickettsiae ehrlichia, anaplasma.

A

Chlamydia-like (RB-EB alternation) in monocytes (Ehr) or granulocytes (Ana)

24
Q

What is structurally unique about Rickettsiae ehrlichia, anaplasma

A

NO PG or LPS

25
Where do Coxiella burnetti grow?
Host cell phagolysosome
26
What should you never treat coxiella burnetti with?
Sulfonamides -- they enhance the growth
27
Clinical presentation of Rickettsiae Typhus group?
Parasite of BV endothelium Vasculitis, Rash (Chest-->Extremities) Weakness, Fever
28
Clinical presentation of Rickettsiae Spotted Fever group?
Rash from extremities (Palms and Soles) --> Trunk | Rocky Mountain Spotted Fever
29
What does Rocky Mountain Spotted Fever entail?
Abrupt fever, headache, nausea, vomiting Muscle, Joint, Ab pains from vasculitis of organs 50% fatal untreated
30
Clinical presentation of Rickettsiae Ehrlichia chaffeensis (monocytic erlyichiosis, HME)
Headache, Myalgia, Thrombocytopenia, lymphopenia, Marrow Granuloma Like RMSF< but no vasculitis
31
What cells does Rickettsiae ehrlichia chaffeensis infect?
Monocytes/Macrophages
32
What tends to cause the primary pathology of Rickettsiae ehrlichia chaffeensis?
Immune Response | Decrease in TNF-a early, Increase late
33
Clinical presentation of Rickettsiae anaplasma phagocytophilum?
Rarely rash, but otherwise like ehrlichosis
34
What cells does Rickettsiae anaplasma phagocytophilum infect?
Neutrophils and Granulocytes
35
Other name for Coxiella burnetti
Q-Fever
36
Clinical presentation of Coxiella burnetti?
Typically: Fever w/ Pneumonia/Hepatitis 2-3 week post exposure Can be: - Chronic infections leading to endocarditis in pts w/ defective heart valves - Granulomas in liver, spleen, BM
37
How is Rickettsiae Typhus Group spread?
Human Louse or Rat Flea Transmit Human-Louse-Human Rats are also reservoir
38
Where is Rickettsiae Typhus Group typically seen?
People together with low hygiene. | POWs, refugees
39
How is Rickettsiae-Spotted Fever Group spread?
Bite of Dog-tick or Wood-tick
40
How is Rickettsiae-Spotted Fever group maintained in reservoir?
Transovarian cycle
41
What part of the country is most prone to dvelop Rickettsiae-Spotted Fever group? What time of year?
Southeast US | Summer, Fall
42
How is Rickettsiae-Ehrlichia/Anaplasma spread? | Where is it commonly found?
Ticks. | WI, MN
43
How is Coxiella burnetti spread to humans?
Via dust or aerosols from infected animals | Especially in placental aerosols
44
Common carriers of Coxiella burnetti include...
Goats Cattle Sheep Cats
45
Pathogenesis of Rickettsial diseases?
Arthropod bite site --> Endothelium Multiply Intracellularly and Spread to other tissues Phospholipase A targets Cell Membranes
46
What does Rickettsiae phospholipase A do?
Lyses blood vessels (rash) and other epithelial cells
47
How does R. Rickettsii one up the norman Rickettsiae vessel lysis?
It lyses smooth muscle cells
48
How are Rickettsial diseases controlled?
Remove Vector Contact | Vaccine for Q-fever (only in Australia)
49
How are Ricketsial diseases treated?
Tetracycline/Doxycycline