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Micro Exam #2 > Vector-Borne Transmission > Flashcards

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
Q

Where do Coxiella burnetti grow?

A

Host cell phagolysosome

26
Q

What should you never treat coxiella burnetti with?

A

Sulfonamides – they enhance the growth

27
Q

Clinical presentation of Rickettsiae Typhus group?

A

Parasite of BV endothelium
Vasculitis, Rash (Chest–>Extremities)
Weakness, Fever

28
Q

Clinical presentation of Rickettsiae Spotted Fever group?

A

Rash from extremities (Palms and Soles) –> Trunk

Rocky Mountain Spotted Fever

29
Q

What does Rocky Mountain Spotted Fever entail?

A

Abrupt fever, headache, nausea, vomiting
Muscle, Joint, Ab pains from vasculitis of organs
50% fatal untreated

30
Q

Clinical presentation of Rickettsiae Ehrlichia chaffeensis (monocytic erlyichiosis, HME)

A

Headache, Myalgia, Thrombocytopenia, lymphopenia, Marrow Granuloma

Like RMSF< but no vasculitis

31
Q

What cells does Rickettsiae ehrlichia chaffeensis infect?

A

Monocytes/Macrophages

32
Q

What tends to cause the primary pathology of Rickettsiae ehrlichia chaffeensis?

A

Immune Response

Decrease in TNF-a early, Increase late

33
Q

Clinical presentation of Rickettsiae anaplasma phagocytophilum?

A

Rarely rash, but otherwise like ehrlichosis

34
Q

What cells does Rickettsiae anaplasma phagocytophilum infect?

A

Neutrophils and Granulocytes

35
Q

Other name for Coxiella burnetti

A

Q-Fever

36
Q

Clinical presentation of Coxiella burnetti?

A

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
Q

How is Rickettsiae Typhus Group spread?

A

Human Louse or Rat Flea
Transmit Human-Louse-Human
Rats are also reservoir

38
Q

Where is Rickettsiae Typhus Group typically seen?

A

People together with low hygiene.

POWs, refugees

39
Q

How is Rickettsiae-Spotted Fever Group spread?

A

Bite of Dog-tick or Wood-tick

40
Q

How is Rickettsiae-Spotted Fever group maintained in reservoir?

A

Transovarian cycle

41
Q

What part of the country is most prone to dvelop Rickettsiae-Spotted Fever group? What time of year?

A

Southeast US

Summer, Fall

42
Q

How is Rickettsiae-Ehrlichia/Anaplasma spread?

Where is it commonly found?

A

Ticks.

WI, MN

43
Q

How is Coxiella burnetti spread to humans?

A

Via dust or aerosols from infected animals

Especially in placental aerosols

44
Q

Common carriers of Coxiella burnetti include…

A

Goats
Cattle
Sheep
Cats

45
Q

Pathogenesis of Rickettsial diseases?

A

Arthropod bite site –> Endothelium
Multiply Intracellularly and Spread to other tissues
Phospholipase A targets Cell Membranes

46
Q

What does Rickettsiae phospholipase A do?

A

Lyses blood vessels (rash) and other epithelial cells

47
Q

How does R. Rickettsii one up the norman Rickettsiae vessel lysis?

A

It lyses smooth muscle cells

48
Q

How are Rickettsial diseases controlled?

A

Remove Vector Contact

Vaccine for Q-fever (only in Australia)

49
Q

How are Ricketsial diseases treated?

A

Tetracycline/Doxycycline

Micro Exam #2 (15 decks)

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