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Immuno mikro eng > Zoonotic & Vector-Borne Infections > Flashcards

Zoonotic & Vector-Borne Infections Flashcards

1
Q

What is the causative agent of Lyme disease and what is the reservoir? Transmission?

A

Borrelia burgdorferi

Reservoir: white-tailed dear and white-footed mouse

Transmitted in northeast US by Ixodes tick

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2
Q

What is the first stage of Lyme disease?

A

Erythema chronicum migrans -> bulls-eye lesion at site of tick bite, often accompanied by fatigue and fever

Happens about 1 week after bite

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3
Q

What is the second stage of Lyme disease?

A

Bacteria spread to CNS and joints: Bilateral bell’s palsy and heart block (conduction defects). Possible early arthritis

Happens weeks to months after tick bite

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4
Q

What is the third stage of Lyme disease?

A

Migratory polyarthritis and encephalitis (CNS defects), occurring months to years after tick bite

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5
Q

What type of bacteria is Borrelia burgdorferi and how is it detected?

A

Spirochete

Detected via blood, CSF, or synovial sample with immunofluorescence showing spirochete.

Can also PCR/ELISA.

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6
Q

What causes relapsing fever?

A

Borrelia recurrentis, a spirochete with antigenic variation causing intermittent relapse

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7
Q

What is the mechanism of Borrelia recurrentis antigen switching? Why is this relevant to treatment?

A

VMP - Variable major protein, a cell surface serotype

Release of VMP during treatment with penicillins will cause Jarisch-Herxheimer reaction

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8
Q

What causes epidemic relapsing fever? What is the bacteria’s host?

A

Transmission of Borrelia recurrentis by human lice vector Pediculus, happens in poor sanitation. Gets into bite site.

Humans are the only animal reservoir

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9
Q

What are the symptoms of relapsing fever?

A

Bacteremia will cause high fever / chills for 3-5 days, with possible delirium, arthralgia, and myalgia

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10
Q

What causes endemic relapsing fever?

A

A soft tick vector carries Borrelia species, with rodent reservoir.

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11
Q

What stain can be used to detect all Borrelia spirochetes?

A

Giemsa stain

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12
Q

How is Leptospirosis transmitted?

A

Via drinking urine-contaminated water, typically during watersports in the tropics.

The organism chronically infects animal kidneys, and will be excreted in animal urine, especially dogs

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13
Q

What are the common clinical findings of Leptospirosis?

A

Fever and headache, and conjunctival suffision (redness of conjunctiva without inflammation)

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14
Q

What can Leptospirosis progress to?

A

Weil’s disease -> marked by kidney damage, liver damage and associated jaundice / conjunctival hemorrhage

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15
Q

What is the morphology of Leptospira and how can it be tested for clinically?

A

Spirochetes -> detected by dark-field microscopy or serotype-specific antibody titers

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16
Q

What organism is often passed via dog bite? What is its morphology / lab test?

A

Pasteurella multocida, found in nasopharynx of many animals

Gram negative, oxidase-positive bacillus

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17
Q

What infection does Pasteurella cause?

A

A skin cellulitis 1-2 days post cat scratch or dog bite

Can cause chronic respiratory infection in patients with chronic lung disease

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18
Q

What causes Rocky Mountain Spotted Fever?

A

Rickettsia ricketssii

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19
Q

How and where is RMSF transmitted?

A

Transmitted via tick vector in southeastern US.

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20
Q

Where does Rickettsia live?

A

Lives in vascular endothelium of lung, spleen, brain, and skin as an obligate intracellular organism (internalized via phospholipase)

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21
Q

What is the pattern of rash from RMSF? What type of rash is it?

A

Starts on the extremities, including palms and soles, and spreads inwards towards trunk. It is a petechial or maculopapular rash

22
Q

What causes high morality in RMSF?

A

Release of LPS from the gram negative cell wall, and splenomegaly + neurological symptoms from blood clots

23
Q

What is the morphology of Rickettsia?

A

Poorly-staining gram negative coccobacillus

24
Q

What test was used to detect Rickettsia?

A

Weil-Felix test -> ability to agglutinate Proteus vulgaris

25
Q

What tests now detect Rickettsia?

A

Indirect immunofluorescence with rickettsial antigens, or IgG/IgM detected

26
Q

What is Cat Scratch Disease and how is it transmitted? How is it seen clinically?

A

Disease caused by cat scratch, bite, or lick. Caused by Bartonella henselae

Seen clinically with fever and swelling of regional lymph nodes, usually in axilla

27
Q

What does Bartonella henselae cause in immunocompromised?

A

Bacillary angiomatosis

Raised, red lesions after cat scratch due to vascular infection. Dissemination is via sepsis, and looks like Kaposi’s sarcoma.

28
Q

What is the most severe manifestion of Bartonella?

A

Hepatic / splenic peliosis -> spread to liver or spleen, will show as cystic, blood-filled lesions and elevated Alk-Phos levels

29
Q

What is the morphology of Bartonella?

A

Gram negative, slightly curved rods

30
Q

What is the basic difference between Category A, B, and C bioterrism threats?

A

A - easily disseminated, high mortality, can cause panic
B - moderately easy to disseminate, moderate mortality
C - organisms which can be engineered in the future of high mortality (none listed)

31
Q

What are the major category A agents?

A

Anthrax, botulism, plague, smallpox, tularemia, hemorrhagic fever viruses: filoviruses, arenaviruses, bunyaviruses, flaviviruses

32
Q

What are the two anthrax toxins and their structure?

A

They are both AB toxins, with B subunit = Protective antigen (PA), used for vaccine

A1 = Edema factor, disrupts cellular metabolism via raising cAMP, uses calmodulin like invasive adenylate cyclase of B. pertussis

A2 = Lethal factor - metalloprotease which cleaves MAP kinases to short circuit transduction pathways in monocytes

33
Q

Where are anthrax spores typically found?

A

Soil or contaminated animal products (sheep, cattle, other herbivores)

34
Q

Why is it so hard to get rid of anthrax?

A

Spores can remain viable for >50+ years

35
Q

How does anthrax infection usually start and how does it kill you?

A

Starts when spores contaminate scratch or abrasion and germinate, forming black eschar. If it spreads from ulcer to lymphatics it can get to blood and kill you

36
Q

What is Woolsorter’s disease? How does it kill you? Why is it hard to diagnose?

A

Inhalation of spores of anthrax, causing bacilli to germinate in lungs.

Death by massive pulmonary edema and mediastinal hemorrhage.

Hard to diagnose because symptoms are nonspecific low grade fever and cough.

37
Q

What is the morphology and lab ID of anthrax?

A

Gram positive bacillus, but interestingly non-hemolytic and non-motile

38
Q

Other than the Type 3 secretion system used to disrupt macrophages and PMNs, what other two virulence factors does Yersinia pestis have?

A
  1. Invasins - inducing actin rearrangement and uptake of bacteria into nonprofessional phagocytes
  2. Plasminogen activator - plasminogen will dissolve fibrin clots and prevent chemotaxis of PMNs
39
Q

What are the two forms of plague and which is of higher concern? Why?

A
  1. Bubonic plague
  2. Pneumonic plague

pneumonic plague is a bigger concern because there is person-to-person transmission, and aerosolization = adaptation to human host

Bubonic only transmitted by fleas, lower virulence

40
Q

What are the features of bubonic plague?

A

Lymphadenitis “buboes”, vasculitis, bruising, and gangrenous necrosis of “acral” or very distal regions of periphery “black death”

41
Q

How does pneumonic plague originally develop?

A

Comes from bubonic or primary septicemic plague (bubonic with no buboes, multiple organ failure)

Represents an adaption by Yersinia pestis to a more virulent phenotype

42
Q

What is the appearance of Yersinia pestis on gram stain? How are samples taken?

A

Safety pin appearance -> stains at the poles.

Gram negative rod

Sputum samples or aspirate from buboes

43
Q

Are vaccines available for plague and anthrax?

A

Yes! for high risk groups

44
Q

What are Yops?

A

Yersinia outer membrane proteins - exotoxins with kinase and phosphatase activity which are injected by Type 3 secretion system

45
Q

What typically carries Francisella tularensis, and what is the other name for the disease?

A

Other than tularemia, it is called Rabbit Fever, because it is carried by wild rodents like rabbits

46
Q

How can humans become infected with Tularemia?

A
  1. Being bitten by infected insect
  2. Handling of infected animal carcasses
  3. Eating or drinking contaminated food / water
  4. Inhalation of bacteria
47
Q

Why is tularemia so scary?

A

Highly infectious, infectious dose is similar to Shigella

48
Q

What is the morphology of Francisella tularensis?

A

Gram negative coccobacillary rod

-> not grown in lab due to infection risk.

49
Q

What are the different types of tularemia? Which is most common?

A
  1. Ulceroglandular - cutaneous ulcer with lymphadenopathy, skin infection from tic bite
  2. Oculoglandular - conjunctivitis with lymphadenopathy
  3. Oropharyngeal
  4. Pneumonic
  5. Systemic with septicemia (50% mortality)
50
Q

What is the growth pattern of Francisella?

A

Intracellular, enters via skin lesion (i.e. tic bite), then travels to lymph nodes in macrophages before disseminating

Immuno mikro eng (56 decks)

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