Pod Zoonosis

Front 1

How is the Black Plague, Yersinia pestis, transmitted?

Back 1

Via flea bites

Front 2

Pneumonic plague or bubonic plague?
Rapid, person to person spread

Back 2

Pneumonic
Direct exposure of yersinia pestis from a mamalian source expresses the F1 capsule causing a more acute disease.

Front 3

Pneumonic plague or bubonic plague?
NO person2person spread

Back 3

Bubonic plague

Front 4

When does the yersinia pestis NOT express the F1 capsule?

Back 4

At temps below the mammalian body temp. Therefore our body temp effects how the bacteria behaves.

Front 5

Are zoonoses typically transmittable from person to person?

Back 5

No

Front 6

T or F
zoonoses are disease transmitted from animal to humans under any condition.

Back 6

No, only under normal conditions.

Front 7

Neutrophils and macrophages phagocytose and kill the majority of yersina pestis. So, what is the problem?

Back 7

The remaining yersinia pestis produce the F1 capsule and are therefore antiphagocytic AND can degrade complement

Front 8

Which version of yersinia pestis has a 2-7 day incubation, and which has a 2-3 day incubation?

Back 8

Bubonic plague has a 2-7 incubation and Pneumonic plague has a 2-3 day incubation.

Front 9

Why can you use chloramphenicol, tetracycline or aminoglycosides against yersinia pestis (plague)? Which is recommended for initial therapy?

Back 9

Because they are all active against Gram neg bacteria.

High doese of tetracycline are recommended for initial therapy.

Front 10

Compare and contrast septcemic plague and pestis minor?

Back 10

Both are transmitted via a flea bite (like bubonic plague) BUT, septemic bypasses lymphatic involvement, has 100% mortality rate untreated and is systemic. Pestis minor has 0% mortality rate and is localized.

Front 11

What pet should further your suspicion of yersinia pestis?

Back 11

Cats

Front 12

What is the mortality rate for bubonic plague and pneumonic plague?

Back 12

Bubonic is 60-90% UNtreated
Pneumonic is 100% TREATED

Front 13

Sudden fever, chills, nausea, emesis. Two days later lymphodenopathy. Two days later severe systemic disease.

Back 13

Bubonic plague, yersinia pestis

Front 14

Where does yersini pestis multiply?

Back 14

In the lungs

Front 15

Lymph nodes markedly necrotic and may ulcerate and drain due to lymphadenitis. What are these called?

Back 15

Buboes

Front 16

Vasculitis can often result due to plague, can produce a rash and can cause infarction leading to:

Back 16

Gangrene of toes, fingers, ears and distal penis.

Front 17

Fastidious, rabbits

Back 17

Tuluremia

Front 18

Brucella melitensis requires direct contact with the organism by inhalation, ingestion or skin exposure. Where is it found?

Back 18

Africa, Asia and the Mediterranean, but foodborne is increasing in the USA.

Front 19

What are typical, and severe signs of brucellosis?

Back 19

Typical: Flu-like
Severe: Orcitis, arthritis, endocarditis, glomerularnephritis, intermittent fever.
(brucellosis, big balls)

Front 20

Why is brucellosis so difficult to treat?

Back 20

Long incubation period, and vague, no specific symptoms.

Front 21

How do you treat brucella? Why do you have to treat it for such a long time?

Back 21

Treat with tetracycline, specifically doxycycline bc it can penetrate cell mem.
Must treat for up to 3 mo bc of the intracellular location of the bacteria.

Front 22

Cat scratch fever (Bartonella henseala)can show up as:

Back 22

a small pustule

Front 23

What two groups are at the greatest risk if infected with toxoplasma?

Back 23

Immunocompromised and pregnant.

Front 24

How is toxoplasma treated in the immunocomp?
Preg?
What is used as long term prophylaxis in supressed pt?

Back 24

Pyrimethamine
Clindamycin (Linda was preggers)
Trimethoprim/Sulfamethoxazole

Front 25

Coxiella burnetti is extremly environmentally resistant, can infect invertebrates and vertebrates, and has many reservoir hosts. How is one typically infected?

Back 25

Contact w/ afterbirth of infected animals
Consumption of unpasturized milk
Exposure to research animals, especially sheep

Front 26

Are most cases of Q fever diagnosed?
Incubation of coxiella burnetti?

Back 26

No, most go misdiagnosed
7-40 days
*causes bacteremia and syptoms are flu-like.

Front 27

Entamoeba histolytica - Amoebic Dysentery (India)
Alternates btwn cyst and trophozoite form.
Where does it bind?
How may it spread?
Binding triggers trophozoites to produce proteinases which are:

Back 27

Where does it bind? Colonic mucous mem
How may it spread? hepatic portal system
Binding triggers trophozoites to produce proteinases which are: cytolytic for human cells.

Front 28

Spread via a tsetse fly in Africa.
Tender nodule and febrile.
What allows this organism to twart the immune defense so well?

Back 28

It is the African Typanosomiasis.
Variant Surface Glycoprotein (VSG), provides an endless suppply of antigenically distinct parasites.

Front 29

D. latum or Echinococcus
Both are tapeworm infections, which one will lead to B12 deficiency and pernicious anemia?

Back 29

D. latum

Front 30

How are D. latum or Echinococcus contracted?

Back 30

Ingestion

Front 31

Big or little?
D. latum or Echinococcus

Back 31

D. latum can reach 30 feet with up to 3000 proglotids
Echinococcus walls itself off and causes problems by the space it takes up.

Front 32

Echinococcus cysts, if they rupture, can cause hypotension, syncope and fever. Why?

Back 32

It is anaphylaxis due to previous patient sensitization and IgE production.

Front 33

How come we can't fight off Echinococcus cysts well?

Back 33

Bc the cyst wall serves as a barrier to the cells of the immune system.

Front 34

What are the three phases, and what do you do to help in each stage, of rabies?

Back 34

Incubation: post-exposure prophylaxis
Prodromal: Onset of clinical disease, can no longer administer vaccine.
Neurologic: Call the morgue

Front 35

What is the incubation period for rabies?
What three factors will cause it to be shorter?

Back 35

Can be 5days to 2years.
Closer to CNS, deeper bite, heavier viral load.

Front 36

Viral infection of the unmyelinated axon occurs when the virus multiplies at the site of initial infection. Retrograde axonal transport carries virus towards the CNS. Transport from the post-synaptic neuron to the pre-synaptic neuron is by endocytosis.

Back 36

Rabies (Rhabdoviridae)

Front 37

Bullet shaped RNA, enveloped, single stranded, negative sense, w/ at least 7 serotypes.

Back 37

Rabies (Rhabdoviridae)

Front 38

Incubation, Prodromal or Neurologic. In which phase(s) has the virus reached the CNS?

Back 38

Prodromal and Neurologic

Front 39

What are the two presenations in neurologic period of rabies infection?

Back 39

Furious phase
Paralytic phase

Front 40

Explain the minor details of a rabies vaccination.

Back 40

5 shots over 1 month
Serious adverse rxns are rare
Killed virus
Immunity is short lived.

Front 41

Clinical findings include tachypnea, tachycardia, hypotention, crackels or rales on lung exam, bilateral interstitial infiltrates, PLEURAL EFFUSION.

Back 41

Hantavirus. Typical symptoms inclue myalgia, fever, nausea, cough.

Front 42

How are you infected with Hantavirus?

Back 42

I'm not, that's nasty.

Ok, seriously,...via inhalation of dust containing virus that was excreted in urine and feces of infected rodents.
See, I told you it was nasty.

Front 43

What is ecchymosis a fancy word for?

Back 43

Bruise

Front 44

What is the underlying cause of Hemorrhagic fever?

Back 44

Coagulopathy (or lack there of)

Front 45

How is ebola passed?

Back 45

Through direct contact

Front 46

Filovirus(2members of the family that we know)

Back 46

Marburg virus and Ebola virus

Front 47

What is one cause of classic viral hemorrhagic fever?

Back 47

Marburg Virus
Filovirus, since they LL filaments.

Front 48

Slow and inevitable progression, exposure usually via ingestion of nervous system tissue containing prion agent, no immune response, no treatment. Aka, you're screwed.

Back 48

Prions