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CMBM exam 6 > Emerging infections > Flashcards

Emerging infections Flashcards

1
Q

What is an emerging infection?

A

Not occurred in human before
Occurred previously but only effected a small amount of peeps
Occurred through history but only recognized as a distinct disease due to an infectious agent

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2
Q

Where do most emerging infections come from?

A

Animals - zoonosis (75%)

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3
Q

What has contributed to emergence?

A 
Mass food production systems (HUS - E. coli)
Evolution of a strain (cholera)
Pig-duck stuff (pandemic flu) 
Refusal of vax (pertussis) 
Break in health measures (rabies)
Antibiotic resistance (TB)
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4
Q

Severe Acute Respiratory Syndrome (SARS) Coronavirus (CoV) characteristics

A

Enveloped (+) ssRNA virus

Readily transmissible and serve in the 21st century

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5
Q

Describe the emergence of SARS.

A

Chinese people on 2002 left in 2003
Spread via international travel
Fatal in 15% unless over 50 yrs (50%)

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6
Q

What is the natural reservoir for SARS?

A

Bats

Intermed host = Palm civet

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7
Q

What is the pathogenesis of Middle East Respiratory Syndrome (MERS)?

A

Beta-coronavirus

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8
Q

How is MERS transmitted?

A

Person-to-person

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9
Q

How is MERs prevented?

A

Surveillance for severe acute respiratory infections (SARI)

Diagnostic testing

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10
Q

What was the emergence of A/H1N1 swine flu?

A

Mixing vessel hypothesis
2009
Triple reassortment in swine

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11
Q

How was mostly effected by A/H1N1?

A

Young people

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12
Q

How is A/H1N1 prevented?

A

Vaccine

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13
Q

What are the subtypes of A/H5N1 avian influenza (AI)?

A

H5 and H7

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14
Q

What are the factors contributing to A/H5N1?

A

Globalization and international trade
Marketing and farming practices
Wild birds
HPAI (highly pathogenic avian influenza)

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15
Q

How is A/H5N1 transmitted?

A

Direct contact with gross birds and poop

Farm movement of birds

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16
Q

What are the clinical presentations of A/H5N1?

A

Aggressive clinical course with deterioration and high fatality
Incubation 2 -8 days
Early symptoms: LRT illness, respiratory distress, sometimes bloody sputum

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17
Q

How is A/H5N1 prevented?

A

Surveillance measures

Biosecurity

18
Q

When did cholera re-emerge?

A

2010

19
Q

What is the pathogenesis of cholera?

A

Toxigenic O1 and O139 bacteria
Free-living organism
Found in fresh and brackish water

20
Q

What are the clinical presentation of cholera?

A

Mild cholera: asymptomatic or causes a mild gastroenteritis
Severe cholera: Acute, profuse watery diarrhea “rice water”, vomit
Hypovolemic shock and death
Tachycardia, loss of skin turgor, dry mucous, hypotension
Muscle cramps, electrolyte imbalances

21
Q

How is cholera prevented?

A

Improved sanitation
Education of the people
Currently no vaccine

22
Q

When did cholera emerge in the US?

A

Transportation of bird, mosquitoes

23
Q

How is cholera transmitted?

A 
Bite of mosquito
Culex pipiens (east US)
Culex tarsalis (midwest + west)
Culex quinquefasciatus (southeast)
24
Q

What is the clinical presentation of pertussis?

A

Effects infants and young children
7 - 10 day incubation
Mild fever, runny nose, paroxysmal cough with whooping, apnoea
Pneumonia

25
Q

How can bordatella pertussis be prevented?

A

DTaP - vaccine for babies

26
Q

What is the treatment for Bordatella pertussis?

A

Antibiotics

27
Q

What were the factors in the emergence of Pertactin-Negative bordatella pertussis in 2013?

A

Outbreak and epidemics when the vaccine wears off

Possibly change in pertussis vaccine

28
Q

Is the pertactin-negative pertussis antibiotic resistant?

A

No

29
Q

What is the vaccine resistant genotype of pertussis?

A

prn2-ptxP3

30
Q

What are some of the issues with current vaccination of the prn2-ptxP3?

A

Maybe be causing powerful clones

Vaccine uptake near 95% but needs frequent boosters

31
Q

When did S. aureus develop resistance to penicillin?

A

1940s-1950s

32
Q

What class of penicillin-like antibiotics is Methicillin resistant to?

A

Beta-lactams

33
Q

When was the first documented case of vanc resistant S. aureus?

A

2002

34
Q

What is N. gonorrhea resistant to?

A

Quinolone, penicillin and tetracyclin

3rd gen cehalosporins in Japan and US

35
Q

Where is Enterococci normally found?

A

Human Gi and female genital tract

36
Q

What are the types of Enterococci that are problematic?

A

E. faecium and E. faecalis

37
Q

How is Enterococci transmitted?

A

Person-to-person by body fluid
Indirect by hand contact w/o open wounds or fomites
Nosocomial infections

38
Q

When did vancomycin resistant enterococci appear?

A

1986, first case 1989

39
Q

What are the two best antibiotics that doesn’t work against multidrug-resistant TB?

A

Isoniazid and rifampin

40
Q

Why is extensively drug-resistant TB dangerous?

A

Less common but resistant to isoniazid and rifampin and most alternative drugs

CMBM exam 6 (16 decks)

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