public health exam 3

What types of infections in hospitals are common?

blood infections- IV/central lines

UTIs- catheters

Pneumonia- ventilators

surgical sites

common causative agents in hospitals?

Clostridium difficle

MRSA/VRSA

VRE (vancomycin resistant enterococci)

Klebsiella sp.

Acinetobacter sp.

Explain the mechanism of methicillin resistance for MRSA

Starts with acquisition of mecA gene

The gene encodes PBP2a proteins (non-native) and enables them to be methicillin resistant

Beta-lactam abx target the penicillin binding proteins in cell walls of bacteria, but are unable to do so when they are PBP2a

describe the emergence/history of community-acquired MRSA

Resistance to methicillin in US reported in 1961 (resistance to penicillin first)

1982 in Michigan, first vague reports of CA MRSA

1990 W. Australia

Late 1990s- Midwestern US- 4 healthy children died from invasive MRSA

CA-MRSA vs HA-MRSA

CA

skin infetions

-strains are more virulent and more transmissible

-affect otherwise healthy individuals

In Australia, only resistant to B-lactams

-crowded places: gyms, dorms, jail, military, athletic facilities

-open wounds

-skin to skin contact

-contamination of items and surfaces

-poor hygiene

HA

severe infections- nosocomial

-immunocompromised individuals

-invasive

-resistant to additional antibiotics (erythromycin, clindamycin, and tetracycline)

What are problems associated with S.aureus carriers?

higher risk of invasive staph in hospital (80% matches nose strain)

CARRIERS SHED

Diagnosis process for MRSA

Should consider for any skin infection

-obtain cultures

-determine antibiotic susceptibility (can be difficult bc of heteroresistance)

-test against oxacillin and cefoxitin bc more stable and less likely to be heteroresistant

-PCR detection of mecA -hard bc mecA variation

methicillin testing isn’t available bc it doesn’t last

to determine HA vs CA

-time, medical history, and risk factors

current treatments for MRSA

antibiotics (determine susceptibility profile)

drainage by healthcare worker

Severe- see a disease specialist, surgery

Why is vrsa a concern?

vancomycin is typically a last resort drug

explain the process of a C. diff infeciton

on people or surfaces

fecal oral route

spores are ingested, they germinate in the SI, vegetative cells grow and colonize in colon, toxin production begins

Toxin A, B or a combination of both

risk factors for nosocomial c. diff infection

older individuals >65

antibiotics in the last few months

receive medical care and are not fully healing'

-possibly acid blockers

-additional illness

Risk factors for CA C. diff

younger <65

more females

less likely than HA to have been on abx, acid blockers, or have other illnesses

what are options for recurrent c. diff infections?

new abx

bacteriotherapy - fecal transplant, oral microbiome pills

immunotherapy (toxin vax?)

what characteristics of the NAP1 strain are believed to contribute to the increased incidence, severity, and mortality associated with this strain?

fluoroquinolone resistance

increased production of toxins A & B

-tcdC mutations “off switch” for toxin production

production of a third toxin

How are CA c. diff infection possibly spread?

asymptomatic healthy carriers- infants

domesticated animals- cows, horses, cats, dogs

food and water supply- meat and veg (high % of detectible spores in meat)

How does variation arise in M. tuberculosis?

MBTC (mycobacterium tuberculosis) complex- there are 10 human adapted lineages

not capable of HGT but can genetically change via mutations, deletions, and/or duplications

Does everyone exposed end up with a severe TB infection?

Nope. Some people are asymptomatic

8 stages of TB

can regress or progress (back and forth)

based on host factors

infection vs disease is a spectrum

Why are HIV and TB cases problematic?

immunocompromised individuals will have severe illness

-necrosis of granulomas and entering into bloodstream- causes systemic infection

how is TB spread?

AIRBORNE droplets

how is tb diagnosed?

skin test

sputum culture

smear test

chest xray

blood tests cannot determine stage but measures immune response

molecular based tests (like strep rapid)

how is tb prevented?

BCG vaccine

testing- difficult

What types of disease does strep A cause?

mild

strep throat

impetigo

scarlet fever

severe

NCF
TSS

what organisms commonly cause tss?

STAPH

and strep

symptoms of NCF?

pain (often out of proportion)

swelling with redness (can be hot)- possible ulcers, blisters, or black spots

fever, chills, vomiting, or fatigue

symptoms of TSS?

high fever

aches

malaise

hypotension

rash

nausea and vomiting

possible organ failure, shock, death

What post infection complications occur following GAS infections?

poststreptococcal glomerulonephritis- kidney disease

Rheumatic fever (autoimmune)

-rheumatic heart disease

why is there interest in a vaccine for GAS? What complications exist?

to prevent people from getting an infection

Complications because genetic diversity and cross reactivity of antibodies

25yr ban on vaccine development b/c of rheumatic fever cases

why is it important that highly pathogenic coronaviruses can grow at 37C?

more tolerant of warm temps

can survive lower in respiratory tracts

can cause severe disease

What is the connection between the SARS-CoV from 2002-2003 outbreak and the human enzyme ACE-2?

ACE-2 is an important enzyme that raises BP

expressed on- smooth muscle cells, circulatory system cells, lung cells, kidney cells, and GI cells.

mutation caused binding to human ACE-2 enzyme, allowed the virus to enter host cell and replicate

The virus’s spike (S) protein binds to the extracellular domain of ACE2 via its receptor-binding domain (RBD), initiating infection

How is SARS-CoV thought to have entered the human population in the SARA 2002-2003 outbreak?

novel cases in Guangdong province in China, Fall 2002

From bats to civets to humans

globalization and ease of travel increased spread

How did MERS CoV enter the human population in 2012?

Bats and camels

camel milk, meat, and contact

human to human

What role did superspreading play in the SARS outbreak in 2002-2003?

Beijing superspreader

62 yo woman

74 close contacts

infected 33

many events of superspreading- mining community

What role did superspreading play in the 2015 MERS outbreak?

35yo man who was a traveler, introduced to 2 hospitals and 2 clinics, infected 85 people

83% of cases were associated with superspreading

What is the future of coronaviruses?

They have the potential to be dangerous because they may become harder to identify due to asymptomatic cases and spread. Additionally, there is a large number of strains associated with bats, and these could eventually infiltrate the human and other animal populations.

What’s the R0 value of chicken pox?

around 10

how does chickenpox spread?

via droplets

viral particles from blisters

What are the possible complications of chickenpox?

if older than 12 you have a greater risk of complications:

dehydration

pneumonia

brain infection

skin infection (Strep)

symptoms of chicken pox?

fever, fatigue, headache

RASH- starts face, chest, back, and then out

itchy fluid filled blisters

~500 spots

treatment for chickenpox?

OTC meds- Tylenol (not ASPRIN bc Reyes)

Antivirals when serious complications likely

chickenpox prevention?

VAX

live attenuated- may carry risk of shingles

MMRV- 1st dose of live to prevent febrile seizure

Typical shingles rash?

one sided

face and or body

What is the most common complication with shingles?

PHN
postherpetic neuralgia

long term pain at site of rash (even after it goes away)

Prevention for the shingles

VAX-shingrix

90% protection for at least 7 yrs

How is smallpox spread?

prolonged person to person contact

droplets

bodily fluids

scabs and blisters

possibly air

Basic disease progression for smallpox

Incubation 7-17 days (avg. 12)

Initial symptoms- flu-like- 2-4 days

Early rash- 4 days HIGHLY contagious, tongue, mouth, to arms, legs, hands, and feet

Pustular rash- 5 days “hard rash”

Scabs- 5 days

Scabs resolve in 6 days

how long does a person remain contagious during a smallpox infection?

around 20 days

What problem may be associated with the smallpox vaccine?

can potentially shed live virus

doesn’t have lifelong/long term immunity

What strategies were used to eradicate smallpox?

mass vaccination and ring vaccination

What characteristics of smallpox made eradication possible?

person to person spread only

effective vaccine

no asymptomatic carriers

global engagement

luck

what are the pros and cons associated with destroying the smallpox stocks?

there isn’t a lot known

could potentially develop better vaccine

could develop better treatment

buttttt

risk accidental or intentional release

smallpox research is restricted (hard)

What is dual purpose research? how does it apply to smallpox?

Research intended for benefit but could be misapplied to cause significant harm to public health, safety, and security

scientist reconstituted horsepox via dna fragments

How many polio serotypes commonly cause human disease?

3 serotypes

but since 2015 only serotypes 1 and 3

What are the main difference between the oral vaccine and the inactivated vaccine?

The inactivated vaccine mostly provides protection against paralysis

Oral does well against GI

Oral provides strong lifelong immunity, inactivated lasts years

Oral

incidence of VAPP- vaccine associated paralytic polio

cvdpv- circulating vaccine derived polio virus- in low vaccination areas with poor sanitation and hygiene

What are difficulties in achieving polio erradication?

asymptomatic cases (95%)

vaccination rates

How did awareness for HIV first emerge?

in US 1980s

Kaposi’s sarcoma that was aggressive and invasive

Pneumocystis jiroveci pneumonia- wasn’t expected in healthy adults

Predominately affecting Homosexual men

patients with no immune function left

Africa in 1970s- “slim” disease

How is the HIV virus able to mutate rapidly?

reverse transcription bc it is a retrovirus

high mutation rate and highly error prone and no proofreading

5-10 mistakes per replication cycle