Session 8 Flashcards

(43 cards)

1
Q

What is a common source?

A

Source of infection which can infect multiple people
Source examples: Environmental Legionella pneumophila
Food/water food poisoning organisms –onward transmission possible
Animals rabies –onward transmission possible

Often environmental examples cannot be spread person to person.

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2
Q

Whats person-person transmission?

A

Two types: Direct and Indirect.

Direct:
When a person infects another person.
Person-to-person examples: 
Influenza 
Norovirus 
Neisseria gonorrhoea 

Indirect:
Person infects a vector and then that vector infects another person.
Indirect person-to-person example:
Mosquitos - malaria

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3
Q

What are the possible consequences of transmission?

A
  • Endemic disease - The usual background rate
  • Outbreak - Two or more cases linked in time and place
  • Epidemic - A rate of infection greater than the usual background rate.
  • Pandemic - Very high rate of infection spreading across many regions, countries, continents
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4
Q

What is R0

A

Basic reproduction number
•Ro -the average number of cases one case generates over the course of its infectious period, in an otherwise uninfected, nonimmune population

  • If Ro >1 increase in cases
  • If Ro =1 stable number of cases
  • If Ro <1 decrease in cases
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5
Q

What are the reasons for outbreaks, epidemics and pandemics?

A

New pathogen (antigens, virulence factors, antibacterial resistance)

New hosts (non-immunes, healthcare effects)

New practice (social, healthcare) e.g. change in law allowed gay sex which increased HIV spread within that population. Or blood transfusions in hospital spreading HIV.

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6
Q

What are the factors affecting transmissibility?

A
•Infectious dose – 
-number of microorganisms required to cause infection 
-Varies by: 
•micro-organism 
•presentation of micro-organism 
•immunity of potential host
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7
Q

What is parasitaemia ?

A

People who have level of immunity to disease so don’t have disease symptoms but parasite can still be detected. They can still pass on the disease through a vector despite not experiencing the disease.

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8
Q

Describe an epidemic curve

A

As people go from susceptible to infected to recovered/died, number of people infected rises to a peak and then falls.

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9
Q

What is the stochastic nature of small scale outbreaks?

A

Random

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10
Q

What kinds of interventions can we use to reduce infection spread?

A

Pathogen (+ vector)
•Reduce/eradicate pathogen
-Anti bacterials including disinfectants
-Decontamination
-Sterilisation
•Reduce/eradicate vector -Eliminate vector breeding sites

Patient
•Improved health 
-nutrition
 -medical treatment 
•Immunity 
-Passive e.g. maternal antibody, intravenous immunoglobulin 
-Active i.e. vaccination
Practice 
•Avoidance of pathogen or its vector 
-Geographic, “Don’t go there” 
-Protective clothing, equipment 
•long sleeves, trousers against mosquito bites 
•Personal protective: equipment in hospitals 
•gowns, gloves, masks
 -Behavioural 
•Safe sex 
•Safe disposal of sharps 
•Food and drink preparation
Place 
•Environmental engineering
 -Safe water 
-Safe air 
-Good quality housing 
-Well designed healthcare facilities
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11
Q

How are new hosts created?

A

Babies after their mothers supply of antibodies runs out are susceptible to disease.
Patients with underactive immune system e.g. bone marrow transplant, until their new bone marrow begins to function fully they are susceptible to disease.

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12
Q

What is herd immunity?

A

the resistance to the spread of a contagious disease within a population that results if a sufficiently high proportion of individuals are immune to the disease, especially through vaccination.

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13
Q

What is herd immunity?

A

The resistance to the spread of a contagious disease within a population that results if a sufficiently high proportion of individuals are immune to the disease, especially through vaccination. Through their immunity they prevent further spread of disease so less likely to reach at risk individuals.

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14
Q

What are the consequences of infection control?

A
GOOD 
•Decreased incidence or elimination of disease/organism 
•Smallpox 
•Polio 
•Dracunculiasis

BAD
•Decreased exposure to pathogen leading to decreased immune stimulus so decreased antibody resulting in increased susceptibles which results in outbreak
•Later average age of exposure which results increased severity -e.g polio, hepatitis A, chicken pox, congenital rubella syndrome

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15
Q

What is hepatitis?

A

•Hepatitis = inflammation of the liver
•Many systemic viruses cause “collateral” liver damage
•Eg EBV, CMV, VZV
•Hepatitis viruses:
- Replication specifically in hepatocytes (hepatotropic)
- Destruction of hepatocytes

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16
Q

What is the structure of viral hepatitis?

A

Hep B is double stranded DNA and enveloped.
Hep C is single positive stranded enveloped and icosahedral.
E and A are non enveloped single positive strand RNA

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17
Q

What are the consequences of leaving hepatitis untreated?

A

Liver cirrhosis (10% in B and 80% in C) and hepatocellular carcinoma

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18
Q

Describe the transmission, incubation and whether it can become a chronic illness of Hepatitis virus.

A
Hepatitis A Faeco-oral 2-6 weeks No 
Hepatitis B Blood/sex/ vertical
6wks-6mths Yes
Hepatitis C Blood (sex) 6-12 weeks Yes 
Hepatitis D Blood/sex/ vertical
6wks-6mths Yes (with Hep B) 
Hepatitis E Faeco-oral 2-6 weeks (Uncommon but possible)

Need to know about C and B

19
Q

What blood tests do we look at when looking at viral hepatitis?

A
Bilirubin
Alanine transaminase (ALT) 
 Alkaline phosphatase (ALP)
20
Q

What is the functional unit of the liver?

21
Q

How does blood flow through liver?

A

Dual blood supple
hepatic artery from aorta 25% and 75% portal vein blood from small bowel,
drain into hepatic vein leading to the vena cava.

22
Q

Function of gall bladder?

23
Q

What is bilirubin?

A

Bilirubin is one of the end products of blood cell metabolism, then binds o albumin and travels to liver where it undergoes conjugation and made into bile
Bile contains water bile salt fat/cholesterol and bilirubin.

24
Q

What is jaundice? What causes it?

A

High bilirubin in blood

types: prehepatic from haemolysis, and cholestatic - intrahepatic which occurs due to structural damage in liver which can be caused by hepatitis, drugs, alcoholic hepatitis, cirrhosis, autoimmune problems etc
- extrahepatic which is in gall bladder or bile duct which could be due to duct stones, carcinoma, biliary stricture etc

25
What are LFTs?
Liver function test • Bilirubin * Liver transaminases * Alanine transaminase (ALT) * Aspartate aminotransferase (AST) * Hepatocyte damage / cellular integrity • Alkaline phosphatase (ALP) • Biliary tract cell damage / cholestasis suggests gall stone rather than liver damage. • Albumin • a protein synthesised in liver seen low in chronic liver damage, when low can see oedema ``` • Tests of coagulation • clotting factors are synthesised in liver • INR (International Normalised Ratio) • Prothrombin time (PT) these are altered in liver damage. ```
26
Who is at risk of Hep B
* Vertical transmission (75% cases globally) * Perinatal transmission in pts from highly endemic areas * Sexual contact * People who inject drugs * Close household contacts * Significant blood exposure * Health care workers via needlestick injuries
27
What are the symptoms of acute hep B?
•Jaundice •Fatigue •Abdominal pain •Anorexia/Nausea/Vomiting •Arthralgia (joint pain)
28
What are some of the important details of acute Hep B?
* Incubation 6wks - 6 months. * AST/ALT in 1000s * Up to 50% - no/vague symptoms * Clear infection within 6 months * <1% - fulminant hepatic failure * Becomes chronic in <10% if infected as adult * 90% if infected in infancy (Asia/China)
29
What are the antigens and antibodies involved in Hep B?
``` Antigen - Antibody • HBsAg  HBsAb (surface) • HBeAg  HBeAb (E) • (HBcAg) not detected in blood.  (Core) HBcAb: IgM and IgG ``` Can look at HBV DNA through PCR.
30
In what order does the serology of Hep B appear?
1) Surface antigen first 1) Within 6/52; Rise in ALT / DNA 2) Followed by e-antigen 1) Highly infectious when present with surface antigen 3) Core antibody (IgM) 1) First antibody to appear 4) Followed by e-antibody 1) Heralds disappearance of e-antigen so less infectivity 5) Surface antibody 1) Last antibody to appear 2) Clearance of virus/recovery 6) Core antibody (IgG) 1) Persists for life
31
What is chronic hep B infection
Definition - Persistence of HBsAg after 6 months. | • 25% chronic infection leads to cirrhosis and ~5% will develop hepatocellular carcinoma
32
What is the treatment for Hep B
* NO CURE – integrates into host genome * Life-long anti-virals to suppress viral replication * Not required for everyone (e.g. “inactive” carrier) * Low VL / normal LFTs / no liver damage
33
Is there a vaccination for Hep B?
* Genetically engineered surface antigen * 3 doses + boosters if required * Effective in most people * Produces surface antibody response * >10 adequate •>100 long-term protection
34
Who is at risk of Hep C?
* People who inject drugs (“Intravenous drug users”) >90% of those with Hep C in UK - IV Heroin / crack / methamphetamines - Crack or heroin smokers * Sexual contact (<1% but higher if HIV co-infected) * Infants born to HCV positive mothers (<5%) * Blood transfusion prior to 1991. * Needlestick injuries to healthcare workers etc.
35
How does Hep C progress?
* ~80% become chronically infected * Of these some will develop chronic liver disease/cirrhosis. Resulting in: * Decompensated liver disease * Hepatocellular carcinoma (primary liver cancer) * Transplant * Death
36
What are the symptoms of Hep C?
``` •80% have no symptoms (acute or chronic) •20% have vague symptoms –Fatigue –Anorexia –Nausea –Abdominal pain (RUQ) ```
37
What blood tests can we use to detect Hep C?
* Serology – anti-Hep C antibody only (doesn't tell you if they currently have had it or if they've cleared it) * Remains positive life-long, even after clearance / cure * Not protective, can get re-infected * Viral PCR * If positive, confirms on-going / chronic infection
38
What is the treatment for Hep C?
* CAN BE CURED! * Directly acting antiviral drug combo * 8-12 weeks * >90% chance of cure * Expensive * Can get re-infected * No vaccine
39
What is the risk of transmission for HIV, Hep B and Hep C from a needlestick injury?
•HIV - 1/300 - Much lower if patient is on ARVs / VL undetectable •Hep C - 1/30 •Hep B - 1/3 -Much lower if recipient has been vaccinated
40
What are the immediate measures taken when someone is exposed to Hepatitis virus
* First aid – bleed and wash wound * Collect blood from patient (with consent) and from med student * Inform Occupational Health * Check med student’s Hep B vaccination status * Assess risk and need for immediate HIV PEP
41
What do we do for HIV post exposure prophylaxis?
* Early initiation of ARVs reduces dissemination and replication of HIV in tissue and bodily fluid * Evidence limited (animal studies / observational human studies) * Assess risk * Give x3 ARVs for 28 days * Start ASAP, max up to 72 hours * HIV test at baseline, 1 month and 3 months
42
What further action needs to be taken after PEP for a blood borne virus?
* Possible for Hep B booster * HIV PEP required for 28 days * Counselling and follow-up required * Advise to use condoms while at risk * No PEP available for Hep C * Repeat HIV and Hep C tests at 12 weeks
43
Give a summary of Hep C and B, and HIV
Acute infection - Prevention - Outcome of infection (untreated) - Treatment HIV - Flu-like symptoms / nil - Condoms, PEP - AIDS Life-long anti-viral therapy Hep B - Jaundice / abdo pain / anorexia - Vaccination - •Cure (majority) •Chronic infection (minority) - Nil OR Lifelong antiviral drug Hep C - Usually nil Risk avoidance only - Chronic infection (majority) - 8-12 weeks of anti-viral drugs