WEEK 3 - Infectious Disease & Resistance

Question 1

What are characteristics of bacteria?

Answer 1

Only have single stranded, circular DNA, no plasma membrane.
No membrane bound organelles.
70S ribosomes for protein production.
No nucleus, DNA lies in the nucleoid.
Flagella for movement towards food and away from immune mechanisms of host.
May have plasmids - additional DNA (usually gram -ve).
Cell wall (peptidoglycans, for maintaining shape and rigidity, for multiplication, may contribute to resistance.

Question 2

What colour do Gram positive bacteria stain and why?

Answer 2

Purple, stain is trapped in thick peptidoglycan wall.

Question 3

What colour do Gram negative bacteria stain and why?

Answer 3

Red, thin peptidoglycan wall does not retain crystal violet, is counterstained with safranin to produce red.

Question 4

What are characteristics of viruses?

Answer 4

Acellular - cannot replicate on own, requires host mechanisms.
Viral genome DNA or RNA packaged into capsid (protein coat).
Capsid = rigid, protects against envi conditions, resistant to acid/drying, helps transmission (faecal-oral).
Some have a lipid membrane envelope in addition to capsid which is only maintained in aqueous solutions (transmission via bodily fluids).

Question 5

When do fungi/parasitic/protozoa infections occur?

Answer 5

When there is disruption in the protective barriers (skin, mucous membranes) or due to defective immune system (immunosuppression).

Question 6

Are fungi, parasites and protozoa prokaryotes or eukaryotes?

Answer 6

Eukaryotes

Question 7

What characteristics do eukaryotes have?

Answer 7

Membrane bound organelles.
Nucleus
Mitochondria
80S ribsomes 
Smooth ER (for detox, lots in liver)
Rough ER
Golgi apparatus

Question 8

What are prions and how are they transmitted?

Answer 8

Completely made up of protein.

Transmitted by electrical transmission, eating food that is contaminated with it, medical procedures.

Question 9

Define pathogen

Answer 9

An agent able to evade the various physiological defences of the human host to cause infection.

Question 10

Define infection

Answer 10

When an infectious agent enters the body, increases in number and causes damage to the host.

Question 11

Define commensalism

Answer 11

Where the host and microbe live together with no effect on each other’s life cycle i.e. normal flora of the skin (Candida albicans protects our skin from other pathogenic agents).

Question 12

Define parasitism

Answer 12

Unequal relationship ‐ one benefits to the detriment of another; this is the case in all infections.

Question 13

Define symbiosis

Answer 13

Where species live together for their mutual benefit i.e. human host and the gut flora ‐ bacteria get warm, moist, protected environment; host cell ‐ digestion.

Question 14

Define opportunistic infection

Answer 14

When the healthy human defences are weakened infection by organisms not generally causing an infection in healthy humans i.e. Pneumocystis carinii (Jirovecii) ‐ known to cause pneumonia in people who have AIDS, won’t happen to a healthy person.

Question 15

Define nosocomial infection

Answer 15

Infections transmitted in hospitals; some may be opportunistic affecting seriously ill (immunocompromised) patients, others occur because of the special nature of the hospital environment i.e. Methicillin‐ Resistant Staphylococcus aureus (MRSA); VRE.

Question 16

What is staphylococcus aureus (golden staph)?

Answer 16

Normally lives on our skin or in the nose, mostly harmless unless it enters the body.
Up to 80% of the population will be carriers.
Common cause of HAI and community acquired infection.

Question 17

What are predictors of carriage of staphylococcus aureus?

Answer 17

Hospital setting:
- Prolonged hospital stay (often > 14 days)
- Preceding antimicrobial therapy 
- Surgical procedure(s); ICU 
- Proximity to a known MRSA case 
Community setting:
- Recent hospitalisation 
- Presence of decubitus ulcer 
- Catheter

Question 18

What are the disease mechanisms of staphylococcus aureus?

Answer 18

Production of toxins or through direct invasion & destruction of tissue.

Question 19

What are the key drivers for antimicrobial resistance?

Answer 19

Prescribing when not necessary eg. for a viral infection.
Prescribing the wrong type - wrong mechanisms of action.
Prescribing for the incorrect duration.

Question 20

What are some mechanisms of resistance that develop?

Answer 20

Changes in the cell wall of gram‐negative bacteria i.e. thickening.
Production of enzymes that alter the antimicrobial/antibiotic structure.
Prevent the antibiotic to bind to its site i.e. modification of target affinity.
Extrusion of the antibiotic from the bacterial cells via efflux pumps - pumps get rid of antibiotics before the drugs can have an effect on the bacterial cell.

Question 21

What’s MDR?

Answer 21

Multi-drug resistant – non‐susceptible to more classes; >1 drug in 3 different classes.

Question 22

Whats XDR?

Answer 22

Extensively drug resistant – resistant to all drugs that have been tested for that infection, need to use something from ages ago eg. colistin.

Question 23

What’s PDR?

Answer 23

Pan‐drug resistant – resistant to all antibiotic classes tested).
No approved antimicrobials; needs combinations, extended infusion times etc.
No guidelines or protocols in place to treat these ones.

Question 24

How does acquired microbial resistance occur?

Answer 24

Results from mutation of endogenous genes, acquisition of exogenous genes and/or DNA and mutation of acquired genes
More likely to be associated with antimicrobial resistance
E.g. exogenous genes scenario: flagella picked up stuff by moving through human host.

Question 25

What is the preferred time period for antimicrobial use?

Answer 25

Short time period.
The longer the period of antibiotic use, more bacteria will be exposed to a drug ‐ increased chance for resistance .
Resistance builds silently, making future treatment difficult.

Question 26

What is HIV?

Answer 26

The Human Immunodeficiency Virus (HIV) is a virus that attacks the immune system.
Damages the body’s ability to fight diseases & infections causing Acquired Immunodeficiency Syndrome (AIDS).

Question 27

What is the aetiology of HIV?

Answer 27

HIV is a RNA blood borne virus transmitted through blood and blood products via:
1. IV drug use – sharing needles or syringes.
2. Unprotected heterosexual and homosexual activity.
3. Blood transfusion/blood products: health care workers (rare transmission) – through needle stick injuries, or coming into contact with an infected patient’s blood; PPE important!
4. Mother‐to‐child (vertical) transmission can occur during 3 major periods: antenatally (through the placenta), intrapartum (around the time of birth) and postpartum (attributable to breastfeeding),
80% intrapartum

Question 28

What are HIV risk factors?

Answer 28

• Needles/syringes are shared during IV drug use.
• Have unprotected sex ‐ anal, oral, vaginal.
• Have unprotected sex with someone who is HIV‐positive or who has any of the risk factors listed.
• Have been given a diagnosis of or been treated for another STD (syphilis, chlamydia, gonorrhoea).
• Have fewer copies of a gene (CCL3L1) that helps fight HIV infection.
• Received a blood transfusion or clotting factor 1978–1985.

Question 29

What is the pathophysiology of HIV?

Answer 29

They use reverse transcriptase, to convert RNA into DNA.
They use integrase to insert the new DNA into the infected cell’s genetic material; DNA that enters the nucleus called a “provirus.”
When HIV enters the bloodstream, the virus starts seeking CD4+ T helper cells.
Once depleted, seeks macrophages, CD8+ cytotoxic C cells, NK cells.
Presence of HIV/antigens activate uninfected T cells making them an easier target.

Question 30

What is the clinical course of HIV/AIDS?

Answer 30

Incubation period:
- Varies: nutrition; health state; further exposure; some asymptomatic.
- But super long, can go for between 1-10 years.
Acute infection:
- 80 to 90% develop an influenza‐like illness called acute HIV infection a month or two after exposure to the virus (fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, mouth/oesophageal ulcers)
Latency stage:
- Can last 2 weeks to 20 years and beyond.
- A strong immune defence reduces the number of viral particles in the blood.
- Shows few or no symptoms but individuals in this phase are still infectious.
AIDS (end stage of HIV infection):
- Symptoms of various opportunistic infections.
- Recurring respiratory tract infections (such as sinusitis, bronchitis, otitis media, pharyngitis, pneumonia), prostatitis, skin rashes; oral ulcerations or thrush, tuberculosis, shingles, Epstein‐Barr virus‐induced B‐cell lymphomas.
Weight loss

Question 31

What are the clinical manifestations of HIV?

Answer 31

Many people are asymptomatic when they first become infected with HIV; some may have a flu‐like symptoms, called HIV sero‐conversion syndrome, a month or two after exposure to virus.
Other symptoms that may occur (non specific):
- Diarrhoea, nausea, vomiting; enlarged liver, spleen, lymph nodes.
- Fever, headache & muscle pain; rash: abdomen, arms, legs and face.
- Sore throat, oral thrush, a common fungal infection caused by Candida.
Infection is one of the most common complications and large lymph nodes (swollen glands) that may be enlarged for more than three months ‐ sometimes the first sign of HIV induced infection process.

Question 32

What is the initial test for HIV?

Answer 32

HIV antibody test.
Relatively accurate & cheap method but not 100%.
HIV antibody test consists of screening with ELISA - enzyme linked immuno-solvent assay

Question 33

What is the 2nd confirmatory HIV test if ELISA is positive?

Answer 33

Western blot assay.
More sensitive, more accurate than ELISA.
If Western blot negative person is not infected with HIV (despite false+ ELISA).

Question 34

What is the main way of stopping HIV?

Answer 34

Prevention and management.
Main method of prevention is avoiding exposure to HIV. A course of antiretroviral treatment administered as quickly as possible after exposure, known as post‐exposure prophylaxis to reduce the risk of infection.

Question 35

What is the main treatment for HIV?

Answer 35

Highly active antiretroviral therapy or HAART.

Question 36

What are the current HAART options?

Answer 36

Combinations of 3 or more drugs belonging to at least two different classes of antiretroviral agents.