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Sandra Phase 2a > Microbiology and Infectious disease > Flashcards

Microbiology and Infectious disease Flashcards

1
Q

Things to consider when looking at bacteria as causes of disease

A

Pathogen
Commensal
Opportunist pathogen
Virulence/pathogenicity
Asymptomatic carriage

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2
Q

What is a pathogen

A

Organism that causes or is capable of causing disease

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3
Q

What is a commensal?

A

Organism which colonises the host but causes no disease in normal circumstances

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4
Q

What is an opportunist pathogen

A

Microbe that only causes disease if host defenses are compromised

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5
Q

What is meant by virulence/pathogenicity

A

The degree to which a given organism is pathogenic

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6
Q

What is asymptomatic carriage

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease

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7
Q

What bacteria stains pink

A

Gram negative (piNk = Negative)

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8
Q

What bacteria stains purple?

A

Gram positive (Positive = Pink)

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9
Q

Describe bacterial morphology (diagram)

A
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10
Q

Which bacteria has 2 membranes

A

Gram-negative

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11
Q

What is the double membrane of gram-negative bacteria separated by?

A

lipoprotein, periplasmic space and peptidoglycan

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12
Q

What are two bacterial toxins?

A

Endotoxin and exotoxin

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13
Q

What is an endotoxin

A

component of the outer membrane of bacteria, e.g. lipopolysaccharide in gram negative bacteria

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14
Q

What is an exotoxin

A

secreted proteins of gram-positive and gram negative bacteria

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15
Q

What are the genetic variations in bacteria

A

Mutations: Base substitution, deletion and transfer

Gene Transfer: Transformation, e.g. plasmid , Transduction, e.g. via phage, Conjugation, e.g. via sex pilus

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16
Q

What is the classification of bacteria (diagram)

A
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17
Q

How would you do a gram stain?

A
  • Apply a primary stain such as crystal violet (purple) to heat-fixed bacteria
  • Add iodide, which binds to crystal violet and helps fix it to the cell wall
  • Decolourise with ethanol or acetone
  • Counterstain with safranin (pink)
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18
Q

What is the Ziehl-Neelsen stain used for?

A

Identifying mycobacterial infections
Detects acid-fast bacilli (AFB)

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19
Q

What does a coagulase test distinguish?

A

S.aureus from other staphylococci
Shows a coagulase positive test

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20
Q

What are the different types of haemolysis

A

Alpha
Beta
Gamma

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21
Q

What is alpha haemolysis?

A

Haemolysis caused by the production of hydrogen peroxide oxidising haemoglobin – the agar appears green.

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22
Q

What is beta haemolysis

A

haemolysis results because of lysis of red blood cells by haemolysis, such as Streptolysin O produced by S.pyogenes

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23
Q

What is gamma haemolysis?

A

implies no haemolysis

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24
Q

What does an oxidase test for? What does this imply?

A

If a micro-organism contains a cytochrome oxidase
Implies organism able to use oxygen as the terminal electron acceptor

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25
Q

Why do gram-positive bacteria retain their crystal violet purple?

A

because they have a cell wall composed of a thick layer of peptidoglycan

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26
Q

What is an example of a gram-positive bacteria and tested to distinguish this

A

Staphylococcus – coagulase test
-Staph. Aureus – coagulase positive

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27
Q

How can you classify streptococci (3)

A
  1. Haemolysis
  2. Lancefield typing
  3. Biochemical properties
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28
Q

What is Lancefield grouping?

A

Method of grouping catalyse-negative, coagulase-negative bacteria based on bacterial carbohydrate cell surface antigens

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29
Q

What is the catalase test?

A

Demonstrates the presence of catalase, an enzyme that catalyses the release of oxygen from hydrogen peroxide (H2O2).

Used to differentiate those bacteria that produce an enzyme catalase, such as staphylococci, from non-catalase-producing bacteria, such as streptococci.

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30
Q

What is blood agar used for?

A

Blood agar is a non-selective medium that can be made selective for specific pathogens by the addition of antibiotics, chemicals or dyes.

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31
Q

What is an XLD culture?

A

Xylose Lysine Deoxycholate agar (XLD agar) is a selective growth medium used to isolate Salmonella and Shigella species from clinical samples and food.

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32
Q

What is MacConkey agar used for?

A

It is designed to selectively isolate Gram-negative and enteric (typically found in the intestinal tract) bacteria and differentiate them based on lactose fermentation.

Lactose fermenters turn red or pink on MacConkey agar, and non-fermenters do not change colour

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33
Q

Purpose of CLED culture

A

Non-selective medium capable of supporting the growth of most urinary pathogens.

differential medium used for the isolation and enumeration of bacteria from urine

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34
Q

Purpose of Sabouraud Culture

A

Sabouraud agar is a selective medium formulated to allow the growth of fungi and inhibit the growth of bacteria.

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35
Q

Purpose of Lowenstein-Jensen culture

A

growth medium specially used for culture of Mycobacterium species, notably Mycobacterium tuberculosis

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36
Q

What are some important gram-positive bacteria that you need to remember (6)

A

S.aureus
S.epidermis
S.pyogenes
S.pneumoniae
viridian streptococci
C.diphtheriae

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37
Q

What do gram-positive bacteria show

A

Wide range of extracellular and cell-associated virulence factors

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38
Q

How do gram-positive bacteria spread

A

aerosols
surface-to-surface contact
colonization of prostheses

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39
Q

How can you manage gram-positive bacteria

A

antimicrobials and vaccination

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40
Q

What are the four major groups (phyla) of gram-negative pathogens?

A
  1. Proteobacteria – all are rod-shaped
  2. Bacteroids – rod-shaped
  3. Chlamydia – round pleimorphic
  4. Spirochaetes – spiral/ helical
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41
Q

What are the two pathogenicity determinants/ virulence factors of gram-negative bacteria

A
  1. Colonization factors: adhesins, invasins, nutrient acquisition, defence
  2. Toxins (effectors): usually secreted proteins -> damage, subversion
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42
Q

Why are gram-negative bacteria difficult to culture in a lab

A

Due to the dependency of a pathogen on its host

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43
Q

What are the three classifications of parasitic worms (Helminth worms)?

A

Nematodes (roundworms)
Trematodes (flatworms, flukes)
Cestodes (tapeworms)

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44
Q

Where can you find nematodes

A

o Intestinal – ascaris lumbricoides
o Larva migrans
o Tissue (filaria)

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45
Q

Where can you find trematodes

A

o Blood
o Liver
o Lung
o Intestinal

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46
Q

Where can you find cestodes?

A

o Non-invasive
o Invasive

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47
Q

What is the pre-patent period?

A

interval between infection and the appearance of eggs in the stool

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48
Q

Mycobacteria of medical importance (7)

A
  • M.tuberculosis – tuberculosis
  • M.leprae – leprosy
  • M.avium – disseminated infection in AIDS, infections in patients with chronic lung disease
  • M.kansasii – chronic lung infection
  • M.marinum – fish tank granuloma
  • M.ulcerans – buruli ulcer
  • Rapidly growing mycobacteria – skin and soft tissue infections
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49
Q

What is the microbiology of mycobacterium

A
  • Aerobic, non-spore forming, non motile bacillus
  • Cell wall contains high molecular weight lipids
    o Weakly gram-positive or colourless
    o Survive inside macrophages, even in a low pH environment
  • Slow reproduction
  • Slow response to treatment
  • Slow growing
    o M tuberculosis generation time 15-20h vs 1h for common bacterial pathogens
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50
Q

What stain is used to identify myobacteria and why?

A

Acid-fast bacilli as its resistant to gram stain

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51
Q

What do acid-fast bacilli stain?

A

organisms with wax-like, thick cell walls

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52
Q

What is nucleic acid detection used for?

A

Nucleic acid amplification test using PCR
Recommended for rapid diagnosis in TB-endemic countries
Sensitivity 88%, specificity 98%

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53
Q

What conclusion can be concluded from mycobacteria?

A

Mycobacteria are common causes of human disease-causing major human illnesses such a tuberculosis and leprosy

They have unique lipid-rich cell walls, which give them unique staining patterns

They are slow growing so hard to culture

The immune response requires cell-mediated immunity, but many of the features of the disease are associated with an aberrant immune response

Tuberculosis will be covered in your respiratory block

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54
Q

Example of mycobacteria

A

TB

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55
Q

How do viruses replicate?

A

By exploiting the energy and reproductive machinery of cells of higher organisms.

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56
Q

Characteristics of viruses (4)

A

Non-cellular structure – does not have membranes or any cell organelles

Consist of an outer protein coat and a strand of nucleic acid, either DNA or RNA

Come in a variety of shapes.

Do not carry out metabolic reactions on their own – require the organelles and enzymes of a host to carry out such reactions.

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57
Q

What are the shapes and sizes of different bacteria?

A
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58
Q

What is the difference between living and non-living cells

A
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59
Q

Describe viral replication

A
  1. Attachment: viral and cell receptors, e.g. HIV
  2. Cell entry: only the central viral core carrying the nucleic acid and some associated proteins enter the host cell
  3. Interaction with host cells: use cell materials (enzymes, amino acids, nucleotides) for their replication
  4. Replication: may localize in the nucleus, cytoplasm or both
  5. Assembly: occurs in the nucleus, in the cytoplasm or at the cell membrane
  6. Release: bursting open of cell or by leaking from the cell over a period of time
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60
Q

How do viruses cause disease

A
  • Damage by direct destruction of host cells e.g. HIV
  • Damage by modification of host cell structure or function e.g. rotaviruses
  • Damage involving over-reactivity of the host as a response to infection e.g. hepatitis B
  • Damage through cell proliferation and cell immortalization e.g. HPVs
  • Evasion of both extracellular and intracellular host defences
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61
Q

Laboratory methods to diagnose bacterial infections

A
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62
Q

Bacteria growing as single cells

A
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63
Q

Describe the structure of fungi

A
  • Eukaryotic
  • Chitinous cell wall
  • Heterotrophic
  • Move by means of growth or through the generation of spores, which are carried through air or water
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64
Q

Types of fungi

A

Yeast
Mould
Dimorphic fungi

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65
Q

Yeast vs Fungi

A
  • Yeasts are small single-celled organisms that divide by budding
    o Account for <1% of fungal species but include several highly medically relevant ones
  • Moulds form multicellular hyphae and spores
  • Some fungi exist as both yeasts and moulds switching between the two when conditions suit – dimorphic fungi
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66
Q

What are a dimorphic fungi

A

Some fungi exist as both yeasts and moulds switching between the two when conditions suit

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67
Q

What is the aim of antimicrobial drug therapy

A

to achieve inhibitory levels of agent at the site of infection without host cell toxicity

68
Q

What does treating fungal disease rely on

A

identifying molecules with selective toxicity for organism targets

o Target does not exist in humans

o Target is significantly different to the human analogue

o Drug is concentrated in organism cells concerning humans

o Increased permeability to compound

o Modification of compound in an organism or human cellular environment

o Human cells are ‘rescued’ from toxicity by alternative metabolic pathways

More different for fungi than bacteria because they are eukaryotic

69
Q

What is the severity of fungal infection in the ‘healthy.’

A

Mild but troublesome

70
Q

Who is susceptible to severe fungal infections

A

immunocompromised

-can be the initial presentation of the underlying disease

71
Q

Why can fungal infections be challenging to treat?

A

We have relatively few classes of agents effective against them

72
Q

What do immune response patterns vary for

A
  • Viruses
  • Bacteria
  • Protozoa
  • Helminths
73
Q

What are the key attributes of pathogens causing disease

A

Infectivity
Virulence
Invasiveness

74
Q

Define infectivity

A

ability to become established in host, can involve adherence and immune escape

75
Q

Define virulence

A

the ability to cause disease once established

76
Q

Define invasiveness

A

the capacity to penetrate mucosal surfaces to reach normally sterile sites

77
Q

What are virulence factors

A

Microbial factors that cause disease

78
Q

Describe the features of a viral infection

A

Need rapid cell entry

Humoral response
o Antibody (IgA) – blocks binding
o Opsonisation
o Complement

Cell-mediated response
o Antiviral action
o Kill infected cells
o Macrophages

Peaks 7-10 days, then declines

79
Q

What does viral evasion interfere with

A

specific or non-specific defence

80
Q

What does influenza change?

A

coat antigen

81
Q

Define anti-genic drift

A

spontaneous mutations occur gradually, giving minor changes in haemagglutinin and neuraminidase. Epidemics

82
Q

Define anti-genic shift

A

sudden emergence of new subtype different to that of preceding virus. Pandemics

83
Q

How do bacterial infections enter?

A

Via
* Respiratory tract
* Gastrointestinal tract
* Genitourinary tract
* Skin break

84
Q

What determines the defence mechanism employed for bacterial infections

A

Number of organisms and virulence

  • Low number or virulence – phagocytes active
  • High number of virulence – immune response
85
Q

Give 2 examples of bacterial evasion

A
  • Mycobacterium – escape from phagolysosome, live in cytoplasm
  • M.avium – block phagosome
86
Q

What does the immune response of a protozoan infection depend on

A

location of the parasite in the host

  • Blood stage – humoral immunity
  • Tissue stage – cell-mediated immunity
  • Plasmodium fulciparium (malaria) – an anopheles mosquito bite
87
Q

3 points that define a protozoan evasion

A
  • Surface antigen variation
  • Intracellular phase
  • Outer coat sloughing
88
Q

5 characteristics of a worm infection

A
  • Do not multiply in humans
  • Not intracellular
  • Few parasites carried
  • Poor immune response
  • Immune response not sufficient to kill
89
Q

2 characteristics of a worm evasion

A
  • Decreased antigen expression by adult
  • Glycolipid/ glycoprotein coat (host-derived)
90
Q

What are the two different types of immunisation

A

Passive
Active

91
Q

What is passive immunisation?

A

preformed antibody transferred

Can be done via:
* Transplacental transfer
* Colostrum
* Inject preformed antibody

92
Q

What is active immunity

A
  • Achieved by natural infection – vaccine administration
  • Elicitis – protective immunity – immunological memory
93
Q

What are the different types of vaccines (4)

A
  • Inactivated (killed)
  • Attenuated (avirulent)
  • Bacteria or viruses
  • Toxoid vaccines (inactivated toxins)
94
Q

Protozoa: The First Animals (6)

A
  • Classified in a sub-kingdom
  • Single-celled eukaryotic organisms
  • Main biological role: consumers of bacteria, algae, microfungi
  • Important parasitic and symbiotic relationships
  • All engulf food by phagocytosis and then digest it in intracellular
  • An outdated classification – protozoa include both plants and animals and, in reality a group including a variety of clades within eukaryotes
95
Q

What are the 5 major groups when classifying organisms

A
  • Flagellates
  • Amoebae
  • Sporozoans
  • Ciliates
  • Microsporidia
96
Q

Characteristics of flagellates (3)

A
  • Flagellum as main locomotory organelle
  • Usually reproduce by binary fission
  • Intestinal flagellates or other body sites
97
Q

Characteristic of amoeba

A

Move by means of flowing cytoplasm and production of pseudopodia

98
Q

Characteristic of sporozoans (4)

A
  • No locomotory extensions
  • All species parasitic
  • Most intracellular parasites
  • Reproduce by multiple fission
99
Q

Example of sporozoan

A

Malaria

100
Q

Characteristic of ciliates (2)

A
  • Cilia that beat rhythmically at some stage in the lifecycle
  • two types of nuclei – macro/micronucleus
101
Q

Characteristics of microsporidia (3)

A

Production of resistant spores
Unique polar filament; coiled inside spore
Little known about human disease

102
Q

What is malaria

A

Protozoan infection caused by Plasmodia sporozoan.

Five species of sporozoites cause human disease: P.falciparum/ovale/vivax/malariae/knowlesi

103
Q

How is malaria transmitted

A
  1. Transmitted by the bite of female Anopheles mosquitoes
  2. The infected mosquito carries the parasite in the salivary gland as sporozoites.
  3. During feeding, the mosquito will expose the sporozoite to human circulation, travel to the liver and enter the hepatocytes.
  4. The sporozoite will replicate asexually and mature into shizont in the hepatocyte until it bursts into many merozoites.
  5. The merozoites enter human circulation, invade erythrocytes, and multiply again until the cell bursts.
  6. The cycle repeats itself; the merozoite invades RBC, multiplies and then bursts out each time, causing chills, fever and sweating.
  7. After several asexual cycles, merozoites can invade RBC, and instead of replication, they develop into a sexual form of parasite (gametocyte)
  8. Mosquito bites the infected human; it digests gametocytes which will then allow it to develop into gametes
  9. Male and female gametes enter the sporogenic cycle producing more pathogenic sporozoites
  10. Mosquitos (female) can infect another human causing malaria

Infected for life

104
Q

What is the lifespan of malaria?

A

Life span 3-4 weeks

105
Q

Malaria lifecycle

A

The liver stage in P.ovale and P.vivax has an additional hypnozoite stage

Lie dormant and cause late relapse by reactivating months later

Not eradicated by most conventional anti-malarial treatments.

Symptomatic malaria: fever, haemolysis

106
Q

What are the clinical features of malaria

A

Very varied
Fever almost invariable

Another common;
o Chills and sweats
o Headache
o Myalgia
o Fatigue
o Nausea and vomiting
o Diarrhoea

These acute symptoms common to all four species

107
Q

Treatments of malaria

A

Quinines

108
Q

Complications of malaria

A

Splenomegaly
Hepatomegaly
Pulmonary oedema
Renal Failure

109
Q

Define antibiotics

A

agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high-dilution

110
Q

What are antimicrobials

A

Molecules that work by binding a target site on a bacterium.

Defined as points of biochemical reaction crucial to the survival of the bacterium
o Penicillin-binding proteins in cell wall
o Cell membrane
o DNA
o Ribosomes
o Topoisomerase IV or DNA gyrase

The crucial binding site will vary with antimicrobial class.

111
Q

Classes of antibiotics (10)

Antibiotics Can Terminate Protein Synthesis For Microbial Cells Like Germs

A
112
Q

Gram Coverage of antibiotics
Remember GLAM and iotic ending

A
113
Q

Mechanism of Action for different antibiotic classes

A
114
Q

What are the three mechanisms of antibiotic resistance genes

A

Antibiotic degrading enzymes
Production of Efflux pump
Modified antibiotic binding target

115
Q

What are the two ways in which bacteria can acquire antibiotic-resistant genes

A

Vertical gene transfer: resistant gene passed during bacterial replication, e.g. via spontaneous mutation

Horizontal gene transfer: Resistant gene transfer via
-conjugation
-transduction
-transformation

116
Q

How to diagnoses a viral infection

A

Tests:

  1. Cell culture
  2. Cytology
  3. Viral Proteins
  4. Viral Genetic Material: PCR, Southern/Northern Blot
  5. Serology
117
Q

What are the key points mentioned in the health act 2006

A

Infection control is every healthcare worker’s responsibility

No longer just the responsibility of the infection control team

Prosecution possible under H&S law

118
Q

Key components of infection prevention and control at STH

A
  • Infection prevention and control team
  • Ward teams
  • Microbiology/ virology laboratories
  • Trust management
  • Estates
  • Domestic services
  • Pharmacy
119
Q

What are infection control policies

A
  • MRSA
  • Tuberculosis
  • Medical equipment management manual
  • Single-use items
  • Outbreak control plan
120
Q

What is the single most effective method of preventing cross infection?

A

Hand hygiene

121
Q

What is hand hygiene

A

hand washing and/ or alcohol gel

122
Q

When to wash hands

A

o Before and after handling patients/ clients
o After handling any item that is soiled
o After using the toilet
o Before and after an aseptic procedure
o After removing protective clothing, including gloves

123
Q

When to use alcohol gel

A

o Following hand washing prior to a ward-based invasive procedure
o Following hand washing when caring for a patient with barrier precautions

124
Q

When should you wear Personal protective equipment (PPE)

A

Protective equipment must be worn by all stuff, whatever their role or grade when there is a risk of contamination to the person or their clothing

E.g. gloves, aprons etc.

125
Q

What is an endogenous infection? Who is most at risk?

A
  • Infection of a patient by their own flora
  • Important in hospitalized patients, especially those with invasive devices or surgical patients
126
Q

Preventing endogenous HCAI (3)

A
  • Good nutrition and hydration
  • Antisepsis/ skin prep where indicated
  • Control underlying disease
    o Drain pus
    o Remove lines and catheters as soon as clinically possible
    o Reduce antibiotic pressure as much as clinically possible e.g. short courses, narrow spectrum
127
Q

Disposal of sharps (5)

A
  • Disposal is the responsibility of the person using the equipment
  • Sharps bins must be correctly assembled
  • Never re-sheath or bend needles
  • Never overfill a sharps bin
  • Be aware of the needle stick injury policy
128
Q

What are the UNIAIDS 90/90/90 goals – global target of

A

90% of people living with HIV are diagnosed

90% diagnosed with ART (antiretroviral therapy)

90% viral suppression for those on ART by 2020

129
Q

What does the Epstein-Barr Virus cause

A

Usually asymptomatic
However, can cause infectious mononucleosis (glandular fever)
Typically in adolescents, young adults
Transmitted orally via saliva

130
Q

Clinical features of Epstein-Barr Virus

A

Fatigue
Malaise
Fever
Headache
Pharyngotonsiltis
Hepatomegaly -> hepatitis
Cervical Lymphadenopathy
Splenomegaly -> splenic rupture

131
Q

Management of Epstein Barr Virus

A

Symptomatic management:
Paracetamol
Ibuprofen
Rest, fluids, nutrition

Primary EBV infection rarely requires more supportive treatment
Complications: upper airway restriction

132
Q

Cytomegalovirus (CMV) (4)

A

Asymptomatic mostly

Type of herpes

It can cause infection in the immunocompromised, mono-like symptoms. congenital infection

Enters via: Respiratory, Genitourinary, Upper GI tract

133
Q

Difference between meningitis and encephalitis

A

Meningitis: Inflammation of the leptomeninges
Encephalitis: Inflammation of the brain

134
Q

Bacterial causes of meningitis

A

Streptococcus pneumoniae.
Group B Streptococcus.
Neisseria meningitidis.
Haemophilus influenzae.
Listeria monocytogenes.
Escherichia coli.

135
Q

Viral causes of meningitis and encephalitis

A
136
Q

What is HIV

A

Human Immunodeficiency Virus

A retrovirus that infects CD4-T lymphocytes leads to the destruction of these cells.

This impairs cell-mediated immunity and increases the risk of cancer and opportunistic infections

137
Q

What is the most common species of HIV worldwide

A

HIV-1

HIV-2 is restricted to West Africa almost

138
Q

What is the structure of HIV

A

Icosahedral
Conical capsid containing: two RNA strands, enzymes (integrase & Reverse transcriptase)
Lipid membrane

139
Q

Why does the timely diagnosis of HIV remain a major challenge?

A
  • Fewer people are diagnosed with an AIDS-defining illness
  • But the numbers diagnosed late remain high
  • Late diagnosis = ten-fold increased risk of death in the first year of diagnosis
140
Q

HIV transmission routes (3)

A
  • Blood
  • Sexual
  • Vertical
141
Q

Benefits of knowing HIV status (6)

A

Access to appropriate treatment and care

Reduction in morbidity and mortality

Reduction in mother-to-child-transmission (MTCT)

Reduction of sexual transmission

Public health

Cost-effective
o Early diagnosis is cost-effective – savings on social care, lost working days, benefits claimed, costs associated with further onward transmission

142
Q

Recognised risk factors – identifying high-risk behaviours of HIV

A
  • Sexual contact with people from high prevalence groups – MSM, sub-Saharan African/ Thailand
  • Multiple sexual partners
  • Rape in high-prevalence localities
143
Q

Symptoms of HIV

A
  • Acute generalized rash
  • Glandular fever
  • Indicators of immune dysfunction
  • Unexplained weight loss or night sweats
  • Recurrent bacterial infections, including pneumococcal pneumonia
144
Q

Learning points of HIV (6)

A
  • Advantages of diagnosing HIV status far outweigh any potential disadvantages
  • Early diagnosis reduces mortality and morbidity
  • Earlier diagnosis reduces transmission
  • Early diagnosis is cost-effective
  • Encourage asymptomatic screening
  • Routine HIV testing in patients with suggestive symptoms/ conditions e.g. TB
145
Q

HIV Virology

A
  1. Attachment – viral and cell receptors, e.g. HIV
  2. Cell entry – only the central viral ‘core’ carrying the nucleic acid and some associated proteins enter the host cell
  3. Interaction with host cells – use cell materials (enzymes, amino acids, nucleotides) for their replication; subvert host cell defence mechanisms
  4. Replication – may localize in the nucleus in, in the cytoplasm or at both; production of progeny viral nucleic acid and proteins
  5. Assembly – occurs in the nucleus, in the cytoplasm or at the cell membrane
  6. Release – by bursting open of cell; or by exocytosis from the cell over a period of time
146
Q

Replication of HIV summary

A
  1. Attachment: e.g CD4 T-cell
  2. Entry: HIV enters the cell, releasing content
  3. Uncoating
  4. Reverse transcription: reverse transcriptase converts viral RNA -> DNA
  5. Genome integration: Integrase carries viral DNA to nucleus, attaching to host DNA
  6. Transcription of viral RNA: Host RNA polymerase makes viral RNA and genomic viral RNA
  7. Splicing of mRNA and translation into proteins: mRNA is used to make proteins for the virus
  8. Assembly of new virions and release
  9. Maturation: Proteases cleave precursors forming the final HIV
147
Q

What are the only cells that can be infected by the HIV virus?

A

Cells containing CD4 receptors (monocytes, macrophages, dendritic cells, microglial cells, t lymphocytes)

148
Q

In what weeks is the HIV antibody detectable

A

2-4 weeks

149
Q

Summary of acute HIV infection

A

It happens in the first couple of weeks of initial infection

Increase in viral load
HIV p24 antigen is detected
Antibodies against HIV
CD8+ Activation
Seroconversion illness

150
Q

Summary of immune response to HIV

A
  • Vigorous immune response but no demonstrable protective immunity with rare exceptions
  • Excessive immune activation, which favours viral replication
  • Immunological dysfunction with involvement of all elements of host defence
  • Ongoing viral replication with progressive immunological impairment leading to clinical manifestations of immunodeficiency
  • HIV-1 is a retrovirus that evolved from a simian immunodeficiency virus in chimpanzees
  • It replicates in CD4 positive cell
  • The virus copies its RNA into DNA and uses the host cell for gene transcription
  • It results in gradual damage to the immune system, mainly through the depletion of CD4 T-cells
151
Q

HIV receptors

A

HIV infects cells that express CD4, and the interaction between CD4 and gp120 is conserved among all primate lentiviruses

The binding of gp120 to CD4 induces a conformational change in gp120

The co-receptor binding site includes a conserved bridging sheet and also amino acids in the V3 loop.

152
Q

Two markers are used to monitor HIV infection.

A
  1. CD4 cell count
  2. HIV viral load
153
Q

What is AIDS defined as:

A

CD4+ T cell count <200

154
Q

What are some AIDS-defining illnesses?

A

Increased infections
Increased malignancy
Increased other comorbidities

155
Q

Screening and diagnosis of HIV

A
156
Q

Management of HIV (3)

A
157
Q

In a patient with fever, rash and non-specific symptoms of HIV, what do you do?

A
  • Ask about sexual history
  • Think of HIV seroconversion
158
Q

When to do an HIV test?

A

when faced with a common problem in:
* An unexpected patient
* No clear underlying cause
* Recurring infections

159
Q

most common opportunistic infection in HIV

A

PCP (pneumocystis pneumonia)

160
Q

_____ threshold for ______ puncture in a patient with HIV and headache

A

Low
lumbar

161
Q

Good adherence and avoidance of drug interactions are key to .. HIV related

A
  • Suppress HIV replication
  • Avoid drug resistance
162
Q

Who is most at risk of HIV?

A
  • Men who have sex with men
  • Heterosexual women
  • Injecting drug users
  • Commercial sex workers
  • Heterosexual men
  • Truck drivers
  • Migrant workers

50% of all new infections occurring world-wide are in 15-24-year-olds

163
Q

Commitments and targets for 2015

A

1 – condom effectiveness in reducing heterosexual HIV transmission.
* Male circumcision – the risk of heterosexual acquisition by 60%
o Removing the foreskin reduces the ability of HIV to penetrate due to keratinization of the inner aspect of the remaining foreskin

2 – harm reduction as an evidence-based approach to HIV prevention, e.g. needle and syringe programmes

3 – how to reduce mother-to-child transmission

4- antiretroviral treatment – awareness, adherence, clinical services

164
Q

Across the globe which factors have an enormous impact on the spread of and efforts to contain HIV

A

poverty and socio-political

165
Q

Mitigating the HIV pandemic requires a combined effort of

A

prevention, diagnosis, ART provision and ongoing care for those with HIV

Sandra Phase 2a (17 decks)

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