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
Why do gram-positive bacteria retain their crystal violet purple?
because they have a cell wall composed of a thick layer of peptidoglycan
26
What is an example of a gram-positive bacteria and tested to distinguish this
Staphylococcus – coagulase test -Staph. Aureus – coagulase positive
27
How can you classify streptococci (3)
1. Haemolysis 2. Lancefield typing 3. Biochemical properties
28
What is Lancefield grouping?
Method of grouping catalyse-negative, coagulase-negative bacteria based on bacterial carbohydrate cell surface antigens
29
What is the catalase test?
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.
30
What is blood agar used for?
Blood agar is a non-selective medium that can be made selective for specific pathogens by the addition of antibiotics, chemicals or dyes.
31
What is an XLD culture?
Xylose Lysine Deoxycholate agar (XLD agar) is a selective growth medium used to isolate Salmonella and Shigella species from clinical samples and food.
32
What is MacConkey agar used for?
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
33
Purpose of CLED culture
Non-selective medium capable of supporting the growth of most urinary pathogens. differential medium used for the isolation and enumeration of bacteria from urine
34
Purpose of Sabouraud Culture
Sabouraud agar is a selective medium formulated to allow the growth of fungi and inhibit the growth of bacteria.
35
Purpose of Lowenstein-Jensen culture
growth medium specially used for culture of Mycobacterium species, notably Mycobacterium tuberculosis
36
What are some important gram-positive bacteria that you need to remember (6)
S.aureus S.epidermis S.pyogenes S.pneumoniae viridian streptococci C.diphtheriae
37
What do gram-positive bacteria show
Wide range of extracellular and cell-associated virulence factors
38
How do gram-positive bacteria spread
aerosols surface-to-surface contact colonization of prostheses
39
How can you manage gram-positive bacteria
antimicrobials and vaccination
40
What are the four major groups (phyla) of gram-negative pathogens?
1. Proteobacteria – all are rod-shaped 2. Bacteroids – rod-shaped 3. Chlamydia – round pleimorphic 4. Spirochaetes – spiral/ helical
41
What are the two pathogenicity determinants/ virulence factors of gram-negative bacteria
1. Colonization factors: adhesins, invasins, nutrient acquisition, defence 2. Toxins (effectors): usually secreted proteins -> damage, subversion
42
Why are gram-negative bacteria difficult to culture in a lab
Due to the dependency of a pathogen on its host
43
What are the three classifications of parasitic worms (Helminth worms)?
Nematodes (roundworms) Trematodes (flatworms, flukes) Cestodes (tapeworms)
44
Where can you find nematodes
o Intestinal – ascaris lumbricoides o Larva migrans o Tissue (filaria)
45
Where can you find trematodes
o Blood o Liver o Lung o Intestinal
46
Where can you find cestodes?
o Non-invasive o Invasive
47
What is the pre-patent period?
interval between infection and the appearance of eggs in the stool
48
Mycobacteria of medical importance (7)
* 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
49
What is the microbiology of mycobacterium
* 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
50
What stain is used to identify myobacteria and why?
Acid-fast bacilli as its resistant to gram stain
51
What do acid-fast bacilli stain?
organisms with wax-like, thick cell walls
52
What is nucleic acid detection used for?
Nucleic acid amplification test using PCR Recommended for rapid diagnosis in TB-endemic countries Sensitivity 88%, specificity 98%
53
What conclusion can be concluded from mycobacteria?
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
54
Example of mycobacteria
TB
55
How do viruses replicate?
By exploiting the energy and reproductive machinery of cells of higher organisms.
56
Characteristics of viruses (4)
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.
57
What are the shapes and sizes of different bacteria?
58
What is the difference between living and non-living cells
59
Describe viral replication
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
60
How do viruses cause disease
* 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
61
Laboratory methods to diagnose bacterial infections
62
Bacteria growing as single cells
63
Describe the structure of fungi
* Eukaryotic * Chitinous cell wall * Heterotrophic * Move by means of growth or through the generation of spores, which are carried through air or water
64
Types of fungi
Yeast Mould Dimorphic fungi
65
Yeast vs Fungi
* 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
66
What are a dimorphic fungi
Some fungi exist as both yeasts and moulds switching between the two when conditions suit
67
What is the aim of antimicrobial drug therapy
to achieve inhibitory levels of agent at the site of infection without host cell toxicity
68
What does treating fungal disease rely on
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
What is the severity of fungal infection in the 'healthy.'
Mild but troublesome
70
Who is susceptible to severe fungal infections
immunocompromised -can be the initial presentation of the underlying disease
71
Why can fungal infections be challenging to treat?
We have relatively few classes of agents effective against them
72
What do immune response patterns vary for
* Viruses * Bacteria * Protozoa * Helminths
73
What are the key attributes of pathogens causing disease
Infectivity Virulence Invasiveness
74
Define infectivity
ability to become established in host, can involve adherence and immune escape
75
Define virulence
the ability to cause disease once established
76
Define invasiveness
the capacity to penetrate mucosal surfaces to reach normally sterile sites
77
What are virulence factors
Microbial factors that cause disease
78
Describe the features of a viral infection
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
What does viral evasion interfere with
specific or non-specific defence
80
What does influenza change?
coat antigen
81
Define anti-genic drift
spontaneous mutations occur gradually, giving minor changes in haemagglutinin and neuraminidase. Epidemics
82
Define anti-genic shift
sudden emergence of new subtype different to that of preceding virus. Pandemics
83
How do bacterial infections enter?
Via * Respiratory tract * Gastrointestinal tract * Genitourinary tract * Skin break
84
What determines the defence mechanism employed for bacterial infections
Number of organisms and virulence * Low number or virulence – phagocytes active * High number of virulence – immune response
85
Give 2 examples of bacterial evasion
* Mycobacterium – escape from phagolysosome, live in cytoplasm * M.avium – block phagosome
86
What does the immune response of a protozoan infection depend on
location of the parasite in the host * Blood stage – humoral immunity * Tissue stage – cell-mediated immunity * Plasmodium fulciparium (malaria) – an anopheles mosquito bite
87
3 points that define a protozoan evasion
* Surface antigen variation * Intracellular phase * Outer coat sloughing
88
5 characteristics of a worm infection
* Do not multiply in humans * Not intracellular * Few parasites carried * Poor immune response * Immune response not sufficient to kill
89
2 characteristics of a worm evasion
* Decreased antigen expression by adult * Glycolipid/ glycoprotein coat (host-derived)
90
What are the two different types of immunisation
Passive Active
91
What is passive immunisation?
preformed antibody transferred Can be done via: * Transplacental transfer * Colostrum * Inject preformed antibody
92
What is active immunity
* Achieved by natural infection – vaccine administration * Elicitis – protective immunity – immunological memory
93
What are the different types of vaccines (4)
* Inactivated (killed) * Attenuated (avirulent) * Bacteria or viruses * Toxoid vaccines (inactivated toxins)
94
Protozoa: The First Animals (6)
* 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
What are the 5 major groups when classifying organisms
* Flagellates * Amoebae * Sporozoans * Ciliates * Microsporidia
96
Characteristics of flagellates (3)
* Flagellum as main locomotory organelle * Usually reproduce by binary fission * Intestinal flagellates or other body sites
97
Characteristic of amoeba
Move by means of flowing cytoplasm and production of pseudopodia
98
Characteristic of sporozoans (4)
* No locomotory extensions * All species parasitic * Most intracellular parasites * Reproduce by multiple fission
99
Example of sporozoan
Malaria
100
Characteristic of ciliates (2)
* Cilia that beat rhythmically at some stage in the lifecycle * two types of nuclei – macro/micronucleus
101
Characteristics of microsporidia (3)
Production of resistant spores Unique polar filament; coiled inside spore Little known about human disease
102
What is malaria
Protozoan infection caused by Plasmodia sporozoan. Five species of sporozoites cause human disease: P.falciparum/ovale/vivax/malariae/knowlesi
103
How is malaria transmitted
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
What is the lifespan of malaria?
Life span 3-4 weeks
105
Malaria lifecycle
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
What are the clinical features of malaria
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
Treatments of malaria
Quinines
108
Complications of malaria
Splenomegaly Hepatomegaly Pulmonary oedema Renal Failure
109
Define antibiotics
agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high-dilution
110
What are antimicrobials
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
Classes of antibiotics (10) Antibiotics Can Terminate Protein Synthesis For Microbial Cells Like Germs
112
Gram Coverage of antibiotics Remember GLAM and iotic ending
113
Mechanism of Action for different antibiotic classes
114
What are the three mechanisms of antibiotic resistance genes
Antibiotic degrading enzymes Production of Efflux pump Modified antibiotic binding target
115
What are the two ways in which bacteria can acquire antibiotic-resistant genes
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
How to diagnoses a viral infection
Tests: 1. Cell culture 2. Cytology 3. Viral Proteins 4. Viral Genetic Material: PCR, Southern/Northern Blot 5. Serology
117
What are the key points mentioned in the health act 2006
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
Key components of infection prevention and control at STH
* Infection prevention and control team * Ward teams * Microbiology/ virology laboratories * Trust management * Estates * Domestic services * Pharmacy
119
What are infection control policies
* MRSA * Tuberculosis * Medical equipment management manual * Single-use items * Outbreak control plan
120
What is the single most effective method of preventing cross infection?
Hand hygiene
121
What is hand hygiene
hand washing and/ or alcohol gel
122
When to wash hands
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
When to use alcohol gel
o Following hand washing prior to a ward-based invasive procedure o Following hand washing when caring for a patient with barrier precautions
124
When should you wear Personal protective equipment (PPE)
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
What is an endogenous infection? Who is most at risk?
* Infection of a patient by their own flora * Important in hospitalized patients, especially those with invasive devices or surgical patients
126
Preventing endogenous HCAI (3)
* 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
Disposal of sharps (5)
* 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
What are the UNIAIDS 90/90/90 goals – global target of
90% of people living with HIV are diagnosed 90% diagnosed with ART (antiretroviral therapy) 90% viral suppression for those on ART by 2020
129
What does the Epstein-Barr Virus cause
Usually asymptomatic However, can cause infectious mononucleosis (glandular fever) Typically in adolescents, young adults Transmitted orally via saliva
130
Clinical features of Epstein-Barr Virus
Fatigue Malaise Fever Headache Pharyngotonsiltis Hepatomegaly -> hepatitis Cervical Lymphadenopathy Splenomegaly -> splenic rupture
131
Management of Epstein Barr Virus
Symptomatic management: Paracetamol Ibuprofen Rest, fluids, nutrition Primary EBV infection rarely requires more supportive treatment Complications: upper airway restriction
132
Cytomegalovirus (CMV) (4)
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
Difference between meningitis and encephalitis
Meningitis: Inflammation of the leptomeninges Encephalitis: Inflammation of the brain
134
Bacterial causes of meningitis
Streptococcus pneumoniae. Group B Streptococcus. Neisseria meningitidis. Haemophilus influenzae. Listeria monocytogenes. Escherichia coli.
135
Viral causes of meningitis and encephalitis
136
What is HIV
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
What is the most common species of HIV worldwide
HIV-1 HIV-2 is restricted to West Africa almost
138
What is the structure of HIV
Icosahedral Conical capsid containing: two RNA strands, enzymes (integrase & Reverse transcriptase) Lipid membrane
139
Why does the timely diagnosis of HIV remain a major challenge?
* 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
HIV transmission routes (3)
* Blood * Sexual * Vertical
141
Benefits of knowing HIV status (6)
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
Recognised risk factors – identifying high-risk behaviours of HIV
* Sexual contact with people from high prevalence groups – MSM, sub-Saharan African/ Thailand * Multiple sexual partners * Rape in high-prevalence localities
143
Symptoms of HIV
* Acute generalized rash * Glandular fever * Indicators of immune dysfunction * Unexplained weight loss or night sweats * Recurrent bacterial infections, including pneumococcal pneumonia
144
Learning points of HIV (6)
* 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
HIV Virology
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
Replication of HIV summary
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
What are the only cells that can be infected by the HIV virus?
Cells containing CD4 receptors (monocytes, macrophages, dendritic cells, microglial cells, t lymphocytes)
148
In what weeks is the HIV antibody detectable
2-4 weeks
149
Summary of acute HIV infection
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
Summary of immune response to HIV
* 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
HIV receptors
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
Two markers are used to monitor HIV infection.
1. CD4 cell count 2. HIV viral load
153
What is AIDS defined as:
CD4+ T cell count <200
154
What are some AIDS-defining illnesses?
Increased infections Increased malignancy Increased other comorbidities
155
Screening and diagnosis of HIV
156
Management of HIV (3)
157
In a patient with fever, rash and non-specific symptoms of HIV, what do you do?
* Ask about sexual history * Think of HIV seroconversion
158
When to do an HIV test?
when faced with a common problem in: * An unexpected patient * No clear underlying cause * Recurring infections
159
most common opportunistic infection in HIV
PCP (pneumocystis pneumonia)
160
_____ threshold for ______ puncture in a patient with HIV and headache
Low lumbar
161
Good adherence and avoidance of drug interactions are key to .. HIV related
* Suppress HIV replication * Avoid drug resistance
162
Who is most at risk of HIV?
* 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
Commitments and targets for 2015
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
Across the globe which factors have an enormous impact on the spread of and efforts to contain HIV
poverty and socio-political
165
Mitigating the HIV pandemic requires a combined effort of
prevention, diagnosis, ART provision and ongoing care for those with HIV