Fichas
Week 3
Fichas del conjunto (37)
- 1What is the prodromal response?The general effects of the innate immune response to viral infections. It is the same irrespective of the virus. Un-infected cells respond to signals produced by infected cells
- 2Describe the influenza virus-Segmented RNA (7-8 pieces)
-3 main species: A, B, C (A is more severe)
-Acute infection
-Does not establish latency
-Infects both upper/lower (increased mortality) respiratory tracts
-Shows seasonality - 3What are the clinically important genes on the influenza virus?Haemagglutinin (H)
Neuraminidase (N) - 4Describe the immune response to influenza-CD8 T cells protect the respiratory mucosa and establish pneumonitis (inflammation of lungs)
-Virus neutralising antibodies limit the spread of infection within the lungs - 5What is seasonal drift?Where the virus accumulates changes over time. Sudden genetic jumps occur when 2 distinct flu virions are mixed in a single cell and 8 segments of each genome re-arrange at random
- 6What is antigenic drift?-Inherent high mutation rate of the RNA virus means there is a high likelihood of adaptive changes in the dominant antigens Haemagglutinin and Neuraminidase.
-Over many flu seasons, the virus gradually changes into a strain able to evade the previously created antibodies - 7What is antigenic shift?-Co-infection of a single organism can result in re-assortment of the individual strains
-Leads to the emergence of a new strain of influenza with no homology to earlier forms and can cause a pandemic - 8Why isn't this seen in other viruses such as the MMR ones?The genome is not segmented so there is no re-assortment
- 9What are the treatments available?Anti-influenza agents: reduce pathogenicity of the virus, but they have poor effectiveness and resistance is common
Annual vaccination programme - 10Describe the HIV virus-2 distinct species
-Enveloped, single-stranded +ve sense RNA viruses with an integrated DNA immediate
-Latent proviral genomes can persist for years undetected and so cannot be targeted by antivirals
-Encode 3 major genes: gag, pol and env - 11How does the HIV virus infect cells?-Infects CD4+ T cells by binding to CD4 via pg120
-Co-receptors CCR5 and CXCR4 bind to gp120 allowing the viral membrane to fuse with the CD4+ membrane
-Viral capsid is released
-Reverse transcriptase converts viral ddRNA into dsDNA and integrase ligates the viral dsDNA genome (provirus)
-Viral protease is packed into emergent virions which leave the cell - 12How does HIV show antigenic drift?-Adaptive immune system takes 1-2 weeks to respond to viral antigens
-Viral population has accumulated antigenic change during this time - 13What are the 3 phases HIV goes through?1) Acute seroconversion
2) Asymptomatic infection
3) AIDS - 14What happens during seroconversion?-Infection is established
-Initial proviral reservoir created
-Fever, flu-like symptoms, rash, diarrhoea
-High viral count in blood
-Transient loss of CD4+ T cells - 15What happens during asymptomatic infection?-7-15 years
-Neutralising antibodies and CD8+ T cells reduce viral count to set point (stable)
-No ill health
-Slow decline in CD4 T cell count
-Increasingly immunodeficient - 16What happens during AIDS?-CD4 numbers fall below a critical point
-Immune system fails
-Patient develops a spectrum of infections (opportunistic) - 17What is HAART?Highly Active Anti-Retroviral Therapy
Combines reverse transcriptase, integrase and protease inhibitors - 18Describe the Herpes virus-dsDNA viruses
-Lifelong infection of the host
-Show latency where the viral genome is present but does not replicate
-Genome is reactivated periodically
-Immune response: cytotoxic CD8+, CD4+ T cells
-Only Herpes vaccine is Varicella Zoster Virus (chicken pox/shingles) - 19Describe HSV 1,2,3-HSV1/2: produce cold sores, genital sores
-HSV3: itchy rash of spots which turn into fluid-filled blisters
-Group together as they infect neurons and reactivate periodically in response to stress factors - 20Describe the Epstein Barr Virus (EBV)-Infects B cells to give mild form of lymphoma
-B cell lymphoma common in patients lacking T cells
-Childhood EBV is asymptomatic
-After puberty can lead to infectious mononucleosis (glandular fever) - 21Describe the CMV-Generally gives rise to asymptomatic infection
-Tropism is broad: infects lungs, liver, endothelium and myeloid cells
-Immune response: CD8+ and CD4+ T cells - 22Define disinfectantAntimicrobial agent used only on inanimate objects
- 23Define chemotherapeutic agentsAntimicrobial agent that can be used internally. It is given systemically
- 24What type of toxicity to antibiotics show? Why?Selective toxicity
They target enzymes or molecules that are only found in bacteria - 25What are the basic sites of antibiotic activity?-Cell wall synthesis (effective since we don't have peptidoglycans)
-DNA replication
-RNA synthesis
-Protein synthesis (30/50S)
-Antimetabolites - 26Describe how prontosil acts as an antibiotic-Active product is the metabolite (sulphanilamide)
-Metabolite is a competitive inhibitor to the precursor of folic acid which is needed by bacteria
-Resistance emerged rapidly - 27How to Beta Lactam antibiotics work?-Normally penicillin binding proteins (PBPs) cross-links peptidoglycan lattices
-Beta Lactams block and inactivate PBPs - 28What is MIC?Minimal Inhibitory Concentration
The concentration of antibiotic which inhibits growth - 29Define antimicrobial resistanceRelative or complete lack of effect of antimicrobial against a previously susceptible microbe.
The MIC increases - 30How is resistance quantified?Preparing doubling dilutions of the antimicrobial in a broth which allows growth of the bacterium you are testing. Each tube is inoculated with that bacterium. The tube that fails to show growth is the MIC
- 31How did Staphylococcus develop resistance against penicillin?-Produce penicillinase enzyme
-This breaks the beta lactam ring which prevents penicillin from binding
-Enzymes needed to make crosslinks in the peptidoglycan polymer are free to work - 32How did the drug company get around the penicillin resistance?-Chemically cleaved the side chain from penicillin G to create 6-aminopenicillanic acid
-This is a stable compound so different side chains can be added
-This was used to create methicillin - 33What is the main control strategy for MRSA?-Screening of patients
-Decolonisation
-Isolation preventing hospital cross-infection - 34How did MRSA develop?-The strain produced a different beta lactam target enzyme to synthesise its cell wall
-Bypass mechanism of resistance where the original target enzyme is still present and inhibited, but the new modified target is not inhibited by methicillin/flucloxacillin
-Bacteris is able to produce a cell wall and grow - 35How did E.coli develop resistance to ampicillin?Plasmids were transferred between E.coli strains or completely different bacterium
- 36What has contributed to the growth of antibiotic resistance?-Use of antimicrobials in food production and human medicines
-Existence of megacities
-Poor public health infrastructure
-Unclean water, poor sewage disposal
-Cheap air travel, movement of people - 37Describe inappropriate antimicrobial use-Prescription not taken correctly
-Antibiotics for viral infections
-Over prescribing
-Antibiotics sold without medical supervision
-Spread of resistant microbes in hospitals due to lack of hygiene
Información
- Descripción
- Immune evasion and HIV Antibiotic resistance and HCAIs
- Creado por
- Dolu Falowo
- Visitas
- 2
- Valoración